Estrogens, like other steroid hormones, initiate their action via specific intracellular receptors [1]. The presence of estrogen receptors in the skeletal muscle cell was demonstrated in bovine [2], rabbit [3,4], and rat [5]. Skeletal myoblasts also expressed functional estrogen receptors [6]. The effects of estrogen on skeletal muscle contractility have been diversely reported. A long-term treatment of the developing rat with estrogen reduced the tetanus tension of skeletal muscle [7]. In women, the supplement with a supraphysiological level of estrogen did not affect the contractile force and fatigue process of the first dorsal interosseus muscle [8]. Neither did the administration of estrogen significantly affect the fatigue of the estradiol-injected extensor digitorum longus muscle in rat [9]. In frog skeletal muscle, however, Rana temporaria, the presence of diethyl-stilboesterol, a nonsteroidal estrogen, markedly potentiated the twitch tension, but apparently not the tetanus tension [10], and it also potentiated the tension response of the fatigued Key words: skeletal muscle, contraction, fatigue, 17-estradiol.
Abstract:The effects of 17-estradiol (10an active estrogen, on the tension and fatigue responses of single fiber or fiber bundle prepared from frog skeletal muscle were investigated. The administration of 17-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 17-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 17-estradiol, the time to 50% tension was faster than that of control. The presence of 17␣-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 17-estradiol. A prompt reduction in temperature to 5°C, from 20°C, in the presence of caffeine elicited the tension response, a rapid cooling contracture (RCC). The presence of 17-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 17-estradiol was induced by the increase of myoplasmic-free Ca 2ϩ concentration via an activ...