Effects of lengthening contraction on calcium kinetics and skeletal muscle contractility in humans.

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Bibliographic Details
Title:	Effects of lengthening contraction on calcium kinetics and skeletal muscle contractility in humans.
Authors:	Nielsen, J. S., Madsen, K., JØrgensen, L. V., Sahlin, K.
Source:	Acta Physiologica Scandinavica. Jul2005, Vol. 184 Issue 3, p203-214. 12p.
Subjects:	Calcium metabolism, Human body, Contractility (Biology), Cell contraction, Biomechanics, Creatine
Abstract:	We have tested the hypothesis that the altered muscle contractility after lengthening contractions (LC) is caused by altered calcium (Ca2+) kinetics. Subjects ( n = 8) performed 100 drop jumps and muscle contractility was measured pre- and post-exercise by maximal voluntary contraction (MVC) and transcutaneous electrical stimulation (1, 20 and 50 Hz). Muscle biopsies were analysed for muscle metabolites, rates of SR Ca2+ uptake (CaU) and release (CaR) and myosin heavy chain (MHC) composition. The rates of torque relaxation and CaU were positively related to muscle fibre type composition (% MHC II). Muscle creatine (Cr) decreased and the ratio between phosphocreatine (PCr) and Cr increased 3 and 24 h post-exercise ( P < 0.05 vs. pre-exercise). LC resulted in reduced MVC (−19%), twitch torque (−41%) and 20/50 Hz torque ratio (−30%) and a faster relaxation rate ( P < 0.05). The contractile parameters recovered partially but remained altered 24 h post-exercise ( P < 0.05). The average CaR was unchanged after LC ( P > 0.05). However, the response varied between subjects and the relative post-exercise CaR was significantly related to the degree of LFF (post/pre 20/50 Hz force ratio) and to the decline in twitch force (post/pre twitch ratio). CaU was lower in seven of eight subjects after LC ( P > 0.05). The decline in torque after LC could not be explained by metabolic factors since PCr/Cr ratio increased. The relation between CaR and fatigue suggests that the mechanism of fatigue in part may be attributed to intrinsic changes in the SR Ca2+ release channel. The faster torque relaxation after LC could not be explained by an increased rate of CaU. [ABSTRACT FROM AUTHOR]
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Database:	Psychology and Behavioral Sciences Collection

Description
Abstract:	We have tested the hypothesis that the altered muscle contractility after lengthening contractions (LC) is caused by altered calcium (Ca2+) kinetics. Subjects ( n = 8) performed 100 drop jumps and muscle contractility was measured pre- and post-exercise by maximal voluntary contraction (MVC) and transcutaneous electrical stimulation (1, 20 and 50 Hz). Muscle biopsies were analysed for muscle metabolites, rates of SR Ca2+ uptake (CaU) and release (CaR) and myosin heavy chain (MHC) composition. The rates of torque relaxation and CaU were positively related to muscle fibre type composition (% MHC II). Muscle creatine (Cr) decreased and the ratio between phosphocreatine (PCr) and Cr increased 3 and 24 h post-exercise ( P < 0.05 vs. pre-exercise). LC resulted in reduced MVC (−19%), twitch torque (−41%) and 20/50 Hz torque ratio (−30%) and a faster relaxation rate ( P < 0.05). The contractile parameters recovered partially but remained altered 24 h post-exercise ( P < 0.05). The average CaR was unchanged after LC ( P > 0.05). However, the response varied between subjects and the relative post-exercise CaR was significantly related to the degree of LFF (post/pre 20/50 Hz force ratio) and to the decline in twitch force (post/pre twitch ratio). CaU was lower in seven of eight subjects after LC ( P > 0.05). The decline in torque after LC could not be explained by metabolic factors since PCr/Cr ratio increased. The relation between CaR and fatigue suggests that the mechanism of fatigue in part may be attributed to intrinsic changes in the SR Ca2+ release channel. The faster torque relaxation after LC could not be explained by an increased rate of CaU. [ABSTRACT FROM AUTHOR]
ISSN:	00016772
DOI:	10.1111/j.1365-201X.2005.01449.x