The effect of metabolic alkalosis on central and peripheral mechanisms associated with exercise-induced muscle fatigue in humans

The increased concentration of protons during fatiguing exercise may contribute to increased activation of group III and IV afferents and subsequently reduced central drive, however this has yet to be confirmed in exercising humans. Here we determined whether inducing metabolic alkalosis differentially effects descending central drive following fatiguing exercise, and whether this effect may, in part, be explained by attenuating group III and IV afferent firing. 11 males performed a maximal 2 min voluntary knee extension (MVC) followed by a 2 min rest and subsequent 1 min MVC with an occlusive cuff either under placebo (PLA; 0.3 g·kg-1 BW calcium carbonate) or alkalosis (ALK; 0.3 g·kg-1 BW sodium bicarbonate) condition. Femoral nerve stimulation was applied prior to exercise, after the 2 min MVC and then at 40 to 60 s intervals throughout the remainder of the protocol to explore central and peripheral mechanisms associated with reductions in maximum force and rate of torque development. Although voluntary activation (VA) declined similarly after the 2 min MVC, during the ischemic period VA was higher during ALK (PLA: 57 ± 8%; ALK: 76 ± 5%). Maximal voluntary torque declined at similar rates during the task (203 ± 19 Nm), however maximal rate of torque development was significantly higher in the ALK condition after the 2 min MVC (mean difference of 177 ± 60 Nm·s-1 ). These results demonstrate the effect of pH on voluntary activation as well as maximal rates of torque development after sustained, maximal voluntary knee extension in humans.