EFFECTS OF ESTRADIOL ON CREATINE KINASE RELEASE AND SUBSEQUENT MUSCLE DAMAGE IN THE RAT 594

Abstract

The mechanisms associated with delayed onset muscle soreness (DOMS), including an increase in serum creatine kinase (CK) activity, and subsequent damage to the contractile filaments of the myofibrils remain unknown. Females have been shown to exhibit a lower serum CK activity post-exercise compared to males. This gender difference has been linked to the female sex hormone estradiol (E2). The effects of E2 on CK release and muscle damage was assessed in female rats following eccentric treadmill exercise. Sprague Dawley female rats were ovariectomized prior to sexual maturity and treated with an E2 (n=5) or placebo (n=4) pellet insert for 21 days prior to the exercise bout. Exercise consisted of 60 minutes of -10° treadmill running at a speed of 19 m·min-1. Serum samples for CK activity (U/L @ 30°C) were obtained pre-exercise, and at times 0, 2, 6, 12, 24, and 48 hours post-exercise. Following the 48 hour post-exercise blood sample, rats were sacrificed and the soleus muscle was disected and prepared for light and electron microscopy. Prior to exercise, E2 levels were significantly higher in the E2 treated animals compared to placebo treated animals. Compared to pre-exercise, CK release in the placebo rats was significantly (p<0.05) elevated at times 0, 2, 6, and 24 hours post-exercise, with the peak response occurring at immediately post-exercise (time 0). Compared to pre-exercise, CK release in the E2 treated rats was significantly (p<0.05) elevated at times 0, and 2 hours post-exercise, with the peak response occuring 2 hours post-exercise. Placebo rats exhibited significantly greater CK activities compared to E2 treated rats at time points 0, 6, and 24 hours post-exercise. Evidence of microscopic damage (A-band disruption and Z-line streaming) was limited to two placebo treated animals only. Therefore, it is difficult to speculate on the precise protective mechanism that E2 may exhert on the muscle. The effects of E2 appear limited to CK release and not directly related to that of myofibril damage.