Exercise

Human Anatomy & Physiology Premium Course

Human Anatomy and Physiology Study Course

Get Instant Access

During exercise, cardiac output may increase from a resting value of 5 L/min to a maximal value of 35 L/min in trained athletes. The distribution of this cardiac output during strenuous exercise is illustrated in Figure 14-64. As expected, most of the increase in cardiac output goes to the exercising muscles, but there are also increases in flow to skin, required for dissipation of heat, and to the heart, required for the additional work performed by the heart in pumping the increased cardiac output. The increases in flow through these three vascular beds are the result of arteriolar va-sodilation in them. In both skeletal and cardiac muscle, the vasodilation is mediated by local metabolic factors, whereas the vasodilation in skin is achieved mainly by a decrease in the firing of the sympathetic neurons to the skin (additional mechanisms are described in Chapter 18). At the same time that arterio-lar vasodilation is occurring in these three beds, arte-riolar vasoconstriction—manifested as decreased blood flow in Figure 14-64—is occurring in the kidneys and gastrointestinal organs, secondary to increased activity of the sympathetic neurons supplying them.

Strenuous exercise (ml/min)

Rest (ml/min)

Brain

650 (13%)

Heart

215 (4%)

Skeletal muscle

1030 (20%)

Skin

430 (9%)

Kidney

950 (20%)

Abdominal organs

1200 (24%)

Other

525 (10%)

Total 5000

17,500

FIGURE 14-64

Distribution of the systemic cardiac output at rest and during strenuous exercise. The values at rest were previously presented in Figure 14-9.

Adapted from Chapman and Mitchell.

Skeletal-muscle blood flow Mean arterial pressure

Systolic arterial pressure Diastolic arterial pressure Total peripheral resistance

Cardiac output

Heart rate Stroke volume

End-diastolic ventricular volume

Skeletal-muscle blood flow Mean arterial pressure

Systolic arterial pressure Diastolic arterial pressure Total peripheral resistance

Cardiac output

Heart rate Stroke volume

End-diastolic ventricular volume

Exercise

1175%

+ 15%

1 50%

+ 50%

1120%

t 90%

t 30%

Time

FIGURE 14-65

Summary of cardiovascular changes during mild upright exercise. The person was sitting quietly prior to the exercise.

Vasodilation of arterioles in skeletal muscle, cardiac muscle, and skin causes a decrease in total peripheral resistance to blood flow. This decrease is partially offset by vasoconstriction of arterioles in other organs. Such resistance "juggling," however is quite incapable of compensating for the huge dilation of the muscle arterioles, and the net result is a marked decrease in total peripheral resistance.

What happens to arterial blood pressure during exercise? As always, the mean arterial pressure is simply the arithmetic product of cardiac output and total peripheral resistance. During most forms of exercise (Figure 14-65 illustrates the case for mild exercise), the cardiac output tends to increase somewhat more than the total peripheral resistance decreases, so that mean arterial pressure usually increases a small amount. Pulse pressure, in contrast, markedly increases, because of an increase in both stroke volume and the speed at which the stroke volume is ejected.

The cardiac output increase during exercise is due to a large increase in heart rate and a small increase in stroke volume. The heart rate increase is caused by a combination of decreased parasympathetic activity to the SA node and increased sympathetic activity. The

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Circulation CHAPTER FOURTEEN

Circulation CHAPTER FOURTEEN

increased stroke volume is due mainly to an increased ventricular contractility, manifested by an increased ejection fraction and mediated by the sympathetic nerves to the ventricular myocardium.

Note, however, in Figure 14-65 that there is a small increase (10 percent) in end-diastolic ventricular volume. Because of this increased filling, the Frank-Starling mechanism also contributes to the increased stroke volume, although not to the same degree as the increased contractility does. The increased contractility also accounts for the greater speed at which the stroke volume is ejected, as noted in the previous discussion of pulse pressure.

We have focused our attention on factors that act directly upon the heart to alter cardiac output during exercise, but it would be incorrect to leave the impression that these factors, by themselves, are sufficient to account for the elevated cardiac output. The fact is that cardiac output can be increased to high levels only if the peripheral processes favoring venous return to the heart are simultaneously activated to the same degree. Otherwise, the shortened filling time resulting from the high heart rate would lower end-diastolic volume and stroke volume by the Frank-Starling mechanism.

Factors promoting venous return during exercise are: (1) increased activity of the skeletal-muscle pump, (2) increased depth and frequency of inspiration (the respiratory pump), (3) sympathetically mediated increase in venous tone, and (4) greater ease of blood flow from arteries to veins through the dilated skeletal-muscle arterioles.

What are the control mechanisms by which the cardiovascular changes in exercise are elicited? As described previously, vasodilation of arterioles in skeletal and cardiac muscle once exercise is underway represents active hyperemia secondary to local metabolic factors within the muscle. But what drives the enhanced sympathetic outflow to most other arterioles, the heart, and the veins, and the decreased parasym-pathetic outflow to the heart? The control of this autonomic outflow during exercise offers an excellent example of what we earlier referred to as a preprogrammed pattern, modified by continuous afferent input. One or more discrete control centers in the brain are activated during exercise by output from the cerebral cortex, and according to this "central command," descending pathways from these centers to the appropriate autonomic preganglionic neurons elicit the firing pattern typical of exercise. Indeed, these centers begin to "direct traffic" even before the exercise begins, since a person just about to begin exercising already manifests many of these changes in cardiac and vascular function; thus, this constitutes a feedforward system.

Once exercise is underway, local chemical changes in the muscle can develop, particularly during high levels of exercise, because of imperfect matching between flow and metabolic demands. These changes activate chemoreceptors in the muscle. Afferent input from these receptors goes to the medullary cardiovascular center and facilitates the output reaching the au-tonomic neurons from higher brain centers (Figure 14-66). The result is a further increase in heart rate, myocardial contractility, and vascular resistance in the nonactive organs. Such a system permits a fine degree of matching between cardiac pumping and total oxygen and nutrients required by the exercising muscles. Mechanoreceptors in the exercising muscles are also stimulated and provide input to the medullary cardiovascular center.

Finally, the arterial baroreceptors also play a role in the altered autonomic outflow. Knowing that the mean and pulsatile pressures rise during exercise, you might logically assume that the arterial baroreceptors will respond to these elevated pressures and signal for increased parasympathetic and decreased sympathetic outflow, a pattern designed to counter the rise in arterial pressure. In reality, however, exactly the opposite occurs; the arterial baroreceptors play an important role in elevating the arterial pressure over that existing at rest. The reason is that one neural component of the central command output goes to the arterial barore-ceptors and "resets" them upward as exercise begins. This resetting causes the baroreceptors to respond as though arterial pressure had decreased, and their output (decreased action-potential frequency) signals for decreased parasympathetic and increased sympathetic outflow.

Table 14-10 summarizes the changes that occur during moderate endurance exercise—that is, exercise (like jogging, swimming, or fast walking) that involves large muscle groups for an extended period of time.

In closing, a few words should be said about the other major category of exercise, which involves maintained isometric contractions, as in weight-lifting. Here, too, cardiac output and arterial blood pressure increase, and the arterioles in the exercising muscles undergo vasodilation due to local metabolic factors. However, there is a crucial difference: During isometric contractions, once the contracting muscles exceed 10 to 15 percent of their maximal force, the blood flow to the muscle is greatly reduced because the muscles are physically compressing the blood vessels that run through them. In other words, the arteriolar vasodi-lation is completely overcome by the physical compression of the blood vessels. Thus, the cardiovascular changes are ineffective in causing increased blood flow to the muscles, and isometric contractions can be

PART THREE Coordinated Body Functions

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

III. Coordinated Body Functions

14. Circulation

© The McGraw-Hill Companies, 2001

PART THREE Coordinated Body Functions

Brain "exercise centers"

Arterial baroreceptors

Reset upward

Medullary cardiovascular center

Afferent input

Exercising skeletal muscles

Contractions n

Stimulate ] mechanoreceptors in the muscles

Local chemical changes

Afferent input i Parasympathetic output to heart t Sympathetic output to heart, veins, and arterioles in abdominal organs and kidneys

Stimulate chemoreceptors in the muscles

Dilate arterioles in the muscle t Muscle blood flow t Cardiac output t Vasoconstriction in abdominal organs and kidneys

FIGURE 14-66

Control of the cardiovascular system during exercise. The primary outflow to the sympathetic and parasympathetic neurons is via pathways from "exercise centers" in the brain. Afferent input from mechanoreceptors and chemoreceptors in the exercising muscles and from reset arterial baroreceptors also influence the autonomic neurons by way of the medullary cardiovascular center.

maintained only briefly before fatigue sets in. Moreover, because of the blood-vessel compression, total peripheral resistance may go up considerably (instead of down, as in endurance exercise), contributing to a large rise in mean arterial pressure.

Maximal Oxygen Consumption and Training

As the magnitude of any endurance exercise increases, oxygen consumption also increases in exact proportion until a point is reached when it fails to rise despite a further increment in work load. This is known as maximal oxygen consumption (VO2max). After VO2max has been reached, work can be increased and sustained only very briefly by anaerobic metabolism in the exercising muscles.

Theoretically, VO2max could be limited by (1) the cardiac output, (2) the respiratory system's ability to deliver oxygen to the blood, or (3) the exercising muscles' ability to use oxygen. In fact, in normal people (except for a few very highly trained athletes), cardiac output is the factor that determines VO2max. With increasing workload (Figure 14-67), heart rate increases progressively and markedly until it reaches a maximum. Stroke volume increases much less and tends to level off when 75 percent of VO2max has been reached (it actually starts to go back down in elderly people). The major factors responsible for limiting the rise in stroke volume and, hence, cardiac output are (1) the very rapid heart rate, which decreases diastolic filling time, and (2) inability of the peripheral factors

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

Circulation CHAPTER FOURTEEN

Circulation CHAPTER FOURTEEN

TABLE 14-10 Cardiovascular Changes in Moderate Endurance Exercise

Variable

Change

Explanation

Cardiac output

Increases

Heart rate and stroke volume both increase, the former to a much greater extent.

Heart rate

Increases

Sympathetic nerve activity to the SA node increases, and parasympathetic nerve activity decreases.

Stroke volume

Increases

Contractility increases due to increased sympathetic nerve activity to the ventricular myocardium; increased ventricular end-diastolic volume also contributes to increased stroke volume by the Frank-Starling mechanism.

Total peripheral resistance

Decreases

Resistance in heart and skeletal muscles decreases more than resistance in other vascular beds increases.

Mean arterial pressure

Increases

Cardiac output increases more than total peripheral resistance decreases.

Pulse pressure

Increases

Stroke volume and velocity of ejection of the stroke volume increase.

End-diastolic volume

Increases

Filling time is decreased by the high heart rate, but this is more than compensated for by the factors favoring venous return—venoconstriction, skeletal-muscle pump, and increased inspiratory movements.

Blood flow to heart and skeletal muscle

Increases

Active hyperemia occurs in both vascular beds, mediated by local metabolic factors.

Blood flow to skin

Increases

Sympathetic nerves to skin vessels are inhibited reflexly by the increase in body temperature.

Blood flow to viscera

Decreases

Sympathetic nerves to the blood vessels in the abdominal organs and the kidneys are stimulated.

Blood flow to brain

Unchanged

Autoregulation of brain arterioles maintains constant flow despite the increased mean arterial pressure

favoring venous return (skeletal-muscle pump, respiratory pump, venous vasoconstriction, arteriolar va-sodilation) to increase ventricular filling further during the very short time available.

A person's t'O?max is not fixed at any given value but can be altered by the habitual level of physical activity. For example, prolonged bed rest may decrease tc>2max by 15 to 25 percent, whereas intense long-term physical training may increase it by a similar amount. To be effective, the training must be of an endurance type and must include certain minimal levels of duration, frequency, and intensity. For example, jogging 20 to 30 min three times weekly at 5 to 8 mi/h definitely produces a significant training effect in most people.

At rest, compared to values prior to training, the trained individual has an increased stroke volume and decreased heart rate with no change in cardiac output (see Figure 14-67). At yc2max, he or she has an increased cardiac output, compared to pretraining values; this is due entirely to an increased maximal stroke volume since maximal heart rate is not altered by training (see Figure 14-67). The increase in stroke volume is due to a combination of (1) effects on the heart (the mechanism is unknown but may include a thicker myocardium and increased ventricular contractility), and (2) peripheral effects, including increased blood volume and increases in the number of blood vessels in skeletal muscle, which permit increased muscle blood flow and venous return.

Training also increases the concentrations of ox-idative enzymes and mitochondria in the exercised muscles (Chapter 12). These changes increase the speed and efficiency of metabolic reactions in the muscles and permit large increases—200 to 300 percent— in exercise endurance, but they do not increase VO2max because they were not limiting it in the untrained individuals.

Aging is associated with significant changes in the heart's performance during exercise. Most striking is a decrease in the maximum heart rate (and hence cardiac output) achievable.

PART THREE Coordinated Body Functions

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition

PART THREE Coordinated Body Functions

Work rate
Work rate

O2 consumption

FIGURE 14-67

Changes in cardiac output, heart rate, and stroke volume with increasing work in untrained and trained persons.

O2 consumption

FIGURE 14-67

Changes in cardiac output, heart rate, and stroke volume with increasing work in untrained and trained persons.

Was this article helpful?

0 0
Push Your Limits

Push Your Limits

Get All The Support And Guidance You Need To Be A Success At Getting In Top Shape... Today. This Book Is One Of The Most Valuable Resources In The World When It Comes To Unleash Your Body Power and Increase Your Body Endurance.

Get My Free Ebook


Responses

  • NADINE
    What happens to total peripheral resistance during exercise?
    8 years ago
  • alexander
    What happens to mean arterial pressure during exercise?
    8 years ago
  • Bobby
    What happens as exercise mean arterial pressure and total peripheral resistance?
    8 years ago
  • vera
    What happens to total peripheral blood flow during exercise?
    8 years ago

Post a comment