Control of exercise hyperpnea during hypercapnia in humans

Abstract

Previous studies have yielded conflicting results on the ventilatory response to CO2 during muscular exercise. To obviate possible experimental errors contributing to such variability, we have examined the CO2-exercise interaction in terms of the ventilatory response to exercise under conditions of controlled hypercapnia. Eight healthy male volunteers underwent a sequence of 5-min incremental treadmill exercise runs from rest up to a maximum CO2 output (VCO2) of approximately 1.5 l . min-1 in four successive steps. The arterial PCO2 (PaCO2) at rest was stabilized at the control level or up to 14 Torr above control by adding 0-6% CO2 to the inspired air. Arterial isocapnia (SD = 1.2 Torr) throughout each exercise run was maintained by continual adjustment of the inspired PCO2. At all PaCO2 levels the response in total ventilation (VE) was linearly related to exercise VCO2. Hypercapnia resulted in corresponding increases in both the slope (S) and zero intercept (V0) of the VE-VCO2 curve; these being directly proportional to the rise in PaCO2 (means +/- SE: delta S/ delta PaCO2, 2.73 +/- 0.28 Torr-1; delta V0/ delta PaCO2, 1.67 +/- 0.18 l . min-1 . Torr-1). Thus the ventilatory response to concomitant hypercapnia and exercise was characterized by a synergistic (additive plus multiplicative) effect, suggesting a positive interaction between these stimuli. The increased exercise sensitivity in hypercapnia is qualitatively consistent with the hypothesis that VE is controlled to minimize the conflicting challenges due to chemical drive and the mechanical work of breathing (Poon, C. S. In: Modelling and Control of Breathing, New York: Elsevier, 1983, p. 189-196).

Effects of negative pressure assisted ventilation on dyspnoeic sensation and breathing pattern

“…This concept of optimization of breathing patterns during addition of respiratory loading is also compatible with the hypothesis proposed by MEAD [20] that breathing patterns are adjusted to the level at which the work of breathing is minimal. In this regard, POON and GREENE [21] suggested that changes in the work of breathing may be sensed as changes in the sense of effort. TACK et al [22] also showed that respiratory sensation changes as a function of both pressure and volume changes so that it is related to respiratory work.…”

Ventilation response to CO 2 and exercise-induced hypoxaemia in master athletes

“…One other explanation should be considered. The eects of hypercapnia and muscle exercise on E are well established, and Poon and Greene (1985) have shown the interaction of hypercapnia and exercise in the overall control of breathing in untrained subjects. We can speculate that this interaction may have been dierent in our two groups of subjects, but other studies are necessary to con®rm it.…”

Integrated characterization of the human chemoreflex system controlling ventilation, using an equilibrium diagram

“…Each FICO 2 trial ran for 15 min at approximately 10-15 min intervals. This duration is long enough to permit CO 2 to reach its new steady-state value at the central chemoreceptors (Honda et al 1983;Poon and Greene 1985;Pianosi et al 1994;Teppema et al 2000). During the interval periods, the subjects inspired room air.…”

“…This is to say that if the characteristics of the central controller remain unaltered, exercise must increase P a CO 2 . However, the fact that P a CO 2 ordinarily does not change much during exercise (Oren et al 1981;Dempsey et al 1984;Poon and Greene 1985;Wasserman et al 1986;Whipp and Pardy 1986) suggests that exercise concurrently sensitizes the respiratory chemoreflex, thereby keeping P a CO 2 fairly constant in healthy subjects.…”