Faculty Opinions recommendation of Effects of ovarian hormones and estrogen receptor α on physical activity and skeletal muscle fatigue in female mice.

Estrogen (E2) is reported to regulate skeletal muscle mass and contractile function; whether E2 exerts its effects through estrogen receptor-α (ERα) or -β (ERβ) is unclear. We determined the effect of ERα or ERβ elimination on muscle mass and contractile function in multiple muscles of the lower limb, muscles with different locomotor tasks and proportions of fiber types I and II: soleus (Sol), plantaris (Plan), tibialis anterior (TA), and gastrocnemius (Gast) in mature female mice. To determine E2 elimination effects on muscle, we also used aromatase (Ar) knockout (KO) and wild-type (WT) mice. ERα and ArKO body weights were ∼10 and 20% higher than WT. Although muscle mass tended to show a commensurate increase in both groups, only the TA was significantly larger in ERα ( P < 0.05). Ratios of muscle mass to body mass revealed significantly lower values for Gast and TA in ArKO mice ( P < 0.05). Tetanic tension (Po) per calculated anatomical cross-sectional area (aCSA) in ERα KO was lower in TA and Gast than in WT. Lower Po/aCSA in ERα KO Gast and TA was also supported histologically by significantly less Po/fiber areas ( P < 0.05). ArKO mice also had lower Po/aCSA in Gast and TA compared with WT. ERβ KO and WT mice were comparable in all measures. Our results support the hypothesis that E2 effects on skeletal muscle are mediated in part via the ERα but that E2 effects may be mediated via more than one mechanism or receptor.

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Skeletal muscle fatigue does not affect shooting accuracy of handball players

Isokinetics and Exercise Science ◽

10.3233/ies-193178 ◽

2019 ◽

Vol 27 (4) ◽

pp. 253-259

Author(s):

Beyza Akyüz ◽

Pınar Arpınar Avşar ◽

Murat Bilge ◽

Gökhan Deliceoğlu ◽

Feza Korkusuz

Keyword(s):

Skeletal Muscle ◽

Muscle Fatigue ◽

Skeletal Muscle Fatigue

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Skeletal muscle fatigue in normal subjects and heart failure patients. Is there a common mechanism?

Acta Physiologica Scandinavica ◽

10.1046/j.1365-201x.1998.0343f.x ◽

1998 ◽

Vol 162 (3) ◽

pp. 215-228 ◽

Cited By ~ 19

Author(s):

P. K. LUNDE ◽

E. VERBURG ◽

N. K. VØLLESTAD ◽

O. M. SEJERSTED

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Muscle Fatigue ◽

Normal Subjects ◽

Common Mechanism ◽

Heart Failure Patients ◽

Skeletal Muscle Fatigue

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Skeletal muscle action of estrogen receptor α is critical for the maintenance of mitochondrial function and metabolic homeostasis in females

Science Translational Medicine ◽

10.1126/scitranslmed.aad3815 ◽

2016 ◽

Vol 8 (334) ◽

pp. 334ra54-334ra54 ◽

Cited By ~ 87

Author(s):

Vicent Ribas ◽

Brian G. Drew ◽

Zhenqi Zhou ◽

Jennifer Phun ◽

Nareg Y. Kalajian ◽

...

Keyword(s):

Skeletal Muscle ◽

Estrogen Receptor ◽

Oxidative Metabolism ◽

Mitochondrial Fission ◽

Estrogen Receptor Α ◽

Glucose Disposal ◽

Mitochondrial Morphology ◽

Metabolic Dysfunction ◽

Mtdna Replication ◽

Primary Tissue

Impaired estrogen receptor α (ERα) action promotes obesity and metabolic dysfunction in humans and mice; however, the mechanisms underlying these phenotypes remain unknown. Considering that skeletal muscle is a primary tissue responsible for glucose disposal and oxidative metabolism, we established that reduced ERα expression in muscle is associated with glucose intolerance and adiposity in women and female mice. To test this relationship, we generated muscle-specific ERα knockout (MERKO) mice. Impaired glucose homeostasis and increased adiposity were paralleled by diminished muscle oxidative metabolism and bioactive lipid accumulation in MERKO mice. Aberrant mitochondrial morphology, overproduction of reactive oxygen species, and impairment in basal and stress-induced mitochondrial fission dynamics, driven by imbalanced protein kinase A–regulator of calcineurin 1–calcineurin signaling through dynamin-related protein 1, tracked with reduced oxidative metabolism in MERKO muscle. Although muscle mitochondrial DNA (mtDNA) abundance was similar between the genotypes, ERα deficiency diminished mtDNA turnover by a balanced reduction in mtDNA replication and degradation. Our findings indicate the retention of dysfunctional mitochondria in MERKO muscle and implicate ERα in the preservation of mitochondrial health and insulin sensitivity as a defense against metabolic disease in women.

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