In this article we will discuss about the changes which occurs in cardiovascular system during exercise.
I. Heart and Exercise:
Prolonged and systematic exercise causes enlargement of the heart, and this is happens only to cope with the excessive work load imposed upon the heart during work. There is a lot of misunderstanding that prolonged exercise may cause dilatation of the heart similar to that happens in heart disease. But the hypertrophy of the heart in athletes is caused by physiological processes.
The nature of processes is similar to the hypertrophy of skeletal muscle resulting from systematic exercise. Thus hypertrophied athletic heart is more powerful, efficient and capable of greater increase in stroke volume but the dilated diseased heart is less efficient and has a limited capacity for work.
II. Heart Rate Changes during Exercise (Fig. 7.112):
The acceleration of the heart is observed immediately following exercise. It has been observed that the heart rater is increased slightly even before onset of exercise and it is presumably due to influence of the cerebral cortex on the medullary cardiac centre. A short rise of heart rate is observed at first minute of exercise but after that this rate of rise is slight decreased.
Within 4 to 5 minutes of exercise the maximal rise is more or less achieved. A ‘plateau’ is observed if the exercise is further continued. But the time is variable from individual to individual and even with different degrees of work load. In athletes, the rate of rise of the heart will be slower.
Besides these, maximal heart rate that is reached during exercise and the rapidity with which the maximal value is attained depends upon several factors which are:
(a) Emotional,
(b) Environmental temperature and humidity, and
(c) Physical conditions of the subjects.
There is no satisfactory explanation of the increase of heart rate in man during exercise. The explanation is mostly based on the animal experimentation. It is claimed that both nervous and chemical factors are playing in such process. Initial rise of heart rate (anticipatory heart rate) just before exercise is due to the influence of cerebral cortex and other higher brain centres.
With the onset of exercise the rise of heart rate may be due to:
(a) Reflexes originating in the receptors of moving joints or contracting muscle,
(b) Stimulation of chemoreceptors in muscles by the acid metabolites,
(c) Sympathetico-adrenal activation causing section of much larger amounts of epinephrine in the blood,
(d) Rise of body temperature, and
(e) Stimulation of stretch receptors in atrium by the rapid venous return in heart thus causing Bainbridge reflex.
There is controversial opinion regarding the Bainbridge reflex. None does believe that the increase of heart rate during exercise is due to the effect of such reflex, because during the right atrial pressure does not rise and if it is so then instead of rise there is possibility of increase of heart rate.
Regarding the return of heart rate to initial resting level depends upon the intensity of work load and also on the physical condition of the individual. The rapidity with which the heart rate returns to the resting level following cessation of exercise is considered as a test for physical fitness. In trained individual or in physically fit person the recovery period is very short.
III. Cardiac Output:
During exercise the cardiac output is greatly increased. In trained athletes, it may achieve a maximal output of 30 litres per minute, at an O2 uptake of 4 litres per minute but in non-athletes, the output may be average 22 litres at an O2 uptake of 3.3 litres per minute. The exercise in cardiac output during exercise is the result of the increase in stroke volume and heart rate.
It has been claimed for a long time that the increased stroke volume during exercise is due to functioning of Starling law of heart. But Starling law of heart cannot hold good because modern technique claims that the diastolic size of the heart is not increased during exercise. Instead, the diastolic size of the heart is decreased during exercise so that the increased stroke volume cannot be caused by greater stretching.
Besides this, Rushmer (1959) has claimed that the increased cardiac output during exercise does not necessarily involve increase in stroke volume and heart rate. He claimed that the stroke volume during exercise is increased no doubt, but by about the same amount on changing from standing to the supine position. He claimed that increase in cardiac output is mostly due to increase of heart rate.
IV. Venous Return:
Venous return is greatly increased during exercise for the following reason:
(a) Milking or Massaging Action of Skeletal Muscles:
During exercise, the alternate contraction and relaxation of the muscle act as a booster pump for flowing blood towards the heart. Due to presence of valves in the veins, the blood is squeezed out from the vein towards the heart during contraction and allowed to fill blood during relaxation of the muscle. This pumping mechanism depends upon intensity and type of exercise,
(b) Respiratory Movements:
Respiratory movements exert a sucking effect over the right heart and great veins so that greater venous return may occur. Visa fronte is the consequence causing of the above effect during respiratory effort. During inspiration the thoracic cavity is enlarged causing fall of intrathoracic pressure. This fall of intrathoracic pressure as well as increase of pressure on the anterior abdominal wall due to descent of diaphragm cause rapid return of blood into the heart. Expiration has got the opposite effect, and
(c) Contraction of Limb Veins:
It is claimed that limb veins undergo reflex vasoconstriction during exercise thus facilitating rapid venous return to the heart.
V. Blood Pressure:
Blood pressure is raised with the onset of exercise. There may be an anticipatory blood pressure due to nerve impulses originating from the cerebral cortex to the medullary cardiac and vasoconstrictor centres. Other factors that may participate in the rise of blood pressure during exercise are due to activation of sympathetico adrenal systems causing shifting of blood from the splanchnic beds to the other parts of the body.
So the rise of arterial blood pressure during exercise is due to:
(a) Increase of cardiac output, causing greater distention of aorta and large arteries,
(b) Increase of heart rate, and
(c) Compensatory vasoconstriction in the non-active organs (splanchnic beds and skin) and vasodilatation in the active organs so as to perfuse the active organs with a greater pressure.
The nature of blood pressure rise cannot be generalised because the pressure changes mostly depend upon the type, speed and duration of the activity and also of the physical condition of the subject.
VI. Circulatory Status During Exercise:
During exercise, the circulation is adjusted in such a way that the active muscles as well as the vital organs get blood supply to a greater proportion than that of the inactive organs and the non-vital organs. It has been observed that the active muscle gets more blood supply during exercise and the circulation is increased more than about 30 times (Fig. 7.113).
It is claimed that this greater supply is due to decrease of vascular resistance caused by locally accumulated metabolites. During exercise sudden lack of O2 caused the increased accumulation of CO2, lactic acid, adenosine, intracellular K+ and histamine. These substances may cause hyperaemia (reactive hyperaemia) and thus the resistance to blood flow is decreased.
As the work load of the heart is increased tremendously during exercise, the coronary flow is increased accordingly to its own nourishment, otherwise hypoxia may prevail. So in moderate exercise, coronary flow is increased according to the O2 requirement of the cardiac muscle. But in severe exercise, the coronary flow may be increased no doubt, but the cardiac muscle due to tremendous increase of heart rate, will fail to maintain its O2 according to its need and the subject may feel anginal pain.
Pulmonary circulation during exercise is increased in proportion to the increase in venous return to the heart. But with the increase of pulmonary circulation, the pulmonary arterial pressure is insignificantly increased possibly due to distensibility of its blood vessels. Blood flow to the brain is relatively under normal state and remains mostly unaltered during exercise.
During exercise the blood flow in the active muscle, lung, heart is increased, but the same in the abdominal organ, kidneys and in the skin; (initially) is greatly decreased due to compensatory vasoconstriction. This happens possibly through the chemoreceptor reflex initiated by the accumulated metabolites during exercise so as to cause redistribution of blood from abdominal organs to the exercising muscle, heart, lung and skin (later stage). Skin blood flow is initially decreased but as the work is continued and the body temperature is increased the skin blood flow is also increased only to eliminate excess heat produced by the contracting muscle.