Intracellular Ca2+ transients in mouse soleus muscle after hindlimb unloading and reloading

Muscle Biology Laboratory, Department of Health and Kinesiology, Texas A & M University, College Station, Texas 77843-4243 The objective of this study was to determine whether altered intracellular Ca 2+ handling contributes to the specific force loss in the soleus muscle after unloading and/or subsequent reloading of mouse hindlimbs. Three groups of female ICR mice were studied: 1 ) unloaded mice ( n = 11) that were hindlimb suspended for 14 days, 2 ) reloaded mice ( n = 10) that were returned to their cages for 1 day after 14 days of hindlimb suspension, and 3 ) control mice ( n = 10) that had normal cage activity. Maximum isometric tetanic force (P o ) was determined in the soleus muscle from the left hindlimb, and resting free cytosolic Ca 2+ concentration ([Ca 2+ ] i ), tetanic [Ca 2+ ] i , and 4-chloro- m -cresol-induced [Ca 2+ ] i were measured in the contralateral soleus muscle by confocal laser scanning microscopy. Unloading and reloading increased resting [Ca 2+ ] i above control by 36% and 24%, respectively. Although unloading reduced P o and specific force by 58% and 24%, respectively, compared with control mice, there was no difference in tetanic [Ca 2+ ] i . P o , specific force, and tetanic [Ca 2+ ] i were reduced by 58%, 23%, and 23%, respectively, in the reloaded animals compared with control mice; however, tetanic [Ca 2+ ] i was not different between unloaded and reloaded mice. These data indicate that although hindlimb suspension results in disturbed intracellular Ca 2+ homeostasis, changes in tetanic [Ca 2+ ] i do not contribute to force deficits. Compared with unloading, 24 h of physiological reloading in the mouse do not result in further changes in maximal strength or tetanic [Ca 2+ ] i . fluo 3; fura red; atrophy; injury; excitation-contraction coupling