Cardiovascular responses to acute exercise - part I

Numerous cardiovascular changes occur during dynamic exercise. All share a common goal: to meet the increased demands necessary to perform exercise. To better understand the changes that occur, we must look more closely at specific cardiovascular functions. Following changes will be examined here in the cardiovascular system:

• Heart rate
• Stroke volume
• Cardiac output
• Blood pressure
• Blood flow
• Blood.

Heart rate

Heart rate(HR) is one of the simplest and yet most informative of the cardiovascular parameters. Measuring HR involves simply taking the subject’s pulse, usually at the radial or carotid artery. Heart rate is a good indicator of the intensity of exercise.

Resting heart rate

Resting heart rate(RHR) averages 60 to 80 beats/min in most individuals. In highly conditioned, endurance-trained athletes, resting rates as low as 28 to 40 beats/min have been reported. This is mainly due to an increase in vagal tone that accompanies endurance exercise training. Resting heart rate can also be affected by environmental factors, for example, it increases with extremes in temperature and altitude.

Just before the start of exercise, preexercise HR usually increases above normal resting values. This is called an anticipatory response. This response is mediated through release of the neurotransmitter norepinephrine from the sympathetic nervous system and the hormone epinephrine from the adrenal medulla. Vagal tone probably also decreases. Because preexercise HR is elevated, reliable estimates of the true RHR should be made only under conditions of total relaxation, such as early in the morning before the subject rises from a restful night’s sleep.

Heart rate during exercise

When exercise begins, HR increases directly in proportion to the increase in exercise intensity(see picture below), until near-maximal exercise is achieved. As maximal exercise intensity is approached, HR begins to plateau even as the exercise workload continues to increase. This indicates that HR is approaching a maximum value. The maximum heart rate(HR_max) is the highest HR value achieved in an all-out  effort to the point of exhaustion. This is a highly reliable value that remains constant from day to day. However, this value changes slightly from year to year due to the normal age-related decline in HR_max.

HR_max is often estimated based on age because HR_max shows a slight but steady decrease of about one beat per year beginning at 10 to 15 years of age. Subtracting one’s age from 220 provides an approximation of one’s average HR_max. However, this is only an estimate – individual values vary considerably from this average value. To illustrate, for a 40-year-old person, HR_max would be estimated to be 180 beats/min(HR_max = 220-40). However, 68% of all 40-year-olds have actual HR_max values between 168 and 192 beats/min(mean ±1 standard deviation), and 95% fall between 156 and 204 beats/min(mean ±2 standard deviations). This demonstrates the potential for error in estimating a person’s HR_max. A more accurate equation has been developed to estimate HR_max from age. In this equation, HR_max = 208 – (0.7 x age).

When the rate of work is held constant at a submaximal intensity, HR increases fairly rapidly until it reaches a plateau. This plateau is the steady-state heart rate, and it is optimal HR for meeting the circulatory demands at that specific rate of work. For each subsequent increase in intensity, HR will reach a new steady-state value within 2 to 3 min. However, the more intense the exercise, the longer it takes to achieve this steady-state value.

The concept of steady-state heart rate forms the basis for several tests that have been developed to estimate physical fitness. In one such test, individuals are placed on an exercise device, such as a cycle ergometer, and then perform exercise at two or three standardized exercise intensities. Those in better physical condition(i.e., those with better cardiorespiratory endurance capacity) will have a lower steady-state HR at each exercise intensity than those who are less fit. Thus, steady-state HR is a valid predictor of cardiorespiratory fitness: A lower steady-state HR reflects greater cardiorespiratory fitness.

Figure below illustrates results from a submaximal exercise test performed by two different individuals of the same age. Steady-state HR is measured at three to four distinct workloads, and a line of best fit is drawn through the data points. Because there is a consistent relationship between intensity and energy demand, steady-state HR can be plotted versus the corresponding energy(VO₂) required to do work on the cycle ergometer. The resultant line can be extrapolated to the age-predicted HR_max to estimate an individual’s maximal exercise capacity. In this picture, subject A has a higher fitness level than subject B because at any given submaximal intensity, his HR is lower; and extrapolation to age-predicted HR_max yields a higher estimated maximal exercise capacity(VO_2max).

Stroke volume

Stroke volume(SV) also changes during acute exercise to allow the heart to meet the demands of exercise. At near-maximal and maximal exercise intensities, SV is a major determinant of cardiorespiratory endurance capacity.

Stroke volume is determined by four factors:

1)      The volume of venous blood returned to the heart(the heart can only pump what returns: preload)

2)      Ventricular distensibility(the capacity to enlarge the ventricle, for maximal filling)

3)      Ventricular contractility(the inherent capacity of the ventricle to contract)

4)      Aortic or pulmonary artery pressure(the pressure against which the ventricles must contract: afterload).

The first two factors influence the filling capacity of the ventricle, determining how much blood is available for filling the ventricle and the ease with which the ventricle is filled at the available pressure. This is reffered to preload. The last two factors influence the ventricle’s ability to empty, determining the force with which blood is ejected and the pressure, or afterload, against which it must be expelled into the arteries. These four factors directly control the alterations in SV in response to increasing exercise intensity.

Stroke volume increase with exercise

Stroke volume increases above resting values during exercise. Most researchers agree that SV increases with increasing rates of work, but only up to exercise intensities somewhere between 40% and 60% of maximal capacity. At that point, SV typically plateaus, remaining essentially unchanged up to and including the point of exhaustion in the picture below. However, other researchers have reported that SV continues to increase up through maximal exercise intensities. 

When the body is in an upright position, SV can almost double from resting to maximal values. For example, in active but untrained individuals, SV increases from about 60 to 70 ml/beat at rest to 110 to 130ml/beat during maximal exercise. In highly trained endurance athletes, SV can increase from 80 to 110ml/beat at rest to 160 to 200ml/beat during maximal exercise. During supine exercise, such as recumbent cycling, SV also increases but usually by only about 20% to 40% - not nearly as much as in an upright position. Why does body position make such a difference?
When the body is in the supine position, blood does not pool in the lower extremities. Blood returns more easily to the heart in a supine posture, which means that resting SV values are higher in the supine position than in the upright position. Thus, the increase in SV maximal exercise is not as great in the supine position than in the upright position. Thus, the increase in SV with maximal exercise is not as great in the supine position as in the upright position because SV starts out higher. Interestingly, the highest SV attainable in upright exercise is only slightly greater than the resting value in the reclining position. The majority of the SV increase during low to moderate intensities of exercise in the upright position appears to be compensating for the force of gravity that causes blood to pool in the extremities.

Explanations for the stroke volume increase

One explanation for the increase in SV with exercise is that the primary factor determining SV is increased preload or the extent to which the ventricle fills with blood and stretches. When the ventricle stretches more during filling, it subsequently contracts more forcefully. For example, when a larger volume of blood enters and fills the ventricle during diastole, the ventricular walls stretch. To eject that greater volume of blood, the ventricle responds by contracting more forcefully. This is reffered to Frank-Starling mechanism. Additionally, SV can increase during exercise if the ventricle’s contractility is enhanced by an increase in neural stimulation, an increased release of circulating catecholamines(epinephrine, norepinephrine), or both, even without an increased end-diastolic volume. These mechanisms combine to increase SV during dynamic exercise.

Some clinically used cardiovascular diagnostic techniques have made it possible to determine exactly how SV changes with exercise. Echocardiography(using sound waves) and radionuclide techniques(“tagging” of red blood cells with radioactive tracers) have elucidated how the heart chambers respond to increasing oxygen demands during exercise. With either technique, continuous pictures can be taken of the heart at rest and up to near-maximal intensities of exercise.

Figure below illustrates the results of one study of normally active but untrained subjects. In this study, participants were tested during both supine and upright cycle ergometry under four conditions, which are depicted on the x-axis:

• Rest
• Low-intensity exercise
• Intermediate-intensity exercise
• Peak-intensity exercise.

Going from resting conditions to exercise of increasing intensities, there is an increase in left ventricular end-diastolic volume(a greater filling or preload), indicating that the Frank-Starling mechanism is operating. There is also a decrease in the left ventricular end-systolic volume(greater emptying), indicating an increased degree of contractility.

This figure shows that both the Frank-Starling mechanism and increased contractility are important in increasing SV during exercise. The Frank-Starling mechanism appears to have its greatest influence at lower exercise intensities, and contractility has its greates effects at higher exercise intensities.

Recall that HR also increases with exercise intensity. The plateau or small decrease in left ventricular end-diastolic volume at higher exercise intensities could be caused by reduced ventricular filling time. One study showed that ventricular filling time decreased from about 500 to 700ms at rest to about 150ms at higher HRs(about 150-200 beats/min). Therefore, with increasing work rates approaching HR_max, the diastolic filling time could be shortened enough to limit filling. As a result, end-diastolic volume might plateau or start to decrease.

For the Frank-Starling mechanism to work, left ventricular end-diastolic volume must increase by an increase in venous blood return to the heart. This happens through redistribution of blood by sympathetic through redistribution of blood by sympathetic activation of arteries and arterioles in inactive areas of the body such as in the renal and splanchnic circulations. Also, the muscle and respiratory pumps aid in increasing venous return.

Thus, two factors that can contribute to an increase in SV with increasing intensity of exercise are increased venous return(preload) and increased ventricular contractility. A third factor also contributes to the increase in SV during exercise -  a decrease in afterload placed on the heart through a decrease in total peripheral resistance. Total peripheral resistance decreases because of vasodilatation of the blood vessels going to exercising skeletal muscle. This decrease in afterload allows the left ventricle to expel blood against less resistance, facilitating emptying of the blood from this chamber.