Oxidative stress in exercise training: the involvement of inflammation and peripheral signals

被引:62
作者
Magherini, Francesca [1 ]
Fiaschi, Tania [1 ]
Marzocchini, Riccardo [1 ]
Mannelli, Michele [1 ]
Gamberi, Tania [1 ]
Modesti, Pietro [2 ]
Modesti, Alessandra [1 ]
机构
[1] Univ Florence, Dept Biomed Expt & Clin Sci Mario Serio, Viale Morgagni 50, Florence, Italy
[2] Univ Florence, Dept Expt & Clin Med, Florence, Italy
关键词
Inflammation; oxidative stress; peripheral signals; training stress; GLUCOREGULATORY HORMONE RESPONSES; PLASMA ADIPONECTIN RESPONSE; DES-ACYL GHRELIN; GROWTH-FACTOR-I; SKELETAL-MUSCLE; RESISTANCE EXERCISE; PHYSICAL-ACTIVITY; RECEPTOR EXPRESSION; PEDIATRIC OBESITY; MAXIMAL EXERCISE;
D O I
10.1080/10715762.2019.1697438
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The evidence about the health benefits of regular physical activity is well established. Exercise intensity is a significant variable and structured high-intensity interval training (HIIT) has been demonstrated to improve both whole-body and skeletal muscle metabolic health in different populations. Conversely, fatigue accumulation, if not resolved, leads to overwork, chronic fatigue syndrome (CFS), overtraining syndrome up to alterations of endocrine function, immune, systemic inflammation, and organic diseases with health threat. In response to temporary increases in stress during training, some athletes are unable to maintain sufficient caloric intake, thus suffering a negative energy balance that causes further stress. The regulation of the energy balance is controlled by the central nervous system through an elaborate interaction of the signalling that involves different tissues such as leptin, adiponectin and ghrelin whose provide important feedback to the hypothalamus to regulate the energy balance. Although exercise-induced reactive oxygen species are required for normal force production in muscle, high levels of ROS appear to promote contractile dysfunction. However, a high level of oxidative stress in may induce a rise in inflammatory markers and a disregulation in expression of adiponectin, leptin and grelin.
引用
收藏
页码:1155 / 1165
页数:11
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