Cardiovascular and pulmonary system health in populations with neurological disorders





Abstract:


This chapter provides an overview of basic physiological principles related to cardiovascular responses to exercise testing, much of the evidence for which was derived several decades ago. A summary of the evidence of cardiopulmonary fitness levels in adults and children with neurological disabilities is followed by a description of factors that contribute to the deconditioned state. Possible mechanisms responsible for reduced exercise capacity are then reviewed. Adaptive responses to aerobic training in patients with neurological conditions are examined, as are factors underlying these responses. The chapter closes with a summary of guidelines for the design of exercise programs that can be used to improve cardiopulmonary health and fitness.




Keywords:

aerobic training, cardiovascular fitness, deconditioning, exercise tolerance, rating of perceived exertion

 




Objectives


After reading this chapter the student or therapist will be able to:



  • 1.

    Explain the physiological principles related to cardiovascular responses to exercise testing.


  • 2.

    Describe the factors that contribute to the deconditioned state in adults with neurological disorders.


  • 3.

    Explain the adaptive responses to aerobic training in populations with neurological disorders and the factors underlying these responses.


  • 4.

    Discuss general guidelines for designing exercise programs to improve cardiovascular health and fitness.





The cardiovascular and pulmonary health of individuals with residual movement dysfunction after a neurological insult has become a topic of great interest in neurorehabilitation. In traditional practice, the state of the neuromuscular system preoccupied the attention of clinicians in the quest to optimize neurological recovery. Most interventions were based on strategies to improve the capacity of that system—an approach that has met with limited success in terms of restoring functional independence. It is now clear that recovery cannot be explained solely on the basis of improved neuromuscular function—three decades ago Roth and colleagues determined that less than one-third of the variance in functional limitations after a stroke can be explained by the extent of neurological impairment. Nevertheless, the current approach to neurorehabilitation is somewhat perplexing. Evidence has accumulated indicating that many people with neurological disabilities are woefully deconditioned. There has been widespread acknowledgement of the central role that aerobic exercise plays in improving cardiopulmonary health and fitness. Furthermore, application of the principles of exercise physiology in cardiac rehabilitation has been widely endorsed. Yet neurorehabilitation clinicians have been observed to practice without full knowledge of their patients’ cardiac status or without monitoring heart rate (HR) and blood pressure (BP). , Moreover, there is evidence to suggest that patients with neurological insults have not been challenged enough in therapy to induce the metabolic stress needed to enhance their cardiopulmonary fitness. A troubling explanation offered for these observations is that clinicians lack either an understanding or an appreciation of the basic physiological principles of exercise. ,


Fortunately, attention has turned to the introduction of interventions that encompass the neuromuscular, cardiovascular, and pulmonary systems and promote a more holistic approach to neurorehabilitation. The challenge of improving cardiopulmonary health and fitness in these populations is not trivial. For individuals with chronic conditions, fitness is affected by a host of interacting influences such as the location and extent of the lesion, the presence of comorbidities (particularly cardiovascular disease), and the premorbid activity level. To complicate matters further, testing and training protocols for individuals with compromised motor and postural control need to be tailored to ensure safety and effectiveness.


This chapter begins with an overview of basic physiological principles related to cardiovascular responses to exercise testing, much of the evidence for which was derived several decades ago. A summary of the evidence of cardiopulmonary fitness levels in adults and children with neurological disabilities is followed by a description of factors that contribute to the deconditioned state. Possible mechanisms responsible for reduced exercise capacity are then reviewed. Adaptive responses to aerobic training in patients with neurological conditions are examined, as are factors underlying these responses. The chapter closes with a summary of guidelines for the design of exercise programs that can be used to improve cardiopulmonary health and fitness. Appendix 29.A at the end of this chapter clearly identifies the meanings of the abbreviations used throughout the chapter.




Physiological responses to exercise


At rest the human body consumes roughly 3.5 mL of oxygen (O 2 ) per kilogram per minute, or 1 metabolic equivalent (MET). In the resting state, skeletal muscle activity accounts for less than 20% of the body’s total energy expenditure; the brain, making up only 2% of body weight, also consumes 20% of the available O 2 . Activities at rest, such as breathing and contracting of the heart, can be sustained indefinitely because the power demands of these activities are met by the rate of energy turnover. In other words, these activities occur well below the critical power of the muscles, defined as the maximal rate of work that can be endured indefinitely. Any physical activity beyond the resting state requires more O 2 ; the increase is dependent on the intensity of the effort involved. The rise in metabolism relies on O 2 transport by the pulmonary and circulatory systems and O 2 usage by the active skeletal, cardiac, and respiratory muscles to convert chemical potential energy to mechanical energy. The components of the O 2 transport system are outlined in Fig. 29.1 .




Fig. 29.1


Diagrammatic Representations of the Components of the O 2 Transport System.

(1) During inspiration O 2 from the air is delivered to the alveolar gas space by the process of respiration. (2) O 2 diffuses across the blood-gas barrier into the pulmonary capillary blood, where almost all of the O 2 is bound to hemoglobin. (3) The heart acts as a pump, and (4) the vascular system acts as the plumbing to transport O 2 to the various tissues, including the exercising muscle, (5) where it diffuses from the red blood cells into the mitochondria within the myocytes. Reduced conductance of any component impairs O 2 transport, whereas improved conductance of any component augments O 2 transport.


Selective distribution of the increased blood flow to regions with heightened metabolic demands—the working muscles—is largely a result of local vasodilation mediated mainly by metabolites acting on the vascular smooth muscle (e.g., carbon dioxide [CO 2 ], hydrogen ions [H + ], nitric oxide, potassium ions, adenosine) and vasoconstriction in tissues with low metabolic demands. Blood flow to other vascular beds (e.g., renal and splanchnic bed) either is unchanged or decreases through active vasoconstriction resulting primarily from increased sympathetic discharge. Cerebral autoregulation maintains regional and total cerebral blood flow and normal tissue oxygenation over a wide range of BPs ; thus cerebral blood flow and O 2 delivery during exercise either remain stable , or increase slightly. , As exercise intensity increases, systolic BP (SBP) increases markedly, whereas diastolic BP (DBP) either remains unchanged or lowers slightly, resulting in a moderate increase in mean arterial pressure.


Extraction of O 2 from the muscle capillary blood to mitochondria is dependent on an adequate O 2 -diffusion gradient. During a progressive increase in workload, the arterial hemoglobin saturation and arterial O 2 content remain relatively constant, whereas the venous O 2 content decreases substantially as a result of increased O 2 extraction in the active muscles. As the metabolic rate rises, the minute ventilation (i.e., respiratory rate multiplied by the tidal volume) increases to remove CO 2 and to regulate pH balance of the active muscles. At low-intensity exercise, ventilation (mainly tidal volume) increases in a linear manner relative to the volume of O 2 use (Vo 2 ) and CO 2 production (Vco 2 ). Above the critical power, the energy demand of the muscle exceeds the capacity of the aerobic process to supply energy for muscle contraction; the additional energy is supplied by the anaerobic glycolytic system.


During more intense exercise, ventilation is extremely variable among individuals; the respiratory rate usually increases without a substantial change in tidal volume. The point at which the rate of glycolysis exceeds that of oxidative phosphorylation is called the anaerobic threshold (which approximates the ventilatory threshold or lactate threshold). Pyruvic acid is converted to lactic acid, which completely dissociates to lactate and H + , resulting in a rise in blood lactate levels and a fall in intramuscular pH. Exercise-induced muscular fatigue is caused by the exponential accumulation of lactate and a drop in intramuscular pH, with negative effects on the actin-myosin turnover rate, enzyme activities, and excitation-contraction coupling.


Maximal oxygen consumption (Vo 2 max) is defined as the highest O 2 intake an individual can attain during physical work. The Fick equation describes the relationship between cardiovascular function and Vo 2 max:


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Vo2max=Qmax×a-vO2diffmax


where Qmax is the maximal cardiac output and a-vO 2 diffmax is the maximal arteriovenous O 2 difference. Given that Qmax equals the product of maximal HR (HRmax) and maximal stroke volume (SVmax),


<SPAN role=presentation tabIndex=0 id=MathJax-Element-2-Frame class=MathJax style="POSITION: relative" data-mathml='Vo2max=HRmaxSVmax×a-vO2diffmax’>Vo2max=HRmaxSVmax×a-vO2diffmaxVo2max=HRmaxSVmax×a-vO2diffmax
Vo2max=HRmaxSVmax×a-vO2diffmax


Thus Vo 2 max reflects both O 2 transport to the tissues and O 2 usage by the tissues. Increases in Vo 2 during exercise are caused by increases in both cardiac output and a-vO 2 diff, with HR and stroke volume (SV) increasing progressively over the lower third of the workload range. Thereafter HR continues to increase while SV remains essentially constant, , resulting, at maximal effort, in a cardiac output three to six times greater than baseline levels. An increase in SV (50% over resting volume) is caused by enhanced myocardial contractility and increased venous return resulting from compression of the veins by contracting muscles and reduced intrathoracic pressure. At low-intensity exercise, the increase in HR is mainly a result of decreased vagal tone, but as exercise intensifies, sympathetic stimulation and circulating catecholamines play a greater role, yielding, at maximal workloads, a rise in HR 200% to 300% above the resting level.




Measurement of cardiopulmonary fitness


Exercise (aerobic) capacity is the principal determinant of the ability to sustain the power requirements of repetitive physical activity. Vo 2 max is generally accepted as the definitive index of exercise capacity and cardiopulmonary fitness. Vo 2 max is a relatively stable measurement; variability of repeated measures of Vo 2 max has been reported to be 2% to 4% or 0.2 L/min. Accurate determination of Vo 2 max requires (1) adequate duration and work intensity by at least 50% of total muscle mass, (2) independence from motivation or skill of the subject, and (3) controlled environmental conditions. Also, because test performance is sensitive to time of day, the time of repeat testing should be consistent.


Before any fitness test, a 3- to 5-minute warm-up of slow treadmill walking on a level grade or unloaded pedaling that raises the metabolic rate twofold (i.e., 2 METs) above resting should be performed. A proper warm-up prevents excessive local muscle fatigue from occurring before Vo 2 max has been attained. Furthermore, a 3- to 5-minute cool-down should follow test completion to aid in venous return to prevent blood pooling in the peripheral vasculature and a subsequent drop in DBP. The intensity of exercise can be increased in a continuous progressive manner (i.e., step or ramp protocol) or, less commonly, in a discontinuous progressive manner (i.e., subject rests between stages). Throughout testing, continuous monitoring of the electrocardiogram and periodic monitoring of BP are essential. The optimal duration of a graded exercise test is 8 to 12 minutes, with testing terminated when the subject can no longer generate the required power, is limited by symptoms, or is unable to continue safely. Variables of interest during exercise testing include Vo 2 max expressed in absolute terms (liters of O 2 per minute) or relative to body mass (milliliters of O 2 per kilogram of body weight per minute), MET level, percent of predicted HRmax, respiratory exchange ratio (RER; ratio of Vo 2 to CO 2 ), peak power, minute ventilation, tidal volume, respiratory rate, and rating of perceived exertion (RPE) according to the Borg scale. Because there is considerable variability in HRmax among healthy individuals, the percent of predicted HRmax attained is not a robust indicator of exercise capacity. Similarly, because both total exercise time and peak exercise intensity (or power attained; i.e., peak treadmill speed and grade or peak power on bike) are dependent on the test protocol, neither is a reliable measure of exercise capacity. , In addition, noninvasive estimation of the anaerobic threshold by identifying the point of nonlinear increases in minute ventilation and Vco 2 can be highly subjective and thus unreliable.


The principal marker of exercise capacity is attainment of a plateau in Vo 2 , beyond which there is a change of less than 100 mL/min, with further increases in workload dependent solely on anaerobic metabolism. In cases in which a Vo 2 plateau is not observed (typically in deconditioned or elderly individuals or in patients with heart disease), the preferred term for the value obtained is peak Vo 2 (Vo 2 peak). Criteria for attainment of Vo 2 peak include achieving the age-predicted HRmax, RER in excess of 1.15, minute ventilation greater than the predicted maximal voluntary ventilation, tidal volume greater than 90% of the inspiratory capacity, and obvious patient exhaustion.


Testing modality


The modality of testing (e.g., treadmill walking, cycling, stepping, arm cranking) can affect Vo 2 max values. The treadmill has the greatest potential to recruit sufficient muscle mass to elicit a maximal metabolic response, particularly in deconditioned individuals. Bike ergometry yields 85% to 90%, and arm ergometry 70%, of the Vo 2 max achieved with a treadmill. Ideally the mode of exercise should be consistent with the patient’s typical activity. Thus the treadmill is often preferred because the pattern of muscle activation during treadmill walking is similar to that for most mobility tasks. In patients with neuromuscular conditions, however, impaired balance and motor control often preclude the use of standard treadmill testing protocols. To resolve this limitation, we devised and validated an exercise protocol using a body-weight support system to permit safe and valid testing of Vo 2 max early after stroke. For subjects with paraplegia, tests with wheelchair treadmills are more functionally relevant than those using arm ergometry.




Predicting maximal oxygen consumption with use of submaximal exercise tests


Although submaximal tests do not measure the systemic response, they are inexpensive to administer and have a low risk of adverse events. The essentially linear relationship between Vo 2 and HR permits the estimation of Vo 2 max from HR measurements taken during submaximal exercise. For example, for people without physical disability the HR increases approximately 50 beats per uptake of 1 L of O 2 , independent of sex and body size. For unfit individuals and patients with cardiac impairment, the increases in HR are greater per liter, except for patients taking β-blockers, who demonstrate blunting of the HR response throughout exercise. The Åstrand-Ryhming nomogram has been used to predict Vo 2 max from submaximal HR. The HR-Vo 2 relationship is independent of the exercise protocol. However, HR, unlike Vo 2 max, is markedly affected by many stresses (e.g., dehydration, changes in body temperature, acute starvation), resulting in substantial error and inaccurate Vo 2 max estimations. In fact, discrepancies between estimated and measured Vo 2 max in individuals with low exercise capacity can be as high as 25%.




Fitness levels in populations with neurological disorders


Documentation of exercise capacity in populations with neurological disorders has been hindered by the lack of testing protocols that can safely and effectively accommodate the motor and balance disturbances common to these populations. Not surprisingly, the evidence to date suggests that most individuals with neurological disabilities are significantly deconditioned. Variability results from a multitude of factors, including differences in testing protocols, as discussed in the previous section, and differences in subject characteristics; these points are discussed in the following section.


Impact of low fitness levels on health of people with neurological disorders


People with high fitness levels use only a small fraction of the physiological fitness reserve of the cardiovascular, respiratory, and neuromuscular systems to respond to the metabolic challenge of activities of daily living (ADLs). , Thus small declines in exercise capacity may not be noticeable in carrying out ADLS. In contrast, relatively minor reductions in capacity can substantially influence performance of ADLs by deconditioned individuals. Light instrumental ADLs require approximately 10.5 mL of oxygen per kilogram per minute (3 METs), whereas more strenuous activities have metabolic costs of about 17.5 mL/kg per minute (5 METs). Cress and Meyer reported that the Vo 2 peak of 20 mL/kg per minute is needed for older adults to meet the physiological demands of independent living. It is evident that many people living with neurological disabilities (particularly stroke, tetraplegia, and postpoliomyelitis syndrome) do not have the level of fitness required for the more strenuous ADLs and independent living. Moreover, relative exercise capacities (expressed as a percentage of normative values) are of concern, given that Vo 2 peak values less than 84% of normal are considered pathological.


For individuals with neurological disabilities, the minimum Vo 2 requirements for ADLs are actually greater than the previously mentioned levels because of the increased energy requirements resulting from gross motor inefficiencies and other related factors. In other words, the percentage of Vo 2 peak required for activity at a fixed submaximal workload (termed fractional utilization ) is increased. When the anaerobic threshold is exceeded prematurely and lactate accumulation is accelerated, accomplishment of low-intensity ADLs is unsustainable for extended periods and achievement of mid- to upper-intensity ADLs is virtually impossible. Moreover, the combination of poor exercise capacity and elevated energy demands results in diminished reserves to support other activities. For example, in the case of people with postpoliomyelitis syndrome, the energy costs of walking are about 40% higher than for healthy peers and are highly correlated with lower-extremity muscle strength. Thus in the calculation of fractional utilization for walking, the numerator (Vo 2 during walking) is increased and the denominator (Vo 2 peak) is decreased, increasing fractional utilization substantially.


Of the neurological populations, people post-stroke are the largest consumer group in need of rehabilitation services. This group also has received the most attention in the literature with regard to functional capacity. Exercise capacities documented in this population are consistently low—with a reported range of 8.3 mL/kg per minute in the sub-acute period to 22.0 mL/kg per minute in the chronic period. As much as 75% to 88% of Vo 2 peak (almost twice that of the healthy control subjects) is required to perform household chores, and one and a half to three times the Vo 2 levels of nondisabled people are needed to walk on level ground. , , Not surprisingly, as many as 70% of patients complain of fatigue after stroke, with poor energy levels rated as the area of greatest personal concern in comparison to mobility limitations, pain, emotional reactions, sleep disturbances, and social isolation.


In addition to contributing to reduced ADL performance and increased fatigability, low fitness levels are associated with higher mortality. Exercise capacity has been reported to be an independent predictor of mortality in persons with coronary artery disease (CAD), a comorbidity prevalent in some populations of people with neurological conditions. , Those with a Vo 2 peak <21 mL/kg per minute are classified as the high-mortality group and with greater than 35 mL/kg per minute as the excellent-survival group. Thus determining an individual’s Vo 2 peak is of clinical value. Individuals who are being encouraged, or are internally motivated, to perform beyond their capacity and beyond the capabilities of the interaction of multiple systems are in a high-risk category. Conversely, individuals who are undermotivated or depressed and are performing below their capacity can be trained to self-monitor, which empowers them to reach goals that are safe and have the potential to improve the quality of their lives.


Factors affecting fitness levels in people with neurological disorders


To identify appropriate measures to improve fitness levels in people with neurological disorders, the myriad factors at play that contribute to the deconditioned state must be considered. A useful conceptual framework to discuss the interaction of these factors is the International Classification of Functioning, Disability and Health (ICF) (see Chapter 1 ). The ICF uses a biopsychosocial approach to organize factors related to the health conditions into two components: (1) personal and environmental contextual factors and (2) functioning and disability, which are further subdivided into components of body functions and structures, activity, and participation ( Fig. 29.2 ). Through application of the ICF framework, the complexity of interacting influences on cardiovascular and pulmonary health and fitness becomes more understandable.




Fig. 29.2


Interaction of the Various Components of the International Classification of Functioning, Disability and Health (ICF).

The ICF is a conceptual framework that uses a biopsychosocial approach to organize factors related to health condition into two components: (1) personal and environmental contextual factors and (2) functioning and disability, which are further subdivided into components of body functions and structures, activity, and participation.


Personal and environmental contextual factors


For both able-bodied and disabled people, personal contextual factors contributing to individual differences in exercise capacity include age, sex, race, and lifestyle habits.


Age


A decline in Vo 2 max of approximately 1% per year (0.4 to 0.5 mL/kg per minute per year) occurs from 25 to 75 years of age. In accordance with the Fick equation, a reduction in Vo 2 max is caused by reductions in both O 2 transporting (i.e., Qmax) and O 2 utilization capacity (i.e., a-vO 2 diffmax) 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. 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. Older adults also have a smaller SVmax, and BP and systemic vascular resistance are higher during maximal exercise in older versus young adults.


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. Age-related decline in oxidative capacity of the working muscles and hence decreased a-vO 2 diff during peak exercise have been attributed to alterations in mitochondrial structure and distribution, oxidative enzyme activity, and skeletal muscle microcirculation, as well as sarcopenia resulting from a reduced number and size of fibers, particularly type II fibers. 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, age is a significant independent predictor of recurrent stroke. 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. In the case of people with Down syndrome, however, Baynard and colleagues found that age-related changes in exercise capacity did not follow the typical pattern of decline after the age of 16 years. Older people with spinal cord injury (SCI) are at an increased risk for cardiac and respiratory complications.


Sex


The absolute and relative Vo 2 max of women is typically about 77% of that of men, after adjustment for body weight and activity level. However, no significant gender differences have been reported in the percentage of exercise-induced improvement in Vo 2 max of older adults. Although older men and women generally exhibit similar responses to maximal exercise, older women tend to have lower SBP during maximal exercise.


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 post-stroke.


Lifestyle factors


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


The relationship between cardiovascular disease and diet has attracted international attention. Indeed, obesity increases the risk of cardiovascular risk factors such as impaired glucose tolerance and type 2 diabetes, hypertension, and dyslipidemia. Abdominal obesity not only increases the risk of atherosclerotic disease but also the risk of primary ischemic stroke. , In addition, when compared with corresponding normal-weight populations, overweight youth with SCI and spina bifida (SB) have lower cardiovascular fitness.


The lifestyle factor that has received the most attention in the literature is sedentary behavior. The evidence of the link between physical activity and cardiopulmonary health and fitness is irrefutable. , 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. Cardiovascular alterations resulting from physical inactivity (i.e., reduced Vo 2 max 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%. 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 have been reported to spend as little as 2% of their walking time participating in leisure physical activity, making them among the most sedentary members of society. Some people with multiple sclerosis (MS) avoid physical activity to prevent elevated body temperature and minimize symptoms of fatigue. , Inactivity can lead to increased cardiovascular risk factors such as hypertension and dyslipidemia, as seen in youth with chronic disabilities (including CP and SCI). Bernhardt and colleagues 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 recumbency and a 28% reduction in healthy young subjects after 3 weeks. Inactivity-induced reductions in Vo 2 peak 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).


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. However, the influence of such factors on cardiovascular and pulmonary fitness of people with neurological disabilities has garnered little attention in the literature.


Health condition


Exercise capacity reflects both systemic capacity and the health of the component systems. Thus differences in Vo 2 peak among individuals with neurological disabilities are a result of not only the contextual factors discussed previously but also pathological conditions involving the neuromuscular, cardiovascular, and pulmonary systems.


Neuromuscular system


For most individuals with neurological conditions, the existence of neuromuscular impairments confounds interpretation of Vo 2 peak 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 atrophy and changes in muscle fiber composition ) affect the response to exercise. As a result, people with neurological disabilities manifest not only metabolic but also biomechanical deficiencies, 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 Vo 2 peak over a 3- to 5-year period was 12% greater than the predicted decline ).


Paresis reduces the pool of motor units available for recruitment during physical work, thereby reducing the metabolically active tissue and lowering the oxidative potential. In the case of stroke, on average about 50% of the normal number of motor units are functioning, and a strong relationship between muscle mass and Vo 2 peak has been reported. In addition, along with altered joint kinematics and decreased postural reactions, 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 Vo 2 peak. Thus when compared with able-bodied individuals, children with CP experience greater levels of fatigue at slower walking speeds. For people with postpoliomyelitis syndrome, muscle weakness of the lower extremities is strongly associated with energy expenditure of walking. In fact, when compared with healthy age- and sex-matched subjects, the energy cost of walking is found to be significantly higher (40%) for people with postpoliomyelitis syndrome.


Altered fiber composition and recruitment patterns of paretic muscle may also contribute to poor fitness. 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. Although relatively equal proportions of slow and fast MHC isoforms are found in the vastus lateralis of healthy individuals, 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. 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 Vo 2 peak. Furthermore, alterations in the structure of mitochondria and reduced activity of oxidative enzymes (e.g., succinate dehydrogenase) 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 leading causes of death in persons with stroke, MS, and SCI. As many as 75% of patients who have had a stroke are hypertensive, and the same proportion of patients have underlying cardiovascular dysfunction. In fact, most persons who have had a stroke have atherosclerotic lesions throughout their vascular system, and a high correlation has been reported between the number and degree of stenotic lesions in the coronary and carotid arteries. 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).


Metabolic syndrome is a usual construct in identifying patients at high risk for future vascular events (e.g., a second stroke, myocardial infarction). Metabolic syndrome refers to a constellation of markers of metabolic abnormalities (i.e., hypertension, abdominal obesity, abnormal lipid profile) that interact to accelerate the progression of atherosclerosis and increase the risk of development of cardiovascular or cerebrovascular disease. 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.


Factors that elevate HR for a given Vo 2 , such as CAD, result in attainment of a peak HR (HRpeak) at a Vo 2 peak 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 exercise and chronotropic incompetence—the inability to increase HR in proportion to the metabolic demands of exercise. 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 O 2 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 post-stroke. , In addition, despite near-normal (above 0.90) mean ankle brachial index values, arterial diameter has been found to be reduced post-stroke. Potential mechanisms responsible for reduced blood flow on the hemiparetic side include altered autonomic function, enhanced sensitivity to endogenous vasoconstrictor agents, and altered histochemical and morphological features of the vascular network itself. 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.


Trauma to the spinal cord may disrupt the autonomic reflexes and sympathetic vasomotor outflow required for normal cardiovascular responses to exercise. As a result, reduced venous return and cardiac output (referred to as circulatory hypokinesis ) impair delivery of O 2 and nutrients to and removal of metabolites from working muscles, intensifying muscle fatigue. 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, 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. Nevertheless, at maximal workloads as much as 10% of Vo 2 max is needed to support the mechanical work of the diaphragm, accessory inspiratory muscles, and abdominal muscles. In contrast, people with neurological impairments may have limited O 2 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). , 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.


As previously mentioned, minute ventilation is closely associated with Vco 2 during exercise. At peak exercise, a ratio of minute ventilation to Vco 2 above between 35 and 40 indicates an abnormal ventilatory response. Neu and colleagues reported an 87% incidence of obstructive pulmonary dysfunction in patients with Parkinson disease, despite the finding that Vo 2 peak levels in this patient group tend to be in the normal range. , For children with CP, reduced exercise capacity may be partly caused by respiratory muscle spasticity resulting in reduced breathing efficiency. 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). , Impaired respiration may be attributed to cardiovascular dysfunction or lifestyle factors (e.g., physical inactivity, high incidence of smoking) 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. Impaired breathing mechanics with restricted and paradoxical chest wall excursion and depressed diaphragmatic excursion have been also reported. , Expiratory dysfunction appears to be related to the extent of motor impairment (e.g., abdominal muscle weakness), whereas inspiratory limitations appear to be related to the gradual development of rib cage contracture.


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 colleagues 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 Vo 2 max. They concluded that further study is needed to determine the clinical implications of this finding.

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Apr 22, 2020 | Posted by in NEUROLOGY | Comments Off on Cardiovascular and pulmonary system health in populations with neurological disorders

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