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).