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The Mammalian Myosin Heavy Chain Gene Family and Muscle Fiber Types
View research View latest news Sign up for updates. However, it remains unclear why these effects are sex- and species-specific, because the loss of STAT5B retards growth in girls, but not in male mice. STAT5B appears to mediate GH signalling in skeletal muscles of male mice at all ages, but only until puberty in female mice. Sexually dimorphic growth of skeletal muscle is evident in most mammals from puberty, with males developing a larger body size and muscle mass, with more fast-twitch and less slow-twitch myofibres than females [ 1 , 2 ]. Of the two, STAT5B appears to be the principle transcription factor regulating sexually dimorphic growth, because removal of STAT5B reduces body mass and the absolute mass of skeletal muscles in male mice to that in female mice [ 7 , 8 , 9 ]. While IGF1 is the major anabolic post-natal growth factor, myostatin restricts the development of skeletal muscle and promotes the development of adipose tissue by inhibiting the signalling of IGF1 [ 10 , 11 , 12 ]. In contrast to mice, it is not clear why inactivating mutations in the Stat5b gene in humans reduce growth and circulating concentrations of IGF1 in both sexes [ 13 ]. Sexually dimorphic growth of skeletal muscle has been attributed to opposing actions of the gonadal steroids, with androgens promoting and oestrogens inhibiting growth [ 16 , 17 ]. Sexually dimorphic growth has also been shown to be due to differences in the inhibition of GH signalling between sexes by suppressor of cytokine signalling 2 SOCS2 and cytokine-inducible SH2-containing protein CIS [ 22 , 23 ].
Skeletal muscle health is a strong predictor of overall health and longevity. Pathologies affecting skeletal muscle such as cancer cachexia, intensive care unit treatment, muscular dystrophies, and others are associated with decreased quality of life and increased mortality. Recent research has begun to determine that these muscular pathologies appear to present and develop differently between males and females. However, to our knowledge, there has yet to be a comprehensive review on musculoskeletal differences between males and females and how these differences may contribute to sex differences in muscle pathologies. Herein, we present a review of the current literature on muscle phenotype and physiology between males and females and how these differences may contribute to differential responses to atrophic stimuli. In general, females appear to be more susceptible to disuse induced muscle wasting, yet protected from inflammation induced such as cancer cachexia muscle wasting compared to males.
