COMPARISON OF ARTERIAL POTASSIUM AND VENTILATORY DYNAMICS DURING SINUSOIDAL WORK RATE VARIATION IN MAN

1. The mechanisms underlying the exercise hyperpnoea have been difficu lt to define. Recently it has been suggested that exercise ventilation (V-E) changes in proportion to changes in arterial potassium concentr ation ([K+](a)). Similar V-E and [K+](a) time courses following work r ate changes have been cited as supporting evidence. This study compare d [K+](a) and V-E dynamics during moderate exercise in man. 2. We obse rved V-E and gas exchange responses in five healthy men to sinusoidal work rate variation between 25 and similar to 105 W. Tests of similar to 30 min duration were performed at sinusoidal periods of 9, 6 and 3 min and in the steady state. In each test, during two or three sine pe riods, arterial blood was sampled (24 per test) and analysed for [K+] and blood gases. Response amplitude and phase (relative to work rate) mere determined for each variable. 3. [K+](a) fluctuated in response t o sinusoidal work rate forcing with mean-to-peak amplitude averaging 0 .15 mmol l(-1). However, among tests, V-E amplitude and phase were not highly correlated with [K+](a) (r = 0.36 and 0.67, respectively). Fur ther, average [K+](a) amplitude in the 9 and 6 min sinusoidal studies tended to exceed the steady-state amplitude, while average V-E amplitu de fell progressively with increasing forcing frequency. The dissimila r dynamics of [K+](a) and V-E seem inconsistent with a major role for [K+](a) as a proportional controller of ventilation during non-steady state moderate exercise in man. 4. Among tests, V-E and CO2 output (V- CO2) amplitude and phase were closely correlated (r = 0.87 and 0.94, r espectively). Further, arterial CO2 pressure (P-a,P-CO2) and arterial pH (pH(a)) did not fluctuate significantly in ten of twenty and thirte en of twenty studies, respectively. In tests where sinusoidal fluctuat ion was detected, amplitude averaged 1.1 mmHg and 0.008 units, respect ively. Thus V-E demonstrated a close dynamic coupling to CO2 output, w ith consequent tight regulation of P-a,P-CO2 and pH(a).