2012
DOI: 10.7600/jpfsm.1.505
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Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation

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Cited by 11 publications
(6 citation statements)
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“…Exercise-induced muscle damage is associated with decrements in force production resulting from disruption of the sarcomere and impaired excitation-contraction coupling [ 24 ]. Eccentric resistance exercise has been shown to impair force generating capacity up to 50-65% compared to pre-exercise values [ 25 , 26 ].…”
Section: Discussionmentioning
confidence: 99%
“…Exercise-induced muscle damage is associated with decrements in force production resulting from disruption of the sarcomere and impaired excitation-contraction coupling [ 24 ]. Eccentric resistance exercise has been shown to impair force generating capacity up to 50-65% compared to pre-exercise values [ 25 , 26 ].…”
Section: Discussionmentioning
confidence: 99%
“…Muscle fatigue and EIMD are multifactorial phenomena which involve several factors that are not well established [27]. Among them, it is proposed that metabolic perturbations (e.g., adenosine triphosphate (ADP), Pi, H + , reactive oxygen species ROS), impairment of Ca 2+ release and uptake from the SR and changes in E-C coupling within the muscle participate in these processes [27,28]. As higher levels of glycogen ensure adequate muscle function [26] and lower metabolic perturbations, it is reasonable to hypothesize that maintaining adequate muscle glycogen during exercise could limit EIMD and, therefore, improve recovery.…”
Section: Introductionmentioning
confidence: 99%
“…However, it has been found that increased intracellular calcium ion (Ca 2+ ) over time as a consequence of stretch-activated Ca 2+ channels plays a key role in the permeability of the sarcolemma ( Allen et al, 2010 ). Considering a perspective applicable to the day-to-day sports practice, transient sarcoplasmic oxidation by-products and Ca 2+ upregulation derived from damaging exercises results in a mild FGC loss as a consequence of failures in the excitation-contraction coupling process ( Kano et al, 2012 ). Given that the mitochondria modulate Ca 2+ overload through the mitochondrial calcium uniporter located in the inner mitochondrial membrane ( Rossi et al, 2019 ), mild decreases in muscle function might be preserved by amino acids and/or micro-nutrients intake, e.g., Vitamin D, owning to the maintenance of the muscle mitochondria structural integrity and function ( Drummond et al, 2009 ; Salles et al, 2022 ).…”
Section: Introductionmentioning
confidence: 99%
“…Finally, sarcomeres and mitochondria impairment caused by eccentric contractions during sprinting results in long-lasting decreases in FGC ( Kano et al, 2012 ; Hyldahl and Hubal, 2014 ), which is a fundamental source for the loss of performance described in both sportswomen ( Keane et al, 2015 ) and men ( Howatson and Milak, 2009 ) after a RST. Accordingly, there is a need for practitioners to monitor FGC and range of motion (ROM) using simple, time and cost-effective sprint-specific muscle function tests associated with biochemical markers using an integrative-based approach.…”
Section: Introductionmentioning
confidence: 99%