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Human menopause is widely associated with impaired skeletal muscle quality and significant metabolic dysfunction. These observations pose significant challenges to the quality of life and mobility of the aging population, and are of relevance when considering the significantly greater losses in muscle mass and force-generating capacity of muscle from post-menopausal females relative to age-matched males. In this regard, the influence of estrogen on skeletal muscle has become evident across human, animal, and cell-based studies. Beneficial effects of estrogen have become apparent in mitigation of muscle injury and enhanced post-damage repair via various mechanisms, including prophylactic effects on muscle satellite cell number and function, as well as membrane stability and potential antioxidant influences following injury, exercise, and/or mitochondrial stress. In addition to estrogen replacement in otherwise deficient states, exercise has been found to serve as a means of augmenting and/or mimicking the effects of estrogen on skeletal muscle function in recent literature. Detailed mechanisms behind the estrogenic effect on muscle mass, strength, as well as the injury response are beginning to be elucidated and point to estrogen-mediated molecular cross talk amongst signalling pathways, such as apoptotic signaling, contractile protein modifications, including myosin regulatory light chain phosphorylation, and the maintenance of muscle satellite cells. This review discusses current understandings and highlights new insights regarding the role of estrogen in skeletal muscle, with particular regard to muscle mass, mitochondrial function, the response to muscle damage, and the potential implications for human physiology and mobility. [ABSTRACT FROM AUTHOR]

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Estrogen and hormone replacement therapy (HRT) have been demonstrated to have significant benefits to metabolic health and skeletal muscle function in animal models. More recently these benefits have also been reproduced in post-menopausal human females. Estrogen and HRT will diminish exercise induced muscle damage and inflammation via stabilizing effects on muscle membranes and calcium channels. Estrogen and HRT will also enhance muscle repair and augment muscle size via effects on satellite cell activation and proliferation. In addition estrogen and HRT will augment muscle strength through direct action on myosin which will enhance myosin strong binding during muscular contraction. These benefits could be important in the longer term maintenance of health, muscle functioning and independent living in older post-menopausal females. The use of HRT should be considered in some of these individuals in the context of the overall health advantages versus drawbacks this population. [ABSTRACT FROM AUTHOR]

Copyright of Applied Physiology, Nutrition & Metabolism is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The aim of this study was to examine specific and interactional effects of estradiol and progesterone on the time-to-fatigue of eccentrically contracted plantarflexor muscles and on the percent of plantarflexor isometric torque remaining immediately after an eccentric contraction (EC) protocol. Ovariectomized 6- to 8-week-old C57BL/6 mice were implanted with 21-day 0.05 mg-placebo, 0.05 mg-17-β estradiol (OE),15 mg-progesterone (OP), or estradiol and progesterone pellets (OEP). On the 16th day of hormone treatment, the isometric torque of the left plantarflexor muscles was measured. The left plantarflexor muscles then underwent 1 set of 150 ECs followed by 2 immediate post-EC isometric torque measurements. A group of ovarian-intact female mice of a similar age underwent the same isometric torque measurements and EC protocol. Plantarflexor muscle fatigue during ECs took 30%-41 % longer to occur in the OP group (n = 9) than it did in the intact (n = 8, P = 0.02), OC (n =11, P = 0.003), and OEP (n = 9, P = 0.007) groups. Peak active isometric torque had decreased immediately after ECs at 2 time points (M1 and M2). The OP group exhibited the greatest percent of isometric torque remaining immediately after ECs (M1, P = 0.03; M2, P = 0.04). These findings suggest that progesterone reduces muscle fatigue in response to ECs and that this progesterone effect is blunted when estradiol also is present. Therefore, ovarian hormone status may need to be considered when evaluating a response to physical activities, especially those activities involving ECs. [ABSTRACT FROM AUTHOR]

We hypothesized that estrogen administration would attenuate skeletal muscle neutrophil infiltration, indices of muscle membrane disruption, and muscle calpain activity shortly after the termination of exercise. Ovariectomized female rats were implanted with either an estogen pellet (25 mg β-estradiol) or a placebo pellet. Two weeks post-implant, animals were killed either at rest or 1 h after running exercise (60 min at 21 m·min[sup –1] , 12% grade). The 4 experimental groups (n = 12) used were: unexercised placebo (UP), unexercised estrogen (UE), exercised placebo (EP), and exercised estrogen (EE). Blood samples were analyzed for creatine kinase (CK) activity and estradiol content. Plantaris and gastrocnemius muscles were removed and histochemical determination of neutrophil content or biochemical determination of myeloperoxidase (MPO), glucose-6-phosphate dehydrogenase (G6PD), and calpain-like activity determined. Estrogen supplemented animals had 10–20-fold higher circulating estradiol levels than placebo animals. EP animals had significantly higher (P < 0.05) circulating CK activities than EE or unexercised animals. Muscle neutrophil concentrations were significantly (P < 0.01) elevated in EP and EE groups compared with unexercised controls, with EP muscle neutrophil levels also being over 60% greater (P < 0.05) than in EE animals. EP animals also had higher (P < 0.05) muscle MPO activities than unexercised or EE animals. Muscle G6PD activities were not significantly different between any groups. Muscle caplain-like activities were 80% higher (P < 0.01) in EP animals than EE animals with calpain-like activities in EE animals similar to unexercised groups. These results indicate that estrogen supplementation in ovariectomized rats attenuated 1-h post-exercise serum CK activities, muscle neutrophil infiltration, MPO activities, and calpain-like activities when compared with exercised, unsupplemented animals. This supports the possibility of a relationship between estrogen, calpain dependent production of neutrophil chemo-attractant peptides, and 1-h post-exercise skeletal muscle neutrophil infiltration.Key words: neutrophils, calpain, estrogen, skeletal muscle, muscle damage.On a émis l'hypothèse que l'administration d'œstrogène atténuerait l'infiltration de neutrophiles musculaires squelettiques, indices de rupture de la membrane musculaire et d'activité de la calpaïne musculaire peu après la fin d'un exercice. On a inséré un pellet d'œstrogène (25 mg β-œstradiol) ou de placebo sous la peau de rats femelles ovariectomisées. Deux semaines plus tard, on a sacrifié les animaux, au repos ou 1 h après une course (60 min à 21 m·min[sup –1] , pente 12 %). Ainsi, on a utilisé quatre groupes (n = 12) aux fins de l'expérience : placebo sédentaire (PS), œstrogène sédentaire (OS), placebo actif (PA), œstrogène actif (OA). On a analysé des échantillons sanguins pour déterminer l'activité de la créatine kinase (KC) et la teneur en œstradiol. On a prélevé les muscles plantaires et gastrocnémiens, et déterminé la teneur en neutrophiles par une méthode histochimique et les activités de la myéloperoxydase (MPO), de la glucose-6-phosphate déshydrogénase (G6PD) et de type calpaïne par une méthode biochimique. Les animaux ayant reçu le supplément d'œstrogène ont eu des taux d'œstradiol circulant d'un facteur 10–20 fois plus élevé que les animaux ayant reçu le placebo. Les animaux PA ont eu des activités de CK circulante significativement plus élevées (P < 0,05) que les animaux OA ou sédentaires. Les concentrations de neutrophiles musculaires ont été significativement plus élevées (P < 0,01) chez les groupes PA et OA que chez les témoins sédentaires, les taux de neutrophiles musculaires des PA étant 60 % plus élevés (P < 0,05) que ceux des animaux OA. Les activités de la MPO musculaire ont aussi été plus élevées (P < 0,05) chez les animaux PA que chez les animaux sédentaires ou OA. Les activités de la G6PD musculaire n'ont pas différé significativement entre les groupes. Les activités de type calpaïne ont été 80 % plus élevées (P < 0,01) chez les animaux PA que chez les animaux OA, les activités de type calpaïne des animaux OA étant similaires à celles des groupes sédentaires. Ces résultats indiquent que la supplémentation en œstrogène chez les rats femelles ovariectomisées a atténué, 1 h après l'exercice, les activités de la CK sérique, l'infiltration de neutrophiles musculaires, les activités de la MPO et les activités de type calpaïne comparativement a ce qui a été observé chez les animaux actifs n'ayant reçu aucun supplément. Ces résultats soutiennent l'hypothèse d'une relation possible entre l'œstrogène, la production dépendante de la calpaïne de peptides chimio-attractifs pour les neutrophiles et l'infiltration de neutrophiles musculaires squelettiques 1 h après un exercice.Mots clés : neutrophiles, calpaïne, œstrogène, muscle squelettique, dommage musculaire.[Traduit par la Rédaction] [ABSTRACT FROM AUTHOR]