Ischemia of active skeletal muscle elicits a powerful pressor response, termed the muscle metaboreflex. We recently reported that the muscle metaboreflex pressor response acts to partially restore blood flow to the ischemic active skeletal muscle. However, because this reflex is activated by reductions in O₂ delivery rather than blood flow per se, gain of the muscle metaboreflex as analyzed on the basis of blood flow alone may underestimate its true strength if this reflex also acts to increase arterial O₂ content. In conscious dogs chronically instrumented to measure systemic arterial pressure, cardiac output, and hindlimb blood flow, we activated the muscle metaboreflex via graded, partial reductions in hindlimb blood flow during mild (3.2 km/h) and moderate (6.4 km/h, 10% grade) workloads. At rest, during free-flow exercise, and with metaboreflex activation, we analyzed arterial blood samples for Hb concentration and O₂ content and compared muscle metaboreflex gain calculations based on the ability to partially restore flow with those based on the ability to partially restore O₂ delivery (blood flow × arterial O₂ content). During both mild and moderate exercise, metaboreflex activation caused significant increases in arterial Hb concentration and O₂ content. Metaboreflex gain quantified on the ability to partially restore O₂ delivery was significantly greater than that based on restoration of blood flow during both mild and moderate workloads (0.52 ± 0.10 vs. 0.39 ± 0.08, P < 0.05, and 0.61 ± 0.05 vs. 0.46 ± 0.04, P < 0.05, respectively). We conclude that the muscle metaboreflex acts to increase both arterial O₂ content and blood flow to ischemic muscle such that when combined, O₂ delivery is substantially increased and metaboreflex gain is greater when analyzed with a more integrative approach.

sympathetic nervous system; hemoglobin; arterial blood gases; muscle blood flow

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