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 important for cardiovascular, neuroendocrine, and extramuscular fuel-mobilization responses in exercise. Furthermore, because hypoxia results in exaggerated metabolic changes in contracting muscle, the present study evaluated whether enhancement of cardiovascular and neuroendocrine responses by hypoxia during exercise is influenced by neural feedback from contracting muscle. Seven healthy males cycled at 46% maximal O(2) uptake for 20 min both during normoxia and at 11.5% O(2), and both without and with epidural anesthesia (EA; 20 ml 0.25% bupivacain, resulting in cutaneous hypesthesia below T10-T12 and 25% reduction in maximal leg strength). Exercise to exhaustion was also performed at 7.8% O(2). The exercise-induced increases in heart rate; cardiac output; leg blood flow; plasma concentrations of growth hormone, adrenocorticotropin, cortisol, and catecholamines; renin activity; glucose production and disappearance; norepinephrine spillover 2, 190 +/- 341 ng/min (exercise at 11.5% O(2)) vs. 988 +/- 95 ng/min (exercise during normoxia); lactate 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 muscle, concentrations of lactate, creatine, and inosine 5'-monophosphate were higher, and those of phosphocreatine were lower after exercise in hypoxia compared with normoxia. The exercise-induced increase in mean arterial blood 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 more pronounced during severe hypoxia compared with normoxia. Apart from this, time to exhaustion at extreme hypoxia, circulatory responses, concentrations of neuroendocrine hormones, and extramuscular substrate mobilization were not diminished by EA. In conclusion, in essence the hypoxia-induced enhancement of systemic adaptation to exercise is not mediated by neural feedback from working muscle in humans.