Intracellular Ca21 transients in mouse soleus muscle after hindlimb unloading and reloading

Ingalls, Christopher P., Gordon L. Warren, and R. B. Armstrong. Intracellular Ca21 transients in mouse soleus muscle after hindlimb unloading and reloading. J. Appl. Physiol. 87(1): 386–390, 1999.—The objective of this study was to determine whether altered intracellular Ca21 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 5 11) that were hindlimb suspended for 14 days, 2) reloaded mice (n 5 10) that were returned to their cages for 1 day after 14 days of hindlimb suspension, and 3) control mice (n 5 10) that had normal cage activity. Maximum isometric tetanic force (Po) was determined in the soleus muscle from the left hindlimb, and resting free cytosolic Ca21 concentration ([Ca]i), tetanic [Ca]i, and 4-chloro-m-cresolinduced [Ca]i were measured in the contralateral soleus muscle by confocal laser scanning microscopy. Unloading and reloading increased resting [Ca]i above control by 36% and 24%, respectively. Although unloading reduced Po and specific force by 58% and 24%, respectively, compared with control mice, there was no difference in tetanic [Ca]i. Po, specific force, and tetanic [Ca]i were reduced by 58%, 23%, and 23%, respectively, in the reloaded animals compared with control mice; however, tetanic [Ca]i was not different between unloaded and reloaded mice. These data indicate that although hindlimb suspension results in disturbed intracellular Ca21 homeostasis, changes in tetanic [Ca]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]i.