Ingalls C P, Warren G L, Armstrong R B
Muscle Biology Laboratory, Department of Health and Kinesiology, Texas A & M University, College Station, Texas 77843-4243, USA.
J Appl Physiol (1985). 1999 Jul;87(1):386-90. doi: 10.1152/jappl.1999.87.1.386.
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+)), tetanic Ca(2+), and 4-chloro-m-cresol-induced Ca(2+) were measured in the contralateral soleus muscle by confocal laser scanning microscopy. Unloading and reloading increased resting Ca(2+) 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+). P(o), specific force, and tetanic Ca(2+) were reduced by 58%, 23%, and 23%, respectively, in the reloaded animals compared with control mice; however, tetanic Ca(2+) 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+) 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+).
本研究的目的是确定细胞内钙离子处理的改变是否导致小鼠后肢卸载和/或随后重新加载后比目鱼肌中特定力量的损失。研究了三组雌性ICR小鼠：1）卸载组小鼠（n = 11），后肢悬吊14天；2）重新加载组小鼠（n = 10），后肢悬吊14天后放回笼中1天；3）对照组小鼠（n = 10），在笼中正常活动。测定左后肢比目鱼肌的最大等长强直力（Pₒ），并通过共聚焦激光扫描显微镜测量对侧比目鱼肌的静息游离胞质钙离子浓度（[Ca²⁺]i）、强直收缩时的[Ca²⁺]i以及4-氯间甲酚诱导的[Ca²⁺]i。卸载和重新加载分别使静息[Ca²⁺]i比对照组升高36%和24%。尽管与对照组小鼠相比，卸载分别使Pₒ和比肌力降低了58%和24%，但强直收缩时的[Ca²⁺]i没有差异。与对照组小鼠相比，重新加载组动物的Pₒ、比肌力和强直收缩时的[Ca²⁺]i分别降低了58%、23%和23%；然而，卸载组和重新加载组小鼠之间的强直收缩时的[Ca²⁺]i没有差异。这些数据表明，尽管后肢悬吊会导致细胞内钙离子稳态紊乱，但强直收缩时[Ca²⁺]i的变化并不导致力量不足。与卸载相比，小鼠24小时的生理性重新加载不会导致最大力量或强直收缩时[Ca²⁺]i的进一步变化。
