Interaction of physiological mechanisms during exercise.

Abstract

obtained from such studies is often difficult to interpret because the precise work intensity is not known and/or the duration of the exercise is too short for cardiorespiratory function to stabilize and a “Steady state” of exercise to be achieved. WASSERMAN, KARLMAN, ANTONIUS L. VAN KESSEL, AND GEORGE G. BURTON. Interaction of physiological mechanisms during exercise. J. Appl. Physiol. 22(1): 71-85. rg67.-The effects of work intensity and duration on the metabolic circulatory and ventilatory response to exercise are quantitated in healthy male subjects during cycle ergometer exercise. There is a wellordered relationship between work rate and oxidatve energy sources. Steady-state time for 02 consumption (Vo,) is dependent on work intensity (the time arterial blood lactate concentration stops increasing). At moderate work, anaerobic metabolism is a very small part of credit oxidation, while at very heavy work, the pyruvate-lactate mechanism is the major creditor. The increase in gas exchange ratio (R) reflecting the production of CO2 from bicarbonate (buffering of lactic aid) is transient. After the steady state is reached, R decreases. The heart rate increase during constant-load exercise parallels the increase in vo,. Physiological dead space/tidal volume ratio decreases from .33 to .17 during exercise. The reduction is independent of work duration and only slightly reduced as work intensity increases. Arterial 02 tension does not decrease during exercise at sea level even at maximal rates of 02 transport. Arterial-end tidal CO2 tension differences suggest a fluctuation in pulmonary capillary CO2 tension of approximately 8 mm Hg during the respiratory cycle of the exercising subject. Changes in minute ventilation are best predicted from the rate of CO2 production and the extent of respiratory compensation for metabolic acidosis.