Dodd S L, Herb R A, Powers S K
Department of Exercise and Sport Sciences, University of Florida, Gainesville.
Sports Med. 1993 Jan;15(1):14-23. doi: 10.2165/00007256-199315010-00003.
Three principal cellular mechanisms have been proposed to explain the ergogenic potential of caffeine during exercise: (a) increased myofilament affinity for calcium and/or increased release of calcium from the sarcoplasmic reticulum in skeletal muscle; (b) cellular actions caused by accumulation of cyclic-3',5'-adenosine monophosphate (cAMP) in various tissues including skeletal muscle and adipocytes; and (c) cellular actions mediated by competitive inhibition of adenosine receptors in the central nervous system and somatic cells. The relative importance of each of the above mechanisms in explaining in vivo physiological effects of caffeine during exercise continues to be debated. However, growing evidence suggests that inhibition of adenosine receptors is one of the most important, if not the most important, mechanism to explain the physiological effects of caffeine at nontoxic plasma concentrations. Numerous animal studies using high caffeine doses have reported increased force development in isolated skeletal muscle in both in vitro and in situ preparations. In contrast, in vivo human studies have not consistently shown caffeine to enhance muscular performance during high intensity, short term exercise. Further, recent evidence supports previous work that shows caffeine does not improve performance during short term incremental exercise. Although controversy exists, the major part of published evidence evaluating performance supports the notion that caffeine is ergogenic during prolonged (> 30 min), moderate intensity (approximately 75 to 80% VO2max) exercise. The mechanism to explain these findings may be linked to a caffeine-mediated glycogen sparing effect secondary to an increased rate of lipolysis.
为了解释咖啡因在运动过程中的促力作用，人们提出了三种主要的细胞机制：(a) 增加肌丝对钙的亲和力和/或增加骨骼肌肌浆网中钙的释放；(b) 由环磷酸腺苷 (cAMP) 在包括骨骼肌和脂肪细胞在内的各种组织中积累所引起的细胞作用；以及 (c) 由中枢神经系统和体细胞中腺苷受体的竞争性抑制介导的细胞作用。上述每种机制在解释运动过程中咖啡因的体内生理效应方面的相对重要性仍在争论中。然而，越来越多的证据表明，抑制腺苷受体是解释咖啡因在无毒血浆浓度下生理效应的最重要机制之一，如果不是唯一最重要的机制的话。许多使用高剂量咖啡因的动物研究报告称，在体外和原位制备的分离骨骼肌中，力量发展有所增加。相比之下，体内人体研究并未一致表明咖啡因能在高强度、短期运动中增强肌肉表现。此外，最近的证据支持了之前的研究结果，即咖啡因在短期递增运动中并不能提高运动表现。尽管存在争议，但大部分评估运动表现的已发表证据支持这样一种观点，即咖啡因在长时间（> 30分钟）、中等强度（约75%至80%最大摄氧量）的运动中具有促力作用。解释这些发现的机制可能与咖啡因介导的糖原节省效应有关，这种效应继发于脂肪分解速率的增加。
