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Received April 10, 2002
Accepted after revision August 2, 2002
1 Department of Kinesiology (Exercise Metabolism Research Group), McMaster University, Hamilton, ON L8S 4K1, Canada
2 Department of Kinesiology (Exercise Metabolism Research Group), McMaster University, Hamilton, ON L8S 4K1, and Department of Medicine (Neurology and Rehabilitation), McMaster University, Hamilton, ON, Canada L8N 3Z5
3 Department of Kinesiology, IWC, AB116, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K
* To whom correspondence should be addressed. E-mail: phillis{at}mcmaster.ca.
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 'damage protocol', during which subjects performed 300 maximal isokinetic (0.52 rad s-1) 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 infiltration into skeletal muscle at both 4 h and 24 h post-damage for macrophages, 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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