Some of my fellow colleagues and I recently read a few articles relating to the topic of VO2max. One of the articles briefly mentioned Respiratory Compensation Rate. We have been unable to find any additional information on this specific subject. Do you have any insight?
Excellent question. Before we jump into the mix with Respiratory Compensation Rate (RCR), let's revise some basic exercise physiology dealing with VO2max and regulation of acid-balance during exercise. Maximal oxygen consumption (VO2max) is the measure of the capacity of the cardiovascular system. VO2max is the product of maximum cardiac output and maximum arteriovenous oxygen difference. Theoretically, VO2max is the point at which oxygen consumption fails to rise despite an increased exercise intensity or power output. This is outlined in the following equation by Brookes, Fahey and White:
- VO2max = Qmax (a – v)O2max
- VO2max = maximal oxygen uptake (ml·min-1)
- Qmax = maximal cardiac output (ml·min-1)
- (a – v)O2max = maximal arteriovenous oxygen difference (ml O2·dl-1)
During the final stages of an incremental exercise test or during near-maximal exercise of short duration, there is a decrease in both muscle and blood pH primarily due to the increase in the production of lactic acid by the muscle. The pH of your body fluids reflects interactions among all the acids, bases, and salts in solution. The pH normally remains within relatively narrow limits, usually from 7.35-7.45. Any deviation outside the normal range is extremely dangerous, because changes in hydrogen ions (H+) concentrations disrupt the stability of cell membranes, alter protein structure, and change the activities of important enzymes.
When the pH of plasma falls below 7.35, acidemia exists. The physiological state that results is called acidosis. When the pH of plasma rises above 7.45, alkalemia exists. The physiological state that results is called alkalosis. Acidosis and alkalosis affect virtually all body systems, but the nervous system and cardiovascular system are particularly sensitive to pH fluctuations. For example, severe acidosis (pH below 7.0) can be deadly, because (1) central nervous system function deteriorates, and the individual may become comatose; (2) cardiac contractions grow weak and irregular, and symptoms of heart failure may develop; and (3) peripheral vasodilation produces a dramatic drop in blood pressure, and circulatory collapse can occur.
How does the body regulate acid-base balance during exercise?
Since the primary source of H+ released during exercise is lactic acid produced within the working muscles, it is reasonable that the first line of defence against a rise in acid production would reside in the muscle itself. Intracellular proteins contribute as much as 60 percent of the cell’s buffering capacity, with an additional 20 to 30 percent of the total buffering capacity comes from muscle bicarbonate. The final 10 to 20 percent comes from intracellular phosphate group. Although buffer systems can tie up excess H+, they provide only a temporary solution. The hydrogen ions have not been eliminated but merely rendered harmless. For homeostasis to be preserved, the captured H+ must ultimately be removed from body fluids. The problem is that the supply of buffer molecules is limited. Suppose that a buffer molecule prevents a pH change by binding a hydrogen ion that enters the extracellular fluid (ECF). The buffer is then tied up, reducing the capacity of the ECF to cope with any more H+. Eventually, all the buffer molecules will be bound to H+, and pH control will be impossible.
The situation can be resolved only by removing the H+ from the ECF, thereby freeing the buffer molecules, or by replacing the buffer molecules. Similarly, if a buffer provides a hydrogen ion to maintain normal pH, either another hydrogen ion must be obtained or the buffer must be replaced. The maintenance of acid–base balance thus includes balancing H+ gains and losses. This balancing act involves coordinating the actions of buffer systems with respiratory mechanisms and renal mechanisms. The respiratory and renal mechanisms support the buffer systems by (1) secreting or absorbing H+, (2) controlling the excretion of acids and bases, and, when necessary, (3) generating additional buffers. It is the combination of buffer systems and these respiratory and renal mechanisms that maintains your pH within narrow limits.
Stringer, Casaburi & Wasserman demonstrated that as blood lactic acid concentration increases, blood bicarbonate concentration decreases proportionally. Also, at approximately 50 to 60 percent of VO2max, blood pH begins to decline due to the rise in lactic acid production. This increase in H+ concentration stimulates the carotoid bodies, which then signal the respiratory control centre to increase alveolar ventilation (i.e., ventilatory threshold). An increase in alveolar ventilation results in a reduction of blood PCO2 and therefore acts to reduce the acid load produced by exercise. The overall process of respiratory assistance in buffering lactic acid during exercise is referred to as respiratory compensation for metabolic acidosis.
Respiratory compensation is a change in the respiratory rate that helps stabilise pH of the ECF. Respiratory compensation occurs whenever your pH strays outside normal limits. This compensation is effective, because respiratory activity has a direct effect on the carbonic acid–bicarbonate buffer system. Increasing or decreasing the rate of respiration alters pH by lowering or raising the PCO2. When the partial pressure of carbon dioxide (PCO2) rises, the pH falls, because the addition of CO2 drives the carbonic acid–bicarbonate buffer system to the right. When the PCO2 falls, the pH rises because the removal of CO2 drives that buffer system to the left.
As previously mentioned chemoreceptors of the carotid and aortic bodies are sensitive to the PCO2 of the circulating blood. Other receptors, located on the ventrolateral surfaces of the medulla oblongata, monitor the PCO2 of the cerebrospinal fluid (CSF). A rise in PCO2 stimulates the receptors; a fall in the PCO2 inhibits them. The stimulation of the chemoreceptors leads to an increase in the respiratory rate. As the rate of respiration increases, more CO2 is lost at the lungs, so the PCO2 returns to normal levels. When the PCO2 of the blood or CSF declines, respiratory activity becomes depressed and the breathing rate decreases. This decrease causes an elevation of the PCO2 in the ECF.
Hope this helps. Good luck with your training!
- Brooks, G.A. Fahey, T.D. & White, T.P. 1996, Exercise Physiology. 2nd edn. Human Bioenergetics and its Application. Mayfield Publishing, Mountain View, California.
- Hultman, E. & Sahlin, K. 1980, Acid-base balance during exercise. In: Exercise and Sport Sciences Reviews, vol 8, eds. R. Hutton and D. Miller. Frankiln Institute Press, Philadeliphia. pp. 41-128.
- Katz, A. & Sahlin, K. 1988, Regulation of lactic acid production during exercise. J. Appl. Physiol. 65 (2): pp. 509-518.
- Martini, F.H. 2001, Fundamentals of Anatomy and Physiology. 5th edn. Prentice Hall, Upper Saddle River, NJ.
- Powers, S.K. & Howley, E.T. 2001, Exercise Physiology: Theory and Application to Fitness and Performance. 4th edn. McGraw-Hill, New York.
- Stringer, W.R. Casaburi, R. & Wasserman, K. 1992, Acid-base regulation during exercise and recovery in humans. J. Appl. Physiol. 72 (3): pp. 954-961.