Cardiovascular and neuroendocrine responses to exercise in hypoxia during impaired neural feedback from muscle

Reflex mechanisms from contracting skeletal muscle have been shown to be im portant for cardiovascular, neuroendocrine, and extramuscular fuel-mobiliza tion responses in exercise. Furthermore, because hypoxia results in exagger ated metabolic changes in contracting muscle, the present study evaluated w hether enhancement of cardiovascular and neuroendocrine responses by hypoxi a during exercise is influenced by neural feedback from contracting muscle. Seven healthy males cycled at 46% maximal O-2 uptake for 20 min both durin g normoxia and at 11.5% Ca, and both without and with epidural anesthesia ( EA; 20 ml 0.25% bupivacain, resulting in cutaneous hypesthesia below T10-T1 2 and 25% reduction in maximal leg strength). Exercise to exhaustion was al so performed at 7.8% O-2 The exercise-induced increases in heart rate; card iac output; leg blood flow; plasma concentrations of growth hormone, adreno corticotropin, cortisol, and catecholamines; renin activity; glucose produc tion and disappearance; norepinephrine spillover [2,190 +/- 341 ng/min (exe rcise at 11.5% O-2) vs. 988 +/- 95 ng/min (exercise during normoxia)]; lact ate release from and glucose uptake in the leg; and the decreases in plasma insulin and free fatty acids were exaggerated in hypoxia (P < 0.05). In mu scle, concentrations of lactate, creatine, and inosine 5'-monophosphate wer e higher, and those of phosphocreatine were lower after exercise in hypoxia compared with normoxia. The exercise-induced increase in mean arterial blo od pressure was not affected by hypoxia, but it was reduced by EA [108 +/- 4 mmHg (control) vs. 97 +/- 4 mmHg (EA); P < 0.05], and the reduction was m ore pronounced during severe hypoxia compared with normoxia. Apart from thi s, time to exhaustion at extreme hypoxia, circulatory responses, concentrat ions of neuroendocrine hormones, and extramuscular substrate mobilization w ere not diminished by EA. In conclusion, in essence the hypoxia-induced enh ancement of systemic adaptation to exercise is not mediated by neural feedb ack from working muscle in humans.