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Purpose: 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. Methods: 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. Results: 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. Conclusions: 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. [ABSTRACT FROM AUTHOR]

Reactive oxygen and nitrogen species are important signal molecules for adaptations to training. Due to the antioxidant properties of vitamin C and E, supplementation has been shown to blunt adaptations to endurance training. In this study, we investigated the effects of vitamin C and E supplementation and endurance training on adaptations in endogenous antioxidants and heat shock proteins (HSP). Thirty seven males and females were randomly assigned to receive Vitamin C and E (C + E; C: 1000 mg, E: 235 mg daily) or placebo (PLA), and underwent endurance training for 11 weeks. After 5 weeks, a subgroup conducted a high intensity interval session to investigate acute stress responses. Muscle and blood samples were obtained to investigate changes in proteins and mRNA related to the antioxidant and HSP system. The acute response to the interval session revealed no effects of C + E supplementation on NF κB activation. However, higher stress responses to exercise in C + E group was indicated by larger translocation of HSPs and a more pronounced gene expression compared to PLA. Eleven weeks of endurance training decreased muscle GPx1, HSP27 and αB-crystallin, while mnSOD, HSP70 and GSH remained unchanged, with no influence of supplementation. Plasma GSH increased in both groups, while uric acid decreased in the C + E group only. Our results showed that C + E did not affect long-term training adaptations in the antioxidant- and HSP systems. However, the greater stress responses to exercise in the C + E group might indicate that long-term adaptations occurs through different mechanisms in the two groups. [ABSTRACT FROM AUTHOR]