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Sarcopenia, the loss of muscle mass and strength associated to age, has been linked to impairment of the cytosolic Ca2+ peak that triggers muscle contraction, but mechanistic details remain unknown. Here we explore the hypothesis that a reduction in sarcoplasmic reticulum Ca2+ concentration ([Ca2+]SR) is at the origin of this loss of Ca2+ homeostasis. We engineered Drosophila melanogaster to express the Ca2+ indicator GAP3 targeted to muscle SR, and we developed a new method to calibrate the signal into [Ca2+]SR in vivo. [Ca2+]SR dropped with age from ∼600 µM down to 50 µM in close correlation to muscle function, which declined monotonically when [Ca2+]SR was &amp;lt;400 µM. [Ca2+]SR results from the pump-leak steady-state at the SR membrane. However, changes in expression of the SERCA pump and of the ryanodine receptor leak, were too modest to explain the large changes seen in [Ca2+]SR. Instead, these changes are compatible with increased leakiness through the ryanodine receptor as the main determinant of the [Ca2+]SR decline in aging muscle. In contrast, there were no changes in endoplasmic reticulum [Ca2+] with age in brain neurons.

Sarcoplasmic reticulum Ca2+ decreases with age and correlates with the decline in muscle function in Drosophila