The heart is an incredible organ, not only delivering a constant, reliable stream of life-giving oxygen and nutrients, but also responding instantly to challenges like stress, cardiovascular workouts and high-intensity bursts of energy.

Without the heart’s extraordinary ability to react immediately to physical overload, the flow of oxygen to the working muscles would cease and an exercise session would come to a quick halt. A better understanding of the structure, function and physiology of the heart may help exercise professionals assess and design more-effective training programs.

Anatomy 101: Structure and Function of the Human Heart

The heart (see Figure 1) is a hollow, pear-shaped organ that lies behind the sternum and between the lungs. In an adult, it’s about the size of a fist. On most people the apex, or pointed end, of the heart is slightly to the left of the body’s midline. The heart sits comfortably within a protective pericardial sac, which permits normal heart contractions with little friction or resistance. The outer layer of the pericardial sac is anchored to the diaphragm and the sternum.

The adult human heart usually weighs less than 1 pound. Its four chambers include two atriums (from Latin atrium for “entrance hall”) and two ventricles (from Latin ventriculus for “little belly”) that divide the heart into two independent pumping systems. The right side of the heart collects oxygen-depleted blood from the body and then sends it to the lungs to pick up fresh oxygen and to release carbon dioxide. Oxygen is used in the majority of life-sustaining reactions, and carbon dioxide is the metabolic waste produced as cells synthesize energy in the form of ATP during specific steps of metabolism. The left side of the heart propels the oxygen-saturated blood to all of the organs, tissues and cells of the body.

At rest, an average heart will beat about 72 times per minute, with a stroke volume (amount of blood pumped with each beat) of about 70 milliliters. Completing the math:

  • 70 ml of blood x 72 bpm x 60 minutes x 24 hours = 7,257 liters, or 1,917 gallons, of blood pumped each day.
  • 1,917 gallons per day x 365 = 699,705 gallons per year. If someone lives to be 75 years old, that would be 52,477,875 + 34,506 (leap years)—over 52.5 million gallons the heart has pumped. Pretty impressive for an organ that is only as big as your fist.
Clinical Application

Exercise professionals often need to explain to clients that exercise triggers a normal, healthy adaptation called cardiac hypertrophy, in which the heart adapts to training by developing a thicker left ventricle. With training, the significant increase in the myocardium (heart muscle) mass of the left ventricle corresponds to a very meaningful increase in its pumping capacity. Thus, progressively challenging cardiovascular training makes the heart stronger so it can pump more blood. Regular anaerobic exercise, such as resistance training, increases the heart muscle’s contractile ability to send blood to the working muscles.

There’s also an unhealthy hypertrophy called pathological hypertrophy, which results from disease, stress, hypertension and muscle damage to the left ventricle. With this pathological hypertrophy, muscle mass increases significantly, but there is no corresponding increase in the left ventricle’s pumping capacity. Without intervention, this pathological hypertrophy eventually renders the heart unable to supply adequate blood to the body.

Blood Pressure 101: An Amazing Pump May Also Become a Silent Killer

The surge of blood leaving the left ventricle during ejection—or systole—creates a powerful force against the arterial walls and sends a pressure wave of blood through the body. A person’s systolic blood pressure at rest provides an estimate of the heart’s working ability and the strain it imposes on the arteries.

The walls of the large arteries and veins can expand (greater diameter allows swifter blood flow) and recoil in response to changes in blood pressure, a concept called vascular compliance. During diastole, the heart’s relaxation phase, the ventricles are refilling. Diastolic pressure indicates how easily the blood flows from the arteries to arterioles to capillaries; this is called total peripheral resistance. If total peripheral resistance is high, meaning there is a lot of resistance to blood flowing in the blood vessels, the blood pressure within the arteries after ejection is not lowering as it should, and this may indicate a number of unhealthy factors, some of which are associated with kidney function. Categories of blood pressure are presented in Table 1.

The high blood pressure that is widespread in the American population is referred to as essential hypertension, a disease condition that is currently unexplained. Another type of high blood pressure—associated with fluctuating blood pressure readings—is called labile hypertension, caused by brain injury, adrenal gland tumors and brain tumors.

Arterial blood pressure is largely controlled by cardiac output and total peripheral resistance. Cardiac output is essentially a function of how much blood is being pumped from the heart per minute—and thus is determined by multiplying stroke volume (blood per beat) by heart rate (per minute).

Clinical Application

Exercise professionals are encouraged to check clients’ blood pressure regularly. According to the Centers for Disease Control and Prevention, high blood pressure is a serious condition that affects 1 in 3 American adults (or 68 million people) and can lead to coronary heart disease, heart failure, stroke, kidney failure and other health problems. Less than half of the people with high blood pressure (46%) have it under control (CDC 2011).

High blood pressure is called the silent killer because it can be present for years without causing any other symptoms. Factors that can contribute to high blood pressure include stress, alcohol consumption (more than 1–2 drinks per day), chronic kidney disease, adrenal and thyroid gland disorders, obesity, smoking, inactivity, genetics, aging and too much salt in the diet. Exercise professionals should be aware that asthma and cold-relief products sometimes contain chemicals that may elevate blood pressure. Also, in some women, birth control pills, pregnancy or hormone therapy may elevate blood pressure.

For prevention of high blood pressure, the NHLBI (2012) encourages people to limit sodium and alcohol intake, stay physically active, quit smoking, maintain a healthy weight, and learn how to manage stress effectively.

What Does Resting Heart Rate Tell the Personal Trainer?

Every personal trainer completes physiological assessments with clients, including determining their resting heart rates. Initially, the exercise professional is establishing a baseline, presumably to make it possible to measure progress down the road. What does an RHR measurement tell us? More important, how can this value help in providing training recommendations for a client?

One of the more important factors related to RHR is its association with cardiovascular disease and mortality. A longitudinal study of 1,827 men and 2,929 women determined that elevated RHR (independent of cardiovascular disease risk factors) is positively associated with cardiovascular mortality (Mensink & Hoffmeister 1997). Recent research indicates that an elevated RHR (above 90 bpm) significantly increases the risk of cardiovascular disease (causing a twofold rise in men and a threefold rise in women) (Cooney et al. 2010).

Ker (2010) points out that elevated RHR may increase the shear stress on the inside of blood vessels, which may cause plaque to rupture. Ruptured plaque may result in a blood clot, which can block a coronary artery, cutting off blood flow to an area of heart muscle and leading to cell damage and/or death. A drug-lowering therapy that attains heart rates >50 bpm but <70 bpm appears to reduce this mortality risk, says Ker. Higher RHRs have been identified as a risk factor for cardiovascular disease in both men and women (Cooney et al. 2010).

Clinical Application

Resting heart rate can also be an indicator of cardiovascular fitness; people with a lower resting heart rate tend to have a greater maximal oxygen consumption (O2) value than those with a higher resting heart rate (Nauman et al. 2012). As a result of cardiovascular training, fitness level improves and RHR may decline. Clinically and functionally, why does this occur? Clearly, in response to endurance training, there is a marked adaptation that directly affects the heart. In fact, researchers found that in response to short-term endurance training (as little as 6 days cycling 2 hours per day at 65% of aerobic capacity), RHR fell by approximately 7%, owing to an increase in ventricle filling and more efficient stroke volume (Goodman, Liu & Green 2005).

How Hard Does the Heart Work During Exercise?

Thanks to the heart, personal trainers can understand the relative intensity of an exercise without having to invest in expensive equipment. In fact, measuring heart rate and blood pressure during exercise makes it is possible to estimate myocardial oxygen consumption—in other words, how hard the heart is working.

We can estimate the heart’s oxygen consumption, or workload, by determining an exerciser’s rate pressure product, where RPP = heart rate x systolic blood pressure. Before diving into this subject, we need to review general oxygen consumption principles.

An individual consuming a lot of oxygen is thought to be working harder or expending more calories than someone consuming less oxygen. Working harder causes muscles to consume more oxygen, making it much more challenging for the cardiovascular system to maintain the intensity over a prolonged period of time.

As the cardiovascular system adapts to repeated, progressively increasing bouts of exercise, eventually the same bout of exercise will require less oxygen consumption. If a person runs at 6 miles per hour on a treadmill and initially consumes 35 milliliters of oxygen per kilogram of body weight per minute, after a consistently challenging training program the same person exercising at 6 mph will consume less than 35 ml O2/kg/min. Therefore, at a given intensity (the same speed on a treadmill), this person will consume less oxygen and have a lower energy cost. In that sense, the oxygen consumption of skeletal muscle is similar to that of the heart muscle (myocardium).

Clinical Application

Let’s assume that while jogging on a treadmill at a low intensity (speed), an individual has a heart rate of 110 bpm at the beginning of a training program and can undergo a blood pressure check while exercising. Let’s now assume that the individual follows the training program and then exercises at the same speed on the treadmill but reaches a steady-state heart rate of only 100 bpm. Heart rate is highly correlated with oxygen consumption in the body and is thus used in numerous prediction equations to determine oxygen consumption.

The personal trainer now has evidence of several physical adaptations in the heart and cardiovascular system. At the same speed of work, the heart rate has declined after the training program in this example. It is also likely that blood pressure has decreased from pretraining to posttraining. Therefore, the trainer can use a more sophisticated measurement of heart work, known as the rate pressure product, introduced above.

Myocardial metabolic demand (workload on the heart) has generally been used in clinical settings to measure relative cardiac work because of its high association with the heart’s oxygen consumption and coronary blood flow. But this measure can also be most valuable for the personal trainer who needs to understand and assess clients. It can help show how—with consistent cardiovascular training—heart rate and blood pressure decrease in response to the same challenging work bout; thus workload on the heart also decreases.

Clinically and functionally, this tells the personal trainer that after enduring a cardiovascular training program, the heart doesn’t have to work quite as hard at a given speed while running or walking on a treadmill or cycling on an ergometer. Thus the heart has adapted to the training by becoming much more efficient. So, the exercise professional can now track a client’s RPP changes over time in order to see more specifically how the exercise program design is improving heart efficiency.

Here is a sample RPP calculation. Remember, RPP = heart rate x systolic blood pressure. In a steady-state bout on a cycle ergometer exerciser, a client’s heart rate is 125 bpm and has a systolic blood pressure of 145 mm HG. RPP = 125 bpm x 145 mm Hg, which = 18,125 mm Hg x bpm.

Since RPP is quite relative to a person’s fitness level and exercise intensity, the best way for a personal trainer to track RPP is to assess a client on the exact same workload after the client has trained for a few months, and then compare changes in RPP over time. With training, the heart should become much more efficient, which will be evidenced by a lower RPP on the retest. At maximal or near-maximal intensity, RPP may be 200 bpm x 200 mm Hg, which = 40,000 mm Hg x bpm.

Continuous Cardiovascular Exercise or High-Intensity Interval Training?

Burgomaster et al. (2008) found that 6 weeks of high-intensity interval training (HIIT) (four to six 30-second “all-out” Wingate Tests separated by 4.5 minutes of recovery), completed 3 days per week, led to similar cardiovascular and metabolic adaptations to those seen in subjects who completed a standard cardiovascular endurance training routine 5 days per week, exercising 40–60 minutes at ~65% of maximal aerobic capacity.

Although both training programs produced similar adaptations, this study shows that less training time is needed to produce these changes when subjects follow a HIIT program. Thus a personal trainer should take into account that both programs are equally effective in improving heart efficiency—but when limited time is a factor for a client, HIIT is a meaningful option as long as the trainer is careful about preventing too much fatigue from client overexertion and overtraining.

With a greater understanding of the heart’s structure, function and physiology, fitness professionals are in a much better position to assess and design safer, more-effective training programs for clients.

Figure 1. The Human Heart and Its Cardiac Cycle

The cardiac cycle describes three phases of a single heartbeat:

  • Phase 1 (diastolic). Ventricular filling occurs during the diastolic phase. Blood moves passively (70%) (as the tricuspid and mitral valves open) and by atrial contraction (30%) from the atria into the right and left ventricles.
  • Phase 2 (systolic). For a brief instant, the heart closes all of its valves and begins to create a forceful contraction (called an isovolumetric contraction). This is followed immediately by systolic ejection of blood through the aorta and pulmonary semilunar valves into the systemic (entire body except lungs) and pulmonary (lungs) arteries.
  • Phase 3. For only a brief moment, the heart closes all valves and goes into relaxation (called isovolumetric relaxation). It then repeats the cardiac cycle beginning at Phase 1.
Table 1. Categories for Blood Pressure in Adults

How Does the Heart Generate Heart Beats?

The heart’s unique ability to self-regulate and to generate its own heartbeats occurs through electrochemical messages originating from the sinoatrial node, or pacemaker (see Figure 2 for a diagram). This node is “polarized” when not sending a message, meaning it is in an electrically relaxed state with a negative charge in the cells’ interior as compared to a positive charge outside the cell membranes.

Through a unique autoconducting cell membrane mechanism, the sinoatrial node triggers a rush of positive sodium ions into the cell, depolarizing the node (i.e., making the interior of the cell very positive). This depolarization then spreads rapidly through the heart (cell by cell), signaling all other autoconduction cells in the heart to depolarize. This messaging system activates a contraction in the contractile cells of the heart, which then initiates the cardiac cycle (explained in Figure 1).

An extrinsic neural and hormonal response influences this autorhythmic characteristic of the heart. In fact, prior to an exercise bout, the brain will elicit “feed-forward” impulses from the motor cortex (or central command), which raises heart rate in anticipation of the motor unit recruitment necessary for exercise. Additionally, neural stimulation of the brain’s adrenal medulla activates a hormone response from epinephrine, which directly activates some specialized receptors (beta-1 andrenergic receptors). This increases heart rate, force of contraction and signal conduction velocity in the heart, preparing it for the ensuing workout.

5 Questions and Answers About the Heart

1. Does heart rate recovery indicate anything about a person’s health?

Yes. Cole et al. (1999) showed that a delayed decrease in heart rate (less than 12 beats slower) during the first minute after a maximal graded exercise may indicate decreased vagal nerve activity and is a powerful predictor of overall mortality.

2. Does exercise training improve recovery heart rate?

Yes. Seiler, Haugen & Kuffel (2007) showed that recovery heart improvement (faster recovery) occurs as fitness level progressively increases.

3. Does cardiovascular training improve blood flow to the heart muscle?

For cardiac patients and noncardiac patients alike, cardiovascular training causes structure and functional changes in the heart that improve blood flow to the heart muscle (myocardium). These changes may provide some protection to the heart.

4. What is a heart arrhythmia, and why is it dangerous?

An arrhythmia is an abnormal heart rhythm. When arrhythmias become long-lasting or severe, they begin to compromise the heart’s ability to pump enough blood to the body, and in some cases they may be life-threatening.

5. What is atrial fibrillation?

Atrial fibrillation is a heart condition in which the upper atriums of the heart begin to beat too rapidly. A person can sustain life with atrial fibrillation, but it may lead to chronic fatigue, heart failure and even stroke. Depending on its severity, atrial fibrillation can be treated with medicine, surgery or a pacemaker.

Figure 3. Blood Pressure Measurement

Special Focus: Understanding the Korotkoff Sounds of Blood Pressure Measurement

As the personal trainer inflates the blood pressure cuff, the bladder inside the cuff puts pressure on the arm. This compression tightens the arm muscles over the brachial artery, occluding blood flow to the forearm and wrist. As the pressure in the cuff is gradually released, a point is reached where the highest blood pressure during systole (ejection) overcomes the resistance of the deflating blood pressure cuff. As the blood pushes through the semi-occluded artery, it thrusts into motionless blood, creating a turbulence that is audible in a stethoscope and known as the first Korotkoff sound; deflating the cuff produces the second and third Korotkoff sounds. When the cuff no longer occludes the artery, normal blood flow is reestablished, producing the fourth and fifth sounds, an audible muffling followed by the disappearance of the Korotkoff sounds (diastole).

Tips for Accurate Blood Pressure Measurement

An accurate blood pressure assessment is essential for detecting a client’s health status and potential cardiovascular risk. Potential errors include using a blood pressure cuff that is either too big or too small. To assess resting blood pressure, follow these steps:

1. Ask the client to sit with his or her back against a chair and both feet flat on floor.

2. Have the person sit in a calm environment for at least 5 minutes before taking the measurement.

3. Use an appropriate-sized blood pressure cuff. The inflatable part of the cuff should cover about 80% of the circumference of the client’s upper arm. The cuff should cover two-thirds of the distance from elbow to shoulder.

4. Align the pressure cuff so the center of the interior bladder is directly over the brachial artery.

5. Place the head of the stethoscope over the brachial artery, just above and medial to the bend in the elbow.

6. Rapidly inflate the manometer to 200 mm Hg or approximately 20 mm Hg higher than the estimated systolic blood pressure.

7. Slowly open the inflator bulb valve and deflate the bladder about 2 mm Hg per second until you hear the first Korotkoff sound (named for the Russian medical doctor Nikolai Korotkov, who in the early 1900s first explained the thumping sound the heart makes during blood pressure measurement). The value on the manometer corresponding to this first sound is the systolic blood pressure.

8. Continue deflating the bulb at the same speed until you hear the muffling (fourth Korotkoff sound) and then disappearance of the beating sound (the fifth Korotkoff sound). Use the fifth Korotkoff sound for the diastolic pressure reading. (For more on understanding the Korotkoff sounds, see Figure 3.)

9. Obtain a second reading ≥1 minute later.

10. Remember that a single-setting measurement indicating high blood pressure is not sufficient. Confirmation of true elevated blood pressure should be completed on several settings.

Figure 2. The Heart’s Electrical Conduction System and ECG Diagram

The heart’s electrical conduction system is depicted and interpreted on an electrocardiogram. As the sinoatrial node depolarizes, it spreads its signaling message to the atrioventricular node and left atrial (via Bachmann’s electrical bundle). This event is seen as the P wave inscription on the ECG. The atrioventricular node sends the electrochemical signal to the ventricles (via the left and right bundle branches and Purkinje fibers), depolarizing the ventricles. This is depicted with the QRS complex on the ECG. Not seen on the ECG is the repolarization of the atria, which occurs at the same time as the QRS complex. The repolarization of the ventricles is shown with the T wave on the ECG.


Burgomaster, K.A., et al. 2008. Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. Journal of Physiology, 586 (1), 151–60.
CDC (Centers for Disease Control and Prevention). 2011. Vital signs: Prevalence, treatment, and control of hypertension—United States, 1999-2002 and 2005–2008. Morbidity and Mortality Weekly Report, 60 (04), 103–108.
Cole, C.R., et al. 1999. Heart-rate recovery immediately after exercise as a predictor of mortality. The New England Journal of Medicine, 341 (18), 1351–57.
Cooney, M.T., et al. 2010. Simplifying cardiovascular risk estimation using resting heart rate. European Heart Journal, 31 (17), 2141–47.
Goodman, J.M., Liu, P.P., & Green, H.J. 2005. Left ventricular adaptations following short-term endurance training. Journal of Applied Physiology, 98 (2), 454–60.
Ker, J.A. 2010. Resting heart rate and cardiovasucular events: Risk factor or risk marker? South African Family Practice, 52 (2), 128–29.
Mensink, G.B.M., & Hoffmeister, H. 1997. The relationship between resting heart rate and all-cause, cardiovascular and cancer mortality. European Heart Journal, 18 (9), 1404–10.
Nauman, J., et al. 2012. A prospective population study of resting heart rate and peak oxygen uptake (the HUNT Study, Norway). PLoS ONE, 7 (9), e45021.
NHLBI (National Heart, Lung and Blood Institute, U.S. Department of Health and Human Services). 2012. What is high blood pressure?; retrieved Nov. 5, 2012.
Seiler, S., Haugen, O., & Kuffel, E. 2007. Autonomic recovery after exercise in trained athletes: Intensity and duration effects. Medicine & Science in Sports & Exercise, 39 (8), 1366–73.

Colin Carriker, MS

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