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Muscle afferent activation causes ventilatory and cardiovascular responses during concurrent hypercapnia in humans
Author(s) -
Bruce Richard M.,
White Michael J.
Publication year - 2012
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2011.061606
Subject(s) - hypercapnia , medicine , anesthesia , circulatory system , ventilation (architecture) , respiratory minute volume , cardiology , respiratory system , heart rate , blood pressure , engineering , mechanical engineering
Respiratory and cardiovascular responses to muscle mechanoreflex (passive calf stretch) and metaboreflex activation (local circulatory occlusion) were examined during inhalation of a hypercapnic gas mixture in four trials. These controlled for the effects of central command, metabolite sensitization of muscle afferents and hypercapnia‐induced elevation of central respiratory drive. In an isokinetic dynamometer, with circulation through the right leg occluded by inflation of a thigh cuff, 13 participants either rested (control trial; CON) or plantarflexed their ankle at 50% maximal force for 1.5 min (voluntary exercise trial; EX). Thereafter, circulatory occlusion was maintained and the calf passively stretched before return to the resting position. Both trials were performed while breathing air, as well as while breathing a normoxic, hypercapnic (5% CO 2 ) gas mixture (CO 2 trial and CO 2 +EX trial). Hypercapnic gas inhalation increased baseline minute ventilation (), heart rate and mean arterial pressure (+27.67 ± 1.74 l min −1 , +7 ± 0.85 beats min −1 and +13 ± 3.41 mmHg, respectively; means ± SEM) above control values (9.78 ± 0.86 l min −1 , 62 ± 2.3 beats min −1 and 88 ± 2.6 mmHg, respectively). Voluntary exercise further increased these variables from baseline during both trials ( P < 0.05). During the continued circulatory occlusion after voluntary exercise, mean arterial pressure remained significantly elevated ( P < 0.05). Minute ventilation returned to baseline during circulatory occlusion following exercise in the EX trial, but in the CO 2 +EX trial the remained elevated at end‐exercise levels during this period (+7.12 ± 1.13 l min −1 ). Passive stretch caused further increases in during CO 2 +EX and CO 2 trials but not in CON and EX. These results indicate that in the absence of central command, either muscle metaboreflex and/or mechanoreflex activation stimulates ventilation during concurrent hypercapnia.