BackgroundPrevious studies have evaluated the effectiveness of branched-chain amino acid (BCAA) supplementation for preventing delayed onset muscle soreness (DOMS) and muscle damage induced by eccentric exercise, their findings have been inconclusive. Since taurine has anti-inflammatory and anti-oxidative effects, the present study investigated the combined effect of BCAA and taurine on DOMS and muscle damage.MethodsThirty-six untrained male subjects (22.5 ± 3.8 years) were assigned to four groups (placebo + placebo [placebo], BCAA + placebo, placebo + taurine, and BCAA + taurine [combined]) and given a combination of 3.2 g BCAA (or placebo) and 2.0 g taurine (or placebo), three times a day, for two weeks prior to and three days after eccentric elbow flexor exercises. DOMS and muscle damage in the biceps brachii were subjectively and objectively evaluated using the visual analogue scale (VAS), upper arm circumference (CIR), and blood parameters (creatine kinase, lactate dehydrogenase [LDH], aldolase, and 8-hydroxydeoxyguanosine [8-OHdG]).ResultsIn the combined group, VAS and 8-OHdG two days after exercise, CIR two and three days after exercise and LDH from one to three days after exercise were significantly lower than the placebo group. The area under the curve from before exercise to four days later for CIR, LDH, and aldolase was also significantly lower in the combined group than in the placebo group.ConclusionA combination of 3.2 g BCAA and 2.0 g taurine, three times a day, for two weeks prior to and three days after exercise may be a useful nutritional strategy for attenuating exercise-induced DOMS and muscle damage.

Sulforaphane (SFN) plays an important role in preventing oxidative stress by activating the nuclear factor (erythroid derived 2)-like 2 (Nrf2) signalling pathway. SFN may improve exercise endurance capacity by counteracting oxidative stress-induced damage during exercise. We assessed running ability based on an exhaustive treadmill test (progressive-continuous all-out) and examined the expression of markers for oxidative stress and muscle damage. Twelve- to 13-week-old Male wild-type mice (Nrf2 +/+) and Nrf2-null mice (Nrf2 −/−) on C57BL/6J background were intraperitoneally injected with SFN or vehicle prior to the test. The running distance of SFN-injected Nrf2 +/+ mice was significantly greater compared with that of uninjected mice. Enhanced running capacity was accompanied by upregulation of Nrf2 signalling and downstream genes. Marker of oxidative stress in SFN-injected Nrf2 +/+ mice were lower than those in uninjected mice following the test. SFN produced greater protection against muscle damage during exhaustive exercise conditions in Nrf2 +/+ mice than in Nrf2 −/− mice. SFN-induced Nrf2 upregulation, and its antioxidative effects, might play critical roles in attenuating muscle fatigue via reduction of oxidative stress caused by exhaustive exercise. This in turn leads to enhanced exercise endurance capacity. These results provide new insights into SFN-induced upregulation of Nrf2 and its role in improving exercise performance.

Regular physical exercise is central to a healthy lifestyle. However, exercise-related muscle contraction can induce reactive oxygen species and reactive nitrogen species (ROS/RNS) production in skeletal muscle. The nuclear factor-E2-related factor-2 (Nrf2) transcription factor is a cellular sensor for oxidative stress. Regulation of nuclear Nrf2 signaling regulates antioxidant responses and protects organ structure and function. However, the role of Nrf2 in exercise- or contraction-induced ROS/RNS production in skeletal muscle is not clear. In this study, using differentiated C2C12 cells and electrical pulse stimulation (EPS) of muscle contraction, we explored whether Nrf2 plays a role in the skeletal muscle response to muscle contraction-induced ROS/RNS. We found that EPS (40 V, 1 Hz, 2 ms) stimulated ROS/RNS accumulation and Nrf2 activation. We also showed that expression of NQO1, HO-1 and GCLM increased after EPS-induced muscle contraction and was remarkably suppressed in cells with Nrf2 knockdown. We also found that the antioxidant N-acetylcysteine (NAC) significantly attenuated Nrf2 activation after EPS, whereas the nitric oxide synthetase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) did not. Furthermore, Nrf2 knockdown after EPS markedly decreased ROS/RNS redox potential and cell viability and increased expression of the apoptosis marker Annexin V in C2C12 myotubes. These results indicate that Nrf2 activation and expression of Nrf2 regulated-genes protected muscle against the increased ROS caused by EPS-induced muscle contraction. Thus, our findings suggest that Nrf2 may be a key factor for preservation of muscle function during muscle contraction.

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