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

The objective of this study was to determine whether altered intracellular Ca2+ handling contributes to the specific force loss in the soleus muscle a fter unloading and/or subsequent reloading of mouse hindlimbs. Three groups of female ICR mice were studied: 1) unloaded mice (n = 11) that were hindl imb 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 forc e (P-0) was determined in the soleus muscle from the left, hindlimb, and re sting free cytosolic Ca2+ concentration ([Ca2+](i)), tetanic [Ca2+](i), and 4-chloro-m-cresol-induced [Ca2+](i) were measured in the contralateral sol eus muscle by confocal laser scanning microscopy. Unloading and reloading i ncreased resting [Ca2+](i) above control by 36% and 24%, respectively. Alth ough unloading reduced P-0 and specific force by 58% and 24%, respectively, compared with control mice, there was no difference in tetanic [Ca2+](i). P-0, specific force, and tetanic [Ca2+](i) were reduced by 58%, 23%, and 23 %, respectively, in the reloaded animals compared with control mice; howeve r, tetanic [Ca2+](i) was not different between unloaded and reloaded mice. These data indicate that although hindlimb suspension results in disturbed intracellular Ca2+ homeostasis, changes in tetanic [Ca2+](i) do not contrib ute to force deficits. Compared with unloading, 24 h of physiological reloa ding in the mouse do not result in further changes in maximal strength or t etanic [Ca2+](i).