Contraction‐induced muscle damage in humans following calcium channel blocker administration
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abstract
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 (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.
