Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation

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  • Kano Yutaka
    Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications
  • Sonobe Takashi
    National Cerebral and Cardiovascular Center Research Institute, Department of Cardiac Physiology
  • Inagaki Tadakatsu
    National Cerebral and Cardiovascular Center Research Institute, Department of Cardiac Physiology
  • Sudo Mizuki
    Central Research Institute for Physical Activity, Fukuoka University
  • Poole David C
    Departments of Anatomy & Physiology and Kinesiology, Kansas State University

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Contraction-induced compromise of muscle function and, in the extreme, muscle damage has been linked to loss of Ca2+ homeostasis and resultant sustained elevation of intracellular Ca2+ ([Ca2+]i). Against a background of in vitro approaches, a novel in vivo model permits investigation of the impact of different contraction types (e.g., isometric, ISO; eccentric, ECC) on [Ca2+]i accumulation profiles. [Ca2+]i elevation of ECC-contracted muscle is more rapid and greater in magnitude compared to ISO. Stretch-activated channels (SAC) are responsible, in large part, for this ECC contractions-induced [Ca2+]i elevation. Transient Ca2+ accumulation in the cytosol incurs loss of force production, whereas continuous high levels of [Ca2+]i, especially following ECC contractions, lead to muscle damage, including disrupted sarcomeres and membranes, and proceed, subsequently, to muscle regeneration via apoptosis and necrosis.

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