Sarcoplasmic reticulum in aged skeletal muscle

A decrease in muscle mass and strength and a slowing of muscle contraction are common features of the ageing process. Recent advances in basic biochemical knowledge have provided new insights into pathogenetic mechanisms underlying age‐related changes in the excitation–contraction coupling process, Ca2+‐transients and isometric twitch‐contraction time. Sarcoplasmic reticulum (SR) Ca2+‐pumps are not basically altered in physiological ageing, but several aspects of the Ca2+‐transport system remain controversial, regarding phosphorylation‐dependent regulation in slow‐twitch muscles, in particular. It seems that conflicting reports and divergent interpretations concerning the effect of ageing on SR Ca2+‐release arise from the type of muscle, the stage of the ageing process and the animal species. A cause–effect relationship between the decrease in dihydropyridine receptors and in muscle strength is strongly suggested by studies in transgenic mice, but is unsupported by our studies with fast‐twitch and slow‐twitch muscles of old rats. Our experimental evidence also seems to exclude the occurrence of age‐related changes in the number and in the functional behaviour of Ca2+‐release channels/ryanodine receptors (RyR1), based on [3H]‐ryanodine binding studies. There is emerging, although only suggestive evidence, so far, that modulation of RyR1 by SR luminal protein calsequestrin, or the functional coupling of RyRs by FKBP‐12, may be altered in ageing skeletal muscle.