Blood Flow
and Ischemia/Hypoxia in Exercising Muscles
Michael J. Joyner and Darren P. Casey
Department of
Anesthesiology, Mayo Clinic,
When oxygen delivery to contracting muscles is reduced by hypoxia, blood flow increases due to vasodilation in a way that tends to maintain oxygen delivery at "normal" levels. We have termed this "compensatory vasodilation" and recently shown in humans that beta-adrenergic mechanisms in conjunction with nitric oxide (NO) play a key role in this response during systemic hypoxia. In this context, little is known about how blood vessels in exercising human muscles respond to hypoperfusion (ischemia) during exercise. To study these responses, and determine if hypoperfusion evokes compensatory vasodilation, we have developed a catheter balloon system that can be deployed in the brachial artery during exercise to reduce blood flow to contracting forearm muscles. Our work to date suggests that a compensatory dilator response occurs in response to hypoperfusion and that NO play a role in this response. Additionally, we have been surprised that hypoperfusion in contracting human forearm muscles does not evoke a systemic "muscle chemoreflex" mediated rise in arterial pressure. Finally, the role of vasodilation in collateral vessels around the elbow in restoring blood flow to hypoperfused forearm muscles can be marked in some subjects. The extent to which the mechanisms that govern the compensatory dilator response to hypoperfusion are similar or different than those operating during hypoxia is a major focus of our work going forward.
Supported by
NIH HL-46493, NCRR U54-1, and NIH AR-55819.
Key words: exercise hyperemia, vasodilation, oxygen delivery