Received July 14, 2006
Revised August 8, 2006
Accepted after revision September 14, 2006

¹ University of South Carolina

^* To whom correspondence should be addressed. E-mail: carsonj{at}gwm.sc.edu.

	Abstract

Resumption of normal muscle loading after a period of disuse initiates cellular processes related to mass accretion. The renewed loading also induces a significant amount of muscle damage and subsequent inflammation. Ovarian hormone depletion delays atrophied myofiber mass recovery. Ovarian hormones are also global regulators of immune system function. The purpose of this study was to determine if ovarian hormone depletion-induced deficits in myofiber re-growth after disuse atrophy are related to the induction of muscle damage and the associated inflammatory response. We hypothesized that soleus muscle immune cell infiltration and inflammatory gene expression would be both accentuated and prolonged in ovarian hormone depleted rats during the first week of recovery from disuse atrophy. Intact and ovariectomized (OVX) female rats were subjected to hindlimb suspension for 10-days and then returned to normal ambulation for a recovery period, and the soleus muscle removed for analysis. Although reloading increased both circulating creatine kinase and myofiber membrane disruption, there was no effect of ovarian hormones on these processes during recovery. Muscle neutrophil concentration was increased above baseline regardless of hormone status at days 1 & 3 of recovery. However, the induction was 43% greater at day 3 in the OVX group. Muscle ED1+ and ED2+ macrophage concentrations were induced during recovery in both groups. However, the OVX group remained elevated at day 7 of recovery, while the intact group returned to control levels. Cyclooxygenase-2, interleukin-6, and interleukin-1 Beta muscle mRNA expression increased similarly during recovery, regardless of ovarian hormone status. These results demonstrate that the initial myofiber damage and inflammatory gene expression induced during muscle recovery from disuse atrophy are independent of ovarian hormone status. However, the muscle response to the damage and inflammatory signaling may be an important for ovarian hormone regulation of muscle mass recovery from disuse.

Key Words: Hormones, Macrophage, Muscle