Cardiovascular responses to acute exercise - part II

 PART I

Cardiac output

If we recall that cardiac output is the product of heart rate and stroke volume(Q = HR x SV), cardiac output predictably increases with increasing exercise intensity(figure below). Resting cardiac output is approximately 5.0 L/min, but varies in proportion to the size of the person. Maximal cardiac output varies between 20(sedentary person) and 40(elite endurance athlete) L/min and is a function of both body size and endurance training. The linear relationship between cardiac output and intensity of exercise is predictable because the major purpose of the increase in cardiac output is to meet the muscles’ increased demand for oxygen. Like VO_2max, when cardiac output approaches maximal exercise intensities it may reach a plateau. In fact, it is likely that VO_2max is limited by this leveling off of cardiac output.

The integrated cardiac response to exercise

To see how HR, SV, and Q vary under various conditions of rest and exercise, consider the following example. An individual first transitions from a reclining position to a sitting position and then to standing. Next the person begins walking, then jogging, and finally breaks into a fast-paced run. How does the heart respond?

In a reclined position, HR is ~50 beats/min; it increases to about 55 beats/min during sitting and to about 60 beats/min during standing. When the body shifts from a reclining to a sitting position and then to a standing position, gravity causes blood to pool in the legs, which reduces the volume of blood returning to the heart and thus decreases SV. To compensate for the reduction in SV, HR increases in order to maintain cardiac output; that is, Q = HR x SV.

During the transition from rest to walking, HR increases from about 60 to about 90 beats/min. Heart rate increases to 140 beats/min with moderate-paced jogging and can reach 180 beats/min or more with a fast-paced run. The initial increase in HR up to about 100 beats/min is mediated by a withdrawal of vagal tone. Further increases in HR are mediated by th sympathetic nervous system. Stroke volume also increases with exercise, further increasing cardiac output. These relationships are shown in the picture below.

During the initial stages of exercise in untrained individuals, increased cardiac output is caused by an increase in both HR and SV. When the level of exercise exceeds 40% to 60% of the individual’s maximal exercise capacity. SV either plateaus or continues to increase, but at a much slower rate. Thus, further increases in cardiac output are largely the result of increases in HR. Stroke volume increases are likely to contribute more to the rise in cardiac output during the higher intensities of exercise in those people who are highly trained.

Blood pressure

During dynamic exercise, mean arterial blood pressure increases substantially. However, systolic and diastolic blood pressure do not increase to a similar degree. With whole-body endurance exercise, systolic blood pressure increases in direct proportion to the increase in exercise intensity. However, diastolic pressure does not change significantly, and may even decrease. A systolic pressure that starts out at 120mmHg in a normal healthy person at rest can exceed 200mmHg at maximal exercise. Systolic pressures of 240 to 250mmHg have been reported in normal, healthy, highly trained athletes at maximal intensities of aerobic exercise.

Increased systolic blood pressure results from the increased cardiac output(Q) that accompanies increasing rates of work. This increase in pressure helps facilitate the increase in blood flow through the vasculature. Also, blood pressure(that is, hydrostatic pressure) determines how much plasma leaves the capillaries, entering the tissues and carrying needed supplies. Thus increased systolic pressure aids substrate delivery to working muscles.

Blood pressure reaches a steady state during submaximal steady-state endurance exercise. As work intensity increases, so does systolic blood pressure. If steady-state exercise is prolonged, the systolic pressure might start to decrease gradually, but diastolic pressure remains constant. The slight decrease in systolic blood pressure, if it occurs, is a normal response and simply reflects increased arteriole dilation in the active muscles, which decreases the total peripheral resistance or TPR(since blood pressure = cardiac output x total peripheral resistance).

Diastolic blood pressure changes little during submaximal dynamic exercise; however, at maximal exercise intensities, diastolic blood pressure increases slightly. Remember that diastolic pressure reflects the pressure in the arteries when the heart is at rest(diastole). With dynamic exercise there is an overall increase in sympathetic neural tone to the vasculature, causing overall vasoconstriction. However, this vasoconstriction is blunted in the exercising muscles by the release of local vasodilators. Thus, there is a balance between vasoconstriction to inactive regions and vasodilatation in the active skeletal muscle; therefore diastolic pressure does not change substantially. However, in some cases of cardiovascular disease, increases in diastolic pressure of 15mmHg or more occur in response to exercise and are one of several indications for immediately stopping a diagnostic exercise test. Figure below illustrates a typical blood pressure response to leg and arm cycling exercise with increasing exercise intensities.

As seen in figure, upper body exercise causes a greater blood pressure response than leg exercise at the same absolute rate of energy expenditure. This is most likely attributable to the smaller muscle mass and vasculature of the upper body compared with the lower body, plus an increased energy demand to stabilize the body during arm exercise. This difference in the systolic blood pressure response to upper and lower body exercise has important implications for the heart. Myocardial oxygen uptake and myocardial blood flow are directly related to the product of HR and systolic blood pressure. This value is referred to as the rate-pressure product or double product(DP = HR x SBP). With static or dynamic resistance exercise or upper body work, the rate-pressure product is elevated , indicating increased myocardial oxygen demand. This relationship between rate-pressure product and myocardial oxygen demand is important in clinical exercise testing.

Blood pressure responses to resistance exercise, such as weighlifting, are exaggerated. With high-intensity resistance training, blood pressure can reach 480/350mmHg. In such exercise, use of the Valsalva maneuver is quite common. This maneuver occurs when a person tries to exhale while the mouth, nose, and glottis are closed. This action causes an enormous increase in intrathoracic pressure. Much of subsequent blood pressure increase results from the body’s effort to overcome the high internal pressures created during the Valsalva maneuver.