Recent scientific efforts have focused on the detrimental effects that obesity has on the metabolic function of skeletal muscles and whether exercise can improve this dysfunction. In this regard, adiponectin, with important metabolic functions (e.g. insulin-sensitizer and anti-inflammatory), has been recently described as a myokine that acts in an autocrine/paracrine manner. Earlier studies reported that muscle adiponectin could be induced by pro-inflammatory mediators (e.g. lipopolysaccharide), cytokines, and high-fat diets, providing a protective mechanism of this tissue against metabolic insults. However, when metabolic insults such as high-fat diets are sustained this protective response becomes dysregulated, making the skeletal muscle susceptible to metabolic impairments. Recent studies have suggested that exercise could prevent or even reverse this process. Considering that most scientific knowledge on adiponectin dysregulation in obesity is from the study of adipose tissue, the present review summarizes and discusses the literature available to date regarding the effects of obesity on skeletal muscle adiponectin induction, along with the potential effects of different exercise prescriptions on this response in an obesity context.

中文翻译：

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肥胖和运动中骨骼肌脂联素的诱导。

最近的科学努力集中于肥胖对骨骼肌代谢功能的有害影响以及运动是否可以改善这种功能障碍。在这方面，最近已将具有重要代谢功能（例如胰岛素增敏剂和抗炎药）的脂联素描述为以自分泌/旁分泌方式起作用的肌动蛋白。较早的研究报道肌肉脂联素可以由促炎性介质（例如脂多糖），细胞因子和高脂饮食诱导，从而为这种组织提供了防止代谢损伤的保护机制。但是，当持续坚持高脂饮食等代谢损害时，这种保护性反应就会失调，从而使骨骼肌易受代谢损伤的影响。最近的研究表明，锻炼可以预防甚至逆转这一过程。考虑到肥胖中脂联素失调的大多数科学知识来自于脂肪组织的研究，本综述总结并讨论了迄今为止有关肥胖对骨骼肌脂联素诱导的影响的文献，以及不同运动处方对肥胖的潜在影响。在肥胖情况下的这种反应。