Contraction-induced muscle damage in humans following calcium channel blocker administration
Following contraction-induced damage of skeletal muscle there is a loss of calcium homeostasis. Attenuating the damage-induced rise in myocellular calcium concentration may reduce proteolytic activation and attenuate other indices of damage; calcium channel blockers have been shown to be effective i...
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Published in | The Journal of physiology Vol. 544; no. 3; pp. 849 - 859 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
The Physiological Society
01.11.2002
Blackwell Publishing Ltd Blackwell Science Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Following contraction-induced damage of skeletal muscle there is a loss of calcium homeostasis. Attenuating the damage-induced
rise in myocellular calcium concentration may reduce proteolytic activation and attenuate other indices of damage; calcium
channel blockers have been shown to be effective in this regard. The effect of administration of a calcium channel blocker
(CCB), amlodipine, on indices of muscle damage following a unilateral âdamage protocolâ, during which subjects performed 300
maximal isokinetic (0.52 rad s â1 ) eccentric contractions with the knee extensors was investigated. The design was a randomized, double-blind crossover. On
one occasion, prior to the damage protocol, subjects consumed CCB for 7 days prior to and for 7 days following the damage
protocol. Biopsies were taken from the vastus lateralis prior to (baseline) and following the damage protocol at 4 h and 24
h post-damage. Isometric peak knee extensor torque was reduced ( P < 0.05) immediately post-, 24 h post- and 48 h post-damage protocol compared to pre-exercise values with no effect of treatment.
Desmin disruption was attenuated ( P < 0.05) with CCB versus placebo at 4 h post-damage. Z-band streaming was significantly ( P < 0.05) elevated compared to baseline at both times post-damage, but was lower with CCB at 4 h ( P < 0.05). Damage resulted in increased inflammatory cell (macrophage) infiltration into skeletal muscle at both 4 h and 24
h post-damage, with no effect of CCB. Neutrophil number was elevated by the damage protocol, but was higher at 24 h post-damage
in the CCB condition ( P < 0.05). Creatine kinase (CK) activity was higher ( P < 0.05) at 24 h and 48 h following the damage protocol compared to baseline, with no effect of treatment. In conclusion,
the reduction in desmin disruption and Z-band streaming indicates that CCB attenuated, or delayed, the contraction-induced
damage to sarcomeric proteins. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 ObjectType-News-3 content type line 23 |
ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.2002.022350 |