EVIDENCE FOR AN INTRAMUSCULAR VENTILATORY STIMULUS DURING DYNAMIC EXERCISE IN MAN

During incremental work rate exercise, ventilation (VE) typically incr eases in proportion to the metabolic rate until the onset of a progres sive 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 t heir limit of tolerance at different levels of lower-body positive pre ssure (LBPP) at 0, 15, 30, and 45 Torr in order to determine if LBPP c ould alter the occurrence of the ventilatory threshold. Ventilatory re sponses and pulmonary gas exchange variables were measured breath-by-b reath while 'arterialized'-venous blood was sampled from the dorsum of the heated hand for determination of [lactatel, pH, and [K+]. The ven tilatory threshold was progressively reduced with increasing levels of LBPP: Ventilatory threshold = 2.33 - (0.0173.LBPP); (r2 = 0.59, P<0.0 01). Ventilatory equivalents for oxygen (VE/V(O2)) and carbon dioxide (VE/V(CO2)) were systematically elevated at work rates above 50 W by i ncreases in respiratory frequency which also resulted in lower PET(CO2 ) and higher PET(O2) values. As [lactate] was only slightly elevated a bove control (DELTAlactate<1 mEq.L-1) while pH and [K+ ] were unchange d, 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-i nduced reduction in perfusion with the subsequent accumulation of intr amuscular metabolites at the working limb and/or a direct effect of in creased intramuscular tissue pressure.