These changes are described below under the following headings:
1. Changes in Respiration:
i. Pulmonary Ventilation:
Pulmonary ventilation in moderate exercise is always linear with the amount of O2 absorbed. It has been observed that a linear relationship between the work load and the pulmonary ventilation is maintained until the work load is so increased that the steady state is not achieved. It has been so observed that the pulmonary ventilation is increased without appreciable increase in O2 consumption with graded increase of work load.
This shows that pulmonary ventilations do not limit the work load but the O2 consumption limits work load because the cardiac output is not increased accordingly. It then indicates that with the increase of work load, pulmonary ventilation is still capable of further adjustment when the cardiovascular system has reached to its limit.
ii. Breathing:
With the increase of O2 demand during exercise the rate and depth of respiration are increased.
These effects may be due to:
(a) Direct effect (centrogenic) of increased CO2, produced by the working muscle, on the respiratory centre,
(b) Indirect effect (reflexogenic) of metabolites on respiratory centre through chemoreceptors (carotid body and aortic body),
(c) Proprioceptive impulses from the joints of the extremities,
(d) Stimulation of chemoreceptors present in pulmonary aorta,
(e) Increase of temperature causing rise of breathing by- (1) direct stimulation of respiratory centre, (2) stimulation of cortical centre or carotid and aortic bodies, and (3) other reflex pathways.
None of the above factors is solely responsible for increase in breathing during exercise and possibly multifactor are responsible for it. Other factors that may take part in increasing the respiration during exercise are the impulses from the cortex and adrenaline liberated into the blood.
a. Nature of Second Wind:
During violent exercise initially there is developed a frequent feeling of distress but if the exercise is further continued then this sense of distress is replaced by a sense of great relief, which is called second wind.
The distresses that precede the second wind are:
(a) Breathlessness,
(b) Throbbing of the head,
(c) Fluttering and irregular pulse,
(d) Muscle pains, and
(e) Feeling of sensation of constriction around the chest.
With the onset of second wind, the facial distress disappears and breathlessness other than discomforts disappears. The subject feels a sense of comfort. The second wind should not be confused with the steady state which is the condition in which oxygen need and oxygen supply are balanced in such a way that the lactic acid and oxygen debt do not take place
The physiological basis of second wind is not clear and it is a complex phenomenon in which different types of physiological adjustments take place.
b. Oxygen Exchange during Exercise:
It has been described by Morehouse and Miller (1967) that in light and moderate exercises 400 and 700 kg-m/minute respectively, both the alveolar and the arterial O2 tension rise. The differences between the alveolar and the arterial O2 tension fall from 14.7 mm Hg to 11.0 mm Hg during exercise.
With the increase of cardiac output during exercise, the velocity of blood flow is not increased but the volume flow of blood in each minute is increased and this permits oxygen exchange in the lungs quite adequately so as to bring about normal saturation of blood with O2 so long as the oxygen uptake does not exceed 4 litres per minute.
In moderate exercise the amount of lactic acid formed, can be fully disposed of the muscle buffers and the greater amount of oxygen supplied by increased blood flow. But in severe exercise the rate of oxygen supply lags behind and lactic acid rapidly accumulates. It enters the blood stream and causes acidosis. Thus in severe exercise the lactate content of blood may go up to 100—200 mg% (10-20 mg% resting).
In order to dispose of these excess metabolites and lactic acid extra amount of O2, is needed. This is called oxygen debt (energy debt). During the first few minutes of recovery period, the lactate content of plasma or muscle does not diminish-showing that O2 is used or the re-synthesis of creatine phosphate and ATP during recovery period. The oxygen used for this purpose is called alactic acid debt. Alactic acid debt is paid at a much faster rate than the lactic acid debt.
iii. R.Q:
It varies according to the degree of exercise. In moderate exercise R.Q varies from 0.85 to 0.89, i e. more or less same as in rest. If exercise be prolonged with a high fat diet, R.Q falls to 0 7.
But in severe exercise:
(a) The R.Q. of excess metabolism (i.e., gaseous exchange over and above the resting) during the period of exercise rises above unity and may go up to 1.5 to 2. This is due to the fact that, the H-ion concentration is much greater in this case than in moderate exercise—being partly due to excess CO2, and partly to the entry of lactic acid from the muscles. Lactic acid combines with bicarbonates liberating more carbonic acid.
Hence, respiration is much more stimulated in this case and more CO2 is liberated without any corresponding oxygen utilisation. Thus R.Q rises above unity. The extent to which it rises above unity is a measure of the severity of the exercise and extent of lactic acid formation.
(b) Late in the recovery period, R.Q falls to 0.5, because respiration is depressed and CO2 is retained to form the lost bicarbonates. This CO2 comes from the burning of the lactic acid part of Na+-lactate in the tissues and combines with the Na+ of the lactate, now left free.
2. Blood Cell Changes during Exercise:
RBC count is increased in the early part of the exercise and it is probably due to haemoconcentration. This haemoconcentration is the cause of transfer of fluid from the blood to the tissues. But with more prolonged exercise the fluid passes back to the blood causing haemodilatation and RBC count is thus lowered. In strenuous exercise there may happen haemolysis.
WBC count is increased significantly at any type of exercise. It has been claimed that the greater rise of the WBC count is related with the degree of stress produced with the exercise. In less fit person the rise is more than in athletes under the same work load. Specific gravity of blood in a muscular activity is increased and it varies directly with the RBC.
3. Body Temperature:
Normally the body temperature is balanced by the rate of the heat production and heat loss. During exercise the heat production is greatly increased and when simultaneous heat loss does not happen then body temperature is raised. In exercise, the body temperature is raised and it is possibly due to the failure of temperature-regulating centre to maintain the normal body temperature.
4. Body Fluid Changes during Exercise:
During exercise acute dehydration is a great problem because there is rapid loss of water through sweating and expired air.
In acute exercise there is haemoconcentration due to:
(a) Shifting of fluid from the blood to the tissue spaces,
(b) Sweating, and
(c) Rapid expiration.
But if the exercise is continued then water loss is partly checked and dehydration may be minimum presumably by the return of fluid from the tissue spaces to the blood. In chronic exercise as in the case of athletes or in subjects undergoing systematic exercise, there appears no permanent shifts of body fluid.
Along with water loss there is excessive loss of salt which deteriorates work performance. If the fluid and salt losses are adjusted by taking water along with salt during the period of exercise then the work performance may be increased. But it is not generally taken as there is a general belief of the coaches and of the trainers that drinking is harmful during exercise.
5. Kidney Function in Exercise:
Alteration in kidney functions that are generally observed during exercise is presumably due to shupting of blood from the kidneys and other abdominal organs to the vital organs and the active muscle.
The renal blood flow is considerably decreased during exercise and this decrease of flow is maintained as long as an hour following cessations of exercise:
Rate of urine formation is greatly diminished due to:
(a) Excessive reabsorption of fluid from the renal tubles with the help of anti-diuretic hormone (ADH) secreted by the posterior pituitary, and
(b) Decreased renal blood flow.
Furthermore, the kidneys excrete excessive acid metabolites that are accumulated in the blood during exercise. Besides these, there is often transient proteinuria with exercise. After strenuous exercise there is accumulation of albumin in the urine and has been considered to be the cause of increased permeability of these substances in the glomerular capillaries.
Some are of opinions that the increased activity of the kidney tissues may alter the kidney functions during exercise. Often Masch Haemoglobinuria a condition in which physical exertion causing formation of red urine containing haemoglobin is observed. This condition is mostly due to intravascular breakdown of RBC during strenuous exercise.
Haemoglobin generally appears 1-3 hours after severe exercise. Exercise myoglobinuria is often encountered after severe exercise. Stahl (1957) has observed black urine formation 24-48 hours after exercise. He has described that breakdown of muscle fibres during exhaustive exercise is the cause of myoglobinuria.
6. Digestive System:
Strenuous exercise inhibits both the motor and secretory functions of the stomach. Campbell and others (1928) have described that moderate exercise inhibits gastric secretion as well as motility of the stomach but the lighter exercise (walking) helps in gastric juice secretion and also in emptying of the stomach.
But after exercise the motility of the stomach and secretion of gastic juice are increased considerably. This shows that the depressed motility and gastic juice secretion during strenuous exercise are balanced by the increased motility of the stomach and gastric juice secretion after the cessation of activity.
7. Endocrine Status:
Andrenal hypertrophy has been observed in animals under prolonged continuous exertion or training programme. Increased utilization of cortical hormones during exercise has been observed by many. Besides this, improvement of work performance after administration of corticoids in adrenalectomised animals has also been observed.
Growth hormone utilization during exercise is increased. It has been observed that during exercise, mobilization of depot fat is increased by the growth hormone secreted in larger quantity. It is claimed that the liberation of growth hormone or STH appears mostly responsible for mobilization of depot fat when the exogenous carbohydrate is not made available during exercise.
As we know that the ADH secretion is increased during physical exercise. This secretion of ADH actually combats against dehydration during exercise. Function of thyroid hormone during exercise is not yet fully worked out. Lashof and others (1954) found no alterations in thyroid hormone functions in moderate exercise.
