The Effects of Exercise


Cardiovascular Physiology

Robert J. Kosinski
Clemson University

Last updated February 2009

The purpose of this page is to help students in Biology 111 at Clemson University write papers on an exercise physiology experiment. It has the following major sections:

Exercise as a Challenge to Homeostasis
Heart Rate and Cardiac Output
The Double Product
Velocity of Blood Flow
Blood Pressure
Resting and Exercising Data for Young Adults
ECG Effects of Exercise
Muscle Fatigue
Literature Cited

Exercise as a Challenge to Homeostasis

Strenuous exercise is a severe test of homeostasis. Oxygen consumption and carbon dioxide production can increase to 10 times normal, mostly due to increased oxygen demand by the muscles (Shepard, 1999). If we were insects, oxygen could diffuse directly to tissues via the tracheal tubes. But because we depend on our circulatory system to deliver oxygen to our tissues, this large increase in gas exchange is a circulatory system story. Blood flow to exercising muscles increases from about 1 L/min at rest to over 20 L/min (Guyton, 1985). This tremendous increase in flow is called exercise hyperemia. Exercise hyperemia comes about mainly because the muscle capillary beds (normally about 20-25% open) all open up. This dramatic change is caused by local adaptation (do you remember what that is?). While resting muscles are high in oxygen and low in carbon dioxide, most precapillary sphincters are contracted. However, when the muscle starts consuming oxygen, the precapillary sphincters open, and blood surges into all the muscle capillaries.

On the other hand, a poorly-conditioned, sedentary person might only be able to increase his oxygen consumption 3 times (rather than 10 times in the trained athlete), mainly because of a circulatory system that can't carry as much blood to the muscles (Laughlin, 1999).

This tremendous increase in oxygen consumption and carbon dioxide production has dramatic consequences for the circulatory system. Heart rate can triple. Mainly because of an increase in heart rate, cardiac output increases by 5 times, or up to 7 times in the trained athlete (Shepard, 1999; Laughlin, 1999). Mostly, this increase is caused by increased venous return, which in turn in caused by decreased resistance in the muscle capillaries, and the fact that working muscles are squeezing the veins and increasing the velocity of blood moving through them (Laughlin, 1999). Pulmonary ventilation increases 10-20 times.

This Web page will look at the effect of exercise (on either a treadmill or an exercise bicycle in most research) on heart rate, blood pressure, and the ECG.

Heart Rate and Cardiac Output

Average resting heart rate is 72-80 beats per minute in a female and 64 to 72 beats per minute in a male. It gets as high as 160 bpm in a fetus. The more physically fit the individual, the slower resting heart rate tends to be. A well-trained athlete can have a resting rate as low as 40 beats per minute, but the heart's stroke volume is higher, so cardiac output stays adequate. In healthy people, a resting heart rate less than 60 bpm (bradycardia) is a sign of good conditioning. On the other hand, tachycardia (a resting heart rate faster than 100 bpm) is a bad sign, and might incline a heart towards ventricular fibrillation (Marieb, 1989). Zhang (2008) reviews data that show that over a broad range of species, a mammal has about 1 billion heartbeats allotted to it, and it can use them up very rapidly (e.g., a mouse, at 600 bpm) or slowly (an elephant, at 25 bpm). The same relationship applies to humans (although we seem to be allotted about 3 billion beats). Humans with high resting heart rates have increased risk of cardiovascular death, especially sudden heart attack death (Jouven et al., 2005):

Fast HR and MI

Fig. 1. The relation between resting heart rate and risk of death. Relative risk has been standardized to 1.0 for heart rates of less than 60 bpm (Jouven et al., 2005).

These data are sobering for those with fast resting heart rates. Note that a person with a "slow" heart rate of 66 bpm has twice the risk of sudden cardiac death as a person with a heart rate less than 60 bpm, and a person with a heart rate of 76 bpm has almost four times as high a mortality risk from sudden heart attack compared with a person with a resting heart rate less than 60 bpm.

Once exercise begins, there is substantial stimulation of the sympathetic nervous system. This sympathetic discharge increases heart rate by increasing the pace of SA node depolarization (Guyton, 1985). Maximum heart rate is a function of age, and is defined by

HRmax = 220 - age

where age is age in years (Goodman, 1999). Training (improvement in condition) does not begin until the heart rate reaches the "target zone," shown below for several different ages:

Fig. 2. The maximum predicted heart rates and target zone heart rates for several different ages. The figures in parentheses are beats per 10 sec. Taken from Goodman (1999), p. 87.
Fig. 2 indicates that for a person of 20, training does not begin until a heart rate of 144 bpm is attained. How close did your subjects come to their target zone? To their maximum heart rate? When you consider that fitness experts recommend getting into your heart rate target zone and staying there for 30 minutes, the minor amount of exercise your section probably did is apparent. Borresen and Lambert (2008) emphasize that the speed of heart rate recovery from exercise is an excellent predictor of general condition, and a slow return of heart rate to resting values is associated with higher mortality.

In addition to heart rate effects, heavy exercise doubles the force of contraction of the heart muscle. More blood returns to the heart, too. Extensive vasodilation in working muscles (see section on blood pressure) and squeezing of the large veins by the muscles returns blood to the heart more quickly, which means an increase in cardiac output (Starling's Law of the Heart; Laughlin 1999). Cardiac output increases from about 5 L/min in the resting adult to about 20 L/min during violent exercise. Some trained athletes can increase their cardiac output up to 35 L/min (Guyton, 1985), and this is the main cause of their greater capacity for aerobic exercise. On the other hand, if the environment is hot, it is harder to exercise as vigorously. One reason for this is that the body threatens to overheat; another is that so many skin capillaries are open to dump heat that there is actually a decrease in blood flowing to the muscles (Laughlin, 1999). Keeping the muscles aerobic with a brisk blood flow is the key to muscular endurance.

The Double Product

The consumption of oxygen by the heart muscle is a clear indication of how hard the heart is working. This consumption is proportional to DP, the double product:

DP = BPsys x HR

where BPsys is the systolic blood pressure in mm Hg, and HR is heart rate in beats per minute (Froelicher and Meyers, 2000). If a person suffers from angina, the angina usually begins at a certain double product (e.g., when the heart is pumping fast, or working against high blood pressure, or both). For example, Sullivan, Genter and Roberts (1984) found that 14 male patients with angina started to experience angina pain on a treadmill when their double products reached 18,900. How close did your subjects come to this double product?

The Velocity of Blood Flow

The fastest blood flow a rest (40-50 cm/sec) is in the aorta. After that, resting blood flow declines to 0.3 cm/sec in the capillaries, and then rises again to about 10-30 cm/sec in the large veins because the veins have a smaller total cross-sectional area than the capillaries (Marieb, 1989).

During exercise, we would expect faster flow rates, at least in the large arteries (that lead to the tip of the finger, for example). If the cardiac output has multiplied by 4-7 times during extreme exercise, and the diameter of the arteries is the same, it follows that blood must be flowing faster. Our exercise could not be called extreme, but it seems reasonable to predict some decrease in pulse lag time.

Blood Pressure

Resting systolic blood pressure varies between 110 and 140 mm Hg in adults, and diastolic pressure varies from 70-80 mm Hg (Marieb, 1989). The sympathetic stimulation that accompanies exercise also causes a powerful vasoconstriction throughout the body outside the exercising muscles, but vasodilation within the working muscles (Guyton, 1985). This increases blood pressure and diverts blood from all parts of the body to the working muscles. This also means that the increase in blood pressure depends on the type of exercise. When only a few muscles are in action, the systolic blood pressure can increase 60-80 mm Hg. When the whole body is in action, the vasodilation in the working muscles nearly cancels out the nonmuscular vasoconstriction, and the increase may be as little as 20 mm Hg (Guyton, 1985).

Systolic blood pressure tends to rise during exercise, but diastolic blood pressure does not, as shown in the following graph, which shows both systolic and diastolic pressures for normal and hypertensive individuals during different types of exercise:

Fig. 3. Systolic (above) and diastolic (below) blood pressures in several types of exercise. The open circles show normal individuals. RR = lying down and resting, RS = standing and resting, 50W = an intermediate level of exercise on a bicycle ergometer, and Max Ex = maximum exercise on a bicycle ergometer. Taken from Tipton (1999), p. 468.
Note that an intermediate level of exercise produced a systolic blood pressure of 155 mm Hg in a normal individual. How close did your subjects come to this?

Resting and Exercising Data for Young Adults

Wilmore et al. (2001) did a large study of 507 "healthy but sedentary" people to determine how much an exercise program helped their cardiovascular health. Surprisingly, it didn't help much. However, the table below shows the pretraining values of heart rate, systolic blood pressure, and diastolic blood pressure for 229 participants who were between the ages of 17 and 29. In other words, these are your age peers. How well do your heart rate and blood pressure compare to theirs? Note that males tend to have slower heart rates and higher blood pressures than females. This may be just a size effect--larger animals also tend to have slower heart rates and higher blood pressures.

Table 1. Pretraining values for 229 healthy volunteers, 17-29 years old. "Moderate" exercise means exercising on a stationary bicycle until oxygen consumption is 60% of the maximum. Heart rate is in beats per minute; blood pressure is measured in mm Hg.

Heart Rate (bpm)
Systolic Blood Press.
Diastolic Blood Press.
Resting males
Resting females
Moderately exercising males
Moderately exercising females
Maximally exercising males
Maximally exercising females

ECG and Exercise

Most of the ECG consequences we saw were due to a speeding of the heart rate. The normal response to exercise includes a shortening of the interval from the beginning of the QRS complex to the end of the T wave, and a great shortening of T-P interval as one beat begins just as another is ending. Other, more subtle features that we didn't monitor are an increase in amplitude of the T wave and a QRS complex that starts with a downward deflection (the Q wave) and whose positive deflection (the R wave) is reduced (Goodman, 1999, p. 72).

Both the P-T interval and the T-P interval should be shortened during exercise. The T-P interval is the "resting period" for the heart, and should almost disappear if the contractions are fast enough. The P-T interval also shortens. For example, a typical heart beating at 75 bpm will have a P-T interval of about 0.5 sec and a T-P interval of about 0.3 sec. Even if the T-P interval became 0 sec, the heart could not beat faster than 120 bpm if the P-T interval remained at 0.5 sec (because 60/0.5 = 120 bpm). To achieve 200 bpm (which is sometimes seen) with a zero T-P interval, the P-T interval would have to shorten from 0.5 sec to 0.3 sec.

We could have seen many more effects of exercise if we had gone into more detail on the ECG. You may remember that we placed the positive electrode on the left arm and the negative electrode on the right arm. An arrangement of electrodes like this is called a "lead," and our arrangement of electrodes is "Lead I." However, a hospital EKG uses 12 different leads, four of which are shown below (taken from Thaler, 1995, pp. 39-40):

Table 2. Electrode arrangement in several ECG leads.
Positive Electrode
Negative Electrode
left arm
right arm
right arm
left arm
left arm
all other limbs

The leads above are all "limb leads," but there are also six "precordial leads" in which electrodes are placed on the chest wall. All of these leads are best at detecting different aspects of the heart's electrical activity.

Lead I is a good, basic lead to use, and Lead I ECGs are usually shown in introductory texts. However, Lead I is not best at detecting effects of exercise other than those related to heart rate. The best lead for this purpose is a precordial lead called V5 (Goodman, 1999). While we didn't use Lead V5, if we had we might have seen a clinically important feature called S-T segment depression, a lowering of the segment from the end of the QRS complex to the beginning of the T wave. This is considered a reliable indicator of ischemia (lack of oxygen in the heart muscle) (Froelicher and Meyers, 2000).

Muscle Fatigue

In prolonged, aerobic exercise such as a marathon, the muscle work output is limited principally by cardiac output and the oxygen supply that the blood brings to the muscles (Guyton, 1985). Fatigue occurs after about 100 minutes due to depletion of muscle glycogen. Recovery from this type of fatigue takes 48 hours (Shepard, 1999).

Exercise that brings about fatigue in 1-2 minutes (like most student experiments in Biology 111) does so by causing anaerobic respiration and a buildup of lactic acid in the muscles. The lactate and hydrogen ions inhibit glycolysis and prevent further production of ATP. The recovery time from this type of fatigue is 15-30 minutes (Shepard, 1999).

Literature Cited

Borresen, J. and Lambert, M. I. 2008. Autonomic control of heart rate during and after exercise: measurements and implications for monitoring training status. Sports Medicine 38(8): 633-646.

Froelicher, V. F and J. N. Myers. 2000. Exercise and the Heart, 4th Ed. W. B. Saunders Co., Philadelphia.

Goodman, J. M. 1999. The assessment of exercise capacity and the principles of exercise prescription. Pp. 59-98 in R. J. Shepard and H. S. Miller, Jr. 1999. Exercise and the Heart in Health and Disease, 2nd Ed. Marcel Dekker, Inc., New York.

Guyton, A. C. 1985. Anatomy and Physiology. Saunders College Publishing, New York, pp. 461-464.

Jouven, X., J. P. Empana, P. J. Schwartz, M. Desnos, D. Courbon, and P. Doucimetiere. 2005. Heart-rate profile during exercise as a predictor of sudden death. New England Journal of Medicine 352: 1951-1958.

Laughlin, M. H. 1999. Cardiovascular response to exercise. The American Journal of Physiology 227(6): S244-S259.

Marieb, E. N. 1989. Human Anatomy and Physiology. The Benjamin-Cummings Publishing Co., Redwood City, CA.

Shepard, R. J. 1999. Physiological, biochemical and psychological responses to exercise and physical activity. Pp. 1-58 in R. J. Shepard and H. S. Miller, Jr. 1999. Exercise and the Heart in Health and Disease, 2nd Ed. Marcel Dekker, Inc., New York.

Sullivan, M. F. Genter and M. Roberts. 1984. The reproducibility of hemodynamic, electrocardiographic, and gas exchange data during treadmill exercise in patients with stable angina pectoris. Chest 86: 375-382.

Thaler,  M.  S. 1995. The Only EKG Book You'll Ever Need. J. B. Lippencott & Co., Philadelphia.

Tipton, C. M. 1999. Exercise and hypertension. Pp. 463-488 in R. J. Shepard and H. S. Miller, Jr. 1999. Exercise and the Heart in Health and Disease, 2nd Ed. Marcel Dekker, Inc., New York.

Wilmore, J. H., P. R. Stanforth, J. Gagnon, T. Rice, S. Mandel, A. S. Leon, D. C. Rao, J. S. Skinner, and C. Bouchard. 2001. Heart rate and blood pressure changes with endurance training: the HERITAGE study. Medicine and Science in Sports and Exercise 33(1): 107-116.

Zhang, G. Q., and W. Zhang. 2008. Heart rate, lifespan, and mortality risk. Ageing Research Reviews 8(1): 52-60.