Received December 18, 2006
Revised January 2, 2007
Accepted after revision January 15, 2007

¹ University of Leeds

^* To whom correspondence should be addressed. E-mail: s.a.ward{at}leeds.ac.uk.

	Abstract

Below the lactate threshold (LT), ventilation (VE) responds in close proportion to CO2 output (VCO2) to regulate arterial PCO2 (PaCO2). While ventilatory control models have traditionally included proportional feedback (central and carotid chemosensory) and feed-forward (central and peripheral neurogenic) elements, the actual mechanisms involved remain unclear. Regardless, putative control schemes have to accommodate the close dynamic "coupling" between VE and VCO2. Above LT, PaCO2 is driven down to constrain the fall of arterial pH by a compensatory hyperventilation, likely of carotid-body origin. When requirements are high (as in highly-fit endurance athletes), can attain limiting proportions. Not only does this impair gas exchange at these work rates, but there may be an associated high metabolic cost for generation of respiratory muscle power which may be sufficient to divert a fraction of the cardiac output away from the muscles of locomotion to the respiratory muscles, further compromising exercise tolerance.

Key Words: Exercise, Ventilation

This article has been cited by other articles:

				S. A. Ward Muscle-energetic and cardio-pulmonary determinants of exercise tolerance in humans: Muscle-energetic and cardio-pulmonary determinants of exercise tolerance in humans Exp Physiol, March 1, 2007; 92(2): 321 - 322. [Full Text] [PDF]