Muscle Na-K-pump and fatigue responses to progressive exercise in normoxia and hypoxia

Abstract

To investigate the effects of hypoxia and incremental exercise on muscle contractility, membrane excitability, and maximal Na+-K+-ATPase activity, 10 untrained volunteers (age = 20 ± 0.37 yr and weight = 80.0 ± 3.54 kg; ± SE) performed progressive cycle exercise to fatigue on two occasions: while breathing normal room air (Norm; FiO2 = 0.21) and while breathing a normobaric hypoxic gas mixture (Hypox; FiO2 = 0.14). Muscle samples extracted from the vastus lateralis before exercise and at fatigue were analyzed for maximal Na+-K+-ATPase (K+-stimulated 3-O-methylfluorescein phosphatase) activity in homogenates. A 32% reduction ( P < 0.05) in Na+-K+-ATPase activity was observed (90.9 ± 7.6 vs. 62.1 ± 6.4 nmol·mg protein−1·h−1) in Norm. At fatigue, the reductions in Hypox were not different (81 ± 5.6 vs. 57.2 ± 7.5 nmol·mg protein−1·h−1) from Norm. Measurement of quadriceps neuromuscular function, assessed before and after exercise, indicated a generalized reduction ( P < 0.05) in maximal voluntary contractile force (MVC) and in force elicited at all frequencies of stimulation (10, 20, 30, 50, and 100 Hz). In general, no differences were observed between Norm and Hypox. The properties of the compound action potential, amplitude, duration, and area, which represent the electomyographic response to a single, supramaximal stimulus, were not altered by exercise or oxygen condition when assessed both during and after the progressive cycle task. Progressive exercise, conducted in Hypox, results in an inhibition of Na+-K+-ATPase activity and reductions in MVC and force at different frequencies of stimulation; these results are not different from those observed with Norm. These changes occur in the absence of reductions in neuromuscular excitability.

Effect of acute severe hypoxia on peripheral fatigue and endurance capacity in healthy humans

“…An additive effect of hypoxia and exercise on M-wave potentiation has been reported previously (21,44) and may be because of a greater recruitment of fast-twitch (type II) motor units (47), which are known to exhibit greater potentiation than type I fibers during fatiguing exercise (22).…”

Skeletal Muscle Fatigue: Cellular Mechanisms

“…An important study on trained humans extends the beneficial effects of NAC to a voluntary submaximal cycling in which the time to volitional fatigue was increased by NAC infusion by 26% (304). In a recent extension of this approach, McKenna et al (303) showed that NAC minimized the reduction in Na ϩ -K ϩ pump activity that usually occurs in exercise (394) and also attenuated the rise in plasma K ϩ . Given that the Na ϩ -K ϩ pump is redox sensitive (184), the authors propose that ionic changes associated with Na ϩ -K ϩ pump contribute to fatigue and can be ameliorated by the ROS scavenger NAC.…”

Effect of arterial oxygenation on quadriceps fatigability during isolated muscle exercise

“…The entire assessment procedure took ϳ8 min. Within-twitch variables included maximal rate of force development (MRFD), maximal rate of relaxation (MRR), contraction time (CT), and onehalf relaxation time (RT 0.5) measured in response to Qtw,unp and Qtw,pot (1,2,45). Each variable is presented as the mean of eight Qtw,unp and three Qtw,pot values.…”

“…Surface electrodes were used to record 1) magnetically evoked compound mass action potentials (M wave) for VL, VM, and RF to evaluate pre-to postexercise changes in membrane excitability and 2) EMG of VL during exercise to estimate changes in motor unit recruitment. To evaluate changes in M-wave properties, we obtained peak amplitude, duration, conduction time, and area (1,2,45). Raw EMG signals (VL) for each muscle contraction during experiment 2 were recorded for later analysis of integrated EMG (iEMG) via a computer algorithm [for details, see Amann et al (1,2)].…”