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Cardiovascular and neuroendocrine responses to exercise in hypoxia during impaired neural feedback from muscle
2 Department of Anesthesia, Copenhagen Muscle Research Center, Rigshospitalet University Hospital; 3 Department of Medical Physiology, Panum Institute; and 1 Sports Medicine Research Unit, Department of Rheumatology H, Bispebjerg Hospital, University of Copenhagen, DK-2400 Copenhagen, Denmark. Re...
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Published in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 1999-07, Vol.277 (1), p.76-R85 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 2 Department of Anesthesia, Copenhagen Muscle
Research Center, Rigshospitalet University Hospital;
3 Department of Medical Physiology, Panum
Institute; and 1 Sports Medicine Research Unit,
Department of Rheumatology H, Bispebjerg Hospital, University of
Copenhagen, DK-2400 Copenhagen, Denmark.
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 |
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ISSN: | 0363-6119 1522-1490 |
DOI: | 10.1152/ajpregu.1999.277.1.r76 |