Chronic effects of β2 agonists on body composition and protein synthesis in the rat

Emery, Peter W.; Rothwell, Nancy J.; Stock, Michael J.; Winter, P de

doi:10.1007/bf01120827

Cited by 278 publications

(180 citation statements)

References 16 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: 59%

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: 59%

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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“…Fenoterol given to lambs in their food for 8 wk did not increase the mass of their infraspinatus or pectoralis profundus muscles (13). Daily subcutaneous injections of fenoterol (1 mg/kg) for 19 days increased the gastrocnemius muscle mass in rats by ϳ12.5% (11). However, no studies have compared the efficacy of fenoterol and clenbuterol treatment on skeletal muscle function in rats.…”

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confidence: 99%

“…However, it became apparent that at high doses ␤ 2 -agonists caused an increase in body mass, which was later attributed to an increase in skeletal muscle mass (11). Not surprisingly, ␤ 2 -agonists such as clenbuterol were examined for possible application in the livestock industry with the aim of promoting muscle growth and hence improving the efficiency of meat production (26,(39)(40)(41).…”

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confidence: 99%

β₂-Agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol

Ryall

Gregorevic

Plant

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

100

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. ␤2-Agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol. Am J Physiol Regul Integr Comp Physiol 283: R1386-R1394, 2002. First published September 5, 2002 10.1152/ajpregu.00324.2002-Potential treatments for skeletal muscle wasting and weakness ideally possess both anabolic and ergogenic properties. Although the ␤2-adrenoceptor agonist clenbuterol has well-characterized effects on skeletal muscle, less is known about the therapeutic potential of the related ␤2-adrenoceptor agonist fenoterol. We administered an equimolar dose of either clenbuterol or fenoterol to rats for 4 wk to compare their effects on skeletal muscle and tested the hypothesis that fenoterol would produce more powerful anabolic and ergogenic effects. Clenbuterol treatment increased fiber cross-sectional area (CSA) by 6% and maximal isometric force (Po) by 20% in extensor digitorum longus (EDL) muscles, whereas fiber CSA in soleus muscles decreased by 3% and Po was unchanged, compared with untreated controls. In the EDL muscles, fenoterol treatment increased fiber CSA by 20% and increased Po by 12% above values achieved after clenbuterol treatment. Soleus muscles of fenoterol-treated rats exhibited a 13% increase in fiber CSA and a 17% increase in Po above that of clenbuteroltreated rats. These data indicate that fenoterol has greater effects on the functional properties of rat skeletal muscles than clenbuterol.

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“…Clenbuterol and other ß2-agonists as anabolic drugs have no effect on GH-or thyroid and insulin-stimulation [38]. They rather act through increasing RNA and protein-synthesis.…”

Section: Discussionmentioning

confidence: 99%

Doping for Chess Performance

Golf¹

2015

J Sports Med Doping Stud

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During a chess game, the needed energy is first derived instantly from ATP and creatine-phosphate, then within a few seconds later from glycogen stores in brain, glycogen, muscle and liver and finally, 1-2 hours later from adipose tissue. Anaerobic oxidation of glucose-derivative from glycogen delivers energy 6 times faster than aerobic oxidation of glucose and oxidation of fatty acids; correspondingly, mental activity can perform as well 6 times faster as long as glycogen is available.The mental profile of chess players correlates with cerebral processes such as attention, conflict solution, memory, motivation and recognition, which together constitute a specific chess-domain expertise.A chess player may compete best when a) regularly physical exercise is carried out to compete in strenuous chess tournaments and to stimulate mental cognition, b) super compensated glycogen is accumulated in brain, muscle and liver by corresponding nutrition and physical and mental activities, and c. an active mental disposition is available for complex brain tasks during chess by complementary treatment schemes e.g., cogni-tive enhancement (CE) by chess training with chess boards, chess books, building chess images, visual observation of chess games, vocational training with chess, metacognitive training, and additionally regular light physical stress. An illicit improvement of brain performance for chess playing may be achieved by several measures:1.Increase of O 2 supply by therapy with erythropoietin (EPO) for chess tournaments at high altitudes and for chess players with lung diseases 2.Increase of body glycogen by therapy with insulin Regular non-medical use of steroid and proteohormones in elevated concentrations and CE-drugs must also consider numerous side effects ranging from simple metabolic disturbances through cardiac problems to cognitive decline to tumorgenesis and sudden death.

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Chronic effects of β2 agonists on body composition and protein synthesis in the rat

Cited by 278 publications

References 16 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

β₂-Agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol

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Chronic effects of β2 agonists on body composition and protein synthesis in the rat

Cited by 278 publications

References 16 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

β2-Agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol

Doping for Chess Performance

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β₂-Agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol