Cardiac output is the most important aspect of heart function and it is determined by the product of heart rate time's stroke volume. It is defined also the amount of blood pumped per minute by the heart, specifically by the left ventricle.

In this article we discuss about the effect of the exercise on cardiac output and also try to find out the cause and factors which are promote to increases the cardiac output.

Many books and research papers from online and offline sources has been reviewed for this paper which has been discussed through out the paper.

Cardiac output is define as the volume of blood pumped by the heart in one minute and is generally expressed in liter/minute or ml/min.

It is the product of heart rate time's stroke volume. It is denoted by Q. It is also calculate by this formula.:

Cardiac output (Q)= Stroke volume × Heart Rate

Q=SV X HR

For example - If heart rate equals 72 beats/min and stroke volume equals 70ml of blood than the

Q=70×72

=5040ml/min or 5.04 lit/min

Stroke Volume is the amount of blood pumped with each beat of the heart.

Cardiac output during rest: - At the rest the normal cardiac output in adult approximately 5lit/min. This is generally  achieved with a heart rate of 70beat/min for the untrained person and 45beats/min for trained person.

The trained person's cardiac output at rest is also five lit/min, then the decrease in heart rate must be offset by an increase in stroke volume, if the cardiac output is to remain normal. It we calculate this following formula-

Q=HR ×SV

Untrained 5,000ml= 70beats/min X 71.43ml

Trained 5,000ml= 45beats/min X 111.12ml

So the cardiac output during rest remain same both trained & untrained person.

Cardiac output during exercise:- During exercise up to 40%to 60% of maximum capacity. Cardiac output in trained athletes may be increased to 40lit/min. whereas untrained subjects may attain outputs of about 20lit/min. At this level of work it is known that this 5 to 7 fold increases in cardiac output is due to increase in cardiac output are mainly a function of heart rate increases.

Untrained 20,000ml = 200beats/min X 100ml

Trained 40,000ml =200beats/min × 200ml

These large increases in cardiac output during exercise are brought about through increases in stroke volume and heart rate.Stroke volume untrained male- 70 & 90ml/beat average and

Maximal value -100 &120ml/beat

Stroke volume trained male-100 & 120 average and Maximal value-150 &170ml/beat,

Maximal Value of stroke volume can be reached 200ml/beat.

So the large cardiac output is brought about an increased maximum strike volume. Maximal heart rate is similar in both trained and untrained athlete, but maximal stroke volume may be double in trained athlete.

Mechanism where stroke volume is increase during exercise was for a long time thought to be result of Starling's law of the heart. This law states that stroke volume increases in response to an increase in the volume of blood filling the heart ventricle during diastole (Ventricle relaxation).

The increase in the awastoxic volume carses a greater stretch on the cardiac fiber, which in turn promotes a more forceful ventricular systole (Contraction). As a result more blood ejected and stroke volume is increase.

But more recently it has been shown that diastolic volume does not increase during exercise. So the significance of this mechanism with respect to increase the stroke volume how?

The answer to this question lies in the facts at rest only about 40% to 50% of the diastolic volume is ejected during each ventricular systole (This is ejection fraction). This means that without increasing diastolic volume a stranger contraction could as much as double stroke volume by more completely empyting the ventricles. In this case the stranger ventricular contraction often referred to as an increase myocardial contractility is mediated through envious and hormonal influences.

Training has a very pronounced effect on heart rate, even at rest, e.g.- highly trained athlete resting heart rate may be as low 40beats/min. In contrast resting heart rate of untrained but healthy individual may be 90beats/min This condition is called bradicardia(decrease heart rate) resulting from training.

Causes of bradicardia is that the heart is supplied by two major autonomic nerves the sympathetic nerves which when stimulated, increase the heart rate and the vagous nerves(parasympathetic nerves) which decrease the rate when stimulated, with this dual nervous system the heart rate can be decrease either by (a) an increase parasympathetic tone (b) a decrease sympathetic influence (c) Combination of both (a) &(b).

There is also another factor of bradicardia the intrinsic rate of the artial pacemaker or S-A mode. If the intrinsic rate of the pacemaker is decrease with exercise training then the heart rate would be slower independently of the influences of autonomic nervous system.

A reduction in the intrinsic rate of the atrial pacemaker, the S-A node is related to the increases amount of acetycholine the(parasympathetic new transmitter) found in atrial tissue,following exercise training and to the increase sensitivity of cardiac tissue to catecholamine's which is also known to occur following training.

Regarding of mechanism that increase cardiac output during exercise the heart can pump only as much blood as it receives, for this reasons cardiac output is ultimately dependent on the amount of blood return to the right heart systemic venous system or venous return.

Saveral mechanism contribute to increase the venous return during exercise-

Muscle Pump

It is a result of the mechanical pumping action produced by rhythmical muscular contracting. As the muscles contract, their veins are compressed and the blood within them is forced toward the heart. Blood is prevented from following backwards because the veins in the limps contain numerous values, which permit flow only towards the heart. When the muscles relax, blood fills the veins again and with the next contraction more blood is forced towards the heart. The next contraction more blood is forced towards the heart. The muscle pump is important when a person doing activity of any type but it is not support at weight lifting or thus type of activity.|

The Respiratory pump

Another similar mechanical action that promotes 'venous return' with this pump the veins of the thorax and refilled during expiration.The reason for this is that intrathoracicpussure decrease during inspiration, and this serves to aspirate the blood in the thoracic veins towards the right heart. The lowering of the diaphragm during inspiration increase abdominal pressure and the veins contained with this cavity are also emptied during inspiration. There pressure effects are reversed during expiration and the vein fill again with more venous blood. Thus morely by breathing venous return is enhanced. This is more effective the greater the respiratory rate of depth.

Venoconstriction

A third way in which venous return is facilitated during exercise is through venconstriction i.e. by reflex constriction of the veins draining the muscles. Venoconstriction reduces the volume capacity of systemic venous system and as a result, blood is forced out toward the heart. As we have indicated, this reflex is one of the many that initiated and controlled by the central nervous system during exercise.

From a functional viewpoint, cardiac output(ml/min) is the most important aspect of heart function. It is determined by the product of heart rate (beats/min) times stroke volume (ml/beat). Endurance training brings about a greater working cardiac output and stroke volume.

While the nerve impulse that causes the heat to contract rhythmically originates within the vagous (parasympathetic) and sympathetic (accelerator) nerves of the autonomic nerves system.

In the control of stroke volume, starling's law of the heart is the principal determinant only when the venous return is altered due to postural and other gravitational changes. During exercise, however, the increase in the stroke volume is due to a greater emptying of the left ventricle.

1. Astarand, I" Depression, Heart rate and Blood pressure During Arm and Leg work, "Scandinavian Journal of clinical laboratory investigation 30:411-14,1972

2. Edington, D.W. and V.R. Edgerton. The Biology of physical Activity, Houghton Mifflin CO. Boston 1976.

3. Braunwald, E., Godblat, A., Harrison, D., and Mason, D. Studies on cardiac dimensions in intact anaesthetized Man III Effects of muscular exercise cisc Des, 13:448,1963

4. Katz. A.M. physiology of the heart, Raven Press, New York 1977.

5. Mathews, D. K., and E. L. Fox. The Physiological Basis of Physical Education and Athletics, 2nd edition, W. B. Saunders Co., Philadelphia, 1976.

6. Roskamm, H. "Myocardial Contractility During Exercise," In J. Keul (Ed.), Limiting Factors of Physical Performance, Georg Thieme, Publishers, Stuttgart, 1973.