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 |
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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 |
| _version_ | 1818670935663706112 |
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| author | Yutaka Kano Takashi Sonobe Tadakatsu Inagaki Mizuki Sudo David C Poole |
| author_facet | Yutaka Kano Takashi Sonobe Tadakatsu Inagaki Mizuki Sudo David C Poole |
| author_sort | Yutaka Kano |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-17T07:16:01Z |
| format | Article |
| id | doaj.art-4ce66213091b452496ae484897a9ed10 |
| institution | Directory Open Access Journal |
| issn | 2186-8131 2186-8123 |
| language | English |
| last_indexed | 2024-12-17T07:16:01Z |
| publishDate | 2012-10-01 |
| publisher | Japanese Society of Physical Fitness and Sports Medicine |
| record_format | Article |
| series | Journal of Physical Fitness and Sports Medicine |
| spelling | doaj.art-4ce66213091b452496ae484897a9ed102022-12-21T21:58:53ZengJapanese Society of Physical Fitness and Sports MedicineJournal of Physical Fitness and Sports Medicine2186-81312186-81232012-10-011350551210.7600/jpfsm.1.505jpfsmMechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulationYutaka Kano0Takashi Sonobe1Tadakatsu Inagaki2Mizuki Sudo3David C Poole4Department of Engineering Science, Bioscience and Technology Program, University of Electro-CommunicationsNational Cerebral and Cardiovascular Center Research Institute, Department of Cardiac PhysiologyNational Cerebral and Cardiovascular Center Research Institute, Department of Cardiac PhysiologyCentral Research Institute for Physical Activity, Fukuoka UniversityDepartments of Anatomy & Physiology and Kinesiology, Kansas State UniversityContraction-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.https://www.jstage.jst.go.jp/article/jpfsm/1/3/1_505/_pdf/-char/enca2+ homeostasisisometric contractioneccentric contractionstretch-activated channelsmuscle regenerationapoptosis |
| spellingShingle | Yutaka Kano Takashi Sonobe Tadakatsu Inagaki Mizuki Sudo David C Poole Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation Journal of Physical Fitness and Sports Medicine ca2+ homeostasis isometric contraction eccentric contraction stretch-activated channels muscle regeneration apoptosis |
| title | Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation |
| title_full | Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation |
| title_fullStr | Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation |
| title_full_unstemmed | Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation |
| title_short | Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation |
| title_sort | mechanisms of exercise induced muscle damage and fatigue intracellular calcium accumulation |
| topic | ca2+ homeostasis isometric contraction eccentric contraction stretch-activated channels muscle regeneration apoptosis |
| url | https://www.jstage.jst.go.jp/article/jpfsm/1/3/1_505/_pdf/-char/en |
| work_keys_str_mv | AT yutakakano mechanismsofexerciseinducedmuscledamageandfatigueintracellularcalciumaccumulation AT takashisonobe mechanismsofexerciseinducedmuscledamageandfatigueintracellularcalciumaccumulation AT tadakatsuinagaki mechanismsofexerciseinducedmuscledamageandfatigueintracellularcalciumaccumulation AT mizukisudo mechanismsofexerciseinducedmuscledamageandfatigueintracellularcalciumaccumulation AT davidcpoole mechanismsofexerciseinducedmuscledamageandfatigueintracellularcalciumaccumulation |