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¹ Department of Physiology and Biophysics, Robert Wood Johnson Medical School, Piscataway, NJ 08854
² Department of Anatomy, Saitama Medical School, Saitama 350-0495, Japan
³ Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH 44106
⁴ Department of Anesthesiology, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, PA 15213
⁵ Department of Biological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto 606-8501, Japan

Correspondence to Jianjie Ma: maj2{at}umdnj.edu

Reduced homeostatic capacity for intracellular Ca²⁺ ([Ca²⁺]_i) movement may underlie the progression of sarcopenia and contractile dysfunction during muscle aging. We report two alterations to Ca²⁺ homeostasis in skeletal muscle that are associated with aging. Ca²⁺ sparks, which are the elemental units of Ca²⁺ release from sarcoplasmic reticulum, are silent under resting conditions in young muscle, yet activate in a dynamic manner upon deformation of membrane structures. The dynamic nature of Ca²⁺ sparks appears to be lost in aged skeletal muscle. Using repetitive voltage stimulation on isolated muscle preparations, we identify a segregated [Ca²⁺]_i reserve that uncouples from the normal excitation–contraction process in aged skeletal muscle. Similar phenotypes are observed in adolescent muscle null for a synaptophysin-family protein named mitsugumin-29 (MG29) that is involved in maintenance of muscle membrane ultrastructure and Ca²⁺ signaling. This finding, coupled with decreased expression of MG29 in aged skeletal muscle, suggests that MG29 expression is important in maintaining skeletal muscle Ca²⁺ homeostasis during aging.

N. Weisleder and M. Brotto contributed equally to this paper.

Abbreviations used in this paper: ANOVA, analysis of variance; CICR, Ca²⁺-induced Ca²⁺ release; E–C, excitation–contraction; EDL, extensor digitorum longus; [Ca²⁺]_o, extracellular Ca²⁺; FDB, flexor digitorum brevis; [Ca²⁺]_i, intracellular Ca²⁺; RyR, ryanodine receptor; SR, sarcoplasmic reticulum; TT, transverse tubule; VICR, voltage-induced Ca²⁺ release; wt, wild-type.

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