Neuromuscular Disorders & Exercise 

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Cerebral Palsy

Neuromuscular Disorder Quiz 1

Exercise Guidelines for Parkinson's

Exercise Guidelines for Cerebral Palsy

Online Presentations

Multiple Sclerosis 


Neuromuscular Disorder Quiz 2

Exercise Guidelines for Multiple Sclerosis 

Exercise Guidelines for Stroke


The nervous system is a multifaceted network of nerves and cells that conduct information from the brain and spinal cord to numerous parts of the body. These nerve cells are responsible for the coordination of all voluntary and involuntary actions and functions of the human body. Fundamentally, the nervous system anatomically consists of the central nervous system (CNS) and the peripheral nervous system (PNS). The PNS refers to segments of the nervous system outside the brain and spinal cord. PNS is divided functionally into the somatic system, which mediates voluntary movements; the autonomic nervous system which is responsible for the control of internal organs and regulates bodily functions; and the enteric nervous system (ENS) which controls the gastrointestinal system. The PNS comprises of sensory (ascending) and motor (descending) neural tracts. 

Neuromuscular disorders (also termed neurological disorders) are a result of the deterioration in the functioning of the body’s muscular system or various nervous systems. These conditions may transpire from genetic defects or biological causes. Additionally, neurological disorders may be caused by acute injuries to the brain or the vertebrae column or by progressive diseases.  The severity and site of the tissue damage determine the immediate outcome of the injury or disease development and ultimately the individual's long-term recovery. For instance, if direct trauma to the brain occurs during pregnancy, during childbirth or within the first three years of life it may result in cerebral palsy. Traumatic brain injury in an adult’s brain may occur due to a disruption of blood flow to the brain resulting feasibly in a stroke. This is contrary to neurological diseases such as Parkinson’s disease and multiple sclerosis that affect the peripheral nerves and the brain tissue.

Neuromuscular disorders can be categorised as progressive or non-progressive disorders. Progressive neurological disorders are conditions that involve a continuing and progressive decline of functioning. These disorders include Parkinson’s disease, multiple sclerosis, and muscular dystrophy. These neuromuscular conditions vary in the rate of development and may have stages of relapse and periods of remission. It is believed that progressive neuromuscular disorders are commonly caused by disease processes or genetic factors. Non-progressive neurological disorders are conditions that do not continue to display deteriorating neurological functioning following an initial episode of disease or mechanical injury. These non-progressive conditions include head injury, spinal cord injury, stroke and cerebral palsy. Non-progressive disorders are mostly a consequence of a traumatic injury to the CNS (either the brain or spinal cord).

Parkinson’s Disease  

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Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease and it is anticipated to inflict a social and economic burden on societies as life expectancy increases (Lonneke and Breteler, 2006). PD is a progressive neurological disorder that affects voluntary movement. This disease progresses slowly and is most prevalent in older individuals (Table 1).  In the UK PD is estimated to affect around 1 in 500 people (NHS, 2019), with an annual incidence rate of approximately 15-20 people per 100,000 (this indicates around a 1:10 ratio with the young-onset). The prevalence of the disease increases with age, with an estimated total of 2% of the entire population over the age of 68 who is estimated to have PD.


As observed in Table 1 PD increases with age. Incidence in individuals aged ≥80 years maybe 1,000 times higher than in individuals <40 years and 10 times higher than the incidence in those in their sixth decade. Scientific interest in PD has grown in recent years with major gene mutations probable only accounting for a small percentage of all PD with about 90% of cases being sporadic. Current thinking is that mitochondrial dysfunction, oxidative stress, and protein mishandling have a fundamental role in PD pathogenesis (Greenamyre and Hastings, 2004) and that in sporadic PD these developments are produced by non-genetic factors, possibly in interaction with susceptibility genes (Lonneke and Breteler, 2006). The most common sign of PD is muscular tremors. However, this disease usually results in muscular stiffness and slow movements. Other symptoms include a lack of facial expression, lack of arm swing during walking, and slurred speech. While there is no known cure for PD at this time, medication may reduce the symptoms.

Table 1.  Age-Specific Prevalence of Parkinson’s Disease from Selected Studies (Adapted from Jankovic and Tolosa, 2015)

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Pathology of Parkinson’s Disease: An Overview

The pathological hallmark of PD is cell death or impairment of dopaminergic neurons within the substantia nigra region of the brain, particularly affecting the ventral component of the pars compacta. By the time of death, this area of the brain has lost 50-to-70% of its neurones compared with the same area in an unaffected person. The initial pathological changes in PD (Braak et al., 2006) have been shown in the medulla oblongata, pontine tegmentum and olfactory bulb (Figure 1). In the initial stages (Braak stages 1 and 2) individuals are pre-symptomatic. As PD advances (Braak stages 3 and 4) the substantia nigra, areas of the midbrain and basal forebrain become involved. Lastly, pathological changes develop in the neocortex (Figure 2).

This staging is founded on the distribution of Lewy bodies. Lewy bodies are the pathological trait of PD. They are a-synuclein-immunoreactive cytoplasmic inclusions made up of numerous neurofilament proteins together with proteins responsible for proteolysis. These include a heat shock protein called ubiquitin which plays a central role in targeting other proteins for breakdown. Mutations in the a-synuclein gene are responsible for several familial forms of PD in which Lewy bodies are also seen. Mutations in the parkin protein produce Parkinsonian syndrome without Lewy bodies in juvenile cases indicating that the parkin protein is essential in the development of the Lewy body. Chung et al., (2001) showed that parkin aids the binding of ubiquitin (ubiquitination) to other proteins such as synphilin-1 (a-synuclein interacting protein) leading to the formation of Lewy bodies. Lewy bodies are found in PD and Dementia with Lewy bodies (DLB) but are not a pathological trait of any other neurodegenerative disease.

Research by Betarbet and associates (2005) have focused attention to single gene defects on the ubiquitin-proteasome system (UPS) in the development of cell death. The UPS is essential for intracellular proteolysis and several intracellular processes that maintain the viability of cells. The UPS achieves this by eradicating unnecessary proteins that are no longer required by the cell.  If the UPS fails to discard these unwanted proteins, then an abnormal accumulation of proteins including a-synuclein which are a key component of Lewy bodies. One of the primary locations for Lewy body accumulation in initial PD is the olfactory bulb (Figure 1). This leads to a disturbance in smell and taste and may be one of the earliest clinical features in PD. This leads to the premise that Lewy body formation may be essential for the activation of pathways leading to neuronal dysfunction and death. The association between UPS and neurodegeneration has been reinforced by the discovery of mutations in genes that code for numerous ubiquitin-proteasome pathway proteins in PD.

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Figure 1. The traditional symptoms of PD occur from degeneration of dopaminergic cells in an area of the brainstem called the substantia nigra (purple) and in the striatum (blue), a structure found in both left and right sides of the brain that is directly linked with the substantia nigra.

While PD is typically regarded as a sporadic disease research has identified several single-gene mutations. So far there has been a minimum of 11 genes that have been mapped by genetic linkage with six genes identified: a-synuclein (SNCA), ubiquitin C-terminal hydrolase like 1 (UCH-L1), parkin (PRKN), LRRK 2, PINK 1 and DJ-1 genes. These single gene defects (except for LRRK 2) are responsible for only a small number of individuals with PD. Importantly, the identification of these genes and the proteins that they encode to provide researchers with a greater insight into the mechanisms that may be responsible for PD and other neurodegenerative diseases. 

Davie (2008) notes that a point mutation of the SNCA gene leads to the early onset of PD in affected members in an autosomal dominant pattern. Duplication or triplication of the SNCA gene in affected members leads to PD symptoms developing in individuals between 40-50 years old. This raises the likelihood that overexpression of SNCA may be a factor in sporadic disease (Davie, 2008).  Gilks et al., (2005) demonstrated that the LRRK 2 gene (PARK8) is the most common cause of familial PD with the occurrence of LRRK2 mutations in individuals with a family history between 5-to-7%. The heterozygous mutation (2877510 g->A) produces a glycine to serine amino acid substitution at codon 2019 (Gly2019 ser). This LRRK2 G2019S mutation is the most frequently described, accounting for the majority of familial cases and around 1.6% of idiopathic PD cases, though the occurrence seems to be variable. The LRRK2 gene encodes for a protein named dardarin.

Lewy bodies have been identified in some LRRK 2 cases. Many of the LRRK2 patients reported have hallmark features of PD with middle or late-onset. Signs and symptoms at onset may be typical of idiopathic PD characterised by unilateral bradykinesia and rigidity, with tremor present in some but not all cases. Several single-gene mutations (e.g., parkin and DJ-1) with an autosomal recessive pattern of inheritance, may have a clinical pattern of earlier age of onset. However, researchers have not been able to identify parkin positive young-onset PD patients from parkin negative patients on clinical features alone. Research into mitochondrial genetics and function in PD has increased with studies identifying abnormalities in Complex 1 of the oxidative phosphorylation enzyme pathway. For example, Gilks et al., (2005) assessed 482 subjects with the PD, with 263 had pathologically confirmed disease, by direct sequencing for mutations in exon 41 of LRRK2. The mutation was present in eight (1·6%) patients. Gilks and associates (2005) showed that a common single Mendelian mutation is associated with sporadic PD.

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Figure 2. The Braak stages of PD. Source: Nature

It has been suggested that the cells of the pars compacta are vulnerable to oxidative damage. Studies focusing on mitochondrial DNA have at present been unable to identify a gene mutation that explains the oxidative phosphorylation defects in PD. Nevertheless, it is conceivable that a mitochondrial defect may play a pivotal role in the pathways leading to cell dysfunction and death. The PINK1 gene codes for a mitochondrial complex and is responsible for an autosomal recessive form of PD, though is not a major risk factor for sporadic disease.

At this time of writing, attempting to detect varying environmental factors that predispose to the development of PD is still elusive. However, living in a rural setting has been suggested by some researchers to increase the risk of PD. Dick (2006) reports a correlation between exposure to pesticide use and wood preservatives. Presently the only consistent environmental factor is a negative correlation between cigarette smoking and the development of PD. 


Effects of Exercise  For Individuals with Parkinson’s

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The American Academy of Neurology promoted the use of exercise as adjunctive therapy for Parkinson’s patients in the 1990s. However, it was later assumed that individuals with PD should not participate in resistance training programs due to the belief that it would increase rigidity (Salgado et al., (2012). Systemic reviews from the Cochrane collaboration released in 2001 found insufficient evidence to support or contest the efficacy of physiotherapy in PD (Deane et al., 2001a; 2001b). 


For example, Deane and associates (2001a) assessed the effectiveness of one physiotherapy intervention compared with the second approach in patients with PD. A total of 43 randomised trials involving 1673 subjects were identified as suitable for the review. However, the methods of randomisation and concealment of allocation were poor or not stated in most trials. Blinded assessors were used in just over half of the trials and only 10 stated that they used intention-to-treat analysis. The most frequently reported physiotherapy outcomes were gait speed (19 trials) and timed up and go (15 trials) with only five of the 43 trials (12%) reported data on falls. The motor subscales of the Unified Parkinson’s Disease Rating Scale and Parkinson’s Disease Questionnaire-39 were the most frequently reported clinician-rated disability and patient-rated quality of life outcome measures, used in 22 and 13 trials respectively. The content and delivery of the physiotherapy interventions varied widely in the trials included within this review, so the authors could not perform a quantitative meta-analysis. 


Deane et al., (2001b) performed a separate systematic review that compared various physiotherapy techniques for patients with PD. Seven studies were identified with a total of 142 patients. All studies used a small number of subjects and the method of randomisation and concealment of allocation was poor or not stated in all of the studies. The methods of physiotherapy varied so significantly that the data could not be combined. Deane and colleagues identified several methodological flaws in many studies and that there was insufficient evidence to support or refute the efficacy of any given form of physiotherapy over another in PD. 


According to Nutt and Wooten (2005), this led to a situation in which physicians were instructed to support the use of regular exercise, despite limited evidence of its efficacy in reducing disease progression or improving activities of daily living. However, more recent studies have found that resistance training in individuals with PD improves numerous outcome measures. Goodwin et al., (2008) systematically reviewed RCTs reporting on the effectiveness of exercise interventions on outcomes (physical, psychological or social functioning, or quality of life) for individuals with PD. Fourteen RCTs were included within the review and the methodological quality of most studies was moderate. Pooled evidence supported exercise as being beneficial with regards to physical functioning, health-related quality of life, strength, balance and gait speed for people with PD. However, there was insufficient evidence to support or refute the value of exercise in reducing falls or depression. Kuroda and colleagues (1992) assessed 438 PD patients over 4.1 years. The subjects were arranged according to the degree of physical exercise they performed, and the ratios of observed to expected deaths were computed. The exercising group showed the lowest ratio of 1.68 (1.45 for patients able to walk independently, and 1.89 for those who could not) while all patients exhibited a ratio of 2.47. Unfortunately, despite the reported benefits of exercise, there is little consensus on the type of exercise dose or types of exercise needed to target the wide range of symptoms that present with PD.


Effects of Resistance Training for Individuals with Parkinson’s 

Cano-de-la-Cuerda (2010) performed a literature review and found that there is a body of evidence that suggests that PD not only leads to impaired motor function but negatively affects muscle strength. Several studies have demonstrated that PD decreases isokinetic muscle strength affecting several muscle groups including the flexors and extensors of the wrist, knee and hip (Durmus et al., 2010; Stevens-Lapsley, Kluger and Schenkman, 2012; Schilling et al., 2009). Additionally, studies have reported that PD may lead to altered isometric ability in the hands (Park et al., 2012; Pedersen et al., 1998; Reck et al., 2009), and trunk muscles (Bridgewater and Sharpe, 1998 of PD patients. This includes the increased time to reach peak torque and contraction, lower rates of force development, and irregular force-time curves, however, these findings are not universal (Koller and Kase, 1986; Jordan, Sagar and Cooper, 1992). While the complete mechanism for this weakness is not fully understood. Brown and associates (1997) suggest it involves decreased motor neuron activation because of inadequate basal ganglia stimulation of cortical motor centres, and incomplete contractions from action tremors initiated by the rhythmic and synchronous discharging of motor units during volitional activity in Parkinson’s patients.


Kakinuma and colleagues (1998) have suggested that muscle weakness may be inherent to PD and influenced by movement speed and not merely a result of ageing or inactivity. Combined with the findings from Hortobagyi et al., (2003) showed that healthy older adults apply close to maximal force production capabilities to climb up and downstairs and rise from chairs, the burden of PD on ADLs from muscle weakness cannot be understated. To improve the strength deficits for individuals living with PD, resistance training has been suggested to be a favourable modality of exercise. Several small studies have shown improvements in muscle strength (Dibble et al., 2006; Hass, Collins and Juncos, 2007), muscular endurance [Scandalis et al., 2001), neuromuscular function (Hass, Collins and Juncos, 2007, Scandalis et al., 2001], muscle force production (Dibble et al., 2006), as well as gait speed and initiation (Hass et al., 2012) and chair rise function Hass, Collins and Juncos, 2007. 

Dibble et al., (2006) examined changes in muscle force production, clinical measures of bradykinesia, and quality of life following 12-weeks of a high-intensity eccentric resistance exercise program in individuals with mild to moderate PD. Twenty subjects with idiopathic PD were matched into an experimental or an active control group. All subjects were tested before and after the 12-week intervention. The experimental group performed high-intensity quadriceps contractions on an eccentric ergometer 3 days a week for 12-weeks. The active control group participated in an evidence-based exercise program of PD. The outcome variables were quadriceps muscle force, clinical bradykinesia measures (gait speed, timed up and go) and disease-specific quality of life (Parkinson's disease questionnaire-39 [PDQ-39]). Results showed significant time by group interaction effects for gait speed, timed up and go, and the composite PDQ-39 score (p <0.05). Muscle force, bradykinesia, and QOL were improved to a greater degree in those that performed high-intensity eccentric resistance training compared to an active control group. 

Hass, Collins and Juncos (2007) assessed the beneficial effects of resistance training with and without creatine supplementation in individuals with mild to moderate PD. Twenty subjects with idiopathic PD were randomised to receive creatine monohydrate supplementation plus resistance training (CRE) or placebo (lactose monohydrate) plus resistance training (PLA), using a double-blind procedure. Both groups participated in 24 resistance training sessions, 2 times per week performing 1 set of 8-12 repetitions of 9 exercises. Results showed significant Group x Time interactions for chest press strength and biceps curl strength with significantly greater improvement for the CRE group. Chair rise performance significantly improved only for CRE (12%, P=0.03). Both PLA and CRE significantly improved 1-RM for leg extension (PLA: 16%; CRE: 18%). Muscular endurance improved significantly for both groups

Scandalis et al., (2001) investigated the effects of resistance training and gait function in individuals with PD. Fourteen subjects with mild-to-moderate PD and six normal control subjects of similar age were recruited. The training consisted of 8-weeks of resistance training 2 times per week with a focus on the lower limbs. Results showed that PD subjects significantly increased in strength similar to those of normal elderly adults. Subjects with PD also had significant gains in stride length, walking velocity, and postural angles compared with pretreatment values.

There is a limited amount of research that has determined the volume dose of training necessary to generate optimal results, however, it is generally accepted that the most advantageous volume of exercise should maximise intensity while minimising fatigue. There have been several small studies that have suggested that in healthy older subjects, three sets of resistance training may produce greater gains than single set training. However, this has given rise to a debate about the set-volume dose required (see critical review on set volume recommendations).


What is apparent is the need for more research on the optimal volume needed for individuals with PD as several current studies evaluating resistance training in PD employ a single set treatment. Contrary to this, Schilling et al., (2010) examined the effects of an 8-week resistance training intervention on strength and function in individuals with PD. Eighteen subjects were randomised to a training or standard care group for the 8-week intervention. The resistance training group performed 3 sets of 5-8 repetitions of the leg press, leg curl, and calf press two times per week. The results showed a significant Group-by-Time effect for maximum leg press strength relative to body mass, with the resistance training group significantly increasing their maximum relative strength (P <0.05). This finding suggests a moderate volume of high-load weight training may be beneficial and manageable for people with PD.


Table 2. Falvo et al., (2007) Resistance training interventions with Clients with PD

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Balance and Stability Training for Individuals with Parkinson’s

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Individuals with PD often have problems with postural stability and balance impairments (Paul et al., 2013). Unfortunately, this contributes to an increased rate of injuries and falls which in turn increases morbidity and mortality (Ashburn et al., 2001). According to Bloem (1996), postural stability in individuals with PD is of concern as the dopamine replacement medications that is prescribed are often insufficient to control these deficits 

There have been several studies that have examined the best types of training to improve balance and reduce falls. Toole et al., (2000) sought to determine if a balance and strength training program could improve balance and strength in individuals with stage 1-3 Parkinsonism. Results from 10 weeks of balance and strength training indicated improvement in equilibrium by two distinct mechanisms: (1) training altered the ability to control the motor system when vestibular cues were the primary source of dependable feedback; (2) training helped subjects to override faulty proprioceptive feedback and utilise consistent visual or vestibular cues. 

Smania et al., (2010) investigated the effects of balance training on postural instability in PD subjects.  Sixty-four subjects were randomly assigned to a balance training (n = 33) or control group of general physical exercise (n = 31). Subjects received 21 treatment sessions lasting 50 minutes each. The Berg Balance Scale Activities, Specific Balance Confidence Scale, postural transfer test, self-destabilisation of the centre of foot pressure test, number of falls, Unified Parkinson’s Disease Rating Scale, modified Hoehn and Yahr Staging Scale, and Geriatric Depression Scale was used to evaluate outcome effects. The results showed that the balance training group showed significant improvements in all outcomes except for Unified Parkinson’s Disease Rating Scale, modified Hoehn and Yahr Staging Scale. Interestingly, these improvements were maintained at the one-month post-treatment in all outcome measures except the Geriatric Depression Scale.


There have been several meta-analytical reviews that examine the effects of neurophysiological functioning, movement and quality of life in individuals with PD. For example, Dibble and associates (2009) found that a moderate body of evidence that suggests physical activity and exercise improves structural in and balance task performance. However, there was inadequate evidence to support an improvement in the quality of life and fall incidents. Likewise, Allen et al., (2011) performed a meta-analysis on the effects of exercise and motor training on the performance of balance-related activities and falls in individuals with PD. The authors found that multifaceted training improved balance-related activity (Hedges' g, 0.33; 95% confidence interval, 0.11-0.55; P=0.003) performance but emphasised that there was no evidence that the number of falls was impacted (risk ratio, 1.02; 95% confidence interval, 0.66-1.58, P=.94).  It was also noted that highly challenging balance training improved the efficacy of the intervention on balance-related activity performance, but the difference was not significant (P=0.166). 

It has been suggested that balance training is supplemented with resistance training to improve balance and stability. Hitsch et al., (2003) examine the immediate and short-term effects of balance and resistance training and balance only for persons with idiopathic PD. The results showed that both training groups improved Sensory Orientation Test performance. Additionally, both groups were able to balance longer before falling with this persisting for at least 4-weeks. Muscular strength, however, increased significantly in the of balance and resistance training group and only marginally in the balance only group and this strength effect persisted for at least 4-weeks. 

Even though there are several studies that exam balance training the long-term effects are still unclear. Allen et al. (2011) suggest the challenging nature of maintaining a challenging training program in a home-based program. However, other studies have suggested several accessible and relatively inexpensive options by which individuals can reduce balance impairments at home. For example, Tousignant and colleagues (2012) suggested that supervised Tai Chi exercise can be an effective alternative to conventional physical therapy for frail older adults. This is supported by a study by Li et al., (2007) who suggested that Tai Chi is an appropriate physical activity for older adults with PD and reduce balance impairments in mild to moderate PD persons. Overall, this suggests that in mild to moderate PD persons, Tai Chi may be more effective than stretching or resistance-training alone in improving postural stability.

NSCA Exercise Recommendations for Clients with Parkinson’s Disease

Individuals with PD may benefit from participation in appropriate designed exercise programs. However, even though there is scientific evidence that supports the use of physical activity and exercise in persons with PD there has not been established specific recommendations for this population group. Therefore, recommendations suggested by NSCA for exercise with PD are centred on the wide-ranging recommendations for older adults. Exercise program design recommendations for clients with PD are shown in Table 2 and Table 3. For example, PD clients may perform resistance training initially with one set of several exercise movements with greater emphasis on the multi-joint exercises. Guidelines suggest that PD clients should train with light to moderate resistance levels of 40-to-80% 1RM for 10-to-12 repetitions per set. The frequency of training may begin with one or two sessions per week with it increasing to three or four weekly sessions if appropriate for the client. 

In addition to an appropriate and client-centred aerobic and resistance training program, PD clients may also benefit from balance training. Exercise professionals should note that clients with PD have difficultly moving their centre of mass outside their base of support and have delayed reaction times, which may result in falls. Modes and client instruction should focus on basic reaching and balance activities and it may not be appropriate for exercise professionals to exercise PD clients on unstable surfaces. PD clients also may become rigid and develop contractures over time. The clients can also benefit from stretching, flexibility, and mobility programs that include all joints and major muscle groups. Specifically, clients with PD tend to develop a kyphotic posture, so exercise professionals should consider activities that stretch the client's anterior trunk muscles (abdominal muscles) rather than performing trunk flexion exercises like crunches.

Table 3. NSCA Exercise Recommendations for Clients with Parkinson’s Disease

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Exercise Precautions, Modifications and Contraindications for Clients with Parkinson’s Disease 

The exercise profession should always consider the safety of any client but especially a person with PD. As has been previously discussed these clients experience alterations in their movement patterns (i.e., reduced walking speed, decreased ability to lift their feet) and impaired balance. In a dynamic environment, PD client finds it difficult to adapt to so it is best, therefore, to train this population group in a quiet room with no apparent trip hazards (exercise equipment, area rugs, power cords etc).

Depending on the specifics of the PD client, they may wish to participate in a group class setting or may need closer 1-to-1- supervision. Importantly, the exercise professional should be nearby in case the client suddenly has a loss of balance. Furthermore, because of tremors and poor motor coordination, upright or free weight exercise may not be fully safe in this population and should be used with caution. Clients should typically use resistance training machines rather than free weights. PD clients should reframe from using a treadmill and instead can benefit from walking over the ground or using a stationary bike with foot straps. 

In addition to safety considerations, clients with PD must ask their physician when the best time is to exercise given their medication schedule. There is a reported window after taking medication during which symptoms are better controlled, therefore this would be the best time for a client to exercise. Clients should also be reminded that it is important to take their medications on time. Additionally, exercise professionals must be familiar with the monitoring of heart rate, blood pressure, and thermoregulation as clients with PD have autonomic nervous system dysfunction. These clients are also at risk for orthostatic hypotension and should be reminded to avoid the Valsalva manoeuvre (breath-holding). Lastly, PD clients, are more vulnerable to fatigue and should be instructed to work at submaximal levels

Multiple Sclerosis

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The nervous system controls and regulates both voluntary and involuntary movements of the human body. The functional units of the nervous system are called neurons and they can generate electrochemical signals that are transmitted along the neuron axon (Figure 1). Some of these neurons are encased by a myelin sheath. This fatty white substance works as an insulating sheath that ensures optimal functioning of the nervous system. Importantly, the myelin sheath increases electrical resistance across the neuron membrane, thus preventing seepage of electrical impulses. 

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Figure 1. Neuron structure and function.

Demyelination is the loss of the myelin sheath (layer) and is the central feature of several neurodegenerative autoimmune diseases in which the deterioration of the myelin sheath severely reduces the electrochemical signals. This substantial loss of myelin reduces or inhibits all electrochemical signals from the brain to the body. The most common of these diseases is multiple sclerosis (MS), which affects either or both of the brain and spinal cord (central nervous system) and the peripheral nervous system. MS is thought to be an immune-mediated disorder, in which the immune system incorrectly attacks healthy tissue in the CNS. Other neurodegenerative autoimmune diseases that involve the loss of myelin sheath include transverse myelitis, Charcot-Marie-Tooth disease, Guillain-Barre syndrome and leukodystrophy. The most common features of these diseases include muscular weakness, numbness, visual impairments, heat sensitivity, reduced coordination and balance, fatigue, and the disturbance of cognitive processes (including speech, memory, or both).

The prevalence of multiple sclerosis (MS) globally is estimated to be around 2 million people. In the UK is approximately 110,000 people with approximately 79,000 females and 31,000 males (approximately a 2.5:1 ratio). There are almost 5000 new cases of MS each year (approximately 8 per 100,000 people in the UK). Multiple sclerosis is a major cause of neurological disability in young and middle-aged adults, with a peak incidence between 40-49 years, but with a peak prevalence of between 50-59.

Pathology of Multiple Sclerosis: An Overview

Multiple sclerosis is a progressive autoimmune disorder characterised by deterioration of the myelin sheath. Myelin encases billions of nerve cells in the human body. The purpose of the myelin sheath is to aid in the speed and transmission of the central nervous systems signals. People with MS have a breakdown in electrochemical transmission due to a substantial loss of the myelin sheath and the neurons experiencing demyelination. 


Individuals with MS may experience a wide range of symptoms that vary between people. These varying symptoms are a consequence of an interruption in nerve signal transmission and differ amongst individuals depending on where the demyelination occurs. Individuals typically report experiences of pain, fatigue, tingling, ambulation difficulties (Crenshaw et al., 2006), impaired balance and coordination (Pula et al., 2013), bladder and bowel dysfunction (DasGupta et at al., 2003), vision difficulties (Balcer et al., 2015), dizziness and vertigo (Pula et al., 2013), sexual dysfunction (Kessler et al., 2009; DasGupta et al., 2003), cognitive dysfunction, emotional changes including depression (Haussleiter et al., 2009). Additionally, there have been other less frequent symptoms reported including speech impairments, swallowing difficulties, headache, loss of hearing, seizures, tremors and breathing difficulties (Bagnato et al., 2011). Despite these symptoms, individuals with MS experience a normal life span.

Individuals affected by MS may experience a range of disease progressions and outcomes. There are four varieties of MS (Figure 2): relapsing-remitting (RRMS), primary progressive (PPMS); secondary progressive (SPMS) and progressive relapsing (PRMS). The Canadian Agency for Drugs and Technology in Health (2016) estimate that eighty-five per cent of cases are diagnosed initially as RRMS. In these cases, individuals experience defined exacerbation or flare-ups. These episodes are typically when the central nervous system experiences inflammation which leads to previously unseen symptoms quickly worsening or even the development of new symptoms. The inflammation varies amongst people and can last anywhere from days or even months.  These episodes are interrupted by a period of remission or when the neurological system functions stabilise and do not further deteriorate. The National Multiple Sclerosis Society (2016) points out that during remission, individuals may return to their pre-exacerbation condition with no symptoms, or they may experience some minor continuing symptoms.

The Canadian Agency for Drugs and Technology in Health (2016) estimate that 15% of MS cases are identified as primary progressive. This is a type of MS in which neurological function deteriorates from the onset of the disease without any significant remissions. These symptoms may provisionally level off or even appear to be briefly improved. Otherwise, these people may experience gradually deteriorating neurological function. Trojano and associates (2003) found that of the 85% of RRMS cases, 50% are considered as secondary progressive within the first 10 years of diagnosis and 90% within 25 years. These people will experience less recovery following bouts and disability advancing over time with diminishing neurological function.


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Figure 2. Four Clinical Subtypes of MS.

Pathophysiology of Multiple Sclerosis

Early research identified that MS is commonly seen in Caucasian individuals (Kurtzke, 1980). Duquette et al., (2015) reported that auto-immune aetiology has a skewed sex distribution with females affected more frequently than males. The authors noted that most population studies demonstrate that the majority of females in MS is almost continuous. Duquette and associates also suggest that MS could be attributed to the recognised hormonal and sex influences on the immune response and also the genetic influences. Pakpoor et al., (2012) performed an interesting meta-analysis that investigated the association between MS and migraines. Eight studies met the pre-set inclusion criteria yielding a total of 1864 subjects and 261563 control subjects. The results suggested a significant association between migraines and MS; however, significant heterogeneity was reported.  Furthermore, MS subjects were more than twice as likely to report migraines as controls. 

Multiple sclerosis is a prevalent neuromuscular disease in young adults and is frequently diagnosed between the 20-to-40 years of age (Frohman (2003). The National Multiple Sclerosis Society (NMSS) estimates that 2.3 million individuals are affected globally (Markowitz, 2013). Although MS is most frequently observed in adults NMSS (2016) estimated that 8,000-to-10,000 people under 18 years of age suffer from this disease. In the UK the prevalence is approximately 110,000 people with around 79,000 women and 31,000 men (approximate 2.5:1 ratio) compared to around 2 million people worldwide. There are approximately 5000 new cases each year (around 8 per 100,000 people in the UK). MS is a major cause of neurological disability in young and middle-aged adults, with a peak incidence between 40-49 years, but with a peak prevalence of between 50-59.

Currently, the cause of MS is not completely understood; however, it is considered to be an autoimmune disease of the CNS. Several epidemiology studies have suggested that individuals with MS may experience an abnormal immune-mediated response in which myelin and nerve fibres are attacked by the body (Rolak, 2002). The myelin sheath, in particular, is attacked by a white blood cell group known as T cells. This causes tissue damage and inflammation leading to scar tissue (sclerosis) and blockage in signal transmission. This obstruction in signal transmission produces distorted or lost messages, leading to the symptoms of MS.

Furthermore, there are multiple areas of inflammatory demyelination with a preference for distribution around the ventricles and vascular spaces. This leads to an immune reaction to myelin (myelin basic protein [MTP]) and myelin oligodendrocyte glycoprotein (MOG). Activated T cells attach to the endothelium of capillaries within the brain and drift into the brains parenchyma where activated macrophages attack and consume the myelin (Figure 3). Numerous cytokines including tumour necrosis factor-alpha (TNF-a), and interferons (IFN-g), as well as IgG, are involved in the immune attack with B cells producing IgG directed at MOG. There is an increased assembly of IgG and an increased occurrence of particular IgG moieties, some of which indicate antiviral IgG. Contemporary studies of total brain N-acetyl aspartate (NAA)- to-creatine ratios have specified loss of axons and evidence for membrane damage (demyelination) as an increase in choline-to-creatine ratio (Gonen et al., 2000). Lesions indicating central regions of inflammatory demyelination may be present in the cerebral hemispheres, brainstem, and spinal cord.

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Figure 3. Multiple Sclerosis and the Myelin sheath.

Environmental and Modifiable Risk Factors for Multiple Sclerosis 


Vitamin D Deficiency 


It has also been hypothesised by Asherio (2007) that MS may be caused [in part] by several environmental factors. MS is most common in countries furthest from the equator, especially in Caucasians in Northern Europe, as the further away from the equator, the less sunlight the body is exposed to. It is the vitamin D, produced naturally when the skin is exposed to daylight, that seems to have a role to play in those who are diagnosed with MS.

In 2016, the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) addressed the subject of environmental and modifiable risk factors for MS. Several factors, including infections, vitamin D deficiency, diet and lifestyle factors, stress and comorbidities, were reviewed. Of interest is the body of evidence that supports the association between vitamin D deficiency and low levels of its metabolite 25-hydroxyvitamin D3 (25(OH)D) in the onset and development of MS (Smolders and Damoiseaux, 2011). The authors demonstrated that vitamin D has potent immunomodulatory activity. This may have an anti-inflammatory role in the second lymphoid organs and the CNS as well as neuro and myelin protective (or even myelin-regenerative) effects in the CNS (Wergeland et al., 2011). Furthermore, genetic effects may be contributed to MS risk as genes are associated with vitamin D metabolism (Niino and Miyazaki, 2015).

This association is a result of epidemiological research based on different study protocols. Collectively, when the results of these studies are pooled the results support the importance of vitamin D in adolescence and adulthood, up to the time of MS onset. Furthermore, Asherio and associates (2007) suggested that vitamin D is important in childhood or even in utero. Recently, a study by Munger et al., (2016) reported that insufficient maternal vitamin D levels during pregnancy were related to a twofold increased risk of MS in the children.  The causality of the relationship between vitamin D and MS risk is further supported by the results of Mendelian randomisation studies (Mokry et al., 2015; Rhead et al., 2016). These results suggest that vitamin D deficiency is an independent risk factor for MS, however, they do not discount a contribution of other aspects. Some uncertainty remains about whether there is a critical timing of exposure to low 25(OH)D levels and what absolute level of 25(OH)D is associated with increased MS risk.

Cigarette Smoking and Multiple Sclerosis Risk

There is wide-ranging evidence that suggests, both active and passive cigarette smoking is risk factors for MS onset. Handel et al., (2011) reported from their meta-analysis that smoking increases the risk of MS by nearly 50% in several epidemiological studies, with a coherent dose-response relationship with an increasing smoking dose (Hedstrom et al., 2013; Salzer et al., 2013). Elevated levels of cotinine (a proxy marker for nicotine) were identified in blood samples taken before the development of MS. This supports current epidemiological evidence on the increased risk of MS in individuals who smoke (Salzer et al., 2013). Variance in smoking over time in behaviour between men (with decreasing numbers of smokers) and women (with a somewhat constant number of smokers) over the last several decades could [in part] explain the increase in the female: male ratio in MS incidence noted in some regions (Palacios et al., 2011). Unfortunately, the period for exposure to cigarette smoke is unclear, with some studies detecting no effect of age (Hedstrom et al., 2013) and others observing increased susceptibility to MS with exposure during adolescence or young adulthood (Salzer et al., 2013).


Body Mass Index and Multiple Sclerosis Risk

Several epidemiological studies had suggested that individuals that are overweight and obese are associated with a two to threefold increased risk of MS (Munger, Chitnis and Ascherio, 2009; Wesnes et al., 2015; Hedstrom, Olsson and Alfredsson, 2012). Interaction with other risk factors, including vitamin D status and genetic susceptibility, has also been acknowledged. Information gathered from the Swedish EIMS study have suggested that individuals with a body mass index (BMI) exceeding 27 kg/m2 at 20 years old had a twofold increased risk of developing MS in comparison with subjects with normal body weight (Hedstrom, Olsson and Alfredsson, 2012). 


Furthermore, Hedstrom and associates (2014) conducted a further study using EIMS and GEMS data and observed a strong association between BMI status and HLA genotype concerning MS risk. The authors also showed that obese individuals with the MS-related HLA genotype (presence of the HLA-DRB1*1501 allele and the absence of the HLA-A*02 allele) had a 16-fold greater probability of developing MS compared to non-obese individuals without this genetic risk factor.

Clinical Signs and Features of Multiple Sclerosis

Long-fibre tracts are commonly involved in the development of demyelination. For instance, it is common for individuals to have posterior column signs, including a loss of vibration sense, and pyramidal signs initially in the development of the disease when it is almost asymptomatic.  A typical characteristic of MS is fatigue often during the daytime (diurnal). This is considered as malaise or a lack of motivation for performance in any form of physical activity. This also includes motor fatigue, which progresses with sustained physical inactivity (Krupp et al., 1988).  Another evident phenomenon is a reduction in heat tolerance (internal and external), which may be accompanied by the development of neurologic symptoms (Freal et al., 1984). Distorted vision in one or both eyes may occur with physical exertion (Uhthoff’s phenomenon). This is because demyelination reduces the efficiency of axonal conduction so there is less current is available for depolarisation at nodes of Ranvier. 

Frequent symptoms of MS include painful blurring or loss of vision in one eye with evidence of deafferentation occurring as the outcome of optic neuritis. Ultimately, there will be evident loss of visual acuity. However, individuals treated with methylprednisolone will have marked improvements in vision within 6-weeks with a reduction in pain (Thompson et al., 1989). There are several other visual conditions including blurred vision with rapid eye movements, difficulty with visual fixation, double vision (diplopia) and diminished night vision. Individuals may further complain of facial numbness or pain typical of trigeminal neuralgia (a chronic pain condition that affects the trigeminal nerve). Additionally, individuals may also experience numbness of the tongue and loss of taste. Often, weakness and loss of coordination initially affect the lower extremities progressing to the upper extremities, occasionally in a hemiparetic pattern. Spastic paraparesis coupled with ataxia is referred to as the “spastic ataxic syndrome.” Early in MS, the neurogenic bladder manifests itself due to the inability of the bladder to retain a sufficient volume of urine. Subsequently, the urinary frequency can exceed 6-times per day, often with incontinence with many individuals reporting increased urination at night (nocturia). There are also high rates of urinary tract infections. 

An array of sensations occurs in the skin especially vibration loss in both feet with position sense preserved until vibration sense loss is severe. Abnormal sensations produced by touching or stroking the skin are also commonly reported (dysesthesias). However, these sensations do not occur throughout the peripheral nerve.  There have also been instances where individuals report abnormal sensations over the trunk, in particular, a band-like sensation around the chest or abdomen region. Patients also report having cognitive difficulties. Several studies have identified that this develops along with the cranial, motor, and sensory symptoms (Herholz, 2006; Gold et al., 2005). Individuals may demonstrate an inability to function when they are required to monitor several activities at the same time. Furthermore, attentiveness is decreased leading to individuals being unable to process information accurately in memory. Emotional lability is also reported with sub frontal demyelination, which produces pseudobulbar palsy. Johnson et al., (1995) have demonstrated that cognitive deficit is greater in people with obvious signs of pseudobulbar palsy or excessive emotional lability. 




For a diagnosis to be firmly established, two or more areas of demyelination (white matter lesions) must be confirmed. Additionally, there must be two or more remissions of neurologic deficits. Krupp and colleagues (1988) stated that this must be accompanied by evidence of the disease identified via magnetic resonance imaging (MRI) with T2-weighted lesions in white matter and confirmation of increased IgG synthesis with positive oligoclonal bands (OCBs) in the cerebrospinal fluid. OCBs occur from a reduction in the number of different migrating species of IgG obtained on electrophoresis. However, other conditions, including bacterial or viral infection, autoimmune diseases, such as systemic lupus erythematosus (SLE), and vasculitis, may also produce increased IgG or oligoclonal bands.

It is often difficult to diagnose MS, as these symptoms can appear similar to symptoms of other diseases. Normally a detailed clinical history is an essential component of the initial diagnosis, as MS requires at least two episodes of neurological impairment combined with evidence from at least one other diagnostic test. Patients often report visual disturbances first, as the nerves supplying the eyes are easily affected by demyelination. The most common tests used for diagnosing MS are as follows:

  • Lumbar puncture: this is where a needle is inserted into the cauda equina space and cerebrospinal fluid is removed. The cerebrospinal fluid is then examined for the presence of proteins, oligoclonal bands (remnants of oligodendrocytes following demyelination) and lymphocytes.

  • Electrophoresis: this test looks for the presence of immunoglobulins in the cerebrospinal fluid (specifically IgG).

  • Evoked potentials: these tests are a form of nerve conduction test, whereby a stimulus of either visual, auditory or somatosensory origin is applied to the body and electrodes on the skull detect brain electrical activity to establish if the nerve is functioning correctly.

  • Magnetic resonance imaging (MRI): this is looking for the presence of inflammation (acute/active disease changes) and/or plaques (old scarring/changes from previous inflammatory episodes) within the brain and/or spinal cord.

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Effects of Exercise in Individuals with Multiple Sclerosis

Active Senior Man

Acute Exercise Responses in Individuals with Multiple Sclerosis

Studies have demonstrated that individuals with MS have a lower maximal aerobic capacity when compared with average age and gender-matched non-disabled adults without MS (Ponichtera-Mulcare,1983; Ponichtera-Mulcare et al.,1995). Ponichtera-Mulcare and associates (1995) showed that maximal aerobic capacity may be inversely related to the level of disability as measured on the Kurtzke Expanded Disability Status Scale (EDSS) (White et al., 2004). According to the EDSS score individuals with a higher EDSS score are indicative of more neurological impairments and have a lower maximal and submaximal aerobic capacity. Even though there is considerable variability in performance a frequently reported side effect of acute exercise in individuals with MS is a heightened sense of fatigue during post-exercise recovery.  However, at present, there is limited evidence that suggests that post-exercise fatigue is reflective of an exacerbation of existing or new MS symptoms. Surakka and colleagues (2004) demonstrated that the level of self-reported postexercise fatigue as measured by the Modified Fatigue Impact Scale (MFIS) can be reduced after training.

Acute Cardiorespiratory Responses


The physiological responses for many individuals with MS to an acute bout of submaximal exercise are comparable to the general population. For example, Ponichtera-Mulcare (1983) showed that there is a linear increase in heart rate, blood pressure, oxygen uptake and minute ventilation to increases workload. Additionally, metabolic and cardiovascular responses are consistent over a broad array of impairment levels (i.e., EDSS). However, this is in contrast when examining the heart rate response to incremental exercise in relation to metabolic cost.

Tantucci et al., (1996) showed that individuals with MS had a significantly lower oxygen pulse compared to healthy subjects. These results appear to be consistent during maximal and submaximal aerobic exercise. A higher heart rate at a specified VO2 may suggest that stroke volume is insufficient to support metabolic demand. Conversely, a case study performed by Fragoso et al., (1995) reported that the patient with MS had respiratory muscle weakness and severely depressed exercise performance. The reduced exercise performance was related to an early anaerobic threshold but a normal central cardiovascular response, suggesting problems in peripheral O2 distribution/utilisation. The respiratory muscle involvement, although substantial, was non-limiting to exercise performance. Cardiovascular autonomic dysfunction (both sympathetic and parasympathetic) has been documented in individuals with MS (Linden, Diehl and Hretzchmar, 1997; Flachenecker et al., 1999; Bonnett et al., 2006).


The use of heart rate as an index of exercise intensity from a clinical standpoint presents potential problems for this population group. Firstly, if oxygen pulse is significantly lower with individuals with MS then the absolute workloads will need to be reduced during exercise. As a result, the exercise intensity is lowered and feasibly a reduction in absolute gains in aerobic capacity. Secondly, due to the reduced cardio acceleration, the standard practice of computing HRmax (220–age) or the Karvonen method for calculating training heart rate should be used with caution. Noble and Roberton (1996) suggested that the perceived exertion scales would be more applicable for this population group with the use of the Category-Ratio Rating of Perceived Exertion. This exertion scale uses individuals perceived stress levels in three categories: peripheral, central, and integrated. This scale may be a useful tool for obtaining information due to unreliable input from “central” (e.g., heart rate) data and has been used effectively with the MS population (Ponichtera-Mulcare,1983).

Several studies have reported that maximal aerobic power (VO2max) varies significantly depending on the level of physical impairment and neurologic symptoms present when measured using indirect calorimetry (Mulcare et al., 2001; Tantucci et al., 1996; Pariser, Madras and Weiss, 2006). Tantucci et al., (1996) showed that MS subjects with minimal impairment performed poorly regardless of what test was performed using the leg, arm or combined arm and leg exercises when compared to healthy adults. Time to fatigue (i.e., aerobic exercise endurance) has been measured using several modes of ergometry and may not be directly related to the individuals level of physical impairment. Ponichtera-Mulcare et al., (1983) noted that a moderate level of exercise (i.e., 50% VO2max) patients with MS have been able to exercise for between 15-to-60 minutes. The correlational analysis found no relationship between endurance time and the level of physical impairment (EDSS).

Chronic Exercise Response with Resistance Training

Research has documented the positive effects of training on muscle performance in individuals with MS (Table 1). Current literature has established that people with MS can improve muscle strength following a supervised resistance training program and aerobic training. Early studies from Petajan et al., (1996) and Ponichtera-Mulcare et al., (1997) have shown that training can yield modest improvements (e.g., 11%–17%) following 15 weeks of training and more significant improvements (29%) after 24 weeks of training in muscle performance. Initial research on resistance training focused principally on detailing absolute muscle performance in individuals with MS.

Contemporary research has concentrated on gait kinematics (Gutierrez et al., (2005) and mobility (White et al., 2004; Taylor et al., 2006). Training protocol duration has typically been 8-to-12 weeks with subjects requiring participating in a minimum of 2 sessions per week with a resistance loading of between 60-80% 1RM (ACSM, 2009). Several studies have shown that MS subjects have improved in walking distance, walking speed and perceived levels of fatigue. However, subjects involved in these studies were generally mobile (EDSS < 5.5 with severely impaired subjects (EDSS >5.5) demonstrating limited improvements (Ponichtera-Mulcare et al.,1997). Therefore, several factors should be considered before the development of any training protocol.

Firstly, there may be neurological changes that the clinician may not have observed affect the exercise training intervention. Therefore, carefully monitoring of these changes should be performed via client interviews to document subjective impressions of the MS grade. Hoogervorst and associated (2003) suggest that The Guy’s Neurologic Disability Scale offers a valid method for recording baseline disability and subsequent levels of disability established on the interviews conducted with the client. This is in comparison to the Kurtzke Expanded Disability Status Scale which requires a physical examination by a trained clinician, most often a neurologist.  Lastly, when implementing any research findings to clients, it should be remembered that training outcomes observed under strict supervision may not necessarily be similar to unsupervised, uncontrolled environments, as in a home exercise program.

The effectiveness of exercise, particularly resistance training, in persons with MS has been recognised (Kjolhde, Wissing and Dalga, 2012). Kjolhe and associates (2012) performed a systematic review of progressive resistance training (PRT) studies and individuals with MS. A total of 16 papers were included in their review. The authors noted that there was strong evidence regarding the benefits of PRT on muscle strength. However, evidence on functional capacity, balance and self-reported measures including fatigue and quality of life were less clear. PRT was reported as having a positive effect on strength for individuals with MS. However, Kjolhe and colleagues noted that there was heterogeneity possibly due to the training protocols, sample sizes, type and severity of MS.

Exercise professionals should be aware that the primary goal of an exercise program for individuals with MS is to improve and maintain vital functions such as activities of daily living (ADL). Participating in exercise or physical activity will not cure or slow the disease progression (de Souza-Teixeira et al., 2009), but it will let individuals experience a higher quality of life (Moradi et al., 2015). PRT has been shown to positively affect strength (Table 1). For instance, Dodd and associates (2011) assigned persons with RRMS to either a PRT group or a control group for 10 weeks. After training two times per week for 10 weeks, the PRT group improved their strength, muscular endurance, fatigue level, and quality of life more than the control group. Dalgas and associates (2009) also demonstrated the effectiveness of PRT in individuals with MS. In this study were again assigned to either a PRT group or a control group. Subjects in the PRT group trained their lower extremity muscles two times per week for 12 weeks. After 12 weeks, the PRT group improved their muscle strength and functional mobility.

Exercise Recommendations for Clients with Multiple Sclerosis

Clients with MS can benefit from performing both resistance and aerobic exercise (Dalgas et al., 2008; 2009). The program recommendations for individuals with MS are detailed in Table 2. Individuals with MS may benefit from using seated resistance exercise machines as opposed to upright free weight activities if they have issues with stability and balance. It has been recommended that the resistance loading should be initiated at the 15RM level with one-to-three sets of four-to-eight exercises performed using a total body regime. The training loading may be increased progressively over time to three-to-four sets per exercise at 8-15RM for two or three sessions per week.

The modalities of aerobic training that the client may use include recumbent cycling, arm–leg ergometry, aquatic exercise, and treadmill walking. The recommendations for aerobic training suggest two-to-three sessions per week at a light-to-moderate intensity with a session duration of between 10-to-40 minutes. Clients with MS may also benefit from performing a general static stretching program of low duration. This is opposed to dynamic stretching as the client may be more prone to spasticity and balance limitations (National Multiple Sclerosis Society, 2016). Furthermore, Rafeeyan et al., (2010) suggested that aquatic-based activity is a beneficial mode of exercise. This can be either swimming or engaging in cardiovascular or resistance training in the pool. If the client prefers this mode of exercise it is suggested that the water temperature should be cool to avoid overheating (less than 85°F [29°C]) (Kargarfard et al., 2012).

Table 2. Program Design Recommendations for Clients With Multiple Sclerosis

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Table 1. RCT Studies on Progressive Resistance Training and Multiple Sclerosis

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Cerebral Palsy

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In the late 1950s, cerebral palsy (CP) was viewed as an unchanging condition of movement and posture that materialised early in life and was caused by a non-progressive brain lesion (Club, 1959). However, the advancement in the understanding of CP had altered this view. CP is now considered a group of nonprogressive, permanent neurological disorders that are caused by a variety of childbirth injuries. These disorders affect the CNS and are mostly categorised by limitations in motor control affecting body movement and posture. 

It is important to add that, although the brain lesion is static, the subsequent movement disorder may not be, and these symptoms could either improve or worsen (Albright, 1996).  For example, Nelson and Ellenberg (1982) founded that 50% of all children diagnosed with CP and 67% of those diagnosed with spastic diplegia by their first year “outgrew” the motor signs of the disorder by seven years of age. However, other studies have demonstrated that the motor skills in children diagnosed with dystonic and athetoid CP can continue to decline for subsequent years. (Arvidsson and Hagberg, 1990)

Prevalence of Cerebral Palsy

In the UK, 1 in 400 children is born with a type of CP, with 1,700 new cases per year (Office for National Statistics, 2018). Prevalence has been suggested to be directly associated with birth weight and gestational age: the lower the weight and more premature the birth, the higher the prevalence. For instance, prevalence has been reported as 90 cases per 1,000 live births in children with a birth weight of 1kg, compared with 1.5 cases per 1,000 live births for children weighing 2.5kg or more (NICE, 2017). When further separated based on socioeconomic class, the prevalence of CP was 3.33 per 1,000 in the poorest socioeconomic quartile compared with 2.08 per 1,000 in the most affluent quartile. This was true for both children of normal birth weight as well as low birth weight children (Odding, Roebroeck and Stam, 2006). 

Pathology of Cerebral Palsy

Cerebral palsy is caused by complications during initial brain development. These complications may arise during pregnancy, during childbirth, or during infancy and up to three years of life (Nelson and Grether, 1999). During pregnancy, several factors can affect the neurological development of the foetus leading to the development of congenital CP. DeLuca (1996) reported that the combination of prematurity and low birth weight was the major cause of CP. The diagnosis of CP has also been related to numerous prenatal causes, including maternal substance abuse, multiple births, congenital brain deformities, viral infections, and certain genetic conditions. Additionally, other perinatal causes include anoxia (absence of oxygen) from traumatic delivery, haemorrhage with direct brain damage from birth trauma, and a rare neurological disorder termed kernicterus (excessive levels of bilirubin in the blood), which may all cause CP. DeLuca (1996) also report that viral and bacterial meningitis, traumatic head injury, anoxia, and toxin-induced encephalopathy are also considered risk factors for CP. Stanley and colleagues (2000) suggest that CP is the outcome of a causal pathway rather than a particular episode. The authors state that various causal factors lead to a child developing CP. For example, they report that multiple births may lead to preterm delivery (babies born before 37 weeks of pregnancy), and preterm delivery can lead to neonatal cerebral damage and, eventually, CP. These causes increase the child’s susceptibility to other causal factors, including intrauterine growth constraints, which may decrease the child’s capacity to manage intrapartum stress.

Classification of CP can be performed using physiologic (Table 1) or anatomic (Table 2) categorisation, or by movement disorder (Table 3). This classification allows for the grouping of CP into subgroups that present specific characteristics. Importantly, for each individual with CP, the type and amount of motor impairment, combined with other effects of brain damage, determines the functional level and the need for a range of intervention services, irrespective of classification. The occurrence of other conditions associated with CP has also been recognised in the scientific literature. For instance, Saito and colleagues (1998) reported a 68% incidence of scoliosis in individuals diagnosed with spastic CP. Scoliosis typically started before the age of 10 and progressed quickly during the children’s growth phase. The authors suggested that risk factors for the progression of scoliosis included having a spinal curve of 40 degrees before the age of 15 years, having total body spasticity, being bedridden, and having a thoracolumbar curve.

Table 1. Physiological Classification of Cerebral Palsy (Onley and Wright, 2006)

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Table 2. Anatomical Classification of Cerebral Palsy (Onley and Wright, 2006)​

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Table 3. Classifications of Cerebral Palsy Founded on Movement Disorder (Davis, 1997)

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Odding et al., (2006) also found an increased prevalence of CP-related impairments. The authors reported that motor deficiency in some form occurred in 100% of children with CP. It was also noted that the incidence of musculoskeletal impairments increased in those with the spastic type of CP and included hip luxation (75%), joint contractures (73%), and scoliosis (72%). It was further found that between 23-to-44% of cases had cognitive. Sensory impairments included decreased proprioception and stereognosis, speech impairments, and dysarthria. Ophthalmic malformations were reported in 62% of children with CP. Urogenital impairments were also noted in 25% of children with CP having primary urinary incontinence. Endocrine impairments included feeding problems, silent aspiration, growth disturbances, body mass issues, and reduced bone mineral density. 

Del Giudice et al., (1999) showed that 92% of children with CP had clinically significant gastrointestinal (GI) symptoms. Furthermore,  60% of children had swallowing disorders, 32% regurgitation and/or vomiting, 32% abdominal pain, 41% episodes of chronic pulmonary aspiration and 74% with chronic constipation. Del Giudice and associates determined that most of these GI clinical symptoms were due to GI motility disorders and were not associated with any specific brain impairment.

Exercise Physiology and  Prescription

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Contemporary evidence is incomplete due to limited research performed on exercise responses with individuals with CP. This lack of research is feasible due to the limited participation in exercise in this specific population group. However, this limited amount of engagement with regards to participation does not necessary construe the lack of desire to participate. Additionally, the lack of participation is also related to a lack of suitable programs that are designed for, or accessible to individuals with disabilities. 

Studies have reported that some children and adolescents with CP have impaired motor function that negatively impacts on their daily physical activity levels leading to diminished function (Bandini et a., 1991; Van den Berg-Emons et al., 1998). Individuals with CP have also reported having increased adiposity (Bandini et al., 1991), low muscular force production (Damiano, Kelly and Vaugh, 1995), reduced aerobic and anaerobic power (Bar-Or, Inbar and Spira, 1976), decreased mechanical efficiency (Bar-Or, Inbar and Spira, 1976) and decreased respiratory function (Hutzler et al., 1998). These factors are indicators of reduced overall physical fitness. This reduction may be associated with poor exercise customs, difficulty performing skilled movements, muscle imbalances, or poor overall functional strength. Laskin, (1998) reported that fatigue and stress associated with a vigorous exercise program can lead to a transient increase in spasticity and discoordination in individuals with CP. 

Unfortunately, it is somewhat difficult to exercise test individuals with CP due to their spasticity and dyskinesia and the uneconomical nature of their mobility often lead to typically higher than anticipated exercise response values. Several studies have assessed individuals with CP physiological responses to submaximal exercise including heart rate, blood pressure, expired air and blood lactate values. Studies have reported that persons with CP  respond with elevated heart and respiratory values and higher blood pressure and lactate levels for a given submaximal work rate compared to individuals without CP. Laskin (2003) noted that individuals with CP peak physiological responses are 10-20% lower than abled-bodies subjects. Additionally, physical work capacity was shown to be 50% that of individuals without CP. However, Bowen and associated (1998) reported that no significant differences in the percentage of variability of physiological cost index, oxygen cost or oxygen consumption between subjects with or without CP at free-walking velocity. The authors observed that oxygen cost was the most reliable oxygen-use measurement with a mean percentage of variability of 13.2% for individuals with CP population and 13.9% for the non-disabled subjects. The physiological cost index was found to be the least reliable measurement with the average percentages of variabilities of the disabled (20.3%) and non-disabled populations (20.5%).

Studies have demonstrated that progressive resistance training in persons with CP leads to significant functional outcomes (Scholtes et al., 2008; Taylor et al., 2013). Scholtes et al., (2008) reported that there is a direct association between lower extremity strength and gait efficiency and gross motor abilities (Taylor et al., 2013). Molik et al., (2010) investigated wheelchair basketball skills in athletes representing the different functional classification levels and various types of disabilities. The results of this study found that regardless of functional classification level athletes with CP constantly performed the poorest. Additionally, the authors found that upper extremity muscular strength and endurance were highly associated with both anaerobic and aerobic wheelchair propulsion.

Several studies have also reported that resistance training in individuals with CP produces improvements in muscular strength, endurance and power comparable to those without disability (Damiano and Abel, 1998; McNee et al., 2009; Park and Kim, 2014). For example, Park and Kim (2014) performed a meta-analysis that investigated evidence on interventions to improve muscle strength and activity in persons with CP.  The main results of the analysis revealed that from the 13 included RCTs (n = 368 [range 12-to-58 years]) that strengthening and electrical stimulation may increase muscle strength and gait for persons with CP, specifically for children or adolescents. Moreover, resistance training programs have been shown to produce gains in fitness levels that are matched by improvements in measures of functional capabilities (Liao et al., 2007; Verschuren et al., 2007). For instance, resistance training has been suggested to improve gait capabilities in ambulatory persons with CP.

Exercise Guidelines for Clients with Cerebral Palsy


As discussed earlier, individuals with CP display considerable lower levels of exercise capacity (i.e., lower muscular strength/ endurance and reduced VO2 peak values). There are also motor limitations that restrict gait efficiency leading to increased energy uptake during ambulation compared to individuals that are not disabled. Strength training programs have also been shown to be effective at improving gait capabilities in individuals with CP. Therefore, both resistance training and upright mobility exercises (i.e., treadmill training and walking over the ground) may be used in training protocols intended to encourage the increased performance of upright activities including independent ambulation. However, it is also advantageous to include exercises that do not require significant gross motor coordination to provide exercise conditioning effects without the restrictions related to discoordination. For example, cycling, steppers, and elliptical machines may offer a means of cardiovascular training without the limitations related to more complex gait activities.

Exercise guidelines have suggested that individuals with CP should perform activities similar to that of the general population.  For example, it has been suggested that individuals with CP should begin aerobic training with an intensity equivalent to 30-to <60% of VO2peak or heart rate reserve for a duration of 15-to-20-minute one to two times per week. However, considerations should be made if the client has limited ability to perform continuous exercise. Therefore, it has been recommended that aerobic training may be separated into multiple shorter sessions of exercise, performed either in the same session with a recovery period included between bouts or in individual training sessions. 

Unfortunately, guidelines on the appropriate dose of resistance training for clients with CP are incomplete. Due to the restricted amount of evidence generated in this area, it is inappropriate to follow general recommendations. This is because the evidence is established on studies centred on children and adolescents with CP. Moreover, disease progression includes a varied group of disorders with a range of levels of physical functioning. Consequently, the general recommendations for adults require modifications to be appropriate for this population group. For example, the use of free weights may not be applicable for many individuals with CP due to limitations in both static and dynamic balance. Likewise, single-joint movements may be more of an appropriate activity for individuals to begin exercise training. Lastly, resistance loading (intensity) should be based on the client’s functional capacity as many individuals with CP exhibit reduced exercise efficiency. Clients with CP should begin at a lower level than the general adult-based recommendations of 60-80% 1RM for 8-to-12 repetitions. It has been suggested that an intensity level of 50-60% 1RM is suitable. Exercise program recommendations for clients with cerebral palsy are summarised in Table 4.

Table 4. Exercise Program Recommendations for Clients with Cerebral Palsy (Barfield et al., 2013; NCHPAD, 2016)

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The cerebrovascular disease commonly referred to as a stroke is the third most common death in Scotland with death rates set amongst the highest in Western Europe (NHS 2008).  In the UK,  approximately 100,000 strokes happen each year that account for about 1.2 million stroke survivors. Public Health England (2018) data indicated almost 32,000 deaths per year in England in 2016 due to a stroke. In Scotland, 5,000 individuals die as a direct result of a stroke.  Alarmingly the incidence of a stroke may further escalate due to the expansion of the elderly population and the rise of non-communicable diseases and the decline in physical activity patterns. 


A stroke is a serious vascular episode involving a loss of neurological functions linked to an acute disturbance of blood flow to the brain. The Royal College of Physicians (2016) has defined a stroke as a disease characterised by rapidly developing clinical signs of local and/or focal origin due to loss of cerebral function that lasts more than twenty-four hours or results in death. Some medical professionals often refer to it as a ‘brain attack’ to relate its symptoms and sequelae with a heart attack (myocardial infarction).

Stroke survivors commonly have physical residues that negatively impacts on their daily physical functioning. Each year almost 15,000 people in Scotland have residue that requires inpatient care. This inpatient care cost equates to approximately 5% of the National Health services annual budget and 7% of inpatient care (Dennis et al., 2002). Stroke is the primary cause of disability in the UK, with approximately two-thirds of survivors leaving the hospital with some form of residue (Jones, 2011).

Stroke Classification

A stroke is considered a heterogeneous condition that may involve the rupturing of a large blood vessel in the brain or the obstruction of a small blood vessel that may affect a specific area of the brain. This disturbance in blood flow leads to cell damage and compromised neurologic function due to restricted blood supply (ischemia) or bleeding (haemorrhage) in the brain tissue (Figure 1). As such, strokes are classified as hemorrhagic or ischemic. Haemorrhagic strokes are subclassified as intracerebral (bleeding directly into the brain) or subarachnoid (bleeding into the spaces and spinal fluid around the brain), depending on where the injury occurs. Depending on where the injury occurs in the brain, haemorrhagic can be subclassified as subarachnoid (bleeding into the spaces and spinal fluid around the brain) or intracerebral (bleeding directly into the brain). Ischemic strokes are separated into two types: thrombotic and embolic.  Haemorrhagic strokes account for approximately 15% of all strokes, whereas the ischemic variety contributes to the remainder (Collins, 2007). The remaining cases of stroke are transient ischemic attacks (TIAs), which are referred to as “mini-strokes” and are a result of temporary blood clots. Risk factors for stroke are identified in Table 1.

Table 1. Risk Factors For Stroke

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Pathology & Pathophysiology of Stroke

Disruption of blood flow impedes the essential delivery of oxygen and nutrients, including glucose, to the brain tissue. The brain uses glucose as the main energy source, and as glucose is not stored in the brain, the time of ischemic blockage is life-threatening. The consequences of a stroke are also associated with the site of the restriction of blood flow and to the amount of brain tissue affected. For example, stroke to the left side of the brain frequently results in paralysis of the right side of the body, limitations in speech, and memory loss (Kleinman et al., 2007) A right-side stroke commonly produces paralysis on the left side of the body, visual limitations, and memory loss (Novitzke, 2008). Paralysis (total or partial) of one side of the body as a consequence of a disease or injury to the central nervous system is referred to as hemiplegia.

Figure 1. Stroke Types

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Several controllable and uncontrollable aspects are associated with the increased risk of developing a stroke. These controllable risk factors include the individual’s lifestyle behaviours that can be modified to decrease risk. Factors that increase the risk of stroke include smoking, high blood pressure, arterial disease, diabetes, abnormal lipid profiles, sedentary lifestyles and obesity (Figure 1). Modifying or reversing any of these controllable risk factors may feasibly reduce the risk of developing a stroke. However, Khaw and Kessler (2006) reported that several risk factors are not controllable, including age, sex, heredity, race, and history of prior stroke. It is important to note that a stroke can occur in individuals with a broad range of these risk factors. However, it has been reported that the risk of stroke is further increased if an individual is older, male (Khaw and Kessler,2006), African American (Howard et al., 2007) or if the person or an immediate family member has a history of stroke (Knottnerus et al., 2011).

Ischemic strokes are caused by three primary mechanisms namely thrombosis, embolism, and global ischemia. Thrombosis refers to an obstruction of blood flow due to a localised occlusion within one or more blood vessels of the brain (Caplan, 2000). Thrombotic infarctions occur when fatty deposits and cholesterol accumulate on the inner lining of blood vessels producing an irritating effect that stimulates the development of clots. Embolic infarction is caused when a blood clot (known as an embolus) that is formed somewhere in the body other than the brain, such as the heart, migrates to the brain via the bloodstream (Walberer and Rueger, 2015). If the embolus, drifts to the brain via the bloodstream, it may restrict the flow of blood through an arterial structure, subsequently causing injury to the brain tissue supplied with blood, oxygen, and nutrients by that specific artery. Global ischemic stroke ensues if blood flow to the whole brain is disturbed by a systemic restriction such as a myocardial infarction. Damage to brain tissue is associated with the time the brain is deprived of oxygen and glucose. Global ischemic stroke can also be caused by low blood pressures produced by drug overdoses and adverse effects that restrict blood flow to the brain (Hoshide et al., 2008; Treadwell and Robinson, 2007).

Haemorrhagic strokes are caused by the rupture of a blood vessel due to damage to the vascular structure, such as cerebral aneurysms or chronic high blood pressure (Smith and Eskey, 2011). Aneurysms are areas of ballooning on a blood vessel due to the weakening of the vessel wall. Over a period, primarily with high blood pressure, the distended area may rupture, causing the blood to leak into the extravascular space within the cranium or the brain tissue. This bleeding damages the brain by cutting off connecting pathways and by causing localised or generalised pressure injury to brain tissue. 

Effects of Exercise in Individuals Who Have Had a Stroke

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The main causes of death following a stroke are coronary arterial disease (CAD) and recurrent strokes. Furthermore, 25-to-50% of individuals require assistance and support in the performance of daily living activities (Ostwald et al., 2008). This inability to accomplish essential daily living activities has been linked to physiological deconditioning, pre-existing cardiovascular disease or reduced gait efficiency and other upright actions (Qureshi et al., 2004). Jorgensen et al., (1995) reported that individuals with stroke hemiplegia exhibit an energy uptake that is two-to-three times greater during walking compared to the general population at the same speed. Several studies have shown that peak oxygen uptake value is nearly 50% of those displayed by healthy individuals of comparable age (Kelly et al., 2003; MacKay-Lyons and Makrides, 2002). Stoller and associates (2014) noted that these problems restrict individuals ability to engage in a more active lifestyle. Ultimately stroke can lead to further physical deconditioning, specifically the cardiovascular system.

Traditionally the rehabilitation procedure following stroke was restricted to the initial six-to-nine months following the acute episode established on the assumption that motor recovery would take place within this time. (Bonita and Beaglehole, 1988; Clafin et al., 2015). The main objectives of stroke rehabilitation include increasing daily activity levels, decreasing the occurrence of recurring strokes, and improving aerobic fitness. In the medical setting, aerobic fitness has been addressed with task-specific activities rather than general exercise conditioning.  Research by Wolf et al., (2006) has suggested that organised physical exercise conditioning programs after the nine months can provide continued development of aerobic fitness, muscular strength, and functional capacity.

Research has suggested that aerobic exercise training (i.e., cycle ergometry and treadmill training) may enhance peak oxygen uptake and workload while decreasing submaximal blood pressure. For example, Potempa et al., (1995) investigated how hemiparetic stroke patients responded to intense exercise and aerobic training. Forty-two subjects were randomly assigned to an exercise training group or a control group. Subjects performed the training protocols three times per week for 10-weeks. Results indicated that there were significant improvements in maximal oxygen consumption, workload, and exercise time. The authors also showed that improvement in sensorimotor function was significantly correlated to the improvement in aerobic capacity. After the training protocol, experimental subjects displayed significantly lower systolic blood pressure at submaximal workloads during the graded exercise test.

Additionally, Macko and associates (2005) study on treadmill training showed comparable increases in peak oxygen uptake values during gait, with reduced energy cost at submaximal effort walking suggesting improved gait efficiency.  The authors also reported a significant association between treadmill training velocity and peak values of VO2. It has been suggested that treadmill training may offer a form of exercise training that transfers directly to gait pace and aerobic endurance. An important positive feature to consider regarding the treadmill is it serves as a means of upright gait training for individuals unable to perform this action with full bodyweight loading. The use of handrails allows for weight distribution and loading via bodyweight harnesses that regulate the loading. This, therefore, adjusts the demand placed on the individual. The training intensity can also be increased with greater treadmill speed or increased elevation; the latter may be beneficial in increasing intensity with a comfortable pace of walking. 

Traditionally, limitations in gait efficiency and motor control of numerous daily tasks were attributed to the state of spasticity or hypertonia commonly found in individuals following stroke (Cussler et al., 2003). An essential goal of rehabilitation with individuals with stroke is the improvement of the regulation and quality of movement, control of spasticity.  However, Pak and Patten (2008) showed that spasticity may not be the main impairment post-stroke; rather, muscular weakness is the main limitation to function poststroke.  Pak and Patten performed an evidence-based review that sought to determine whether [in part] high-intensity resistance training offsets weakness without increasing spasticity in individuals poststroke. The results on spasticity found that four of the 11 studies formally measured spasticity via the Pendulum test (Olney and Lowe, 1979) or modified Ashworth scale (Bohannaon and Smith, 1987). Teixeira-Salmela et al., (1999) reported no increased spasticity as measured by the Pendulum test. Furthermore, Sharp and Brouwer, (1997) Moreland et al., (2003) and Flansbjer et al., (2008) reported no increased spasticity during or post strength training using the modified Ashworth scale.

Contemporary research has shown that resistance training of the lower limbs provides significant improvements in muscle strength, power and endurance in the affected and nonaffected limbs of individuals with post-stroke hemiplegia. For example, Lee et al., (2010) investigated the effects of high-intensity progressive resistance training (PRT) and high-intensity cycling (cycling) on muscle performance and the time course of strength gains in a chronic stroke population. Forty-eight subjects were randomly allocated to one of four groups and performed 30 exercise sessions over 10-to-12 weeks. Results showed that subjects that underwent PRT improved lower limb strength, peak power and endurance compared with sham PRT or cycling only (P = <0.05) and combined exercise (PRT and cycling) was not superior to PRT alone. 


Jorgensen and associates (2010) evaluated the impact of intensive physical training on gait performance and cardiovascular health parameters in persons with stroke. Fourteen subjects with hemiparesis after stroke (mean age= 58.4 years, meantime since injury =25 months) participated in a 12-week training intervention, 5 times per week for 1.5 hours per session.  The intervention consisted of high-intensity, body-weight–supported treadmill training; progressive resistance strength training; and aerobic exercise. Resistance training movements included semi-seated leg press, leg extension, leg curl, and seated leg press, with relative training intensity increasing weekly from 12RM to 4-to-8RM levels. The training was performed unilaterally for three to five sets per exercise with recovery periods of 90 seconds between sets. The main outcome measures were gait performance (Six-Minute Walk Test, 10-Metre Walk Test, and aerobic capacity) and parameters of cardiovascular health (systolic and diastolic blood pressures, body mass index, and resting heart rate). The findings of this study included significant improvements in all outcome measures. Gait speed during the Six-Minute Walk Test increased by 62%, and systolic and diastolic blood pressures decreased by 10% and 11%, respectively. Weekly testing of walking speed showed that most of the increase in the walking speed occurred in the first 8 weeks of training.


Exercise Guidelines for Stroke Clients

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Traditionally emphasis in stroke rehabilitation was during the first 6 months of recovery (Teasell et al., 2006). There have been limited available studies that have examined the most effective mode of improving fitness in stroke survivors after rehabilitation (Meek et al., 2003). The studies that have examined these effects have, however, supported the use of exercise in improving mobility and functional independence and in reducing or preventing further disease and functional impairment in individuals with stroke (Ivey et al., 2005; Ouellette et al., 2004; Patten et al., 2004; Macko et al., 2005). Gordon and associates (2004) reported that during the first six months of rehabilitation most people will see a significant period of recovery. However, other stroke survivors may not see significant improvements for up to a year or possibly longer. Individuals that return home following a stroke will require greater attention to ensure that cardiovascular adaptations are conducted in a safe environment with appropriate supervision.

Cardiorespiratory Endurance Training 

Stroke survivors should perform cardiorespiratory fitness training. Ivey and associates (2005) reported that cardiovascular-related morbidity and mortality is increased post-stroke combined with cardiovascular deconditioning. This deconditioning places added risk on the individual. Several studies have suggested that aerobic exercise training should be an essential part of the recovery process (Macko et al., 1997; Potempa et al., 1996; Macko et al., 2005). For example, Macko et al., (2001) investigate the effects of treadmill training on peak exercise capacity (VO2 peak) and the rate of oxygen consumption during submaximal effort treadmill walking before and after 3 and 6 months of training. Findings showed that subjects who completed 3 months of training increased their VO2peak and lowered their oxygen demands of submaximal effort ambulation, which enabled them to perform the same constant-load treadmill task using 20% less of their peak exercise capacity. Gains in VO2peak and economy of gait plateaued by 3 months, while peak ambulatory workload capacity progressively increased by 39% over 6 months.

Frequency and Duration 

The exercise program should be designed for each specific individuals level of physical health and functioning. Studies have suggested that the optimal duration should be between 30-60 minutes per session most days of the week. However, consideration must also be made regarding any significant barriers that the client may have in participating in physical activity with a lower volume of exercise also valuable given the client's high rate of deconditioning (Rimmer, 2005; Rimmer, Wang and Smith, 2008). If the client is at an increased risk because of cardiovascular comorbidity or falls, it is strongly suggested that the client should exercise under the supervision of a fully qualified staff member, preferably one that is trained in rehabilitation. 

As with other population groups, the cardiovascular exercise program should consist of a warm-up and cool-down. Clients should ideally have their blood pressure values measured at regular intervals before, during, and after the exercise session. Cardiovascular exercise can be continuous or accumulated over the day aiming to achieve between 20–60 minutes (Gordon et al., 2004).  Older or severely deconditioned clients should begin training with smaller doses of physical activity (i.e., 5-to-20 minutes per day). After the client has completed the screening process as described by the ACSM (2021), the first 2-to-4 weeks of training should be used to educate the clients in using the equipment safely and ensuring they are familiar with the exercise program. Individual goals should be established to ensure that the clients are training within their comfort zone while achieving the desired training stimulus.

Cardiorespiratory Training Intensity 


Where feasible the cardiovascular exercise intensity level should be established from the graded exercise test. The American Heart Association (2004) advisory statement on physical activity and exercise recommends that stroke survivors training intensity of 40-to-70% of peak VO2 or heart rate reserve while also monitoring rating of perceived exertion (RPE). There have been limited studies that have been performed on stroke survivors, however, the ones that have been conducted were set at different levels. For example, Rimmer and colleagues (2000) established the intensity level on the subjects peak VO2 values. The heart rate values that the subjects achieved at a respiratory quotient (RQ) of 1.00 was used to set the target heart rate range (THRR). Five beats per minute were subtracted from this value, and the THRR for the subjects was then set from this heart rate to 10 bpm below this heart rate. For example, if a subject’s heart rate was 120 bpm at an RQ = 1.00, subtracting 5 bpm from this value would put the THRR at 105–115 bpm.

In the study of stroke survivors by Potempa et al., (1995) the initial training was set at 40-to-60% of measured peak VO2 for a duration of 30 minutes of continuous or discontinuous exercise. The authors placed emphasis during the initial stages of the program was on duration as opposed to intensity. Once the subjects were able to exercise for 30 minutes, the training intensity was progressively increased to the highest workload tolerance without cardiac symptoms. It is important to be aware that the Potempa and associates used telemetry monitoring with their subjects and were thus able to be more assertive in the training intensity. Macko and associates (1997; 2001; 2005) have performed a substantial amount of research on stroke survivors and treadmill exercise. The investigators training protocols started with subjects performing treadmill training at 40-to-50% HRR for 10-to-20 minutes and increased by 5 minutes every two weeks as tolerated by the subject until they were able to train at 60-to-70% of HRR. In a study by Teixeira-Salmela et al., (1999) on high functioning stroke survivors, an intensity value of 70% of maximum heart rate obtained from an exercise test was used.


Chu et al., (2004) evaluated the effect of an 8-week, water-based exercise program compared with an upper-extremity function program. Twelve subjects with stroke with mild to moderate residual motor deficits participated in this study for 1 hour, 3 times a week. The water-based group exercised in chest-deep water at a specified heart rate value. The upper-extremity function control group performed arm and hand exercises while sitting. The training intensity increased from 50-to-70% HRR (weeks 1–2) to 75% (weeks 3–5), and finally to 80% HRR (weeks 6–8). The results showed that the water-based group significantly improved compared to the upper-extremity function group in cardiovascular fitness, maximal workload, gait speed, and paretic lower-extremity muscle strength. The 8-week program of water-based exercise resulted in a 22% improvement in cardiovascular fitness in subjects with stroke who had a high function. This was one of only a few limited studies that trained stroke survivors at an intensity level of 80%. Interestingly, the authors reported that subjects had a 22% increase in peak VO2 after the exercise intervention which was the highest increase in stroke survivor subjects. 

Rimmer et al., (2000), examined the effects of a 12-week exercise training program in a predominantly African American group of stroke survivors with multiple comorbidities. Subjects who had an abnormal blood pressure response during the exercise test (systolic >221 mm Hg, diastolic >111 mmHg) had modifications to their exercise prescription. Subjects were instructed not to exceed a rate pressure product (RPP) of 200. The RPP was computed by multiplying heart rate multiplied by systolic blood pressure, divided by 100. For instance, if a subject’s blood pressure response during an exercise session was 175 mmHg at a heart rate of 120 bpm, the RPP would be 175 x 120/100 or 210. Because the value is > 200, the subjects would not be allowed to exercise on that day or had to wait until RPP dropped <200. Resting diastolic blood pressure (DBP) should be less than 100 mmHg to begin exercising. If resting DBP is greater than 100 mm Hg, ROM exercises should be performed until the DBP drops below 100. Exercise should be terminated if blood pressure is elevated to 220/110 mmHg or higher and should only be resumed when blood pressure drops below this value. 

It is recommended that clients should begin with intermittent exercise during the initial 4 weeks of the program. At the end of the 4 weeks, most individuals should be able to complete 30 minutes of continuous or discontinuous exercise in their THRR. However, it is important that clients have approval from their doctor before participating in the training program and that the medical professionals are updated on their patient’s performance throughout.

Resistance Training


One of the major symptoms following a stroke is muscle weakness. Research by Sharp and Brouwer, (1997) have shown that torque produced by the ankle plantar flexors, knee extensors and hip flexors is associated with gait performance in stroke survivors. Individuals with reduced levels of muscular strength can have significant functional limitations, compromised stability, increased postural sway and a reduction in walking speed (Morris, Dodd and Morris, 2004). Therefore, the main goal of strength training is to increase functional independence that may include walking, falls prevention and performing basic activities of daily living and instrumental activities of daily living (Patten, Lexell and Brown, 2004).

Resistance Training Intensity

Limited published guidelines and recommendations currently exist for developing resistance training programs for individuals with stroke. Based on the current research, several studies have demonstrated significant improvements in strength using various levels of resistance. For example, Rimmer and associates (2000) initiated a strength training protocol for stroke survivors at 70% of each participant’s 10RM for one set of 15-to-20 repetitions. When subjects achieved 25 repetitions for two consecutive sessions with correct form and lifting technique (i.e., correct biomechanical motion, without Valsalva manoeuvre), the loading was increased by 10% of their 10-RM. Subjects trained using a variety of exercises, including the bench press, leg press, leg curl, triceps pushdown, seated shoulder press, seated row, lateral pull-down, and biceps curl. Results showed that compared with controls, the exercise group showed significant gains in strength (P < 0.01) but no significant difference between exercise and controls on grip strength.

Badics and colleagues (2002) examined the effects of targeted strength training in patients with muscle weakness following a stroke. This was a non-randomised study of 56 patients that undertook a full residential neurologic rehabilitation program for four weeks. This included an exercise program for restoring the extensor strength of the legs and the supporting strength of the arms by leg and arm presses. Results showed that the subjects leg extensor strength increased significantly. The extent of strength gain was positively associated with the intensity and the number of exercising units.

Kim et al., (2020) examined the existing guidelines for individuals with stroke and attempted to harmonise the existing exercise prescriptions. The investigators reported that resistance training frequency should be between 2-to-3 days per week with progression made over time. Additionally, it was suggested that at the initial stages of training resistance training should engage the major muscle groups and include 8-to-10 exercises with 1-to-3 sets between 10-15RM per exercise performed at 30-50% of 1RM. As the individual progresses the intensity may be adjusted within 50-to-80% 1RM. It was suggested that a recovery or rest day should be incorporated between training sessions. These recommendations are supported [in part] by the meta-analysis of Pogrebnoy and Dennett (2020) who reviewed the American Stroke Association physical activity guidelines for individuals post-stroke. The authors reported that a combined exercise program comprising aerobic and resistance training that adheres to the American Stroke Association guidelines is safe and should be prescribed in addition to usual care to improve mobility.

Based on a systematic review by Morris and associates (2004) there is limited evidence that demonstrates that progressive resistance training reduces musculoskeletal impairment after stroke. Eight studies met the author's inclusion criteria however, only three were randomised controlled trials with the remainder being single-case time-series analyses or pre-post trials. The five studies that measured impairments of muscle strength showed positive outcomes for progressive resistance strength training, with large effect sizes (ES = 1.2-to-4.5). Only a few negative effects of strength training were reported, and these were minor. Three of the eight trials that measured activity limitations reported improvements in activities such as walking and stair climbing. 

A general strength training prescription should use a minimum of one set of 8-to-10 lifts using the large muscle groups of the body, lighter weights, and higher repetitions (e.g., 10-to-15 repetitions), and perform them 2-3 days per week. Blood pressure and RPE should be documented after each set until the individual adjusts to the training program. Adaptive gloves and other types of assistive aids may be necessary to ensure that the participant can safely hold or grasp the weight.


Resistance Training Volume


A significant factor to consider for the exercise professional is the resistance training volume in relation to the quantity of functional muscle mass available. For example, individuals with hemiplegia, paralysis, impaired motor control, or limited joint mobility have less functional muscle mass and as a result, will tolerate lower training volume. There may be clients that are unable to move the minimal load on certain resistance machines. Therefore resistance bands or cuff weights should be considered. For instance, it may be necessary for clients to perform an arm or leg lifting exercise against gravity for 15-20 seconds due to the clients low starting strength values.  The volume of loading and training is also client-specific and depends on their health status. Importantly, many individuals post-stroke have spent a large period of time being inactive and may only need a small dose of resistance exercise to obtain a training effect. How the client responds to the prescribed training stimulus is conditional to their current health status and the severity of their stroke. Individuals with low levels of strength may make significant improvements with very light resistance loading. 

Flexibility Training


Clients should be taught to perform a variety of stretching exercises that target both the upper and lower body extremities. Gordon et al., (2004) stated that the main goal of flexibility training for stroke survivors is to increase range of motion and prevent joint contractures. Clients should stretch at the start of each exercise session, and the end of the cardiovascular exercise session, between strength exercises, and after the exercise session. Stretches should be held with mild tension for 15-to- 30 seconds with greater emphasis being placed on stretching the tight (spastic) muscle groups on the hemiparetic side, which includes the finger and wrist flexors, elbow flexors, shoulder adductors, hip flexors, knee flexors, and ankle plantar flexors. 

Key Points


The contemporary literature supports the use of aerobic training in individuals following stroke using exercise modalities that engage the legs, arms, or combined arm and leg activities (Table 2). The suggested aerobic training intensity for this population group is 40-to <60% of VO peak or heart rate reserve. The frequency of training is suggested to be between three to seven days per week with the training duration ranging from 20-to-60 minutes per session.  Short but multiple bouts (intermittent) of treadmill training per session has been suggested as being beneficial for clients that are deconditioned. 

Evidence-based recommendations also suggest that resistance training following a stroke in individuals with hemiparesis should be comparable to programming for individuals who are elderly. Guidelines for resistance training post-stroke include 8-to-10 exercises performed three times per week. Training intensity should begin with 50-to-60% 1RM and progress to 60-to-85% 1RM.  It is recommended to focus on unilateral movements to place suitable stresses on the paretic limb. Most individuals who have sustained a stroke may also present with other comorbidities and are possibly taking medications for those conditions. For instance, many post-stroke clients may also have CAD and hypertension. It is important that the exercise professional designs an individualised exercise program. Consideration should be given for potential compounded effects of multiple comorbidities and also the interaction of prescribed medications. 

There may also be limitations in communication and mental processing for individuals that have sustained a stroke. This includes problems with written communication and also understanding verbal cues. The fitness professional should provide multiple methods of communication to the client including verbal cues and visual examples of each exercise.  

Table 2.  Program Design Recommendations for Post-Stroke (Patten, Lexell and Brown, 2004; Kim et al., 2020; Pak and Patten, 2008).

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