Efficacy of myonuclear addition may explain differential myofiber growth among resistance-trained young and older men and women

Petrella, John K.; Kim, Jeong Su; Cross, James M.; Kosek, David J.; Bamman, Marcas M.

doi:10.1152/ajpendo.00190.2006

Cited by 309 publications

(402 citation statements)

References 65 publications

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“…However, we also observed a strong trend for increased IGF-I mRNA in the non-HMB group (+30%, p = 0.056). Because of this, we could surmise that IGF-I mRNA increased similarly in both experimental groups primarily from the RT stimulus itself, which agrees with numerous investigations demonstrating the induction of muscle IGF-I by high tension loading (Bamman et al, 2001;Kim et al, 2005;Petrella et al, 2006;Sun et al, 2006). For MGF mRNA levels, significant increases were observed in soleus muscles of both the HMB (+32%) and non-HMB (+40%) groups compared to control (p < 0.05).…”

Section: Hmb and Rt Regulation Of Mitogenic And Myogenic Genessupporting

confidence: 90%

β-Hydroxy-β-Methylbutyrate Did Not Enhance High Intensity Resistance Training-Induced Improvements in Myofiber Dimensions and Myogenic Capacity in Aged Female Rats

Kim

Park

Lee

et al. 2012

Molecules and Cells

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Older women exhibit blunted skeletal muscle hypertrophy following resistance training (RT) compared to other age and gender cohorts that is partially due to an impaired regenerative capacity. In the present study, we examined whether β-hydroxy-β-methylbutyrate (HMB) provision to aged female rodents would enhance regenerative mechanisms and facilitate RT-induced myofiber growth. Nineteen-month old female Sprague-Dawley rats were randomly divided into three groups: HMB (0.48 g/kg/d; n = 6), non-HMB (n = 6), and control (n = 4). HMB and non-HMB groups underwent RT every third day for 10 weeks using a ladder climbing apparatus. Whole body strength, grip strength, and body composition was evaluated before and after RT. The gastrocnemius and soleus muscles were analyzed using magnetic resonance diffusion tensor imaging, RT-PCR, and immunohistochemistry to determine myofiber dimensions, transcript expression, and satellite cells/myonuclei, respectively. ANOVAs were used with significance set at p < 0.05. There were significant time effects (pre vs. post) for whole body strength (+262%), grip strength (+17%), lean mass (+20%), and fat mass (-19%). Both RT groups exhibited significant increases in the mean myofiber cross-sectional area (CSA) in the gastrocnemius and soleus (+8-22%) compared to control. Moreover, both groups demonstrated significant increases in the numbers of satellite cells (+100-108%) and myonuclei (+32%) in the soleus but not the gastrocnemius. A significant IGF-I mRNA elevation was only observed in soleus of the HMB group (+33%) whereas MGF and myogenin increased significantly in both groups (+32-40%). Our findings suggest that HMB did not further enhance intense RT-mediated myogenic mechanisms and myofiber CSA in aged female rats.

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Section: Hmb and Rt Regulation Of Mitogenic And Myogenic Genessupporting

confidence: 90%

β-Hydroxy-β-Methylbutyrate Did Not Enhance High Intensity Resistance Training-Induced Improvements in Myofiber Dimensions and Myogenic Capacity in Aged Female Rats

Kim

Park

Lee

et al. 2012

Molecules and Cells

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“…Decreased expression of myostatin in response to resistance exercise has been noted in several investigations [87][88][89][90][91], and is necessary for optimal hypertrophic adaptation [88]. Reductions in myostatin mRNA were reported by Drummond et al [92] following low-intensity resistance exercise with BFR.…”

Section: Intramuscular Signallingmentioning

confidence: 89%

Hypoxia and Resistance Exercise: A Comparison of Localized and Systemic Methods

et al. 2014

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It is generally believed that optimal hypertrophic and strength gains are induced through moderate-or high-intensity resistance training, equivalent at least 60% of an individual's 1-repetition maximum (1RM). However, recent evidence suggests that similar adaptations are facilitated when low-intensity resistance exercise (~20-50% 1RM) is combined with blood flow restriction (BFR) to the working muscles. Although the mechanisms underpinning these responses are not yet firmly established, it appears that localized hypoxia created by BFR may provide an anabolic stimulus by enhancing the metabolic and endocrine response, and increase cellular swelling and signalling function following resistance exercise. Moreover, BFR has also been demonstrated to increase type II muscle fibre recruitment during exercise.However, inappropriate implementation of BFR can result in detrimental effects, including petechial haemorrhage and dizziness. Further, as BFR is limited to the limbs, the muscles of the trunk are unable to be trained under localized hypoxia. More recently, the use of systemic hypoxia via hypoxic chambers and devices has been investigated as a novel way to stimulate similar physiological responses to resistance training as BFR techniques. While little evidence is available, reports indicate that beneficial adaptations, similar to those induced by BFR, are possible using these methods. The use of systemic hypoxia allows large groups to train concurrently within a hypoxic chamber using multi-joint exercises. However, further scientific research is required to fully understand the mechanisms that cause augmented muscular changes during resistance exercise with a localized or systemic hypoxic stimulus.3

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“…However, linkage of myonuclei number and muscle fiber size is the basis of the “myonuclear domain” hypothesis which asserts that a single myonucleus controls the translational and transcriptional regulation of protein synthesis for a limited cell volume known as the myonuclear domain. Although more recent studies indicate that age‐related myofiber atrophy results primarily from reductions in myonuclear domain size instead of the loss of myonuclei numbers (Karlsen et al, 2015; Schwartz, Brown, McLaughlin, Smith, & Bigelow, 2016), other findings show that increased myonuclear fusion facilitates muscle hypertrophy, especially when the myonuclear domain size exceeds a certain threshold (Jo et al, 2012; Petrella, Kim, Cross, Kosek, & Bamman, 2006). The findings in the current study support the possibility that the ablation of TNF‐α contributes to increased myofiber size in aging muscle by increasing the frequency of muscle cell fusion with aging muscle fibers.…”

Section: Discussionmentioning

confidence: 99%

Myeloid cell‐derived tumor necrosis factor‐alpha promotes sarcopenia and regulates muscle cell fusion with aging muscle fibers

et al. 2018

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Sarcopenia is age‐related muscle wasting that lacks effective therapeutic interventions. We found that systemic ablation of tumor necrosis factor‐α (TNF‐α) prevented sarcopenia and prevented age‐related change in muscle fiber phenotype. Furthermore, TNF‐α ablation reduced the number of satellite cells in aging muscle and promoted muscle cell fusion in vivo and in vitro. Because CD68+ macrophages are important sources of TNF‐α and the number of CD68+ macrophages increases in aging muscle, we tested whether macrophage‐derived TNF‐α affects myogenesis. Media conditioned by TNF‐α‐null macrophages increased muscle cell fusion in vitro, compared to media conditioned by wild‐type macrophages. In addition, transplantation of bone marrow cells from wild‐type mice into TNF‐α‐null recipients increased satellite cell numbers and reduced numbers of centrally nucleated myofibers, indicating that myeloid cell‐secreted TNF‐α reduces muscle cell fusion. Transplanting bone marrow cells from wild‐type mice into TNF‐α‐null recipients also increased sarcopenia, although transplantation did not restore the age‐related change in muscle fiber phenotype. Collectively, we show that myeloid cell‐derived TNF‐α contributes to muscle aging by affecting sarcopenia and muscle cell fusion with aging muscle fibers. Our findings also show that TNF‐α that is intrinsic to muscle and TNF‐α secreted by immune cells work together to influence muscle aging.

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Efficacy of myonuclear addition may explain differential myofiber growth among resistance-trained young and older men and women

Cited by 309 publications

References 65 publications

β-Hydroxy-β-Methylbutyrate Did Not Enhance High Intensity Resistance Training-Induced Improvements in Myofiber Dimensions and Myogenic Capacity in Aged Female Rats

β-Hydroxy-β-Methylbutyrate Did Not Enhance High Intensity Resistance Training-Induced Improvements in Myofiber Dimensions and Myogenic Capacity in Aged Female Rats

Hypoxia and Resistance Exercise: A Comparison of Localized and Systemic Methods

Myeloid cell‐derived tumor necrosis factor‐alpha promotes sarcopenia and regulates muscle cell fusion with aging muscle fibers

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