Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation
| Autor: | Tadakatsu Inagaki, David C. Poole, Mizuki Sudo, Yutaka Kano, Takashi Sonobe |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
muscle regeneration
Ca homeostasis Chemistry Physiology apoptosis Stretch activated channels Isometric exercise Anatomy Muscle damage ca2+ homeostasis eccentric contraction Calcium in biology isometric contraction Cell biology Muscle regeneration Apoptosis stretch-activated channels Sports medicine QP1-981 Ca2 homeostasis RC1200-1245 |
| Zdroj: | Journal of Physical Fitness and Sports Medicine, Vol 1, Iss 3, Pp 505-512 (2012) |
| ISSN: | 2186-8123 2186-8131 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|