High-intensity interval training alters ATP pathway flux during maximal muscle contractions in humans.
High-intensity interval training alters ATP pathway flux during maximal muscle contractions in humans.
复制标题
高强度间歇训练会改变人类最大肌肉收缩期间的 ATP 通路通量。
DOI：
10.1111/apha.12275
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Kent,JA
中科院分区：
文献类型：
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作者：
Larsen,RG;Maynard,L;Kent,JA
AimHigh‐intensity interval training (HIT) results in potent metabolic adaptations in skeletal muscle; however, little is known about the influence of these adaptations on energeticsin vivo. We used magnetic resonance spectroscopy to examine the effects of HIT on ATP synthesis from net PCr breakdown (ATPCK), oxidative phosphorylation (ATPOX) and non‐oxidative glycolysis (ATPGLY)in vivoin vastus lateralis during a 24‐s maximal voluntary contraction (MVC).MethodsEight young men performed 6 sessions of repeated, 30‐s ‘all‐out’ sprints on a cycle ergometer; measures of muscle energetics were obtained at baseline and after the first and sixth sessions.ResultsTraining increased peak oxygen consumption (35.8 ± 1.4 to 39.3 ± 1.6 mL min−1kg−1,P= 0.01) and exercise capacity (217.0 ± 11.0 to 230.5 ± 11.7 W,P= 0.04) on the ergometer, with no effects on total ATP production or force–time integral during the MVC. While ATP production by each pathway was unchanged after the first session, 6 sessions increased the relative contribution of ATPOX(from 31 ± 2 to 39 ± 2% of total ATP turnover,P< 0.001) and lowered the relative contribution from both ATPCK(49 ± 2 to 44 ± 1%,P= 0.004) and ATPGLY(20 ± 2 to 17 ± 1%,P= 0.03).ConclusionThese alterations to muscle ATP productionin vivoindicate that brief, maximal contractions are performed with increased support of oxidative ATP synthesis and relatively less contribution from anaerobic ATP production following training. These results extend previous reports of molecular and cellular adaptations to HIT and show that 6 training sessions are sufficient to alterin vivomuscle energetics, which likely contributes to increased exercise capacity after short‐term HIT.
