Gonad-related factors promote muscle performance gain during postnatal development in male and female mice

Ueberschlag-Pitiot, Vanessa; Stantzou, Amalia; Messéant, Julien; Lemaître, Mégane; Owens, Daniel J.; Noirez, Philippe; Roy, Pauline; Agbulut, Onnik; Metzger, Daniel; Ferry, Arnaud

doi:10.1152/ajpendo.00446.2016

Cited by 16 publications

(12 citation statements)

References 68 publications

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“…The sex-related exercise differences disappeared after normalization of exercise performance by size (body mass). This had already been described for muscle strength 17 – 19 , but not for running power and economy. However, body size and muscle strength are well-known secondary sexual characteristics, influenced primarily by the anabolic action of the hormone testosterone, a major determinant of sexual dimorphism 20 .…”

Section: Discussionmentioning

confidence: 84%

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The exercise sex gap and the impact of the estrous cycle on exercise performance in mice

Aguiar

Speck

Amaral

et al. 2018

Sci Rep

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Exercise physiology is different in males and females. Females are poorly studied due to the complexity of the estrous cycle and this bias has created an exercise sex gap. Here, we evaluated the impact of sexual dimorphism and of the estrous cycle on muscle strength and running power of C57BL/6 mice. Like men, male mice were stronger and more powerful than females. Exercise-induced increase of O2 consumption (O2) and CO2 production (CO2) were equal between sexes, indicating that running economy was higher in males. Thermoregulation was also more efficient in males. In females, proestrus increased exercise O2 and CO2 at low running speeds (30–35% female O2max) and estrus worsened thermoregulation. These differences translated into different absolute and relative workloads on the treadmill, even at equal submaximal O2 and belt speeds. In summary, our results demonstrate the better muscle strength, running power and economy, and exercise-induced thermoregulation of males compared to females. Proestrus and estrus still undermined the running economy and exercise-induced thermoregulation of females, respectively. These results demonstrate an important exercise sex gap in mice.

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Section: Discussionmentioning

confidence: 84%

“…Skeletal muscle mass and strength are lower in females 19 , 21 . Likewise, normalization of exercise performance by specific muscle mass (rather than body mass) makes sexual dimorphism disappear 19 , 21 . Male mammals are larger, with larger cross-sectional muscle area 8 , 10 .…”

Section: Discussionmentioning

confidence: 93%

The exercise sex gap and the impact of the estrous cycle on exercise performance in mice

Aguiar

Speck

Amaral

et al. 2018

Sci Rep

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“…Neuromuscular junction immunostaining was performed on isolated muscle fibres as described previously with minor modifications (Messéant et al 2015;Ueberschlag-Pitiot et al 2017). TA muscles were dissected and fixed in 4% paraformaldehyde for 1 h at room temperature.…”

Section: Histology Of Neuromuscular Junctionmentioning

confidence: 99%

Desmin prevents muscle wasting, exaggerated weakness and fragility, and fatigue in dystrophic mdx mouse

Ferry

Messéant

Parlakian

et al. 2020

The Journal of Physiology

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Key points Desmin, similar to dystrophin, is associated with costameric structures bridging sarcomeres to the extracellular matrix. Deletion of the desmin gene in mdx mice [double knockout (DKO) mice] induces marked muscle weakness and fatigue resistance compared to mdx mice. Muscle fragility (higher susceptibility to contraction‐induced injury) was also aggravated in DKO mice compared to mdx mice. By contrast to mdx mice, the DKO mice did not undergo muscle hypertrophy. Desmin cDNA transfer with adeno‐associated virus in newborn mdx mice reduced muscle weakness. Overall, desmin plays important and beneficial roles in muscle wasting, performance and fragility in dystrophic muscle. Abstract Duchenne muscular dystrophy (DMD) is a severe neuromuscular disease caused by dystrophin deficiency. Desmin, similar to dystrophin, is associated with costameric structures bridging sarcomeres to the extracellular matrix that contributes to muscle function. In the present study, we attempted to provide further insight into the roles of desmin, for which the expression is increased in the muscle from the mouse mdx DMD model. We show that a deletion of the desmin gene (Des) in mdx mice [double knockout (DKO) mice, mdx:desmin–/–] induces a marked muscle weakness; namely, a reduced absolute maximal force production and increased fatigue compared to that in mdx mice. Fragility (i.e. higher susceptibility to contraction‐induced injury) was also aggravated in DKO mice compared to mdx mice, despite the promotion of supposedly less fragile muscle fibres in DKO mice, and this worsening of fragility was related to a decreased muscle excitability. Moreover, in contrast to mdx mice, the DKO mice did not undergo muscle hypertrophy, as indicated by smaller and fewer fibres, with a reduced percentage of centronucleated fibres, potentially explaining the severe muscle weakness. Notably, Desmin cDNA transfer with adeno‐associated virus in newborn mdx mice improved specific maximal force normalized to muscle weight. Overall, desmin plays important and beneficial roles in muscle wasting, performance and fragility in dystrophic mdx mice, which differ, at least in part, from those observed in healthy muscle.

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“…The decrease in mature MSTN in males is developmentally regulated by growth hormone (GH) [56], as the GH/IGF-1 axis is the major regulator of postnatal growth [57]. Male gonad related factors (i.e., testosterone) also affect postnatal development and skeletal muscle maintenance [58], and the combination of these factors result in sexually dimorphic muscle growth with age, in favor of males [56,58,59]. It follows, then, that males and females would adapt differently to experimental modulations of a variety of factors, including MSTN.…”

Section: Discussionmentioning

confidence: 99%

“…Our results show that male and female mice respond differently to post-developmental MSTN reduction via DOX treatment, with females significantly increasing their lean mass, and males significantly reducing fat mass accumulation, compared to their respective controls. The reason for the females’ greater increase in lean mass is unclear, but may be related to MSTN reduction counteracting barriers to muscle growth in females (e.g., lower GH/IGF-1 levels and elevated MSTN levels) [56,58,59], while males may already be near optimal muscle growth levels prior to the reduction. Another possibility is that the differences in circulating levels of certain estrogens in females can produce anabolic effects in the absence of myostatin [60].…”

Section: Discussionmentioning

confidence: 99%

Sex differences in body composition but not neuromuscular function following long-term, doxycycline-induced reduction in circulating levels of myostatin in mice

et al. 2019

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Age-related declines in muscle function result from changes in muscle structure and contractile properties, as well as from neural adaptations. Blocking myostatin to drive muscle growth is one potential therapeutic approach. While the effects of myostatin depletion on muscle characteristics are well established, we have very little understanding of its effects on the neural system. Here we assess the effects of long-term, post-developmental myostatin reduction on electrophysiological motor unit characteristics and body composition in aging mice. We used male (N = 21) and female (N = 26) mice containing a tetracycline-inducible system to delete the myostatin gene in skeletal muscle. Starting at 12 months of age, half of the mice were administered doxycycline (tetracycline) through their chow for one year. During that time we measured food intake, body composition, and hindlimb electromyographic responses. Doxycycline-induced myostatin reduction had no effect on motor unit properties for either sex, though significant age-dependent declines in motor unit number occurred in all mice. However, treatment with doxycycline induced different changes in body composition between sexes. All female mice increased in total, lean and fat mass, but doxycycline-treated female mice experienced a significantly larger increase in lean mass than controls. All male mice also increased total and lean mass, but administration of doxycycline had no effect. Additionally, doxycycline-treated male mice maintained their fat mass at baseline levels, while the control group experienced a significant increase from baseline and compared to the doxycycline treated group. Our results show that long-term administration of doxycycline results in body composition adaptations that are distinctive between male and female mice, and that the effects of myostatin reduction are most pronounced during the first three months of treatment. We also report that age-related changes in motor unit number are not offset by reduced myostatin levels, despite increased lean mass exhibited by female mice.

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Gonad-related factors promote muscle performance gain during postnatal development in male and female mice

Cited by 16 publications

References 68 publications

The exercise sex gap and the impact of the estrous cycle on exercise performance in mice

The exercise sex gap and the impact of the estrous cycle on exercise performance in mice

Desmin prevents muscle wasting, exaggerated weakness and fragility, and fatigue in dystrophic mdx mouse

Sex differences in body composition but not neuromuscular function following long-term, doxycycline-induced reduction in circulating levels of myostatin in mice

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