Peake Jonathan M, Markworth James F, Nosaka Kazunori, Raastad Truls, Wadley Glenn D, Coffey Vernon G
School of Biomedical Sciences and Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Australia; Centre of Excellence for Applied Sports Science Research, Queensland Academy of Sport, Brisbane, Australia;
Liggins Institute, University of Auckland, Auckland, New Zealand;
J Appl Physiol (1985). 2015 Aug 1;119(3):172-89. doi: 10.1152/japplphysiol.01055.2014. Epub 2015 May 14.
Hormesis encompasses the notion that low levels of stress stimulate or upregulate existing cellular and molecular pathways that improve the capacity of cells and organisms to withstand greater stress. This notion underlies much of what we know about how exercise conditions the body and induces long-term adaptations. During exercise, the body is exposed to various forms of stress, including thermal, metabolic, hypoxic, oxidative, and mechanical stress. These stressors activate biochemical messengers, which in turn activate various signaling pathways that regulate gene expression and adaptive responses. Historically, antioxidant supplements, nonsteroidal anti-inflammatory drugs, and cryotherapy have been favored to attenuate or counteract exercise-induced oxidative stress and inflammation. However, reactive oxygen species and inflammatory mediators are key signaling molecules in muscle, and such strategies may mitigate adaptations to exercise. Conversely, withholding dietary carbohydrate and restricting muscle blood flow during exercise may augment adaptations to exercise. In this review article, we combine, integrate, and apply knowledge about the fundamental mechanisms of exercise adaptation. We also critically evaluate the rationale for using interventions that target these mechanisms under the overarching concept of hormesis. There is currently insufficient evidence to establish whether these treatments exert dose-dependent effects on muscle adaptation. However, there appears to be some dissociation between the biochemical/molecular effects and functional/performance outcomes of some of these treatments. Although several of these treatments influence common kinases, transcription factors, and proteins, it remains to be determined if these interventions complement or negate each other, and whether such effects are strong enough to influence adaptations to exercise.
兴奋效应包含这样一种观念，即低水平的应激会刺激或上调现有的细胞和分子通路，从而提高细胞和生物体抵御更大应激的能力。这一观念是我们所了解的运动如何塑造身体并诱导长期适应性变化的基础。在运动过程中，身体会暴露于各种形式的应激之下，包括热应激、代谢应激、低氧应激、氧化应激和机械应激。这些应激源会激活生化信使，进而激活各种调节基因表达和适应性反应的信号通路。从历史上看，抗氧化剂补充剂、非甾体抗炎药和冷冻疗法一直被用于减轻或抵消运动诱导的氧化应激和炎症。然而，活性氧和炎症介质是肌肉中的关键信号分子，此类策略可能会减轻对运动的适应性。相反，在运动期间限制膳食碳水化合物摄入和肌肉血流可能会增强对运动的适应性。在这篇综述文章中，我们整合并应用了有关运动适应基本机制的知识。我们还批判性地评估了在兴奋效应这一总体概念下使用针对这些机制的干预措施的理论依据。目前尚无足够证据确定这些治疗是否对肌肉适应产生剂量依赖性影响。然而，其中一些治疗的生化/分子效应与功能/表现结果之间似乎存在某种脱节。尽管其中几种治疗会影响常见的激酶、转录因子和蛋白质，但这些干预措施是相互补充还是相互抵消，以及此类效应是否强大到足以影响对运动的适应性，仍有待确定。
