Chapter 20

Exercise and the Heart

Regular aerobic exercise can: Increase cardiac output Increase HDL Decrease triglycerides Improve lung function Decrease blood pressure Assist in weight control

Conduction system of the heart

SA node, AV node, Bundle of His, Purkinje fibers

Proprioceptors

Sensory receptors, located in the muscles and joints, that provide information about body position and movement.

autorhythmic fibers

Specialized cardiac muscle fibers that repeatedly generate action potentials that trigger heart contractions

influences on the conduction system

The autorhythmic fibers in the SA node are the natural pacemaker of the heart because they initiate action potentials most frequently Signals from the nervous system and hormones (like epinephrine) can modify the heart rate and force of contraction but they do not set the fundamental rhythm

P wave

atrial depolarization

A physically fit person may even exhibit __________ a resting heart rate under 50 beats/min. This is a beneficial effect of endurance-type training because a slowly beating heart is more energy efficient than one that beats more rapidly.

bradycardia

Baroreceptors

detect changes in blood pressure

cardiac accelerator nerves

extend out to the SA node, AV node, and most portions of the myocardium. Impulses in the cardiac accelerator nerves trigger the release of norepinephrine, which binds to beta-1 (β1) receptors on cardiac muscle fibers. This interaction has two separate effects: (1) In SA (and AV) node fibers, norepinephrine speeds the rate of spontaneous depolarization so that these pacemakers fire impulses more rapidly and heart rate increases; (2) in contractile fibers throughout the atria and ventricles, norepinephrine enhances Ca2+ entry through the voltage-gated slow Ca2+ channels, thereby increasing contractility.

Q-T interval

extends from the start of the QRS complex to the end of the T wave. It is the time from the beginning of ventricular depolarization to the end of ventricular repolarization. The Q-T interval may be lengthened by myocardial damage, myocardial ischemia (decreased blood flow), or conduction abnormalities.

Chemical Regulation of Heart Rate

hormones and ions

During surgical repair of certain heart abnormalities, it is helpful to slow a patient's heart rate by_______, in which the person's body is deliberately cooled to a low core temperature. Hypothermia slows metabolism, which reduces the oxygen needs of the tissues, allowing the heart and brain to withstand short periods of interrupted or reduced blood flow during a medical or surgical procedure.

hypothermia

cardiac reserve

is the difference between a person's maximum cardiac output and cardiac output at rest. The average person has a cardiac reserve of four or five times the resting value. Top endurance athletes may have a cardiac reserve seven or eight times their resting CO. People with severe heart disease may have little or no cardiac reserve, which limits their ability to carry out even the simple tasks of daily living.

P-Q interval

is the time from the beginning of the P wave to the beginning of the QRS complex. It represents the conduction time from the beginning of atrial excitation to the beginning of ventricular excitation.

Cardiac Output (CO)

is the volume of blood ejected from the left ventricle (or the right ventricle) into the aorta (or pulmonary trunk) each minute.

cardiac accelerator nerves

part of the sympathetic nervous system that stimulates the SA node to increase heart rate This interaction has two separate effects: (1) In SA (and AV) node fibers, norepinephrine speeds the rate of spontaneous depolarization so that these pacemakers fire impulses more rapidly and heart rate increases; (2) in contractile fibers throughout the atria and ventricles, norepinephrine enhances Ca2+ entry through the voltage-gated slow Ca2+ channels, thereby increasing contractility.

Electrocardiogram (ECG)

recording of the electrical changes that occur in the myocardium during a cardiac cycle

Chemoreceptors

respond to chemicals in solution

Bradycardia

slow heart rate

Preload

the degree of stretch on the heart before it contracts

Contractility

the forcefulness of contraction of individual ventricular muscle fibers

afterload

the pressure that must be exceeded before ejection of blood from the ventricles can occur.

Contractility

the second factor that influences stroke volume is myocardial contractility, the strength of contraction at any given preload. Substances that increase contractility are positive inotropic agents (īn′-ō-TRŌ-pik); those that decrease contractility are negative inotropic agents. Thus, for a constant preload, the stroke volume increases when a positive inotropic substance is present. Positive inotropic agents often promote Ca2+ inflow during cardiac action potentials, which strengthens the force of the next contraction.

QRS complex

ventricular depolarization

T wave

ventricular repolarization and relaxation

S-T segment

which begins at the end of the S wave and ends at the beginning of the T wave, represents the time when the ventricular contractile fibers are depolarized during the plateau phase of the action potential.

By comparing these records with one another and with normal records, it is possible to determine

(1) if the conducting pathway is abnormal, (2) if the heart is enlarged, (3) if certain regions of the heart are damaged, (4) the cause of chest pain.

Two key factors determine EDV

(1) the duration of ventricular diastole (2) venous return, the volume of blood returning to the right ventricle. When heart rate increases, the duration of diastole is shorter. Less filling time means a smaller EDV, and the ventricles may contract before they are adequately filled. By contrast, when venous return increases, a greater volume of blood flows into the ventricles, and the EDV is increased.

cations

. Given that differences between intracellular and extracellular concentrations of several cations (for example, Na+ and K+) are crucial for the production of action potentials in all nerve and muscle fibers, it is not surprising that ionic imbalances can quickly compromise the pumping effectiveness of the heart. In particular, the relative concentrations of three cations—K+, Ca2+, and Na+—have a large effect on cardiac function. Elevated blood levels of K+ or Na+ decrease heart rate and contractility. Excess Na+ blocks Ca2+ inflow during cardiac action potentials, thereby decreasing the force of contraction, whereas excess K+ blocks generation of action potentials. A moderate increase in interstitial (and thus intracellular) Ca2+ level speeds heart rate and strengthens the heartbeat

Regulation of Stroke Volume

1. Preload 2. Contractility 3. Afterload

During embryonic development, only about 1% of the cardiac muscle fibers become autorhythmic fibers; these relatively rare fibers have two important functions:

1.They act as a pacemaker, setting the rhythm of electrical excitation that causes contraction of the heart. 2.They form the cardiac conduction system, a network of specialized cardiac muscle fibers that provide a path for each cycle of cardiac excitation to progress through the heart. The conduction system ensures that cardiac chambers become stimulated to contract in a coordinated manner, which makes the heart an effective pump. As you will see later in the chapter, problems with autorhythmic fibers can result in arrhythmias (abnormal rhythms) in which the heart beats irregularly, too fast, or too slow.

During embryonic development, only about 1% of the cardiac muscle fibers become autorhythmic fibers; these relatively rare fibers have two important functions:

1.They act as a pacemaker, setting the rhythm of electrical excitation that causes contraction of the heart. 2.They form the cardiac conduction system, a network of specialized cardiac muscle fibers that provide a path for each cycle of cardiac excitation to progress through the heart.

pacemaker

A device that delivers electrical impulses to the heart to regulate the heartbeat

Autorhythmic Fibers: The Conduction System

An inherent and rhythmical electrical activity is the reason for the heart's lifelong beat. The source of this electrical activity is a network of specialized cardiac muscle fibers called autorhythmic fibers because they are self-excitable

autorhythmic fibers

An inherent and rhythmical electrical activity is the reason for the heart's lifelong beat. The source of this electrical activity is a network of specialized cardiac muscle fibers called autorhythmic fibers because they are self-excitable. Autorhythmic fibers repeatedly generate action potentials that trigger heart contractions. They continue to stimulate a heart to beat even after it is removed from the body—for example, to be transplanted into another person—and all of its nerves have been cut.

coronary circulation

Blood flow through coronary arteries delivers oxygenated blood and nutrients to the myocardium -Branches arise from the ascending aorta Coronary veins remove carbon dioxide and wastes from the myocardium -Branches converge at the coronary sinus

conduction system

Cardiac muscle cells are self-excitable, and therefore, autorhythmic Cardiac muscle cells repeatedly generate spontaneous action potentials that then trigger heart contractions These cells form the conduction system, which is the route for propagating action potentials through the heart muscle

Preload

Effect of Stretching A greater preload (stretch) on cardiac muscle fibers prior to contraction increases their force of contraction. Preload can be compared to the stretching of a rubber band. The more the rubber band is stretched, the more forcefully it will snap back. Within limits, the more the heart fills with blood during diastole, the greater the force of contraction during systole. This relationship is known as the Frank-Starling law of the heart. The preload is proportional to the end-diastolic volume (EDV) (the volume of blood that fills the ventricles at the end of diastole). Normally, the greater the EDV, the more forceful the next contraction.

Afterload

Ejection of blood from the heart begins when pressure in the right ventricle exceeds the pressure in the pulmonary trunk (about 20 mmHg), and when the pressure in the left ventricle exceeds the pressure in the aorta (about 80 mmHg). At that point, the higher pressure in the ventricles causes blood to push the semilunar valves open.

hormones

Epinephrine and norepinephrine (from the adrenal medullae) enhance the heart's pumping effectiveness. These hormones affect cardiac muscle fibers in much the same way as does norepinephrine released by cardiac accelerator nerves—they increase both heart rate and contractility. Exercise, stress, and excitement cause the adrenal medullae to release more hormones. Thyroid hormones also enhance cardiac contractility and increase heart rate. One sign of hyperthyroidism (excessive thyroid hormone) is tachycardia (tak′-i-KAR-dē-a), an elevated resting heart rate.

Autonomic Regulation of Heart Rate

Nervous system regulation of the heart originates in the cardiovascular (CV) center in the medulla oblongata. This region of the brain stem receives input from a variety of sensory receptors and from higher brain centers, such as the limbic system and cerebral cortex. The cardiovascular center then directs appropriate output by increasing or decreasing the frequency of nerve impulses in both the sympathetic and parasympathetic branches of the AN

cardiac cycle

One cardiac cycle consists of the contraction (systole) and relaxation (diastole) of both atria, rapidly followed by the systole and diastole of both ventricles Electrical events Pressure changes Heart sounds Volume changes Mechanical events

atrial depolarization

P wave

vagus (X) nerves

Parasympathetic nerve impulses reach the heart via the right and left vagus (X) nerves. Vagal axons terminate in the SA node, AV node, and atrial myocardium. They release acetylcholine, which decreases heart rate by slowing the rate of spontaneous depolarization in autorhythmic fibers. As only a few vagal fibers innervate ventricular muscle, changes in parasympathetic activity have little effect on contractility of the ventricles.