Age

A decline in Vo₂max of approximately 1% per year (0.4 to 0.5 mL/kg/min/year) occurs from 25 to 75 years of age.⁶¹ In accordance with the Fick equation, a reduction in Vo₂max is caused by reductions in both O₂ transporting (i.e., Qmax) and O₂ utilization capacity (i.e., a-vO₂diffmax) associated with cardiac, respiratory, and muscular changes. Decreased Qmax is the result of increasing myocardial stiffness and decreased left ventricular contractility, manifested by reductions in both ejection fraction and HRmax—hallmarks of cardiovascular aging.⁶² In fact, the reduction in HRmax, which decreases 6 to 10 beats per minute (bpm) per decade, is responsible for much of the age-associated decline in Qmax.⁶³ Evidence also suggests that older adults have a smaller SVmax⁶³ and that BP and systemic vascular resistance are higher during maximal exercise in older versus young adults.⁶⁴

With advancing age, reduced elastic recoil of the lung and calcification and stiffening of the cartilaginous articulations of the ribs restrict compliance of the lungs, thus limiting increases in minute ventilation during exercise.⁶⁵ Age-related decline in oxidative capacity of the working muscles and hence decreased a-vO₂diff during peak exercise⁶⁶ have been attributed to alterations in mitochondrial structure and distribution, oxidative enzyme activity,⁶⁷ and skeletal muscle microcirculation, as well as sarcopenia resulting from a reduced number and size of fibers, particularly type II fibers.⁶⁸ Nevertheless, despite loss of aerobic capacity with aging, people without chronic health conditions retain adequate reserves for daily activities. However, for aging individuals with a neurological impairment, the decrease in aerobic capacity with age can further reduce their reserves and thus threaten living an independent lifestyle. In fact, in a population-based study, age was found to be a significant independent predictor of recurrent stroke.⁶⁹ Particularly disadvantaged are people with cerebral palsy (CP) or other developmental disabilities as a result of an incomplete development of their musculoskeletal and cardiorespiratory systems at the time of the neurological event, which accelerates the aging process.⁷⁰ In the case of people with Down syndrome, however, Baynard and colleagues⁷¹ found that age-related changes in exercise capacity did not follow the typical pattern of decline after the age of 16 years. People with spinal cord injury (SCI) are at an increased risk for cardiac and respiratory complications with age.⁷²

Sex

The absolute and relative Vo₂max of women is about 77% of that of men, after adjustment for body weight and activity level.⁷³ For nondisabled older adults, Kohrt and colleagues⁷⁴ reported no significant gender difference in the percentage of improvement in Vo₂max; women had an increase in Vo₂max of 26% ± 12% (range 4% to 58%), and men demonstrated a 23% ± 12% (range 0% to 51%) increase. Although older men and women generally exhibit similar responses to maximal exercise, older women tend to have lower SBP during maximal exercise.⁶⁴

Race

Little attention has been paid to the differences in exercise capacity among racial groups; however, in one study no differences were found between 66 black and 52 white stroke survivors in the level of physical deconditioning poststroke.⁷⁵

Lifestyle factors

Smoking is one factor that has been shown to impair exercise capacity in the general population.⁷⁶ Smoking causes increases in HR, myocardial contractility, and myocardial oxygen demand, which can lead to atherosclerosis and acute cardiovascular events.⁷⁷ In the stroke population, smoking doubles the risk of death (equivalent of a 7-year reduction in life span) when compared with the risk in nonsmokers and ex-smokers.⁷⁸

Currently the relationship between cardiovascular disease and diet is receiving international attention.⁷⁹ Indeed, obesity increases the risk of cardiovascular risk factors such as impaired glucose tolerance and type 2 diabetes, hypertension, and dyslipidemia.⁸⁰ Specifically, abdominal obesity not only increases the risk of atherosclerotic disease but also the risk of primary ischemic stroke.^81,82 In addition, when compared with corresponding normal-weight populations, overweight youth with SCI and spina bifida have lower cardiovascular fitness.⁸³ Yet the lifestyle factor that has received the most attention in the literature is habitual activity. There is now irrefutable evidence of the link between physical activity and cardiopulmonary health and fitness.^76,84–86 In fact, in the stroke population, prestroke physical activity has been found to decrease stroke severity as well as to result in better long-term rehabilitation outcomes.⁸⁷ Cardiovascular alterations resulting from physical inactivity (i.e., reduced Vo₂max and Qmax) parallel, in many ways, the changes that occur with aging; in fact, sedentary lifestyles explain a significant proportion of these age-related declines. If physical activity levels and body composition remain constant over time, the expected rate of loss in aerobic power associated with senescence is reduced by almost 50%.⁶⁸ Nonetheless, people with chronic health conditions often rate poorly in terms of daily physical activity, in part because of underlying physical impairments (e.g., paralysis, pain). For example, people with SCI spend as little as 2% of their walking time participating in leisure physical activity,⁸⁸ making them the most sedentary members of society.⁸⁹ Some people with multiple sclerosis (MS) avoid physical activity to prevent elevated body temperature and minimize symptoms of fatigue.⁹⁰ Inactivity can lead to increased cardiovascular risk factors such as hypertension and dyslipidemia as seen in youth with chronic disabilities (including CP and SCI).⁹¹ Bernhardt and colleagues⁹² found that after a stroke, patients spend more than 50% of their time resting in bed. Short periods of bed rest cause rapid decreases in aerobic capacity—a 15% reduction in healthy, middle-aged men after 10 days of recumbency⁹³ and a 28% reduction in healthy young subjects after 3 weeks.⁹⁴ Inactivity-induced reductions in Vo₂peak have been attributed to both central changes (decreased SV from impaired myocardial function and increased venous pooling) and peripheral changes characteristic of aerobically inefficient muscle fibers (decreases in oxidative enzyme concentrations, mitochondria, and capillary density).²²

Environmental factors

Significant associations have been found between physical activity and physical environmental factors such as accessibility, esthetic attributes, and opportunities for activity within the general public.⁹⁵ However, the influence of such factors on cardiovascular and pulmonary fitness of people with neurological disabilities has received little attention in the literature.

Neuromuscular system

For most individuals with neurological conditions, the existence of neuromuscular impairments confounds interpretation of Vo₂peak testing. When people with an intact nervous system are tested, normal biomechanical efficiency is assumed; an impaired nervous system increases the complexity of physiological responses. Both primary effects of upper motor neuron damage (e.g., paralysis, incoordination, spasticity, sensory-perceptual disorders, balance disturbances) and secondary “peripheral” changes in skeletal muscle (e.g., gross muscular atrophy⁹⁶ and changes in muscle fiber composition⁹⁷) affect the response to exercise. As a result, people with neurological disabilities manifest not only metabolic but also biomechanical defficiencies, both of which contribute to reduction in functional capacity. Consequently, the decline in exercise capacity is greater than expected (e.g., in people with postpoliomyelitis syndrome, deterioration in Vo₂peak over a 3- to 5-year period was 12% greater than the predicted decline⁹⁸).

Paresis reduces the pool of motor units available for recruitment during physical work,⁹⁹ thereby reducing the metabolically active tissue and lowering the oxidative potential.¹⁰⁰ In the case of stroke, an estimated 50% of the normal number of motor units are functioning,¹⁰¹ and a strong relationship between bilateral thigh muscle mass and Vo₂peak has been reported.¹⁰² In addition, along with altered joint kinematics and decreased postural reactions,¹⁰³ children with CP exhibit high levels of co-contraction (simultaneous contraction of agonist and antagonist muscle groups), which may prematurely induce skeletal muscle fatigue, further increasing the energy expenditure of walking and decreasing Vo₂peak.^104,105 Thus, when compared with able-bodied individuals, children with CP experience greater levels of fatigue at slower walking speeds.^104,105 For people with postpoliomyelitis syndrome, muscle weakness of the lower extremities is strongly associated with energy expenditure of walking.⁴⁹ In fact, when compared with healthy age- and sex-matched subjects, energy cost of walking is found to be significantly higher (40%) for people with postpoliomyelitis syndrome.⁴⁹

Altered fiber composition and recruitment patterns of paretic muscle may also contribute to poor fitness.^97,106 Skeletal muscles are composed of fibers that express different myosin heavy chain (MHC) isoforms. Slow (type I) MHC isoform fibers have higher oxidative function, are more fatigue resistant, and are more sensitive to insulin-mediated glucose uptake; fast (type II) MHC fibers are recruited for more powerful movements, are more reliant on anaerobic or glycolytic means of energy production, fatigue rapidly, and are less sensitive to the action of insulin.¹⁰⁷ Although relatively equal proportions of slow and fast MHC isoforms are found in the vastus lateralis of healthy individuals,¹⁰⁰ elevated proportions of the fast, more fatigable fibers that are less glucose sensitive have been found in the paretic leg of people after a stroke.⁹⁷ Hence it is likely that reduced insulin sensitivity and increased use of the anaerobic processes during dynamic exercise at the level of the muscle contribute to reductions in Vo₂peak. Furthermore, alterations in the structure of mitochondria¹⁰⁰ and reduced activity of oxidative enzymes (e.g., succinate dehydrogenase)¹⁰⁸ may contribute to the reduced oxidative capacity of paretic muscles.

Cardiovascular system

Cardiovascular comorbidities, prevalent in populations with neurological disorders, contribute to metabolic inefficiency. In fact, cardiovascular complications are the leading cause of death in persons with stroke,¹⁰⁹ MS,¹¹⁰ and SCI.¹¹¹ About 75% of patients who have had a stroke are hypertensive,¹¹² and the same proportion of patients have underlying cardiovascular dysfunction.¹¹³ In fact, most persons who have had a stroke have atherosclerotic lesions throughout their vascular system,¹¹⁴ and a high correlation has been reported between the number and degree of stenotic lesions in the coronary and carotid arteries.^115,116 The high prevalence of CAD in this population should not be surprising because stroke and cardiac disease share similar predisposing factors (e.g., older age, hypertension, diabetes mellitus, cigarette smoking, sedentary lifestyle, and hyperlipidemia) and pathogenic mechanisms (e.g., atherosclerosis).¹¹⁷ Metabolic syndrome is a usual construct in identifying patients at high risk for future vascular events (e.g., a second stroke, myocardial infarction).¹¹⁸ Metabolic syndrome refers to a constellation of markers of metabolic abnormalities (i.e., hypertension, abdominal obsesity, abnormal lipid profile) that interact to accelerate the progression of atherosclerosis and increase the risk of development of cardiovascular or cerebrovascular disease.¹¹⁹ The prevalence of metabolic syndrome in neurological populations is high. A retrospective study reported that about 61% of 200 patients in stroke rehabilitation met the criteria for the syndrome.¹²⁰

Factors that elevate HR for a given Vo₂, such as CAD, result in attainment of a peak HR (HRpeak) at a Vo₂peak below that predicted for that individual. Cardiac dysfunction contributes to a lower aerobic capacity through two principal mechanisms: ischemia-induced reductions in ejection fraction and SV with exercise¹²¹ and chronotropic incompetence—the inability to increase HR in proportion to the metabolic demands of exercise.²¹ For persons who can attain HRmax within 15 bpm of the predicted maximum, limitations in exercise capacity probably do not have cardiovascular causes.

Impaired peripheral blood flow also contributes to reduced cardiovascular fitness. Inadequate blood flow to the periphery impairs O₂ transport and limits energy production in the working muscles, thereby compromising the ability to sustain physical activity. Both resting blood flow and postischemic reactive hyperemic blood flow have been found to be lower (approximately 36% less) in the paretic leg of people poststroke.^122,123 In addition, despite near-normal (above 0.90) mean ankle brachial index values, arterial diameter has been found to be reduced poststroke.¹²² Potential mechanisms responsible for reduced blood flow on the hemiparetic side include altered autonomic function,¹²⁴ enhanced sensitivity to endogenous vasoconstrictor agents,¹²⁵ and altered histochemical and morphological features of the vascular network itself.¹²⁶ However, the relative contribution of each of these factors is unknown. In addition, local metabolic mediators associated with changes in muscle fiber composition in the paretic limb (previously discussed) may contribute to impaired limb blood flow.¹⁰⁰

Trauma to the spinal cord may disrupt the autonomic reflexes and sympathetic vasomotor outflow required for normal cardiovascular responses to exercise.¹²⁷ As a result, reduced venous return and cardiac output (referred to as circulatory hypokinesis) impair delivery of O₂ and nutrients to and removal of metabolites from working muscles, intensifying muscle fatigue.¹²⁸ For people with paraplegia, an exaggerated HR response may occur during exercise in order to compensate for reduced SV. However, adrenergic dysfunction associated with lesions above the T1 sympathetic outflow prevent this compensatory mechanism,¹²⁹ thereby increasing the risk of cardiovascular disease.

Pulmonary system

Typically in able-bodied individuals the pulmonary system does not limit cardiopulmonary fitness, because the lungs of people without chronic health conditions have a large reserve.¹³⁰ Nevertheless, at maximal workloads as much as 10% of Vo₂max is needed to support the mechanical work of the diaphragm, accessory inspiratory muscles, and abdominal muscles.¹²¹ In contrast, people with neurological impairments may have limited O₂ availability for exercise as a result of pathological conditions involving the pulmonary system, either as a direct complication of a neuromuscular condition (e.g., muscle weakness, impaired breathing mechanics) or as a result of cardiovascular dysfunction, comorbidities (e.g., chronic obstructive pulmonary disease), or lifestyle factors (e.g., physical inactivity, smoking habits).^131,132 These impairments can reduce the ventilatory reserve, defined as the difference between the maximal available ventilation and the ventilation measured at the end of exercise.¹³³

As previously mentioned, minute ventilation is closely associated with Vco₂ during exercise. At peak exercise, a ratio of minute ventilation to Vco₂ above between 35¹³⁴ and 40¹³⁵ indicates an abnormal ventilatory response. Neu and colleagues¹³⁶ reported an 87% incidence of obstructive pulmonary dysfunction in patients with Parkinson disease, despite the finding that Vo₂peak levels in this patient group tend to be in the normal range.^137,138 For children with CP, reduced exercise capacity may be partly caused by respiratory muscle spasticity resulting in reduced breathing efficiency.¹⁰⁵ In the case of stroke, pulmonary function is usually affected to only a modest extent, notwithstanding acute respiratory complications (e.g., pulmonary embolism, aspiration pneumonia).¹³¹ Impaired respiration may be attributed to cardiovascular dysfunction or lifestyle factors (e.g., physical inactivity, high incidence of smoking)¹³⁹ or a direct result of the stroke, particularly brain stem stroke. The overwhelming fatigue felt by some persons after a stroke may be partly caused by respiratory insufficiency as manifested by low pulmonary diffusing capacity, decreased lung volumes, and ventilation-perfusion mismatching.¹⁴⁰ Impaired breathing mechanics with restricted and paradoxical chest wall excursion and depressed diaphragmatic excursion have been also reported.^131,141 Expiratory dysfunction appears to be related to the extent of motor impairment (e.g., hemiabdominal muscle weakness), whereas inspiratory limitations appear to be related to the gradual development of rib cage contracture.¹⁴²

To summarize, a host of interacting factors are associated with abnormally low cardiopulmonary fitness in people with neurological disorders. Neuromuscular and respiratory dysfunctions are often superimposed on an already-compromised state as a result of comorbid cardiovascular disease and premorbid health- and lifestyle-related declines. Paresis and the subsequent reduction in lean muscle mass, changes in the muscle fiber phenotype, and increased reliance on anaerobic processes for energy production result in high metabolic costs of moving paretic limbs. As a consequence, cardiac reserves available for meaningful activity-level functions are limited, which in turn has a negative impact on participation-level functions. Collectively, impairments in the neuromuscular, cardiovascular, and pulmonary systems converge to promote a sedentary lifestyle and reduced health-related quality of life, which in turn leads to further inactivity and further reductions in cardiopulmonary fitness. The contribution of skeletal system impairments to this downward spiral has received little attention. Pang and colleagues¹⁴³ studied the relationship between bone health and physical fitness in patients who had had a stroke and found a significant correlation between paretic femur bone mineral density and Vo₂max. They concluded that further study is needed to determine the clinical implications of this finding.

Cardiopulmonary function

Decreases in HR at a fixed submaximal workload after training have been attributed to increases in total blood volume¹⁸³ and vagal activity and to concomitant reductions in sympathetic-adrenergic drive and resting heart rate (HRrest).¹⁸⁴ However, according to Wilmore and colleagues¹⁸³ the decrease in HRrest is of minimal physiological significance. Potempa and colleagues¹⁸⁵ reported reduction in SBP at submaximal workloads after a 10-week training program for people after stroke. Related to this finding, training can also reduce the rate-pressure product (product of HR and SBP) at submaximal loads,⁶³ which reflects improvement in cardiac efficiency.¹⁸⁶ After a 4-week single-limb exercise training program with the hemiparetic limb, Billinger and colleagues¹²² reported significant improvements in femoral artery blood flow and diameter compared with the nonhemiparetic limb poststroke. The authors reasoned that in order to maintain homeostasis, the diameter increased to adjust for the coupling of increases in metabolic demand and improved blood flow.

In patients with CAD, training has resulted in decreased ST segment depression (a marker of myocardial ischemia) during submaximal exercise performed at the same baseline rate pressure product,¹⁶⁸ thus raising the anginal threshold and extending the time that submaximal tasks can be performed without triggering myocardial ischemia. Cardiovascular and muscle adaptations also lower minute ventilation at a given submaximal workload, intimating improved ventilatory efficiency.¹⁸⁷ After training, Vo₂ at a given submaximal workload is either unchanged¹⁹ or modestly reduced¹⁸⁸ because the increased a-vO₂diff in trained muscles is offset by reduced blood flow to the working muscles and a less pronounced decrease in blood flow to the nonexercising muscles resulting from depressed sympathetic reflex activity.¹⁷¹ As a result of improved pulmonary function resulting from targeted expiratory¹⁸⁹ and inspiratory¹⁹⁰ muscle training in people with MS, it may be possible for members of this population to increase exercise tolerance.

Cardiovascular risk factor reduction

Although limited physical activity is an independent predictor of risk of stroke,191–193 the capacity of exercise to confer similar protective benefits against stroke recurrence is unknown. It is clear that endurance exercise training lowers resting BP in both young and older hypertensive adults.¹⁹⁴ Training is also associated with lower fasting and glucose-stimulated plasma insulin levels and with improved glucose tolerance (if initially impaired), insulin sensitivity,¹⁹⁵ and glycemic control in patients with type 2 diabetes.¹⁹⁶ A 6-month treadmill exercise training program reduced insulin resistance in stroke survivors.¹⁹⁷ Evidence suggests that populations with neurological disorders achieve similar training-induced improvements in lipid profile as previously documented for participants in cardiac rehabilitation.¹⁹⁸ Patients with MS showed reductions in triglyceride and very-low–density lipoprotein levels after a 15-week training program.¹⁹⁹ Similarly, an 8-week training program for individuals early after SCI led to improved lipid profiles, with more pronounced changes in response to high-intensity training.²⁰⁰ However, these changes may be a result of training-induced reductions in body fat stores.²⁰¹ The potential for training to reduce intraabdominal fat is particularly significant because it is the body fat depot that increases the most with age and is associated with other cardiovascular disease risk factors.²⁰² Because of the positive effects on glucose homeostasis, lipid lipoprotein profiles, and cardiovascular fitness, exercise training has been found to be effective in reducing the risk of cardiovascular disease and comorbidities (e.g., type 2 diabetes, hypertension, obesity) in people with SCI.¹⁵¹ Stroke survivors participating in a 10-week cardiac rehabilitation program obtained greater improvements in cardiac risk score when compared with stroke patients in usual care.²⁰³

Impairments in body structure and function

The benefits of training to impairments in body structure and function of people with neurological disabilities, other than improved endurance and exercise tolerance, have not been well documented. In patients who have had a stroke, training studies have noted enhanced balance²⁰⁴ and paretic lower-extremity muscle strength.¹⁶⁴ A 15-week aerobic training program for patients with MS resulted not only in improvement in exercise capacity but also in upper- and lower-extremity strength.¹⁹⁹ Children with CP have shown improved gross motor function after participating in an 8-month circuit-training program.²⁰⁵

An exercise training program designed to improve ambulatory efficiency of patients with traumatic brain injury failed to reduce energy costs of walking despite a 15% improvement in Vo₂peak.²⁰⁶ In contrast, two studies reported mean reductions in energy costs of walking of 30%⁵³ and 23% after stroke rehabilitation,⁵⁴ and a pilot study reported a 32% reduction in the energy cost of walking in individuals with incomplete spinal cord lesions after a 12-week program of body-weight–supported treadmill training (BWSTT).¹⁹³ Macko and colleagues⁴⁰ interpreted gains observed in ambulatory workload capacity as a reflection of both improved exercise capacity and greater gross motor efficiency. The investigators postulated that central neural motor plasticity, mediated by the repetitive, stereotypic training, underlay these adaptations. In addition, Luft and colleagues²⁰⁷ suggest that training-induced gains in walking ability^208,209 may be caused by neuroplastic mechanisms involving cerebellum-midbrain circuits.²⁰⁷

In recent years the possible role that dynamic exercise may play in enhancing cognitive function has come under investigation. In fact, in older adult populations without known cognitive impairment and in cardiac populations, there is evidence supporting the benefit of exercise training on improving cognition.210–212 Neeper and colleagues²¹³ observed up-regulation of brain-derived neurotrophic factor (BDNF) in the cerebral cortex of rats housed in an environment with free access to a running wheel. Since then, several researchers have demonstrated increased BDNF production and synaptic plasticity in the brains^214,215 and spinal cords²¹⁶ of rodent models engaged in voluntary running. Tong and colleagues²¹⁷ reported that these responses appear to be dose dependent. Van Praag and colleagues²¹⁸ contributed to this line of inquiry by providing in vitro evidence of neurogenesis in the dentate gyrus of adult mice in response to an enriched environment that included voluntary wheel running. Gordon and co-workers²¹⁹ drew on the findings from these animal studies by suggesting that the improved cognitive function observed in individuals with traumatic brain injury who exercised regularly may be attributable to exercise-induced increases in BDNF or other growth factors. In another animal study, positive effects of aerobic training on neural functioning through the modulation of synaptic plasticity underlying neuroprotective and neuroadaptive processes were found.²²⁰ In terms of fatigue, after an 8-week hospital-based training program, patients with postpoliomyelitis were found to have reduced levels of fatigue. However, limited evidence exists regarding the effect of exercise on fatigue in patients with Guillain-Barré syndrome²²¹ and MS.²²²

Emotional well-being

Increased exercise capacity has been shown to improve mental well-being (reductions in anxiety and depression) in cardiac patients.^223,224 There is moderate evidence regarding the effect of exercise training on improving mood in patients with MS.²²² Very limited evidence exists to support the relationship between aerobic exercise and emotional well-being poststroke. Yet 18% to 68% of stroke survivors are depressed,¹⁹¹ making this population at an increased risk for depression.²²⁵ High levels of physical disability, cognitive impairment, and severity of stroke have been found to be predictors of poststroke depression.²²⁶ Stuart and colleagues²²⁷ reported that stroke survivors participating in an exercise group improved their average score on the Hamilton Rating Scale for Depression, which for the control group remained constant. In addition, Lennon and colleagues²⁰³ found that greater improvements in depressive symptoms were found in poststroke patients who participated in a 10-week cardiac rehabilitation program than in the usual care group.

Activity, participation, and quality of life

Few investigators have studied training-induced changes in activity, participation, and quality of life for people with neurological disabilities. Evidence has been found regarding the positive impact of exercise training on quality of life for people with MS,^199,228,229 CP,^205,230 and postpoliomyelitis.²³¹ Turner and colleagues²²⁸ reported better physical and mental health, as well as social functioning, in veterans with MS who exercised. However, only 26% of the 2996 veterans surveyed reported engaging in physical activity.²²⁸ Dieruf and colleagues²³⁰ found that after a 2-week intensive BWSTT program, children with CP reported improvements on a health-related quality-of-life measure. This finding may indicate that with a physically and psychologically challenging intervention program, along with encouragement from their parents and practitioners, children with CP may gain a better perception of their level of control and health and ultimately improve their quality of life.²³⁰ In stroke survivors gains in walking capacity have been reported in terms of both gait speed^164,204 and walking tolerance.²⁰⁴ However, there is insufficient evidence to support whether cardiovascular exercise improves quality of life after stroke.^225,232 Small improvements in Vo₂peak can have a substantial impact on the ability to perform daily activities, particularly in individuals with limited cardiac or ventilatory reserves, but there is a lack of documentation of these benefits in people with neurological disorders.

Initiation of training

Most of the training studies on populations with neurological disorders have involved patients with chronic neurological impairments; however, the optimal time to introduce training is unknown. Macko and colleagues²⁴⁵ expressed caution about training in the early poststroke period, speculating that abnormal cardiovascular responses to exercise (e.g., hypotension, arrhythmia) may impede perfusion of ischemic brain tissue during the period when cerebral autoregulation is most often impaired. Nevertheless, in one study, training was initiated 8 to 21 days after stroke without complications.⁵⁰ In addition, an exercise rehabilitation trial, also involving patients in the hyperacute stage poststroke, began early mobilization within 24 hours of stroke onset.²⁴⁶ The intervention group receiving early mobilization training reported fewer nonserious adverse events, and there were no differences in the total number of serious adverse events and fall rate when compared with the group receiving usual care.²⁴⁶ Furthermore, because there is increased plasticity (e.g., axonal sprouting and neurogenesis) of the periinfarct cortex during the first month after an ischemic stroke, early training may accelerate functional recovery.²⁴⁷

Training environment

High-risk individuals, such as patients in the early stages of neurological recovery or with cardiac comorbidities, should be trained in a setting with quick access to emergency medical equipment and trained personnel. An adverse event protocol should be posted and rehearsed. Lower-risk individuals, after appropriate screening to ensure an appropriate response to exercise, can be trained in supervised community²⁴⁸ or home-based²⁰⁴ aerobic exercise programs. One study involving postpolio patients reported reductions in fatigue and improvements in quality of life but found no changes in exercise capacity when patients were trained in either a hospital or home setting.²³¹ However, Hassett and colleagues²⁴⁹ reported similar gains in cardiovascular endurance in poststroke patients training in either an unsupervised home-based or a supervised facility-based exercise program. Regardless of the setting, certain safeguards are required. Because thermal dysregulation is common in patients with neurological disability, particularly MS²⁵⁰ and spinal cord injuries,²⁵¹ the ambient temperature should be carefully controlled and fans, spray bottles, towels, and a water cooler are recommended. Hydration before and during exercise and rehydration after exercise should be monitored by use of a water bottle with volumetric indicators. The exercise area should be wheelchair accessible, free of obstacles and blunt objects, and sufficiently large to permit safe transfer to and from exercise equipment.

Preparation of participants

Participants should be advised to avoid eating 2 hours before training and to empty bowel and bladder before training, when possible, especially for patients with SCI above T6 at risk of autonomic dysreflexia. Comfortable clothing and supportive footwear, appropriate for dynamic exercise, prepare the participant both physically and psychologically for training.

Scheduling of sessions

Many patients with neurological involvement report a decline in energy levels in the afternoon. If fatigability is a concern, training should be scheduled for morning hours, when circadian body temperature is at its lowest. For certain patient groups, including people with Parkinson disease, training should be coordinated with the timing of medication to optimize performance.

Duration of program

A meaningful increase in aerobic capacity (i.e., greater than 10% improvement) of individuals without neurological impairment is unlikely to occur in less than 4 weeks.²⁵² The minimal exposure required for people with neurological disabilities has not been fully investigated. However, da Cunha and colleagues⁵⁰ reported a mean improvement of 35% in Vo₂peak after 2 to 3 weeks of treadmill ergometry in six people who had had a stroke less than 1 month previously. Regardless of the minimum, participation in training must be sustained indefinitely to prevent return to the deconditioned state measured at the beginning of the program. Therefore a maintenance program should be followed after termination of formal training sessions.

Frequency and duration of sessions

To optimize aerobic training, three to five sessions per week are required, although fitness can improve with twice-weekly sessions.²⁷ Although a minimum of 20 minutes of exercise within the target zone for training per session is required to elicit a training effect,²⁷ we documented that patients engaged in 1-hour sessions of stroke rehabilitation spent, on average, less than 3 minutes per session within the training zone.⁴ For those with low fitness levels or who are very deconditioned (which would include the majority of patients with neurological involvement) training may be initiated with 5-minute exercise “bouts” with rest periods between bouts. Two additional 5-minute periods are required for warmup and cool down; hence the minimal time required to complete a training session is 30 minutes. Incrementally increasing the duration to a target of 40 to 60 minutes of aerobic training is recommended. However, the greater the intensity of exercise, the shorter the duration needed to achieve improvement in cardiopulmonary fitness; conversely, low-intensity exercise can be compensated for by longer duration.²⁵³ As well, accumulation of 10- to 15-minute periods of activity throughout the day can yield similar physiological improvements, provided that the total volume of training is comparable.²⁵⁴

Mode of training

To induce central adaptations, training must incorporate large muscle mass activities that require elevated levels of Vo₂. Treadmill or overground walking is a preferred mode because of its direct functional nature; however, a variety of disabilities may preclude this approach. Suitable alternatives include the cycle ergometer with toe clips and heel straps, recumbent ergometer, arm-leg ergometer, wheelchair ergometer, and stepping machine and swimming. Indeed, water-based exercise poststroke has shown positive effects on cardiovascular fitness and coping with life after stroke.¹⁶³ In addition, body-weight–supported treadmill training can also be used during early aerobic training poststroke.⁵⁰ Although arm ergometry activates a smaller portion of total muscle mass, its effectiveness in the aerobic training of patients with quadriplegia has been demonstrated.²⁵⁵ Innovative approaches have been introduced to overcome limitations to exercise training imposed by upper motor neuron damage. For example, a combination of electric stimulation of lower-extremity muscles and voluntary upper-extremity rowing has been applied to augment the muscle activation of patients after SCI.¹⁶⁶ Grealy and colleagues²⁵⁶ piloted use of a virtual reality recumbent ergometer with patients after traumatic brain injury, postulating that the interaction between the training apparatus and the participant might enhance attention to the task of exercising and increase the potential of structural changes in the brain.

A continuous, interval, or circuit training regimen may be used. Typically, training studies involving patients with neurological disabilities have used short bouts of exercise with a gradual transition to continuous training. However, it has been recommended for some time that if continuous training results in either a lack of improvement or a plateau in response, interval training should be instituted.^153,257

Muscle strengthening

Traditionally, aerobic training programs emphasized dynamic exercise. However, the addition of resistance training improves outcome.^238,258 Moreover, strength training decreases the cardiac demands of daily tasks such as lifting objects or carrying groceries while simultaneously increasing the endurance capacity to sustain these submaximal activities.²⁵⁹ Muscle strengthening exercises should also be carried out 2 or 3 days per week. Key muscle groups (e.g., triceps, biceps, abdominals, hip and knee flexors and extensors, hip abductors, ankle dorsiflexors, and plantarflexors) should be strengthened with one set of 10 to 15 repetitions starting at a low weight and avoiding a Valsalva maneuver.²⁷ Including strength training with aerobic training may produce greater gains in functional and health outcomes. For example, engaging in a combined strength and aerobic training program has been shown to be more effective in improving Vo₂peak, walking endurance, and lipid profile in people with type 2 diabetes.²⁶⁰ Improved fitness outcomes have also been reported in people who have had a stroke,²³⁸ despite controversy about whether the benefits of strength training of the paretic upper limb poststroke outweigh the potential risk of increased tone and pain, particularly in the shoulder region. However, the meta-analysis by Harris and Eng²⁶¹ found no reported adverse affects after upper-limb strength training and concluded that upper-limb strength training improves upper-limb strength and function in people poststroke. In people with SCI, increases in fitness level and reduction in shoulder pain have been observed after circuit training involving resistance exercises and arm cranking.²⁶²

Intensity of training

Determining an appropriate intensity is the most challenging aspect of exercise prescription. The cardiovascular system responds to overload; hence, the metabolic load must be sufficient to provoke central and peripheral adaptations. However, excessive stress imposed on the heart and contracting skeletal muscles can evoke abnormal clinical signs or symptoms. The initial exercise intensity and progression must be individualized using the participant’s HR or Vo₂peak data (Table 30-4). The RPE can serve as a valid proxy to more physiological measures³⁰; ratings of 11 (“fairly light”) to 13 (“somewhat hard”) on the RPE scale of 6 to 20 are recommended for initiation of training.²⁷ The RPE range associated with physiological adaptation to exercise is 12 to 16 on the Borg (6 to 20) category scale or 4 to 6 on the Borg (0 to 10) scale.²⁷ Despite considerable interindividual variation in RPE,²⁶³ the ratings have been shown to correlate well with exercise intensity, even in patients taking β-blockers.²⁶⁴ When exercise intensity is being established, other variables (e.g., anginal symptoms, arrhythmias) should also be considered. Continuous monitoring of HR and periodic monitoring of BP and RPE will ensure that an appropriate intensity is sustained during training.

In addition to the RPE, another proxy measure of intensity is the talk test, in which the participant’s intensity is regulated by whether he or she can sing (in which case intensity should be increased) or whether he or she is unable to talk (in which case intensity should be decreased). At an appropriate intensity the participant should be able to talk while exercising, as the point of “hearing your breath” while exercising occurs at or near the ventilatory threshold.²⁶⁵ This relationship was confirmed by Foster and colleagues,²⁶⁶ who reported that the exercise intensity at the ventilatory threshold corresponds to the greatest intensity with which a participant can comfortably speak. Recently, the counting talk test (CTT) was introduced as another proxy measure; it measures how high the participant can count aloud without taking a second breath (e.g., “one, one thousand; two, one thousand…”).²⁶⁷ The percentage of resting CTT has been reported to be strongly correlated with the percentage of HR reserve, Vo₂ reserve, and RPE, with moderate intensity coinciding with 50% of CTT.²⁶⁷ It should be noted, however, that the validity of the proxy measures of intensity has yet to be validated in neurological populations. For example, in the SCI population, no association was found between RPE and both HR and Vo₂.¹²⁹

The American College of Sports Medicine guidelines recommend light- to moderate-intensity physical activities to optimize cardiopulmonary health.²⁵⁴ In fact, a meta-analysis revealed that for very unfit patients (which would include many people with chronic neurological conditions), the initial intensity can be much lower than previously recommended.¹⁸² However, the only consistent beneficial cardiovascular response to low levels of training is reduction in BP in older hypertensive adults. To reduce cardiovascular risk factors and increase cardiopulmonary fitness, moderate- or high-intensity exercise appears to be necessary.²⁰² In agreement, Fisher and colleagues²⁶⁸ reported greater consistent improvements in gait parameters (self-selected gait speed, stride length, and step length), hip and ankle joint excursion, and sit-to-stand measures and lengthening of cortical silent period durations measured through transcranial magnetic stimulation in people with Parkinson disease participating in high-intensity BWSTT when compared with low-intensity or zero-intensity exercise programs. Nevertheless, light-intensity to moderate-intensity physical activity programs may prove adequate to reduce the rate of age-associated deterioration in a variety of physiological functions and in the long run may improve both quantity and quality of life.²⁰²

For many people with neurological involvement, determination of an appropriate intensity of exercise is confounded not only by cardiac status but also by the extent of neurological impairment. We have derived guidelines for determining the initial intensity of treadmill training for people after stroke, based on baseline cardiac signs, prescription of β-adrenergic blockade therapy,²⁶⁹ fitness level, and motor control of the involved lower extremity (i.e., Chedoke-McMaster stage of recovery of the leg)²⁷⁰ (Table 30-5).

Music to pace exercise

Music, if properly selected, can be helpful in pacing the repetitive, alternating movements characteristic of aerobic exercise such as walking or cycling. Rossignol and Jones²⁷¹ found that with close matching of the cadence of music and alternating movements, music can potentiate muscle activation. Similarly, McIntosh and colleagues²⁷² reported that music facilitated the gait pattern of people with Parkinson disease. (Refer to Chapters 4, 20, and 39 for additional information.)

Progression of training program

Exercise progression must be individualized because people with neurological disabilities have a wide range of functional capacities. Progression usually occurs over a 3- to 6-month period from an initial conditioning phase to a training phase and then to a maintenance phase. Generally the first goal of training is to reach a target frequency (i.e., a minimum of 3 days per week), then duration (minimum of 20 minutes), and finally an appropriate intensity (40% to 60% of HR reserve, or 11 to 13 on the Borg scale). Subsequently, exercise duration should be increased as tolerated, every 1 to 3 weeks, with a goal of achieving 20 to 30 minutes of continuous exercise before increasing the intensity.²⁷ Patients with higher baseline fitness levels can be progressed more rapidly than those with lower initial capacities.

Laboratory outcome measures

Laboratory tests are useful not only to identify limitations in exercise capacity and establish exercise training protocols but also to evaluate the effectiveness of a training program. The principal indicator of a training effect is attainment of a higher Vo₂peak than was achieved in the pretrained state. The greatest increments occur in individuals with the lowest initial Vo₂peak.¹⁶¹ Ideally, Vo₂peak should be measured directly because indirect methods of predicting exercise capacity are more variable and prone to error. However, because Vo₂peak testing requires special equipment and trained personnel, clinicians often resort to clinical measures of functional capacity.

Clinical outcome measures

Adherence to program

The benefits of training are lost unless some form of training stimulus is maintained; therefore, sustained behavioral change must be an important goal in any exercise program. A decrease in mobility or inactivity can lead to rapid loss of cardiovascular and pulmonary fitness. For example, a 25% reduction in maximum oxygen uptake has been observed in nondisabled young adults after 3 weeks of bed rest.⁹⁴ In secondary prevention of stroke, behavioral modifications may be as beneficial as antihypertensive and cholesterol-lowering agents.⁷⁸ Yet establishing and maintaining a regular fitness regimen in patients with neurological impairments pose challenges. In one study, 39% of 691 patients did not engage in the exercise program created by their physical therapist.²⁸² In addition, 75% of people poststroke reported that they were not ready to incorporate exercise into their lifestyle.^203,283

Some individuals are reluctant to engage in exercise owing to the fear of increasing their symptoms. Indeed, people with Parkinson disease avoid exercise out of fear they will increase their already high levels of fatigue.²⁸⁴ Similarly, people with MS avoid exercising to avert increases in their level of fatigue and body temperature.⁹⁰ Furthermore, the frequency of MS-related symptoms has been found to be significantly and inversely related to physical activity.²⁸⁵ It has been shown that less than 30% of 2995 people with MS reported engaging in any form of exercise,²²⁸ with one study revealing an overall adherence rate of 65%.²⁸⁶ Morris and Williams²⁸⁷ reported that many individual factors (e.g., sex, level of disability), social factors, and environmental factors (e.g., access to facilities, travel) influence the level of engagement in exercise and physical activity in people with mixed disabilities. In addition, numerous psychological, cognitive, and emotional factors have been identified as potential mediators of engagement in physical activity (e.g., self-efficacy, attitude, competence, intention, knowledge of health and exercise benefits, motivation, readiness to change, and the value of exercise benefits).²⁸⁸ One study involving people poststroke reported self-efficacy as an important psychological factor predicting engagement in exercise.²⁸⁹ Snook and colleagues²⁸⁵ reported that self-efficacy was significantly and moderately correlated with physical activity in people with MS.

A better understanding of theoretical frameworks of behavior change [see recent overview²⁹⁰] would be helpful for neurorehabilitation clinicians to increase participant engagement. Garner and Page²⁸³ exposed community-based, chronic stroke survivors to a theoretically based intervention using the transtheoretical model with five stages of change (i.e., precontemplation, contemplation, preparation, action, and maintenance). Change is mediated at each stage by self-efficacy, decisional balance, and processes of change.²⁹¹ In a study by Gillham and Endacott,²⁹² a stroke-specific score based on the transtheoretical model was used to assess readiness to change behavior in patients undergoing enhanced secondary stroke prevention. The authors found that the prevention program, which consisted of conventional rehabilitation plus additional advice, motivational interviewing, and telephone support, improved exercise frequency and increased consumption of fruits and vegetables when compared with the control group receiving conventional rehabilitation.²⁹² They also reported a nonsignificant trend of more patients in the enhanced group progressing from contemplation to action stages of change.²⁹² Several other behavioral theories (i.e., social cognitive theory, theory of reasoned action, theory of planned behavior, health belief model, protection motivation theory, and self-determination theory) may also be useful in facilitating long-term engagement.²⁹³ The American College of Sports Medicine (ACSM)²⁷ acknowledged that assessing the participants’ self-motivation and readiness for change can provide important information toward adapting the exercise program to meet the specific needs of the participants.

In the cardiac rehabilitation literature, Piepoli and colleagues²⁹⁴ recommended that in order for an individual to pursue and engage in an exercise program, both physiological and psychosocial changes are needed. Progression from promotion of physical activity within the patient’s current domestic, occupational, and leisure settings to participating in vigorous and structured exercise programs is recommended.²⁹⁴ In a systematic review also involving people with cardiac conditions, evidence supported the use of educational sessions, spousal and family involvement, flexible and convenient scheduling of sessions, ongoing positive reinforcement and enjoyment (e.g., motivational letters, pamphlets, conversations), and self-management aids (e.g., self-report diets, activity logs, individualized goal setting).²⁹⁵ Other strategies to enhance long-term exercise adherence include gradually progressing the exercise intensity, establishing regularity of training sessions, minimizing the risk of muscular soreness, and exercising in groups. Training sessions should be scheduled at a convenient time and in an accessible location, and if feasible, assistance with transportation and childcare should be offered. With the established emphasis on patient-centered care, it is consistent to have the patient identify individual goals and time frames to achieve these goals. Incorporating physical activity within everyday life will help to promote cardiovascular and pulmonary fitness as a life activity and not solely an exercise program conducted within a medical environment or rehabilitation setting.

Lifestyle modifications

Aerobic training alone is not sufficient to optimize the health and fitness of people with neurological disabilities. Education and counseling regarding daily physical activity, nutrition, energy conservation techniques, smoking cessation, and coping strategies are essential.