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We hypothesised that vagal withdrawal and increased venous return interact in determining the rapid cardiac output (CO) response (phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood distribution to the heart by muscle pump action and reduce resting vagal activity. We expected a larger increase in stroke volume (SV) and smaller for heart rate (HR) at progressively stronger LBNP levels, therefore CO response would remain unchanged. To this aim ten young, healthy males performed a 50 W exercise in supine position at 0 (Control), −15, −30 and −45 mmHg LBNP exposure. On single beat basis, we measured HR, SV, and CO. Oxygen uptake was measured breath-by-breath. Phase I response amplitudes were obtained applying an exponential model. LBNP increased SV response amplitude threefold from Control to −45 mmHg. HR response amplitude tended to decrease and prevented changes in CO response. The rapid response of CO explained that of oxygen uptake. The rapid SV kinetics at exercise onset is compatible with an increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, one acting on SV, the other on HR.

The effects of muscle temperature on the development of muscular power are discussed. Temperature influences power (both metabolic and mechanical) by means of its effects on the rate of ATP hydrolysis and/or resynthesis. One would therefore expect reduced power outputs at cold muscle temperatures in humans. However, this is not the case during submaximal aerobic exercise. In fact, no changes in metabolic power output at any given submaximal work load were found at cold muscle temperatures, despite the reduced rate of ATP resynthesis and/or splitting. To explain this, it has been postulated that the fraction of active muscle mass at any given time instant could increase in the cold, thus compensating for the reduced ATP splitting rate. This means that the aerobic ATP resynthesis in the cold may be carried out at a slower rate by a greater activated muscle mass. This compensation cannot be operational when maximal power is attained, for in this case the instantaneously activated muscle mass is constant and limited. In fact the maximal aerobic power and the maximal instantaneous anaerobic power decrease with decreasing muscle temperature, as indicated by an average Q10 of 1.4 in the physiological muscle temperature range. The reduction in maximal aerobic power in the cold may be the consequence particularly of a decrease in O2 supply associated with reduced maximal cardiac output and muscle blood flow. On the other hand, the Q10 of the maximal anaerobic power should strictly depend on the reduced rate of ATP hydrolysis. The Q10 of the latter, however, according to Arrhenius law, should be 2 to 3 instead of 1.4.(ABSTRACT TRUNCATED AT 250 WORDS)

The time course of phosphocreatine (PC) hydrolysis in humans was measured by 31P-NMR spectroscopy (31P-NMRS) with a time resolution of 10.8 s in the gastrocnemius muscle and a relationship between muscle O2 consumption (VO2) and [PC] was derived from a bioenergetic model. This allowed a direct estimate of the half-time of the intracellular VO2 kinetics (t1/2 VO2) of the contracting human gastrocnemius in aerobic conditions. t1/2 VO2 was found to be approximately 16 s and independent of the work load. This value corresponds to the shortest t1/2 VO2 determined at the mouth of the subject in the absence of lactate accumulation in the rest to work transient. t1/2 VO2 may now be assessed in man at low muscle temperatures. To this aim a procedure was developed allowing corrections of the 31P-NMR spectra based on the muscle temperature profiles obtained by a simultaneously acquired proton image.