Clenbuterol treatment affects myosin heavy chain isoforms and MyoD content similarly in intact and regenerated soleus muscles

Bricout, Véronique-Aurélie; Serrurier, B.; Bigard, A. X.

doi:10.1046/j.0001-6772.2003.01246.x

Cited by 30 publications

(28 citation statements)

References 36 publications

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“…This delicate balance suggests that hypertrophy may provide a means to antagonize skeletal muscle atrophy induced by some physiological and pathological challenges (16). ␤-Adrenergic agonists (BA) are a family of compounds that induce skeletal muscle hypertrophy in rats (7,13,46), mice (21), pigs (12), cattle, and sheep (27). Consistent with the aforementioned thesis, BA antagonize skeletal muscle atrophy in experimentally induced denervation or limb immobilization models (11,21).…”

mentioning

confidence: 60%

Extracellular signal-regulated kinase pathway is differentially involved in β-agonist-induced hypertrophy in slow and fast muscles

Shi

Zeng²,

Ricome³

et al. 2007

American Journal of Physiology-Cell Physiology

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The molecular mechanisms controlling ␤-adrenergic receptor agonist (BA)-induced skeletal muscle hypertrophy are not well known. We presently report that BA exerts a distinct muscle-and muscle fiber type-specific hypertrophy. Moreover, we have shown that pharmacologically or genetically attenuating extracellular signal-regulated kinase (ERK) signaling in muscle fibers resulted in decreases (P Ͻ 0.05) in fast but not slow fiber type-specific reporter gene expressions in response to BA exposure in vitro and in vivo. Consistent with these data, forced expression of MAPK phosphatase 1, a nuclear protein that dephosphorylates ERK1/2, in fast-twitch skeletal muscle ablated (P Ͻ 0.05) the hypertrophic effects of BA feeding (clenbuterol, 20 parts per million in water) in vivo. Further analysis has shown that BA-induced phosphorylation and activation of ERK occurred to a greater (P Ͻ 0.05) extent in fast myofibers than in slow myofibers. Analysis of the basal level of ERK activity in slow and fast muscles revealed that ERK1/2 is activated to a greater extent in fast-than in slow-twitch muscles. These data indicate that ERK signaling is differentially involved in BA-induced hypertrophy in slow and fast skeletal muscles, suggesting that the increased abundance of phospho-ERK1/2 and ERK activity found in fast-twitch myofibers, compared with their slow-twitch counterparts, may account, at least in part, for the fiber type-specific hypertrophy induced by BA stimulation. These data suggest that fast myofibers are pivotal in the adaptation of muscle to environmental cues and that the mechanism underlying this change is partially mediated by the MAPK signaling cascade. muscle fiber type; mitogen-activated protein kinase signaling pathways; mechanism SKELETAL MUSCLE ADAPTATION is triggered by a variety of cues that depend largely on a delicate balance between hypertrophy and atrophy signaling processes converging on the nucleus (34,37,39). This delicate balance suggests that hypertrophy may provide a means to antagonize skeletal muscle atrophy induced by some physiological and pathological challenges (16). ␤-Adrenergic agonists (BA) are a family of compounds that induce skeletal muscle hypertrophy in rats (7, 13, 46), mice (21), pigs (12), cattle, and sheep (27). Consistent with the aforementioned thesis, BA antagonize skeletal muscle atrophy in experimentally induced denervation or limb immobilization models (11, 21). Mechanistically, BA bind to the ␤-adrenergic receptor, a G protein-coupled receptor, and activate the G s protein and PKA signaling pathway. PKA then phosphorylates the ␤-receptor and switches its coupling from G s to G i protein. The ␤␥-subunit of G i protein stimulates the ERK-MAPK through a pathway involving c-Src and Ras (10). The activated receptor is then phosphorylated and bound by ␤-arrestin for degradation, a process called desensitization (29,38). Modulation of receptor desensitization is thought to account for the activation of MAPK in isoproterenol-stimulated cells (24). In addition, the ␤ 2 form of the ...

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confidence: 60%

Extracellular signal-regulated kinase pathway is differentially involved in β-agonist-induced hypertrophy in slow and fast muscles

Shi

Zeng²,

Ricome³

et al. 2007

American Journal of Physiology-Cell Physiology

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“…Evidence comes from the findings of Beitzel et al (31) and Bricout et al (57) who found that administration of a ␤-agonist hastened the functional recovery of regenerating rat skeletal muscles after myotoxic injury with bupivacaine or Notexin, respectively. Daily fenoterol administration to rats (1.4 mg⅐kg Ϫ1 ⅐day Ϫ1 ip) enhanced the force-producing capacity of the injured/regenerating EDL muscles by 19% compared with untreated regenerating muscles at 14 days postinjury.…”

Section: F Improving Muscle Regeneration and Functional Repair Aftermentioning

confidence: 97%

Role of β-Adrenoceptor Signaling in Skeletal Muscle: Implications for Muscle Wasting and Disease

Lynch¹,

Ryall²

2008

Physiological Reviews

362

356

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The importance of beta-adrenergic signaling in the heart has been well documented, but it is only more recently that we have begun to understand the importance of this signaling pathway in skeletal muscle. There is considerable evidence regarding the stimulation of the beta-adrenergic system with beta-adrenoceptor agonists (beta-agonists). Although traditionally used for treating bronchospasm, it became apparent that some beta-agonists could increase skeletal muscle mass and decrease body fat. These so-called "repartitioning effects" proved desirable for the livestock industry trying to improve feed efficiency and meat quality. Studying beta-agonist effects on skeletal muscle has identified potential therapeutic applications for muscle wasting conditions such as sarcopenia, cancer cachexia, denervation, and neuromuscular diseases, aiming to attenuate (or potentially reverse) the muscle wasting and associated muscle weakness, and to enhance muscle growth and repair after injury. Some undesirable cardiovascular side effects of beta-agonists have so far limited their therapeutic potential. This review describes the physiological significance of beta-adrenergic signaling in skeletal muscle and examines the effects of beta-agonists on skeletal muscle structure and function. In addition, we examine the proposed beneficial effects of beta-agonist administration on skeletal muscle along with some of the less desirable cardiovascular effects. Understanding beta-adrenergic signaling in skeletal muscle is important for identifying new therapeutic targets and identifying novel approaches to attenuate the muscle wasting concomitant with many diseases.

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“…[35][36][37][38][39] Among these durations, we selected the most prolonged period, and demonstrated that such stimuli suppresses the phagocytic activity of splenic adherent cells expressing high levels of MARCO. It is necessary to elucidate the mechanisms of β 2 -agonist action by examining in various periods, including the acute experiment.…”

Section: Discussionmentioning

confidence: 99%

β<sub>2</sub>-Agonist Clenbuterol Suppresses Bacterial Phagocytosis of Splenic Macrophages Expressing High Levels of Macrophage Receptor with Collagenous Structure

Shirato

Sato

et al. 2013

Biological & Pharmaceutical Bulletin

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Splenic marginal zone macrophages expressing macrophage receptor with collagenous structure (MARCO) contribute to the clearance of blood-borne pathogens. We determined a splenic adherent cell fraction abundantly containing cells expressing a higher level of MARCO by flow cytometry, and examined the effects of daily administration of an anabolic dose of β2-agonist clenbuterol on the phagocytic capacity of the cells in mice. After 6 weeks of clenbuterol (1.0 mg/kg body weight/d) or vehicle administration to the mice, splenic adherent cells were isolated. These cells were separated into three cell-size subpopulations. Among them, the small-cell subpopulation contained abundantly the cells with markedly higher levels of MARCO and exhibited more intense phagocytic capacity against Escherichia coli, as compared with the other subpopulations. The phagocytic capacity of the small cells was significantly reduced after clenbuterol administration. These results suggest that the utilization of clenbuterol as doping drug impairs bacterial clearance in the spleen.

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Clenbuterol treatment affects myosin heavy chain isoforms and MyoD content similarly in intact and regenerated soleus muscles

Cited by 30 publications

References 36 publications

Extracellular signal-regulated kinase pathway is differentially involved in β-agonist-induced hypertrophy in slow and fast muscles

Extracellular signal-regulated kinase pathway is differentially involved in β-agonist-induced hypertrophy in slow and fast muscles

Role of β-Adrenoceptor Signaling in Skeletal Muscle: Implications for Muscle Wasting and Disease

β<sub>2</sub>-Agonist Clenbuterol Suppresses Bacterial Phagocytosis of Splenic Macrophages Expressing High Levels of Macrophage Receptor with Collagenous Structure

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