The Differential Effect Of Metabolic Alkalosis On Central And Peripheral Mechanisms Associated With Fatigue

Abstract

The increased concentration of protons (H+) in the interstitium and extracellular milieu 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. Theoretically, introducing a buffering agent prior to fatiguing exercise may substantiate whether increased H+ production significantly contributes to afferent activation and subsequent descending central drive. PURPOSE: To determine whether 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. METHODS: On two separate days, 11 recreationally active males (22 ± 3 yrs) performed an exercise protocol consisting of a 2-min maximal voluntary knee extension (MVC) followed by a 2-min rest with an occlusive cuff either under placebo (PLA; 0.3 g·kg-1 BW calcium carbonate) or alkalosis (ALK; 0.3 g·kg-1BW sodium bicarbonate) condition. To ensure adequate fatigue was achieved and to maximise the effect of afferent firing rates, a final 1-min MVC with cuff occlusion was performed after the initial 4-min sequence. Femoral nerve stimulation was applied to explore central and peripheral mechanisms associated with reductions in maximum force and rate of force development, and occurred prior to exercise, after the 2-min MVC and then at 60 s intervals throughout the remainder of the protocol. RESULTS: Maximal voluntary torque (MVT) declined at similar rates during the task (mean decline of 203 ± 19 N; p < 0.001), however maximal rate of torque development (RTDMAX) was significantly higher in the ALK condition after the 2-min MVC (mean difference of 177 ± 60 Nm·s-1; p < 0.05). 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%; p < 0.05). CONCLUSION: Metabolic alkalosis exerts a differential effect on VA after a 2-min MVC followed by ischemia, and attenuates the decline in the rate of torque development but not maximal voluntary torque.