Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation
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 o...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Japanese Society of Physical Fitness and Sports Medicine
2012-10-01
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| Series: | Journal of Physical Fitness and Sports Medicine |
| Subjects: | |
| Online Access: | https://www.jstage.jst.go.jp/article/jpfsm/1/3/1_505/_pdf/-char/en |
| Summary: | 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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| ISSN: | 2186-8131 2186-8123 |