Department of Molecular and Cellular Sport Medicine, Institute of Cardiovascular Research and Sport Medicine, Germany.
PLoS One. 2012;7(11):e49326. doi: 10.1371/journal.pone.0049326. Epub 2012 Nov 16.
While ryanodine receptor 1 (RyR1) critically contributes to skeletal muscle contraction abilities by mediating Ca²⁺ion oscillation between sarcoplasmatic and myofibrillar compartments, AMP-activated protein kinase (AMPK) senses contraction-induced energetic stress by phosphorylation at Thr¹⁷². Phosphorylation of RyR1 at serine²⁸⁴³ (pRyR1Ser²⁸⁴³) results in leaky RyR1 channels and impaired Ca²⁺homeostasis. Because acute resistance exercise exerts decreased contraction performance in skeletal muscle, preceded by high rates of Ca²⁺-oscillation and energetic stress, intense myofiber contractions may induce increased RyR1 and AMPK phosphorylation. However, no data are available regarding the time-course and magnitude of early RyR1 and AMPK phosphorylation in human myofibers in response to acute resistance exercise.
Determine the effects and early time-course of resistance exercise on pRyR1Ser²⁸⁴³ and pAMPKThr¹⁷² in type I and II myofibers.
7 male subjects (age 23±2 years, height: 185±7 cm, weight: 82±5 kg) performed 3 sets of 8 repetitions of maximum eccentric knee extensions. Muscle biopsies were taken at rest, 15, 30 and 60 min post exercise. pRyR1Ser²⁸⁴³ and pAMPKThr¹⁷² levels were determined by western blot and semi-quantitative immunohistochemistry techniques.
While total RyR1 and total AMPK levels remained unchanged, RyR1 was significantly more abundant in type II than type I myofibers. pRyR1Ser²⁸⁴³ increased 15 min and peaked 30 min (p<0.01) post exercise in both myofiber types. Type I fibers showed relatively higher increases in pRyR1Ser²⁸⁴³ levels than type II myofibers and remained elevated up to 60 min post resistance exercise (p<0.05). pAMPKThr¹⁷² also increased 15 to 30 min post exercise (p<0.01) in type I and II myofibers and in whole skeletal muscle.
Resistance exercise induces acutely increased pRyR1Ser²⁸⁴³ and concomitantly pAMPKThr¹⁷² levels for up to 30 min in resistance exercised myofibers. This provides a time-course by which pRyR1Ser²⁸⁴³ can mechanistically impact Ca²⁺handling properties and consequently induce reduced myofiber contractility beyond immediate fatiguing mechanisms.
Ryanodine 受体 1（RyR1）通过介导肌浆网和肌原纤维间隙之间的 Ca²⁺离子振荡，对骨骼肌收缩能力至关重要，而 AMP 激活的蛋白激酶（AMPK）通过 Thr¹⁷² 磷酸化来感知收缩引起的能量应激。RyR1 丝氨酸 2843 位磷酸化（pRyR1Ser²⁸⁴³）导致 RyR1 通道渗漏和 Ca²⁺稳态受损。由于急性抗阻运动在骨骼肌中先引起收缩性能下降，随后 Ca²⁺振荡和能量应激率升高，强烈的肌纤维收缩可能导致 RyR1 和 AMPK 磷酸化增加。然而，目前尚无关于急性抗阻运动后人类肌纤维中 RyR1 和 AMPK 早期磷酸化的时间过程和幅度的数据。
确定抗阻运动对 I 型和 II 型肌纤维中 pRyR1Ser²⁸⁴³ 和 pAMPKThr¹⁷² 的影响及其早期时间过程。
7 名男性受试者（年龄 23±2 岁，身高 185±7cm，体重 82±5kg）进行 3 组 8 次最大离心膝关节伸展运动。运动后 15、30 和 60 分钟分别采集肌肉活检。通过 Western blot 和半定量免疫组织化学技术测定 pRyR1Ser²⁸⁴³ 和 pAMPKThr¹⁷² 水平。
尽管总 RyR1 和总 AMPK 水平保持不变，但 RyR1 在 II 型肌纤维中的含量明显高于 I 型肌纤维。pRyR1Ser²⁸⁴³ 在运动后 15 分钟增加，并在 30 分钟达到峰值（p<0.01），两种肌纤维类型均如此。I 型肌纤维的 pRyR1Ser²⁸⁴³ 水平相对高于 II 型肌纤维，并且在抗阻运动后 60 分钟仍保持升高（p<0.05）。pAMPKThr¹⁷² 在 I 型和 II 型肌纤维以及整个骨骼肌中也在运动后 15 至 30 分钟增加（p<0.01）。
抗阻运动在抗阻运动后的肌纤维中诱导急性增加的 pRyR1Ser²⁸⁴³ 并同时增加 pAMPKThr¹⁷² 水平，持续 30 分钟。这提供了一个时间过程，通过该过程，pRyR1Ser²⁸⁴³ 可以通过机械方式影响 Ca²⁺处理特性，并因此导致肌纤维收缩性降低，超出即时疲劳机制。
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