Evidence for an intramuscular ventilatory stimulus during dynamic exercise in man

During incremental work rate exercise, ventilation (VE) typically increases in proportion to the metabolic rate until the onset of a progressive metabolic acidemia induces an additional compensatory hyperpnea. We examined the control characteristics of this compensatory mechanism in seven healthy subjects performing incremental cycle ergometry to their limit of tolerance at different levels of lower-body positive pressure (LBPP) at 0, 15, 30, and 45 Torr in order to determine if LBPP could alter the occurrence of the ventilatory threshold. Ventilatory responses and pulmonary gas exchange variables were measured breath-by-breath while 'arterialized'-venous blood was sampled from the dorsum of the heated hand for determination of [lactate], pH, and [K+]. The ventilatory threshold was progressively reduced with increasing levels of LBPP: Ventilatory threshold = 2.33-(0.0173.LBPP); (r2 = 0.59, P < 0.001). Ventilatory equivalents for oxygen (VE/VO2) and carbon dioxide (VE/VCO2) were systematically elevated at work rates above 50 W by increases in respiratory frequency which also resulted in lower PETCO2 and higher PETO2 values. As [lactate] was only slightly elevated above control (delta lactate < 1 mEq.L-1) while pH and [K+] were unchanged, it seems unlikely that the LBPP-induced hyperpnea can be attributed to activation of peripheral arterial or central chemoreceptors. These findings suggest a ventilatory stimulus may be generated by an LBPP-induced reduction in perfusion with the subsequent accumulation of intramuscular metabolites at the working limb and/or a direct effect of increased intramuscular tissue pressure.