The effect of physical exercise on the cardiovascular system Essay Example

The Effect of Physical Exercise on the Cardiovascular System

This paper discusses the impact of physical exercise on the cardiovascular system. Generally, during physical exercise the cardiovascular system performs a number of functions including delivering O2 to the working muscles, oxygenating blood by returning it to the lungs, transporting heat from the core to the skin, delivering nutrients and fuel to active tissues, and transporting hormones. This paper thus discusses the changes that occur when the body is subjected to physical exercise in relation the functions of the cardiovascular system. Some of the key points addressed include heart rate, stroke volume, cardiac output, blood flow and blood pressure

Exercise imposes an increased demand on the cardiovascular system, which raises O2 demand sharply. The compensatory cardiovascular response embodies an integration of neural, biochemical, and physiologic factors. The cardiovascular control centre is believed to be positioned in the ventrolateral medulla of the brain and responds to both central and peripheral output. Central impulses originate from somatomotor centres of the brain. On the other hand, peripheral impulses are generated by mechanoreceptors found in joints, muscles and the vascular system; chemoreceptors located in the muscles and the vascular system; and baroreceptors located in the vascular system. The control centre regulates cardiac output and its distribution to organs and tissues according to metabolic demand (Fuster, O’Rourke & Alexander, 2004, p. 2245). Cardiac output refers to the amount of blood ejected from the heart per minute, which is calculated by multiplying heart rate (frequency at which the heart beats) by stroke volume (Thomas & Kotecki, 2006 p. 70).

Before exercise even commences, the heart rate rises in anticipation. This is referred to as the anticipatory response. It is initiated by the release of neurotransmitters known as epinephrineandnorepinephrine (also referred to as adrenaline and noradrenaline respectively) (Aaronson, Ward & Wiener, 2004, p. 61).

After the initial response, heart rate rises proportionately with the level of exercise until the maximum heart rate is attained. As this happens, a series of cardiovascular adaptations occur as the level of dynamic exercise increases, thereby allowing muscles to be supplied with the increased amount of O2 they require. The most significant aspect here is the increase in cardiac output, which increases almost linearly with the rate of O2 consumption by the muscle (work level) as a result of increases in both the heart rate and to a lower extent stroke volume (Aaronson, Ward & Wiener, 2004, p. 64). Stroke volume refers to the amount of blood ejected by each contraction of the heart (Thomas & Kotecki, 2006, p. 70). Increase in cardiac output is also stimulated by increases in systolic blood pressure and myocardial contractile activity (Moore, 2006, p. 326). As exercise begins or is about to begin, impulses from the cerebral cortex act on the medulla to suppress vagal tone, thereby increasing heart rate and cardiac output (Aaronson, Ward & Wiener, 2004, p. 65).

As mentioned above, heart rate is increased by a reduction in vagal tone, as well as by increases in sympathetic nerve firing and circulating catecholamines. The resultant stimulation of cardiac β-adrenoreceptors increases stroke volume by raising the level of myocardial contractility and facilitating more complete systolic emptying of the ventricles. Cardiac output is the limiting factor that determines the maximum capacity of exercise (Aaronson, Ward & Wiener, 2004, p. 64).

Several hormones are involved during physical exercise. Some of them affect the energetics of muscle contraction while others affect physiologic processes related to exercise such as temperature regulation, water balance and cardiorespiratory control. The hormones that affect muscular contraction includeepinephrine, norepinephrine, insulin, glucagon, corticotrophin, cortisol, and the growth hormone. These hormones are released to mobilise fuels for the production of ATP required to support muscle contraction, maintain blood glucose levels, enhance cardiac output, increase blood supply to the active tissues, and to maintain blood pressure by stabilising fluid and electrolyte balance (Brown, Miller & Eason, 2006, p. 83). All these functions are necessary for the normal operation of the cardiovascular system.

Several circulatory adjustments occur in response to physical exercise. Such adjustments involve a complex series of changes due to the resulting increase in cardiac output in line with metabolic demands. The changes are necessary to ensure that the metabolic needs of exercising are met, to ensure that blood flow to essential organs is maintained, and to forestall hyperthermia. Thus, adequate blood flow is channelled to exercising muscles through the increased cardiac output and redistribution of blood flow away from the viscera (Fuster, O’Rourke & Alexander, 2004, p. 2245).

From rest to strenuous exercise, heart rate increases quickly to levels of 160 to 180 beats per minute. During short levels of maximal exercise, the heart rate can go as high as 240 beats per minute. The initial rapid increase is likely due to the effect of the central command or reflex from mechanoreceptors. The immediate increase in heart rate is largely as a result of vagal withdrawal. Later increases occur due to reflex activation of the pulmonary stretch receptors, which cause increased sympathetic tone and more parasympathetic withdrawal (Fuster, O’Rourke & Alexander, 2004, p. 2245).

As mentioned above, heart rate is increased by a reduction in vagal tone, as well as by increases in sympathetic nerve firing and circulating catecholamines. The resultant stimulation of cardiac β-adrenoreceptors increases stroke volume by raising the level of myocardial contractility and facilitating more complete systolic emptying of the ventricles. Cardiac output is the limiting factor that determines the maximum capacity of exercise (Aaronson, Ward & Wiener, 2004, p. 64).

In conclusion, physical exercise increases the O2 demand by the cardiovascular system. The cardiovascular system responds to this through an integration of neural, biochemical, and physiologic factors. To increase the rate at which oxygen reaches the muscles and organs where it is needed most, there is need to achieve a higher blood flow rate. This is achieved through increases in heart rate, stroke volume and cardiac output. Also during exercise, impulses from the cerebral cortex act on the medulla to suppress vagal tone. This is achieved through the control centre as it coordinates central and peripheral pulses. Heart rate is also increased by increases in the sympathetic nerve firing and circulating catecholamines. This leads to stimulation of the cardiac β-adrenoreceptors, which causes an increase in stroke volume by raising the rate of myocardial contractility, resulting in more complete emptying of the ventricles.

References

Aaronson, P I, Ward, J P T & Wiener, C M 2004, The cardiovascular system at a glance, Wiley-Blackwell, New York.

Brown, S P, Miller, W C & Eason, J M 2006, Exercise Physiology: Basis of Human Movement in Health and Disease, Lippincott Williams & Wilkins, Sydney.

Fuster, V, O’Rourke, R A & Alexander, R W 2004, Hurst’s the Heart, Book 2, McGraw-Hill Professional, New York.

Moore, R L 2006, “The cardiovascular system: Cardiac function,” in Tipton, C M ACSM’s advanced exercise physiology, Lippincott Williams & Wilkins, Philadelphia, pp. 326+.

Thomas, D Q & Kotecki, J E 2006, Physical activity & health: An interactive approach (2nd edition), Jones & Bartlett Learning, New York.