Journal of Applied Physiology, Vol 59, Issue 3 792-797, Copyright © 1985 by American Physiological Society
Control of exercise hyperpnea during hypercapnia in humans
C. S. Poon and J. G. Greene
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).
