Parker Lewan, McGuckin Teneale A, Leicht Anthony S
College of Sport and Exercise Science, Victoria University, Melbourne, Vic., Australia; Institute of Sport, Exercise and Active Living, Victoria University, Melbourne, Vic., Australia.
Clin Physiol Funct Imaging. 2014 Sep;34(5):377-83. doi: 10.1111/cpf.12108. Epub 2013 Nov 27.
The aim of the current study was to examine the influence of exercise intensity on systemic oxidative stress (OS) and endogenous antioxidant capacity. Non-smoking, sedentary healthy adult males (n = 14) participated in two exercise sessions using an electronically braked cycle ergometer. The first session consisted of a graded exercise test to determine maximal power output and oxygen consumption (VO(2max)). One week later, participants undertook 5-min cycling bouts at 40%, 55%, 70%, 85% and 100% of VO(2max), with passive 12-min rest between stages. Measures of systemic OS reactive oxygen metabolites (dROM), biological antioxidant potential (BAP), heart rate (HR), VO(2), blood lactate and rating of perceived exertion were assessed at rest and immediately following each exercise stage. Significant (P<0·05) differences between exercise bouts were examined via repeated measures ANOVA and post hoc pairwise comparisons with Bonferroni correction. Increasing exercise intensity significantly augmented HR (P<0·001), VO(2) (P<0·001), blood lactate (P<0·001) and perceived exertion (P<0·001) with no significant effect on dROM levels compared with resting values. In contrast, increasing exercise intensity resulted in significantly (P<0·01) greater BAP at 70% (2427 ± 106), 85% (2625 ± 121) and 100% (2651 ± 92) of VO(2max) compared with resting levels (2105 ± 57 μmol Fe(2+)/L). The current results indicate that brief, moderate-to-high-intensity exercise significantly elevates endogenous antioxidant defences, possibly to counteract increased levels of exercise-induced reactive oxygen species. Regular moderate-to-high-intensity exercise may protect against chronic OS associated diseases via activation, and subsequent upregulation of the endogenous antioxidant defence system.
本研究的目的是检验运动强度对全身氧化应激（OS）和内源性抗氧化能力的影响。不吸烟、久坐不动的健康成年男性（n = 14）使用电子制动的自行车测力计参加了两次运动测试。第一次测试包括一次分级运动试验，以确定最大功率输出和耗氧量（VO₂max）。一周后，参与者在VO₂max的40%、55%、70%、85%和100%强度下进行5分钟的骑行，各阶段之间有12分钟的被动休息时间。在休息时以及每个运动阶段结束后立即评估全身OS活性氧代谢物（dROM）、生物抗氧化潜力（BAP）、心率（HR）、VO₂、血乳酸和主观用力程度。通过重复测量方差分析以及采用Bonferroni校正的事后两两比较，检验各运动阶段之间的显著差异（P<0·05）。与静息值相比，运动强度增加显著提高了心率（P<0·001）、VO₂（P<0·001）、血乳酸（P<0·001）和主观用力程度（P<0·001），而对dROM水平无显著影响。相比之下，与静息水平（2105 ± 57 μmol Fe²⁺/L）相比，运动强度增加导致在VO₂max的70%（2427 ± 106）、85%（2625 ± 121）和100%（2651 ± 92）强度下BAP显著升高（P<0·01）。目前的结果表明，短时间的中高强度运动可显著提高内源性抗氧化防御能力，可能是为了抵消运动诱导的活性氧水平升高。定期进行中高强度运动可能通过激活并随后上调内源性抗氧化防御系统，预防与慢性OS相关的疾病。
