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Kriz et al. (1992)

VÜ2peak: peak oxygen consumption; VÜ2peak % normal: peak oxygen consumption expressed as a percentage of normative values; NR: not reported.

sclerosis is often avoided in order to prevent elevated body temperature and minimize symptoms of fatigue (Ng and Kent-Braun, 1997). Pathologic changes in paretic muscle increase the likelihood of abnormally low exercise capacity. Reduction in the number of recruitable motor units available for physical work (Dietz et al., 1986), altered muscle fiber distribution and recruitment patterns (Jakobsson et al., 1991), and diminished capacity for oxidative metabolism in paretic muscles (Landin et al., 1977) lower the oxidative potential. In addition, central nervous system trauma, particularly involving the spinal cord, may disrupt the autonomic reflexes and sympathetic vasomotor outflow required for normal cardiovascular responses to exercise (Glaser, 1986). Resulting "circulatory hypokinesis" - reduced cardiac output at a given VO2 resulting from reduced venous return - impairs delivery of O2 and nutrients to and removal of metabolites from working muscles, intensifying muscle fatigue (Davis and Shephard, 1988).

Cardiovascular co-morbidity, prevalent in neurologic populations, can restrict exercise capacity. About 75% of patients poststroke have underlying cardiovascular dysfunction (Roth, 1993). Cardiorespira-tory complications are the leading causes of death in persons with stroke (Matsumoto et al., 1973), multiple sclerosis (Sadovnick et al., 1991), and spinal cord injury (Kennedy, 1986). Cardiac dysfunction contributes to lower aerobic capacity through two principal mechanisms: ischemia-induced reductions in ejection fraction and SV with exercise (Clausen et al., 1973) and chronotropic incompetence - the inability to increase HR in proportion to the metabolic demands of exercise (Camm, 1996). Respiratory impairment, either as a direct complication of neuromuscular condition (e.g., muscle weakness, impaired breathing mechanics) or secondary to cardiovascular dysfunction or lifestyle factors (e.g., physical inactivity, smoking habits), may limit O2 availability for exercise (Vingerhoets and Bogousslavsky, 1994; Wiercisiewski and McDeavitt, 1998). Neu et al. (1967) reported an 87% incidence of obstructive pulmonary dysfunction in patients with Parkinson disease; however, despite respiratory compromise in this patient group, VO2peak levels tend to be within the range of normal values (Canning et al., 1997; Stanley et al., 1999).

Long-term adaptations to exercise training

Endurance training using dynamic exercises of adequate intensity, duration, and frequency provokes central and peripheral adaptations in proportion to the stress imposed on the heart and working skeletal muscles, respectively (Clausen et al., 1973). To induce central adaptations, training must incorporate large muscle mass activities in order to attain high levels of VO2. The principal indicator of a training effect during maximal exercise is attainment of a higher VO2max than was achieved in the pre-trained state. Healthy individuals with similar pre-training exercise capacity demonstrate comparable exercise trainability regardless of age or sex (Lewis et al., 1986). However, the greatest increments in VO2max occur with the lowest initial values of VO2max (Saltin, 1969).

Training-induced increases in VO2max are due primarily to improved cardiac output (Hartley et al., 1969). Maximal HR remains unchanged with training; thus, higher SV secondary to enhanced myocar-dial contractility accounts for the higher output (Clausen, 1977). With training, there is decreased vasoconstriction in the non-working muscles and improved venous return, thus, a training-induced increase in Qmax can occur without a concomitant increase in mean arterial pressure (Clausen, 1977). Training does not, however, have a substantial effect on blood hemoglobin content and coronary blood flow (Clausen et al., 1973). Its effect on ejection fraction remains unclear (Franklin et al., 1992). Improved AVO2 difference in the exercising muscle tissue has been attributed to increases in size and number of mitochondria, myoglobin levels, Krebs' cycle enzymes (e.g., succinate dehydrogenase), and respiratory chain enzymes (e.g., cytochrome oxidase) (Whipp, 1994), as well as increased capillary density (Saltin, 1985).

The mechanisms underlying the training-induced bradycardic response at a fixed submaximal workload may be explained by a concomitant elevation in total blood volume (Wilmore et al., 1996), an increase in vagal activity, a reduction in sympathetic-adrenergic drive, or a reduction in resting HR (Casaburi, 1994). However, Wilmore et al. (1996) reported that the small decrease in resting HR is of minimal physiologic significance. Although arterial blood pressure at a given work rate is often unchanged with training, there is lowering of the rate-pressure product (Ogawa et al., 1992), reflecting improved cardiac efficiency (Nelson et al., 1974). In addition, demand for increased anaerobic metabolism is delayed due to the improved capacity for aerobic exercise; thus the lactate threshold is elevated and the VE at a given submaximal workload is reduced (Casaburi, 1994). After training, O2 consumption at a given submaximal workload is either unchanged (Hartley et al., 1969) or modestly reduced (Gardner et al., 1989) because the increased AVO2 difference in trained muscles is offset by reduced blood flow to the working muscles and a less pronounced decrease in blood flow to the non-exercising muscles resulting from depressed sympathetic reflex activity (Clausen, 1977).

Factors limiting the capacity of healthy individuals to respond to physical work have not been identified conclusively. The respiratory system, AVO2 difference, and metabolic capacity of the muscles have not been implicated as principal limiting factors (Rowell, 1974; Andersen and Saltin, 1985); thus, the main limitation appears to be cardiac output.

Long-term adaptations in individuals with neurologic conditions

Controlled trials of the adaptability of the cardiore-spiratory system to exercise after neurologic insult are lacking; hence effective training regimens remain unclear. In the past, emphasis in neurorehabilitation was placed on neuromuscular impairments because motor and postural control was considered the main factor limiting functional recovery. Also, clinicians were apprehensive about increased risk of falls, detrimental cardiac responses, and aggravation of spasticity to the overload needed to achieve a training effect; however, such concerns have not been substantiated (Smith et al., 1999; Teixeira-Salmela et al., 1999; Saunders et al., 2004). In fact, there is evidence from studies of spinal cats (Coté et al., 2003) and humans with spinal cord injury (Trimble et al., 1998) that treadmill training may reduce spasticity by improving stretch reflex modulation.

Traditional modes of aerobic training have been used for patients with neuromuscular conditions -leg ergometer, arm ergometer, and arm-leg ergometer (Fig. 21.2.). In addition, innovative approaches have recently 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 patients post spinal cord injury to augment the muscle activation needed to achieve a training effect (Wheeler et al., 2002). Body weight-supported treadmill training, originally designed for early gait retraining poststroke (Barbeau and Visitin, 2003), has been pilot tested as a training mode for patients early poststroke (da Cunha Filho et al., 2001) (Fig. 21.3). To enhance attention to the task of exercising in patients post traumatic brain injury, Grealy and colleagues (1999) used a virtual reality recumbent ergometer. The authors postulated that the interaction between the training apparatus and the participant might potentiate structural changes in the brain.

The findings of the few training studies that measured VO2peak suggest that improvements in cardiovascular adaptation to physical work are possible in neurologic populations (Table 21.2). In some studies, the magnitude of change in VO2peak was comparable to the 15% gain reported for healthy, sedentary adults (Samitz and Bachl, 1991) and the 13-15% gains for participants in cardiac rehabilitation (Franklin et al., 1978; Mertens and Kavanagh, 1996). Variability in the results is attributable to many factors, including differences in mode and intensity of training, disparities in level of compliance with exercise regime, and variation in neurologic condition, severity and time post insult. The largest increments in VO2peak tended to occur with the most deconditioned subjects, consistent with findings for people without impairments (Saltin, 1969).

Figure 21.2. Examples of modes of exercise training used in neurorehabilitation. (a) The leg ergometer is appropriate for people with adequate lower-extremity control and sitting balance. (b) The arm ergometer may be used when lower-extremity strength is insufficient for leg ergometry; however, a disadvantage with the arm ergometer is the smaller muscle mass activated when movement is restricted to the upper extremities. (c) The recumbent leg ergometer can be used in place of the standard leg ergometer if sitting balance is impaired. (d) The arm-leg ergometer can be propelled by a combination of lower and upper extremities and therefore is suitable for individuals with hemiparesis or quadriparesis.

Figure 21.2. Examples of modes of exercise training used in neurorehabilitation. (a) The leg ergometer is appropriate for people with adequate lower-extremity control and sitting balance. (b) The arm ergometer may be used when lower-extremity strength is insufficient for leg ergometry; however, a disadvantage with the arm ergometer is the smaller muscle mass activated when movement is restricted to the upper extremities. (c) The recumbent leg ergometer can be used in place of the standard leg ergometer if sitting balance is impaired. (d) The arm-leg ergometer can be propelled by a combination of lower and upper extremities and therefore is suitable for individuals with hemiparesis or quadriparesis.

Figure 21.3. Body weight-supported treadmill walking has been introduced as an aerobic training mode for patients in the early stages of neurologic recovery. This patient is walking at a low treadmill speed (0.6 km/h) with 30% body weight support, and manual guidance by two physiotherapists - one to assist advancement of the hemiparetic lower extremity and one to stabilize the pelvis to achieve symmetry of the gait pattern.

Figure 21.3. Body weight-supported treadmill walking has been introduced as an aerobic training mode for patients in the early stages of neurologic recovery. This patient is walking at a low treadmill speed (0.6 km/h) with 30% body weight support, and manual guidance by two physiotherapists - one to assist advancement of the hemiparetic lower extremity and one to stabilize the pelvis to achieve symmetry of the gait pattern.

Most of the training studies in Table 21.2 involved patients with chronic neurologic impairments; however, the optimal time to introduce training is unknown. Macko et al. (1997) expressed caution about training in the early poststroke period, reasoning that abnormal cardiovascular responses to exercise (e.g., hypotension, dysrhythmia) may impede perfusion of ischemic brain tissue during the period when cerebral autoregulation is most often impaired. Nevertheless, in a recent study da Cunha Filho and colleagues (2001) training was initiated 8-21 days after stroke without complications.

In addition to improved exercise capacity, other benefits of training realized by healthy populations are also attainable for individuals with neuromus-cular impairments. For example, a 15-week training program for patients with multiple sclerosis resulted in decreases in skinfold thickness, triglycerides, and very-low-density lipoprotein and improvements in upper- and lower-extremity strength and quality-of-life measures (i.e., depression, fatigue, social interaction) (Petajan et al., 1996). An 8-week training program for patients early after spinal cord injury led to improved lipid profiles, with more pronounced changes in response to high-intensity training (de Groot et al., 2003). Gordon et al (1998) speculated that the improved cognitive function observed in individuals with traumatic brain injury who exercised on a regular basis may be attributed to exercise-induced increases in brain-derived neurotrophic factor (BDNF) or other growth factors. Neeper and colleagues (1995) were the first to note upregulation of BDNF in the cerebral cortex of rats with free access to a running wheel. Since then, several investigators have demonstrated in rodent models that voluntary running induces BDNF production and synaptic plasticity in the brain (Molteni et al., 2002; Farmer et al., 2004) and spinal cord, (Gomez-Pinilla et al., 2002) and that these responses appear to be dose dependent (Tong et al., 2001). Moreover, Van Praag and colleagues (1999) found in vitro evidence of neurogenesis in the dendate gyrus of adult mice exposed to an enriched environment that included voluntary wheel running.

There is a possibility that "spontaneous" increases in exercise capacity can occur during neurologic recovery. Recently, we reported a mean increase of 17% in VO2peak over the course of a stroke rehabilitation program that lacked a specific aerobic training component (MacKay-Lyons and Makrides, 2004). Similar findings of cardiovascular adaptations without formal exercise training have been reported in patients recovering from myocardial infarction

Table 21.2. Long-term cardiorespiratory adaptations to aerobic exercise training programs in individuals with neuromuscular impairments.

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