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高强度运动后积极恢复期间肌纤维中的糖原合成。

Glycogen synthesis in muscle fibers during active recovery from intense exercise.

作者信息

Fairchild Timothy J, Armstrong Alex A, Rao Arjun, Liu Hawk, Lawrence Steve, Fournier Paul A

机构信息

School of Human Movement and Exercise Science, University of Western Australia, Crawley, Western Australia, Australia.

出版信息

Med Sci Sports Exerc. 2003 Apr;35(4):595-602. doi: 10.1249/01.MSS.0000058436.46584.8E.

Abstract

PURPOSE

There is evidence that active recovery impairs glycogen repletion in skeletal muscles of fasted individuals. Our main goal was to examine the impact of active recovery on the glycogen stores of the different muscle fiber types.

METHODS

Eight endurance-trained individuals cycled for 2.5 min at 130% [OV0312]O(2peak) followed by a 30-s all-out cycling sprint. After exercise, the participants were subjected to either a passive recovery or an active recovery protocol that consisted of pedalling for 45 min at 40% [OV0312]O(2peak).

RESULTS

During active recovery, blood lactate and pH returned more rapidly toward preexercise levels than during passive recovery. In contrast, average muscle glycogen content remained at stable levels during active recovery (209 +/- 32 and 202 +/- 30 mmol.kg-1 at 0 and 45 min of recovery, respectively) but increased significantly in response to passive recovery (from 185 +/- 27 to 283 +/- 42 mmol.kg-1). The pattern of change in periodic acid-Schiff staining intensity across muscle fibers suggests that the impact of active recovery on average muscle glycogen content is different from that observed at the levels of the individual muscle fibers, with active recovery having no effect on glycogen resynthesis in Type II muscle fibers but causing glycogen breakdown in Type I muscle fibers. Although active recovery was also associated with higher plasma catecholamines and lower insulin levels, such an unfavorable hormonal environment had no effect on glycogen resynthesis in Type II muscle fibers.

CONCLUSION

Active recovery in comparison to passive recovery does not affect glycogen resynthesis in Type II muscle fibers despite being associated with an unfavorable hormonal environment but results in a marked glycogen mobilization in Type I muscle fibers.

摘要

目的

有证据表明,主动恢复会损害禁食个体骨骼肌中的糖原再填充。我们的主要目标是研究主动恢复对不同肌纤维类型糖原储备的影响。

方法

八名耐力训练个体以130%[OV0312]O₂峰值的强度骑行2.5分钟,随后进行30秒的全力骑行冲刺。运动后,参与者接受被动恢复或主动恢复方案,主动恢复方案包括以40%[OV0312]O₂峰值的强度蹬车45分钟。

结果

与被动恢复相比,主动恢复期间血乳酸和pH值恢复到运动前水平的速度更快。相反,主动恢复期间平均肌肉糖原含量保持在稳定水平(恢复0分钟和45分钟时分别为209±32和202±30 mmol·kg⁻¹),而被动恢复后显著增加(从185±27增加到283±42 mmol·kg⁻¹)。肌纤维间过碘酸-希夫染色强度的变化模式表明,主动恢复对平均肌肉糖原含量的影响与在单个肌纤维水平观察到的不同,主动恢复对II型肌纤维的糖原再合成没有影响,但会导致I型肌纤维中的糖原分解。尽管主动恢复还与较高的血浆儿茶酚胺和较低的胰岛素水平相关,但这种不利的激素环境对II型肌纤维的糖原再合成没有影响。

结论

与被动恢复相比,主动恢复尽管与不利的激素环境相关,但不影响II型肌纤维中的糖原再合成,却导致I型肌纤维中明显的糖原动员。

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