Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway.
Department of Public Health, Sport & Nutrition, University of Agder, Agder, Norway.
Scand J Med Sci Sports. 2022 Jun;32(6):984-996. doi: 10.1111/sms.14148. Epub 2022 Mar 8.
A typical football match leads to neuromuscular fatigue and physical performance impairments up to 72-96 h post-match. While muscle damage is thought to be a major factor, damage on the ultrastructural level has never been documented. The purpose of this study was to investigate post-match cellular muscle damage by quantifying the heat shock protein (HSP) response as a proxy for protein damage.
Muscle biopsies, blood samples, countermovement jumps, and perception of muscle soreness were obtained from twelve semi-professional football players 1, 24, 48, and 72 h after a 90-min football match. Muscle biopsies were analyzed for αB-crystallin and HSP70 in the cytosolic and cytoskeletal sub-cellular fractions by Western blotting. Fiber type-specific αB-crystallin and HSP70 staining intensity, and tenascin-C immunoreactivity were analyzed with immunohistochemistry. Blood samples were analyzed for creatine kinase and myoglobin.
Within 24 h post-match, a 2.7- and 9.9-fold increase in creatine kinase and myoglobin were observed, countermovement jump performance decreased by -9.7% and muscle soreness increased by 0.68 units. αB-crystallin and HSP70 accumulated in cytoskeletal structures evident by a 3.6- and 1.8-fold increase in the cytoskeletal fraction and a parallel decrease in the cytosolic fraction. In type I and II fibers, αB-crystallin staining intensity increased by 15%-41% and remained elevated at 72 h post-match. Lastly, the percentage of fibers with granular staining of αB-crystallin increased 2.2-fold.
Football match play induced a muscular HSP stress response 1-72 h post-match. Specifically, the accumulation of HSPs in cytoskeletal structures and the granular staining of αB-crystallin suggests occurrence of ultrastructural damage. The damage, indicated by the HSP response, might be one reason for the typically 72 h decrease in force-generating capacity after football matches.
一场典型的足球比赛会导致神经肌肉疲劳和身体表现受损,直到赛后 72-96 小时。虽然肌肉损伤被认为是一个主要因素,但从未有研究记录过超微结构水平的损伤。本研究的目的是通过量化热休克蛋白(HSP)反应来研究赛后细胞肌肉损伤,将其作为蛋白质损伤的替代物。
12 名半职业足球运动员在 90 分钟足球比赛后 1、24、48 和 72 小时,采集肌肉活检、血液样本、反跳跳和肌肉酸痛感。通过 Western 印迹法分析细胞质和细胞骨架亚细胞部分的αB-晶体蛋白和 HSP70。用免疫组织化学分析纤维型特异性αB-晶体蛋白和 HSP70 染色强度和 tenascin-C 免疫反应性。分析血液样本中的肌酸激酶和肌红蛋白。
比赛后 24 小时内,肌酸激酶和肌红蛋白分别增加了 2.7 倍和 9.9 倍,反跳跳性能下降了-9.7%,肌肉酸痛增加了 0.68 个单位。αB-晶体蛋白和 HSP70 在细胞骨架结构中积累,这表现为细胞骨架部分增加了 3.6 倍和 1.8 倍,细胞质部分减少。在 I 型和 II 型纤维中,αB-晶体蛋白染色强度增加了 15%-41%,并在赛后 72 小时仍保持升高。最后,αB-晶体蛋白颗粒染色的纤维百分比增加了 2.2 倍。
足球比赛会导致肌肉 HSP 应激反应在赛后 1-72 小时发生。具体来说,HSP 在细胞骨架结构中的积累和αB-晶体蛋白的颗粒状染色表明存在超微结构损伤。这种损伤,表现为 HSP 反应,可能是足球比赛后力量生成能力通常下降 72 小时的原因之一。