Testosterone-induced increase in muscle size in healthy  young men is associated with muscle fiber hypertrophy

Sinha‐Hikim, Indrani; Artaza, Jorge N.; Woodhouse, Linda J.; González‐Cadavid, Néstor F.; Singh, Atam B.; Lee, Martin I.; Storer, Thomas W.; Casaburi, Richard; Shen, Ruoqing; Bhasin, Shalender

doi:10.1152/ajpendo.00502.2001

Cited by 348 publications

(248 citation statements)

References 46 publications

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“…exercise before senescence. Anabolic steroids have been shown to increase the number of nuclei (34,35); thus, the benefits of using steroids might be permanent and should have consequences for the exclusion time after a doping offense.…”

Section: Discussionmentioning

confidence: 99%

Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining

Bruusgaard

Johansen

Egner

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

248

276

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Effects of previous strength training can be long-lived, even after prolonged subsequent inactivity, and retraining is facilitated by a previous training episode. Traditionally, such "muscle memory" has been attributed to neural factors in the absence of any identified local memory mechanism in the muscle tissue. We have used in vivo imaging techniques to study live myonuclei belonging to distinct muscle fibers and observe that new myonuclei are added before any major increase in size during overload. The old and newly acquired nuclei are retained during severe atrophy caused by subsequent denervation lasting for a considerable period of the animal's lifespan. The myonuclei seem to be protected from the high apoptotic activity found in inactive muscle tissue. A hypertrophy episode leading to a lasting elevated number of myonuclei retarded disuse atrophy, and the nuclei could serve as a cell biological substrate for such memory. Because the ability to create myonuclei is impaired in the elderly, individuals may benefit from strength training at an early age, and because anabolic steroids facilitate more myonuclei, nuclear permanency may also have implications for exclusion periods after a doping offense. muscle memory | muscle nuclei | muscle atrophy | muscle hypertrophy | apoptosis

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Section: Discussionmentioning

confidence: 99%

Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining

Bruusgaard

Johansen

Egner

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

248

276

View full text Add to dashboard Cite

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“…They observed that testosterone substitution leads to an increase in muscle mass and muscle strength due to hypertrophy of muscle fibers, while at the same time leading to a decrease in body fat content (2,4,15,16). In some of these studies, MRI was used to determine morphologic changes of the musculature.…”

Section: Discussionmentioning

confidence: 99%

Changes in calf muscle elasticity in hypogonadal males before and after testosterone substitution as monitored by magnetic resonance elastography

et al. 2007

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Purpose: We sought to determine whether differences in muscle elasticity between healthy age-related controls and patients with hypogonadism could be measured by a new, non-invasive method termed magnetic resonance elastography (MRE). Materials and methods: Twelve hypogonadal (21-68 years) and twenty-seven healthy age-related men (20-76 years) were examined. In the hypogonadism group, serum testosterone levels were compared and MRE was conducted prior to and after 6 months of therapy in 6 of the 12 patients. MRE was performed by mechanically exciting the soleus muscle that was used because of its uniformly distributed muscle fibers, size, and accessibility, with a custom designed piezoelectric-actuator using a modified phase-contrast sequence. For mechanical excitation the actuator lever was placed on the anterior surface of the calf. The subjects had to maintain a force of 0-20% of their maximum voluntary contraction against a home-built footplate that was mounted on the MR table. All images were phase unwrapped and reconstructed into shear modulus elastograms using the local frequency estimation technique. Results: Testosterone levels were significantly higher after 6 months of treatment. A statistical difference in the shear modulus was observed prior to and after 6 months of testosterone therapy and was nearly the same as in the healthy age-related control group. Conclusion: MRE seems to be a promising technique for the evaluation of therapeutic effects in patients with hypogonadism and possibly in other diseases with muscular effects.European Journal of Endocrinology 156 673-678

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“…Interestingly, satellite cells express the highest levels of AR in skeletal muscle [63]. Satellites cells are the main target for polyQ-AR toxicity and androgens have been shown to promote proliferation and differentiation, which may account for the hypertrophic effect of androgens on muscle [64]. Conversely, it is possible that androgens trigger toxic response in satellite cells expressing polyQ-AR contributing to muscle deterioration in SBMA [65]: while androgens and AR have remarkable hypertrophic effects on skeletal muscle, they have detrimental effects in SBMA muscle.…”

Section: Pathogenesismentioning

confidence: 99%

Kennedy disease (X-linked recessive bulbospinal neuronopathy): A comprehensive review from pathophysiology to therapy

2017

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Acknowledgments: the authors thank AFM-Téléthon, Téléthon Biobank, Institut pour la Recherche sur la Moelle épinière et l'Encéphale (IRME), Association pour la Recherche sur la SLA (ARSla) and the University of Padova for their research support.Kennedy disease (X-Linked recessive Bulbospinal Neuronopathy): a comprehensive review from pathophysiology to therapy. AbstractKennedy's disease, also known as spinal and bulbar muscular atrophy (SBMA), is a rare, adult-onset, Xlinked recessive neuromuscular disease. It is caused by expansion of a CAG repeat sequence in exon 1 of the androgen-receptor (AR) gene, encoding a poly-glutamine (polyQ) tract. Poly-Q-expanded AR accumulates in nuclei and initiates degeneration and loss of motor neurons and dorsal root ganglia. The disease has been retained to be a pure lower motor neuron disease for a long time, but recently the presence of important hyper-Creatine-Kinase-emia and of myopathic alterations on muscle biopsy has suggested the presence of a primary myopathy underlying a wide proportion of clinical manifestations. The disease, that affects male adults, is characterized by muscle weakness and atrophy localized proximally in the limbs and by bulbar involvement. Sensory disturbances are associated to the motor phenotype but may be subclinical. The most frequent systemic symptom is gynecomastia related to androgen insensitivity, but other abnormalities, such as heart rhythm and urinary disturbances, have also been reported. The course of the disease is slowly progressive with normal life expectancy. The diagnosis of SBMA is based on genetic testing, with 38 CAG repeats retained to be pathogenic. Even though several therapeutic attempts have been made in mouse models, no effective disease modifying therapy is available but symptomatic therapy is beneficial for the management of weakness, fatigability and bulbar symptoms.

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Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy

Cited by 348 publications

References 46 publications

Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining

Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining

Changes in calf muscle elasticity in hypogonadal males before and after testosterone substitution as monitored by magnetic resonance elastography

Kennedy disease (X-linked recessive bulbospinal neuronopathy): A comprehensive review from pathophysiology to therapy

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