Effects of reduced muscle glycogen on excitation–contraction coupling in rat fast-twitch muscle: a glycogen removal study

• Published in: Journal of muscle research and cell motility 2019-12, Vol.40 (3-4), p.353-364
• Main Authors: Watanabe, Daiki, Wada, Masanobu
• Format: Article
• Language: English
• Subjects: Action potential; Animal Anatomy; Biomedical and Life Sciences; Biomedicine; Calcium (reticular); Cell Biology; Contraction; Depolarization; Glycogen; Histology; Life Sciences; Microsomes; Morphology; Muscle contraction; Original Article; Preservation; Proteomics; Ryanodine receptors; Sarcoplasmic reticulum; Skin; Statistical analysis
• ISSN: 0142-4319; 1573-2657
• DOI: 10.1007/s10974-019-09524-y

The aim of this study was to investigate the effects of an enzymatic removal of glycogen on excitation–contraction coupling in mechanically skinned fibres of rat fast-twitch muscles, with a focus on the changes in the function of Na + –K + -pump and ryanodine receptor (RyR). Glycogen present in the skinned fibres and binding to microsomes was removed using glucoamylase (GA). Exposure of whole muscle to 20 U mL −1 GA for 6 min resulted in a 72% decrease in the glycogen content. Six minutes of GA treatment led to an 18 and a 22% reduction in depolarization- and action potential-induced forces in the skinned fibres, respectively. There was a minor but statistically significant increase in the repriming period, most likely because of an impairment of the Na + –K + -pump function. GA treatment exerted no effect on the maximum Ca 2+ release rate from the RyR in the microsomes and the myofibrillar Ca 2+ sensitivity in the skinned fibres. These results indicate that reduced glycogen per se can decrease muscle performance due to the impairment of SR Ca 2+ release and suggest that although Na + –K + -pump function is adversely affected by reduced glycogen, the extent of the impairment is not sufficient to reduce Ca 2+ release from the sarcoplasmic reticulum. This study provides direct evidence that glycogen above a certain amount is required for the preservation of the functional events preceding Ca 2+ release from the sarcoplasmic reticulum.