Ovarian hormone status and skeletal muscle inflammation during recovery from disuse in rats.
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 myofibre mass recovery. Ovarian hormones are also global regulators of immune system function. The purpose of this study was to determine whether ovarian hormone depletion-induced deficits in myofibre regrowth 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, the rats were killed and the soleus muscle removed for analysis. Although reloading increased both circulating creatine kinase and myofibre 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 and 3 of recovery; however, this increase was 43% greater at day 3 in the OVX group. Muscle ED1+ and ED2+ macrophage concentrations were increased during recovery in both groups. However, macropage concentrations remained elevated at day 7 of recovery in the OVX group, whereas they returned to control levels in the intact group. Cyclo-oxygenase-2, interleukin-6 and interleukin-1beta muscle mRNA expression increased similarly during recovery, regardless of ovarian hormone status. These results demonstrate that the initial myofibre damage and inflammatory gene expression induced during muscle recovery from disuse atrophy are independent of ovarian hormone status.
McClung
J M
JM
University of South Carolina, Department of Exercise Science, 1300 Wheat Street, Columbia, SC 29208, USA.
Davis
J M
JM
Carson
J A
JA
D000818:Animals; D052283:Creatine Kinase, MM Form / Q000097:blood; D051546:Cyclooxygenase 2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D016189:Dystrophin / Q000378:metabolism; D004958:Estradiol / Q000097:blood*; D005260:Female; D005786:Gene Expression Regulation; D019417:Hindlimb Suspension; D007249:Inflammation / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D008264:Macrophages / Q000473:pathology; D008407:Mast Cells / Q000473:pathology; D018485:Muscle Fibers, Skeletal / Q000378:metabolism / Q000473:pathology; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D009133:Muscular Atrophy / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D009504:Neutrophils / Q000473:pathology; D009929:Organ Size; D010052:Ovariectomy; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration; D013997:Time Factors; D014867:Water / Q000378:metabolism
D016207:Cytokines; D016189:Dystrophin; D012333:RNA, Messenger; D014867:Water; D004958:Estradiol; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D052283:Creatine Kinase, MM Form