Effects of 17.BETA.-Estradiol on Tension Responses and Fatigue in the Skeletal Twitch Muscle Fibers of Frog.

Abstract

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...

17β-Estradiol-induced enhancement of estrogen receptor biosynthesis via MAPK pathway in mouse skeletal muscle myoblasts

“…In contrast, our previous experiment in frog skeletal muscle revealed the presence of a much faster signaling initiated by the cell membrane ER, where administration of E2 quickly (in minutes) enhanced the twitch tension, presumably because of increased myoplasmic Ca 2? concentration [18]. These findings may suggest, as in other cell types, the presence of distinct nongenomic signalings linked to the cell membrane ERs, which operate in both fast and slow fashions via PLC-and MAPK-mediated pathways, respectively.…”

“…Since we previously found rapid contractile effects of E2 on frog skeletal muscle [18], we were especially interested in the nongenomic actions of estrogen. For this purpose, we explored both total and nonnuclear expression of ER in relation to its biosynthesis and associated cellular signaling cascades in mouse C2C12 myoblasts.…”

Muscle function in monozygotic female twin pairs discordant for hormone replacement therapy

“…This effect was at least partly mediated via regulation of estrogen receptor alpha, both at transcript and protein level. Also Hatae 28 has shown an immediate increasing effect of estradiol administration on twitch force in frog skeletal muscle fibers.…”

“…Hatae 28 suggested that with high levels of E2 the reuptake of released Ca 2+ by sarcoplasmic reticulum could not be accomplished on time resulting in decreases in the following contraction. Thus, the same mechanism of E2 action that is involved in potentiating twitch may contribute to faster fatigability.…”

Estrogen weakens muscle endurance via estrogen receptor-p38 MAPK-mediated orosomucoid (ORM) suppression

“…Notably, acute 17β-estradiol treatment of in vitro frog skeletal muscle facilitated the fatigue response to repetitive tetanus stimuli with high frequency, and this direct and quick effect may be related to an increase in the imbalance of Ca 2+ turnover in the cytoplasm. 46 Estrogen also influences glucose uptake via regulation of GLUT4 expression in muscles. 47 GLUT4-deficient mice exhibit a hastened onset of muscle fatigue.…”