The ‘normal’ adjustment of oxygen delivery to small muscle mass exercise is not optimized for muscle contractile function

Abstract

AbstractOxygen delivery is viewed as tightly coupled to demand in exercise below critical power because increasing oxygen delivery does not increase . However, whether the ‘normal’ adjustment of oxygen delivery to small muscle mass exercise in the heavy intensity domain is optimal for excitation–contraction coupling is currently unknown. In 20 participants (10 female), a remote skeletal muscle (i.e. tibialis anterior) metaboreflex was (Hyperperfusion condition) or was not (Control condition) activated for 4 min during both force of contraction (experimental model 1) and muscle activation‐targeted (experimental model 2) rhythmic forearm handgrip exercise. Analysis was completed on the combined data from both experimental models. After 30 s of remote skeletal muscle metaboreflex activation, mean arterial blood pressure, forearm blood flow and muscle oxygenation were increased and remained increased until metaboreflex discontinuation. While oxygen delivery was elevated, the muscle activation to force of contraction ratio was improved. Upon metaboreflex discontinuation, forearm oxygen delivery and the muscle activation and force of contraction ratio rapidly (within 30 s) returned to control levels. These findings demonstrate that (a) the metaboreflex was effective at increasing forearm muscle oxygen delivery and oxygenation, (b) the muscle activation to force of contraction ratio was improved with increased oxygen delivery, and (c) in the heavy exercise intensity domain, the normal matching of oxygen delivery to metabolic demand is not optimal for muscle excitation–contraction coupling. These results suggest that the nature of vasoregulation in exercising muscle is such that it does not support optimal perfusion for excitation–contraction coupling. imageKey points Oxygen delivery is viewed as tightly coupled to demand in exercise below critical power because increasing oxygen delivery does not increase the rate of oxygen uptake. Whether the ‘normal’ adjustment of oxygen delivery in small muscle mass exercise below critical power is optimal for excitation–contraction coupling is not known. Here we show in humans that increasing oxygen delivery above ‘normal’ improves excitation–contraction coupling. These results suggest that, in the heavy exercise intensity domain, the ‘normal’ matching of oxygen delivery to metabolic demand is not optimal for muscle excitation–contraction coupling. Therefore, the nature of vasoregulation in exercising muscle is such that it does not support optimal perfusion for excitation–contraction coupling.