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Muscle blood flow, hypoxia, and hypoperfusion
Journal article   Open access   Peer reviewed

Muscle blood flow, hypoxia, and hypoperfusion

Michael J Joyner and Darren P Casey
Journal of applied physiology (1985), Vol.116(7), pp.852-857
04/01/2014
DOI: 10.1152/japplphysiol.00620.2013
PMCID: PMC3972742
PMID: 23887898
url
https://doi.org/10.1152/japplphysiol.00620.2013View
Published (Version of record) Open Access

Abstract

Blood flow increases to exercising skeletal muscle, and this increase is driven primarily by vasodilation in the contracting muscles. When oxygen delivery to the contracting muscles is altered by changes in arterial oxygen content, the magnitude of the vasodilator response to exercise changes. It is augmented during hypoxia and blunted during hyperoxia. Because the magnitude of the increased vasodilation during hypoxic exercise tends to keep oxygen delivery to the contracting muscles constant, we have termed this phenomenon "compensatory vasodilation." In a series of studies, we have explored metabolic, endothelial, and neural mechanisms that might contribute to compensatory vasodilation. These include the contribution of vasodilating substances like nitric oxide (NO) and adenosine, along with altered interactions between sympathetic vasoconstriction and metabolic vasodilation. We have also compared the compensatory vasodilator responses to hypoxic exercise with those seen when oxygen delivery to contracting muscles is altered by acute reductions in perfusion pressure. A synthesis of our findings indicate that NO contributes to the compensatory dilator responses during both hypoxia and hypoperfusion, while adenosine appears to contribute only during hypoperfusion. During hypoxia, the NO-mediated component is linked to a β-adrenergic receptor mechanism during lower intensity exercise, while another source of NO is engaged at higher exercise intensities. There are also subtle interactions between α-adrenergic vasoconstriction and metabolic vasodilation that influence the responses to hypoxia, hyperoxia, and hypoperfusion. Together our findings emphasize both the tight linkage of oxygen demand and supply during exercise and the redundant nature of the vasomotor responses to contraction.
 Adaptation, Physiological Signal Transduction Receptors, Adrenergic - metabolism Humans Oxygen Consumption Muscle, Skeletal - metabolism Regional Blood Flow Oxygen - blood Vasodilation Hypoxia - blood Exercise Muscle Contraction Muscle, Skeletal - physiopathology Hypoxia - physiopathology Nitric Oxide - metabolism Muscle, Skeletal - blood supply

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