Merry Troy L, Ristow Michael
Energy Metabolism Laboratory, Swiss Federal Institute of Technology (ETH), 8603, Zurich, Switzerland.
J Physiol. 2016 Sep 15;594(18):5135-47. doi: 10.1113/JP270654. Epub 2016 Jan 18.
A popular belief is that reactive oxygen species (ROS) and reactive nitrogen species (RNS) produced during exercise by the mitochondria and other subcellular compartments ubiquitously cause skeletal muscle damage, fatigue and impair recovery. However, the importance of ROS and RNS as signals in the cellular adaptation process to stress is now evident. In an effort to combat the perceived deleterious effects of ROS and RNS it has become common practice for active individuals to ingest supplements with antioxidant properties, but interfering with ROS/RNS signalling in skeletal muscle during acute exercise may blunt favourable adaptation. There is building evidence that antioxidant supplementation can attenuate endurance training-induced and ROS/RNS-mediated enhancements in antioxidant capacity, mitochondrial biogenesis, cellular defence mechanisms and insulin sensitivity. However, this is not a universal finding, potentially indicating that there is redundancy in the mechanisms controlling skeletal muscle adaptation to exercise, meaning that in some circumstances the negative impact of antioxidants on acute exercise response can be overcome by training. Antioxidant supplementation has been more consistently reported to have deleterious effects on the response to overload stress and high-intensity training, suggesting that remodelling of skeletal muscle following resistance and high-intensity exercise is more dependent on ROS/RNS signalling. Importantly there is no convincing evidence to suggest that antioxidant supplementation enhances exercise-training adaptions. Overall, ROS/RNS are likely to exhibit a non-linear (hormetic) pattern on exercise adaptations, where physiological doses are beneficial and high exposure (which would seldom be achieved during normal exercise training) may be detrimental.
一种普遍的观点认为,线粒体和其他亚细胞区室在运动过程中产生的活性氧(ROS)和活性氮(RNS)会普遍导致骨骼肌损伤、疲劳并阻碍恢复。然而,现在很明显,ROS和RNS作为细胞适应应激过程中的信号具有重要意义。为了对抗ROS和RNS的有害影响,活跃的个体摄入具有抗氧化特性的补充剂已成为常见做法,但在急性运动期间干扰骨骼肌中的ROS/RNS信号可能会削弱有利的适应性。越来越多的证据表明,补充抗氧化剂可以减弱耐力训练诱导的以及ROS/RNS介导的抗氧化能力、线粒体生物发生、细胞防御机制和胰岛素敏感性的增强。然而,这并不是一个普遍的发现,这可能表明在控制骨骼肌对运动的适应性的机制中存在冗余,这意味着在某些情况下,抗氧化剂对急性运动反应的负面影响可以通过训练来克服。更多一致的报道称,补充抗氧化剂对过载应激和高强度训练的反应有有害影响,这表明抗阻运动和高强度运动后骨骼肌的重塑更依赖于ROS/RNS信号。重要的是,没有令人信服的证据表明补充抗氧化剂能增强运动训练适应性。总体而言,ROS/RNS可能在运动适应方面呈现非线性(兴奋效应)模式,即生理剂量是有益的,而高暴露(在正常运动训练中很少会达到)可能是有害的。