Effects of 17beta-estradiol on tension responses and fatigue in the skeletal twitch muscle fibers of frog.

The effects of 17beta-estradiol (10(-5) M), an active estrogen, on the tension and fatigue responses of single fiber or fiber bundle prepared from frog skeletal muscle were investigated. The administration of 17beta-estradiol caused a transient potentiation of tetanus tension by field stimulation at every minute. This potentiation was not affected by the presence of nicardipine, suggesting that the action of 17beta-estradiol would place the excitation-contraction (E-C) coupling beyond T-tubule depolarization. Fatigue was produced by repeated tetanic stimulation every second until tension declined to approximately 40% of the initial level. Fibers were then allowed to recover by having tetani given to them every minute. In the normal Ringer solution, the time to 50% of the initial tetanus tension was 41.7 s. With the presence of 17beta-estradiol, the time to 50% tension was faster than that of control. The presence of 17alpha-estradiol, a stereoisomer, caused no potentiation of tetanic tension to be stimulated every minute, and the rate of decline of fatigued response was almost the same as that of control, suggesting the existence of specific estrogen receptors in the frog muscle. In fatigued muscle with or without estrogen, the tension to field stimulation was transient and not sustained. When the fatigued muscle was again treated with field stimulation at every minute after the more-frequent stimulation, the recovery rate was increased in 17beta-estradiol. A prompt reduction in temperature to 5 degree C, from 20 degree C, in the presence of caffeine elicited the tension response, a rapid cooling contracture (RCC). The presence of 17beta-estradiol inhibited peak tension and maximum rate of rise of the RCC only after the repetitive electrical stimuli. These results suggest that the potentiation of contraction upon the electrical stimulation by 17beta-estradiol was induced by the increase of myoplasmic-free Ca(2+) concentration via an activation of some E-C coupling process. The 17beta-estradiol-induced facilitation of fatigue response to repetitive tetanus stimuli with high frequency may be due to an increase in the imbalance of Ca(2+) turnover in the cytoplasm.