Point:counterpoint Comments

To the Editor: Ventilation (VE) is controlled by the arterial tension of carbon dioxide (PaCO2), but during exercise other mechanisms prevail. At low work rates, the moderate increase in VE represents “hypoventilation” as PaCO2 increases, whereas at 60–70% of work capacity and during intense exercise, the marked increase in VE restores to the resting value, or even lowers, PaCO2 (2). Also, during intense exercise, administration of bicarbonate that eliminates the drop in pH attenuates the hyperpneic response, although PaCO2 increases (3). However, these observations do not undermine the influence of PaCO2. Postexercise muscle ischemia reduces VE, which increases again on release of the cuff(s) in close parallel with PaCO2 (2), and a similar response is elicited by reperfusion of internal organs during surgery. However, in some subjects who experience lively pain, postexercise muscle ischemia is associated with a marked increase in VE (2). If no pain is experienced, neural influence from the working muscles does not influence VE because VE is not influenced by epidural anesthesia (4). Conversely, central command has a marked influence on VE and the neurophysiological background is summarized elegantly by Waldrop and Iwamoto (5). In humans, the classical experiment is to perform exercise with partial neuromuscular blockade as first carried out in Germany and in the well-known study of Asmussen et al. (1). Under such circumstances, VE is larger than during control exercise, indicating that the will to exercise supports the first step of oxygen delivery to working skeletal muscles.