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A 45-year-old male with type 2 diabetes is diagnosed with autonomic neuropathy, which impairs autonomic function. He complains of becoming weak and "light headed" when he performs physical work such as mowing the lawn. Explain how this patient's autonomic dysfunction may account for his inability to be engaged in normal physical activities.

Autonomic neuropathy affects the function of most organ systems of the body because autonomic nerves play a vital role in regulating normal function. In the cardiovascular system, autonomic nerves, particularly sympathetic adrenergic nerves, regulate arterial pressure through their actions on the heart and vasculature. Patients with type 2 diabetes who have impaired autonomic control of the cardiovascular system may have abnormal responses to exercise because heart rate and inotropy may not increase normally and sympathetic stimulation of the arterial and venous system may be impaired. This loss of sympathetic control may result in a fall in arterial pressure during exercise owing to a greater-than-normal reduction in systemic vascular resistance, a decrease in central venous pressure owing to loss of venous tone, and a reduction in cardiac output caused by smaller-than-normal increases in heart rate and stroke volume. Hypotension during exercise impairs muscle perfusion, causing fatigue. Decreased cerebral perfusion caused by hypotension can lead to dizziness, visual disturbances, and syncope.

cannot operate to promote venous return and so cardiac output increases relatively little. Furthermore, the abdominothoracic pump does not contribute to enhancing venous return, particularly if the subject holds his or her breath during the forceful contraction, effectively performing a Valsalva maneuver (see Valsalva in Chapter 5 on CD). Unlike dynamic exercise, static exercise leads to a large increase in systemic vascular resistance, particularly if a large muscle mass is being contracted at maximal effort. The increased systemic vascular resistance results from enhanced sympathetic adrenergic activity to the peripheral vas-culature and from mechanical compression of the vasculature in the contracting muscles. As a result, systolic arterial pressure may increase to over 250 mm Hg during forceful isometric contractions, particularly those involving large muscle groups. This acute hypertensive state can produce vascular damage (e.g., hemorrhagic stroke) in susceptible individuals. In contrast, dynamic exercise leads to only modest increases in arterial pressure.

Body posture also influences how the cardiovascular system responds to exercise because of the effects of gravity on venous return and central venous pressure (see Chapter 5). When a person exercises in the supine position (e.g., swimming), central venous pressure is higher than when the person is exercising in the upright position (e.g., running). In the resting state before the physical activity begins, ventricular stroke volume is higher in the supine position than in the upright position owing to increased right ventricular preload. Furthermore, the resting heart rate is lower in the supine position. When exercise commences in the supine position, the stroke volume cannot be increased appreciably by the Frank-Starling mechanism because the high resting preload reduces the reserve capacity of the ventricle to increase its end-diastolic volume. Stroke volume still increases during exercise although not as much as when exercising while standing; however, the increased stroke volume is resulting primarily from increases in inotropy and ejection fraction with minimal contribution from the Frank-Starling mechanism. Because heart rate is initially lower in the supine position, the percent increase in heart rate is greater in the supine position, which compensates for the reduced ability to increase stroke volume. Overall, the change in cardiac output during exercise, which depends upon the fractional increases in both stroke volume and heart rate, is not appreciably different in the supine versus standing position.

The level of physical conditioning significantly influences maximal cardiac output and therefore maximal exercise capacity. A conditioned individual is able to achieve a higher cardiac output, whole-body oxygen consumption, and workload than a person who has a sedentary lifestyle. The increased cardiac output capacity is a consequence, in part, of increased ventricular and atrial responsiveness to inotropic stimulation by sympathetic nerves. Conditioned individuals also have hy-pertrophied hearts, much like what happens to skeletal muscle in response to weight training. Coupled with enhanced capacity for promoting venous return by the muscle pump system, these cardiac changes permit highly conditioned individuals to achieve ventricular ejection fractions that exceed 90% during exercise. In comparison, a sedentary individual may not be able to increase ejection fraction above 75%. Although the maximal heart rate of a conditioned individual is not necessarily any greater than that of a sedentary individual, the lower resting heart rates of a conditioned person allow for a greater percent increase in heart rate. Heart rate is lower in conditioned individuals because resting stroke volume is increased owing to the larger heart size and increased inotropy. Because resting cardiac output is not necessarily increased in a conditioned person, the heart rate is reduced by increased vagal tone to offset the increase in resting stroke volume, thereby maintaining a normal cardiac output at rest. The enhanced reserve capacity for increasing heart rate and stroke volume enables conditioned individuals to achieve maximal cardiac outputs (and workloads) that can be 50% higher than those found in sedentary people. Another important distinction between a sedentary and conditioned person is that for a given workload, the conditioned person has a lower heart rate. Furthermore, a conditioned person is able to sustain higher workloads for a longer duration and recover from the exercise much more rapidly.

Environmental factors affect cardiovascular responses to exercise. High altitudes, for example, decrease maximal stroke volume and cardiac output. The reason for this is that the pO 2 in arterial blood is reduced at higher elevations because of decreased atmospheric pressure. This decreases oxygen delivery to tissues, particularly to contracting muscle (both skeletal and cardiac), thereby resulting in insufficient oxygenation at lower workloads. Myocardial hypoxia decreases inotropy, which results in reduced stroke volume. Reduced oxygen delivery to exercising muscle reduces exercise capacity in the muscle and results in increased production of lactic acid as the muscle switches over to more anaerobic metabolism in the absence of adequate oxygen; i.e., the anaerobic threshold is reached at a lower workload.

Increased temperature and humidity affect cardiovascular responses during exercise by diverting a greater fraction of cardiac output to the skin to enhance heat removal from the body. This decreases the availability of blood flow for the contracting muscles. With elevated temperature and humidity, maximal cardiac output and oxygen consumption are reached at lower workloads, thereby reducing exercise capacity as well as endurance. Furthermore, dehydration can accompany high temperatures. Dehydration reduces blood volume and central venous pressure, and it attenuates the normal increase in cardiac output associated with exercise. This can lead to a fall in arterial pressure and heat exhaustion. Signs of heat exhaustion include general fatigue, muscle weakness, nausea, and mental confusion; it usually results from dehydration and loss of sodium chloride associated with physical activity in a hot environment— core temperature is not necessarily elevated.

Increased age reduces maximal exercise capacity. Maximal oxygen consumption decreases about 40% between 20 and 70 years of age. Many reasons exist for this decline. With increasing age, maximal heart rate decreases. Maximal heart rate is approximately 220 beats/minute minus the age of a person. Therefore, the maximal heart rate of a 70-year-old person is about 25% lower than the maximal heart rate of a 20-year-old person. Increasing age also reduces maximal stroke volume because of impaired ventricular filling (decreased ventricular compliance) and reduced inotropic responsiveness to sympathetic stimulation. Together, these changes reduce maximal cardiac output substantially. Older individuals have reduced skeletal muscle mass as well as decreased maximal muscle blood flow per unit weight of muscle. Recent research indicates a reduction in vasodilatory capacity of resistance vessels in skeletal muscle in older persons may be related to reduced endothelial production or bioavailability of nitric oxide and altered vascular smooth muscle responsiveness to metabolic vasodilators. Although increasing age inevitably limits exercise capacity, exercise habits and general health can significantly influence the decline in maximal cardiac output with age.

Finally, gender influences cardiovascular responses to exercise. Generally, males can reach and sustain significantly higher workloads and maximal oxygen consumptions than can females. Maximal cardiac outputs are about 25% less in females, although the maximal heart rates are similar. This difference is partly owing to increased skeletal muscle mass and to increased cardiac mass in males.

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