Muscle Blood Flow and Cardiac Output During Exercise; the Coronary Circulation and Ischemic Heart Disease

Blood Flow During Muscle Contractions

Figure 21-1 shows a record of blood flow changes in a calf muscle of a leg during strong rhythmic muscular exercise. Note that the flow increases and decreases with each muscle contraction. At the end of the contractions, the blood flow remains high for a few seconds but then returns to normal during the next few minutes.

The cause of the lower flow during the muscle contraction phase of exercise is compression of the blood vessels by the contracted muscle. During strong tetanic contraction, which causes sustained compression of the blood vessels, the blood flow can be almost stopped, but this also causes rapid weakening of the contraction.

Increased Blood Flow in Muscle Capillaries During Exercise

During rest, some muscle capillaries have little or no flowing blood, but during strenuous exercise, all the capillaries open. This opening of dormant capillaries diminishes the distance that oxygen and other nutrients must diffuse from the capillaries to the contracting muscle fibers; it sometimes contributes a twofold to threefold increased capillary surface area through which oxygen and nutrients can diffuse from the blood to the tissues.

Decreased Oxygen in Muscle Greatly Enhances Flow

The large increase in muscle blood flow that occurs during skeletal muscle activity is caused mainly by chemicals released locally that act directly on the muscle arterioles to cause dilation. One of the most important chemical effects is reduction of the oxygen level in the muscle tissues. When muscles are active, they use oxygen rapidly, thereby decreasing the oxygen concentration in the tissue fluids. This in turn causes local arteriolar vasodilation because low oxygen levels cause the blood vessels to relax and because oxygen deficiency causes release of vasodilator substances. Adenosine may be an important vasodilator substance, but experiments have shown that even large amounts of adenosine infused directly into a muscle artery cannot increase blood flow to the same extent as during intense exercise, and it cannot sustain vasodilation in skeletal muscle for more than about 2 hours.

Fortunately, even after the muscle blood vessels have become insensitive to the vasodilator effects of adenosine, other vasodilator factors continue to maintain increased capillary blood flow as long as the exercise continues. These factors include the following: (1) potassium ions; (2) adenosine triphosphate (ATP); (3) lactic acid; and (4) carbon dioxide. We still do not know quantitatively how much of a role each of these factors plays in increasing muscle blood flow during muscle activity; this subject was discussed in additional detail in Chapter 17 .

Nervous Control of Muscle Blood Flow

In addition to local tissue vasodilator mechanisms, skeletal muscles are provided with sympathetic vasoconstrictor nerves and, in some species of animals, sympathetic vasodilator nerves as well.

The sympathetic vasoconstrictor nerve fibers secrete norepinephrine at their nerve endings. When maximally activated, this mechanism can decrease blood flow through resting muscles to as little as one-half to one-third normal. This vasoconstriction is of physiologic importance in attenuating decreases of arterial pressure in circulatory shock and during other periods of stress, when it may even be necessary to increase blood pressure.

In addition to the norepinephrine secreted at the sympathetic vasoconstrictor nerve endings, the medullae of the two adrenal glands also secrete increased amounts of norepinephrine plus even more epinephrine into the circulating blood during strenuous exercise. The circulating norepinephrine acts on the muscle vessels to cause a vasoconstrictor effect similar to that caused by direct sympathetic nerve stimulation. The epinephrine, however, often has a slight vasodilator effect because epinephrine excites more of the beta-adrenergic receptors of the vessels, which are vasodilator receptors, in contrast to the alpha vasoconstrictor receptors excited especially by norepinephrine. These receptors are discussed in Chapter 61 .

Why Is Increased Arterial Pressure During Exercise Important?

When muscles are stimulated maximally in a laboratory experiment, but without allowing the arterial pressure to rise, muscle blood flow seldom rises more than about eightfold. Yet, we know from studies of marathon runners that muscle blood flow can increase from as little as 1 L/min for the whole body during rest to more than 20 L/min during maximal activity. Therefore, it is clear that muscle blood flow can increase much more than that which occurs in this simple laboratory experiment. What is the difference? Mainly, the arterial pressure rises during normal exercise. Let us assume, for example, that the arterial pressure rises by 30% during heavy exercise. This 30% increase causes 30% more force to push blood through the muscle tissue vessels. However, this is not the only important effect—the extra pressure also stretches the walls of the vessels, and this effect, along with the locally released vasodilators and higher blood pressure, may increase muscle total flow to more than 20 times normal.

Graphic Analysis of Changes in Cardiac Output During Heavy Exercise

Figure 21-2 shows a graphic analysis of the large increase in cardiac output that occurs during heavy exercise. The cardiac output and venous return curves crossing at point A represent the normal circulation, and the curves crossing at point B represent heavy exercise. Note that the great increase in cardiac output requires significant changes in both the cardiac output curve and the venous return curve, as follows.

The increased level of the cardiac output curve is easy to understand. It results almost entirely from sympathetic stimulation of the heart, which causes the following: (1) increased heart rate, up to as high as 170 to 190 beats/min; and (2) increased strength of contraction of the heart to as much as twice normal. Without this increased level of cardiac function, the increase in cardiac output would be limited to the plateau level of the normal heart, which would be a maximum increase of cardiac output of only about 2.5-fold rather than the 4-fold increase that can commonly be achieved by the untrained runner and the 7-fold increase that can be achieved in some marathon runners.

Now study the venous return curves. If no change occurred from the normal venous return curve, the cardiac output could hardly rise at all in exercise because the upper plateau level of the normal venous return curve is only 6 L/min. Yet, two important changes do occur:

• 1.

  The mean systemic filling pressure rises at the onset of heavy exercise. This effect results partly from the sympathetic stimulation that contracts the veins and other capacitative parts of the circulation. In addition, tensing of the abdominal and other skeletal muscles of the body compresses many of the internal vessels, thus providing more compression of the entire capacitative vascular system and causing a still greater increase in the mean systemic filling pressure. During maximal exercise, these two effects together can increase the mean systemic filling pressure from a normal level of 7 mm Hg to as high as 30 mm Hg.

• 2.

  The slope of the venous return curve rotates upward. This upward rotation is caused by decreased resistance in virtually all the blood vessels in active muscle tissue, which also causes resistance to venous return to decrease, thus increasing the upward slope of the venous return curve.

Therefore, the combination of increased mean systemic filling pressure and decreased resistance to venous return raises the entire level of the venous return curve.

In response to the changes in both the venous return curve and cardiac output curve, the new equilibrium point in Figure 21-2 for cardiac output and right atrial pressure is now point B, in contrast to the normal level at point A. Note especially that the right atrial pressure has hardly changed, having risen only 1.5 mm Hg. In fact, in a person with a strong heart, the right atrial pressure often falls below normal during very heavy exercise because of the greatly increased sympathetic stimulation of the heart. In contrast, even a moderate level of exercise may cause marked increases in right atrial pressure in patients with weakened hearts.