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高强度间歇训练过度后骨骼肌过度训练的细胞机制。

Cellular mechanisms underlying overreaching in skeletal muscle following excessive high-intensity interval training.

作者信息

Watanabe Daiki, Wada Masanobu

机构信息

Graduate School of Sport and Health Sciences, Osaka University of Health and Sport Sciences, Osaka, Japan.

Graduate School of Humanities and Social Sciences, Hiroshima University, Hiroshima, Japan.

出版信息

Am J Physiol Cell Physiol. 2025 Mar 1;328(3):C921-C938. doi: 10.1152/ajpcell.00623.2024. Epub 2025 Feb 4.

Abstract

Overreaching (OR) can be defined as a decline in physical performance resulting from excessive exercise training, necessitating days to weeks recovery. Impairments in the contractile function of skeletal muscle are believed to be a primary factor contributing to OR. However, the cellular mechanism triggering OR remains unclear. The purpose of this study was to elucidate the mechanisms underlying OR. Rats' plantar flexor muscles were subjected to repeated electrical stimulations mimicking excessive high-intensity interval training (HIIT) daily for 13 consecutive days, and isometric torques were monitored. The torque was measured one day after HIIT, and subsequently, the physiological function of type II fibers was analyzed by using mechanically skinned-fiber technique. Eleven of 17 rats exhibited torque decline, whereas others did not. Thus, the rats were divided into OR and nonoverreaching (NOR) groups. Skinned fibers from the gastrocnemius (GAS) muscles of both groups showed decreased depolarization-induced force and increased myofibrillar Ca sensitivity. However, the fibers from the OR group, but not the NOR group, exhibited a decrease in myofibrillar maximal force. Biochemical analyses of a superficial region of GAS muscle revealed that α-actinin 2 content was increased in the NOR group, but not in the OR group, whereas calpain-3 autolysis was increased in the OR group, but not in the NOR group. These findings shed light on the cellular mechanism underlying OR: OR following excessive HIIT was induced by a decreased myofibrillar maximal force, whereas Ca sensitivity was increased. An early sign of overtraining is a performance impairment known as overreaching (OR). This study revealed the cellular mechanism underlying OR by combining in vivo fatiguing contractions with mechanically skinned-fiber technique. Thirteen consecutive days of intense training result in myofibrillar force depression in OR. This study provides valuable insights not only for athletes and coaches but also for nonathletes who incorporate exercise into their daily activity.

摘要

过度训练(OR)可定义为因过度运动训练导致身体机能下降,需要数天至数周时间恢复。骨骼肌收缩功能受损被认为是导致过度训练的主要因素。然而,引发过度训练的细胞机制仍不清楚。本研究的目的是阐明过度训练的潜在机制。对大鼠的跖屈肌进行反复电刺激,模拟每日进行的过度高强度间歇训练(HIIT),持续13天,并监测等长扭矩。在HIIT后一天测量扭矩,随后,通过机械去表皮纤维技术分析II型纤维的生理功能。17只大鼠中有11只表现出扭矩下降,而其他大鼠则没有。因此,将大鼠分为过度训练组和非过度训练(NOR)组。两组腓肠肌(GAS)的去表皮纤维均表现出去极化诱导力降低和肌原纤维钙敏感性增加。然而,过度训练组的纤维,而非非过度训练组的纤维,表现出肌原纤维最大力量下降。对GAS肌肉表层区域的生化分析表明,非过度训练组α-辅肌动蛋白2含量增加,而过度训练组未增加,而钙蛋白酶-3自溶在过度训练组增加,而非过度训练组未增加。这些发现揭示了过度训练的细胞机制:过度HIIT后的过度训练是由肌原纤维最大力量下降引起的,而钙敏感性增加。过度训练的早期迹象是一种称为过度训练(OR)的机能损害。本研究通过将体内疲劳收缩与机械去表皮纤维技术相结合,揭示了过度训练的细胞机制。连续13天的高强度训练导致过度训练组肌原纤维力量下降。本研究不仅为运动员和教练,也为将运动纳入日常活动的非运动员提供了有价值的见解。

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