Effect of continuous and intermittent clenbuterol feeding on rat growth rate and muscle

McElligott, Mary Ann; Barreto, Albert; Chaung, L Y

doi:10.1016/0742-8413(89)90215-6

Cited by 37 publications

(23 citation statements)

References 12 publications

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“…Although short-term use of ␤ 2 -adrenoceptor agonists has been recommended for therapeutic purposes related to functional recovery after skeletal muscle trauma (3), chronic administration of sympathomimetics leads to ␤ 2 -adrenoceptormediated skeletal myotoxicity and loss of its potential muscular benefits (21,29). In fact, we observed that chronic sympathetic hyperactivity induced skeletal muscle myopathy in 7-mo-old ␣ 2A /␣ 2C ARKO mice associated with a more extensively prooxidant state marked by increased muscular norepinephrine levels associated with decreased redox balance and increased lipid hydroperoxidation and iNOS expression.…”

Section: Resultsmentioning

confidence: 99%

Sympathetic hyperactivity differentially affects skeletal muscle mass in developing heart failure: role of exercise training

Bacurau¹,

Jardim²,

Ferreira³

et al. 2009

Journal of Applied Physiology

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Ramires PR, Moriscot AS, Brum PC. Sympathetic hyperactivity differentially affects skeletal muscle mass in developing heart failure: role of exercise training. J Appl Physiol 106: 1631-1640, 2009. First published January 29, 2009 doi:10.1152/japplphysiol.91067.2008.-Sympathetic hyperactivity (SH) is a hallmark of heart failure (HF), and several lines of evidence suggest that SH contributes to HFinduced skeletal myopathy. However, little is known about the influence of SH on skeletal muscle morphology and metabolism in a setting of developing HF, taking into consideration muscles with different fiber compositions. The contribution of SH on exercise tolerance and skeletal muscle morphology and biochemistry was investigated in 3-and 7-mo-old mice lacking both ␣2A-and ␣2C-adrenergic receptor subtypes (␣2A/␣2CARKO mice) that present SH with evidence of HF by 7 mo. To verify whether exercise training (ET) would prevent skeletal muscle myopathy in advanced-stage HF, ␣2A/␣2CARKO mice were exercised from 5 to 7 mo of age. At 3 mo, ␣2A/␣2CARKO mice showed no signs of HF and preserved exercise tolerance and muscular norepinephrine with no changes in soleus morphology. In contrast, plantaris muscle of ␣2A/␣2CARKO mice displayed hypertrophy and fiber type shift (IIA 3 IIX) paralleled by capillary rarefaction, increased hexokinase activity, and oxidative stress. At 7 mo, ␣ 2A/␣2CARKO mice displayed exercise intolerance and increased muscular norepinephrine, muscular atrophy, capillary rarefaction, and increased oxidative stress. ET reestablished ␣2A/ ␣2CARKO mouse exercise tolerance to 7-mo-old wild-type levels and prevented muscular atrophy and capillary rarefaction associated with reduced oxidative stress. Collectively, these data provide direct evidence that SH is a major factor contributing to skeletal muscle morphological changes in a setting of developing HF. ET prevented skeletal muscle myopathy in ␣2A/␣2CARKO mice, which highlights its importance as a therapeutic tool for HF. oxidative stress; ␣2A/␣2C-adrenergic receptor knockout mice; cardiac cachexia HEART FAILURE (HF) is a clinical syndrome with poor prognosis characterized by exercise intolerance, early fatigue, and skeletal muscle myopathy associated with atrophy and shift toward fast-twitch fibers (27,28,49). The development of end-stage HF often involves a myocardial insult that reduces cardiac output, which leads to a compensatory increase in sympathetic nervous activity (4, 5). Although beneficial acutely, chronic increase of sympathetic activity leads to further pathological changes in the heart with a progressive deterioration of cardiac function (7,24,38,39), which is closely related to increased cardiac oxidative stress (52).Several lines of evidence suggest that sympathetic hyperactivity also contributes to the skeletal myopathy of HF, since it leads to chronic vasoconstriction in HF patients (22,35,44) associated with skeletal muscle oxidative stress (34,46,53) and increased concentrations of proinflammatory cytokines (12, 23). However, little is known ...

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Section: Resultsmentioning

confidence: 99%

Sympathetic hyperactivity differentially affects skeletal muscle mass in developing heart failure: role of exercise training

Bacurau¹,

Jardim²,

Ferreira³

et al. 2009

Journal of Applied Physiology

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“…Importantly, the SB-mediated increase of muscle strength is induced via direct action on the muscle b 2 -AR, but the CB-mediated increase of muscle strength might involve a mechanism other than the direct muscle b 2 -AR stimulation, such as cerebral b 2 -AR stimulation, although the mechanisms remain poorly understood (19). The histological (Figs.…”

Section: Discussionmentioning

confidence: 99%

“…this study increased the mass of the skeletal and cardiac muscle efficiently without altering the body weight, probably due to the concomitant decrease of fat tissue induced by CB through its lipolytic effect (18,19,26). We also performed electrocardiogram (ECG) recording using a telemetric unit (24,25,27).…”

Section: Effects Of Cb On Other Muscles and Heart Ratementioning

confidence: 99%

“…and these results served as controls. Subsequently, CB (Sigma, St. Louis, MO, USA) treatment was initiated via the drinking water (30 mg/L) for 2 weeks because oral administration of CB might increase the skeletal mass efficiently without altering the body weight (18,19). SB (Sigma) treatment was initiated via intraperitoneal injection (1.15 mg/kg) (20).…”

Section: Emg Recording With Radio-telemetry Systemmentioning

confidence: 99%

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Role of Masseter Muscle β2-Adrenergic Signaling in Regulation of Muscle Activity, Myosin Heavy Chain Transition, and Hypertrophy

et al. 2013

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Abstract. Chronic administration of clenbuterol (CB), a lipophilic b 2 -adrenoceptor (b 2 -AR) agonist, induces skeletal muscle hypertrophy and slow-to-fast fiber-type transitions in mammalian species, but the mechanism and pathophysiological roles of these changes have not been explored. Here, we examined the effects of CB not only on masseter muscle mass, fiber diameter, and myosin heavy chain (MHC) composition, but also on daily muscle activity, a factor influencing muscle phenotype, by means of electromyogram analysis in rats. MHC transition towards faster isoforms was induced by 2-week CB treatment. In addition, daily duty time was increased at 1 day, 1 week, and 2 weeks after the start of CB treatment and its increase was greater at high activity level (6-fold) than at low activity level (2-fold). In order to examine whether these effects of CB were mediated through muscle or CNS b 2 -AR stimulation, we compared these effects of CB with those of salbutamol (SB), a hydrophilic b 2 -AR agonist. SB treatment induced masseter hypertrophy and MHC transition, like CB, but did not increase daily activity. These results suggest that CB-mediated slow-to-fast MHC transition with hypertrophy was induced through direct muscle b 2 -AR stimulation, but the increase of daily duty time was mediated through the CNS.

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“…[44][45][46] Essa desaceleração da taxa de crescimento ocorre pela redução da densidade de receptores β-adrenérgicos, causada pela exposição crônica dos receptores ao agonista. Um estudo demonstrou que o tratamento com clembuterol por 18 dias reduziu 50% da densidade de receptores β2-adrenérgicos na musculatura esquelética.…”

Section: Figura 4: Principais Causas Das Lesões Causadas Ao Organismounclassified

Relevância e tratamento das lesões características da insuficiência cardíaca na musculatura esquelética

Júnior

2009

Medicina (Ribeirão Preto)

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Pacientes com insuficiência cardíaca, a via final das doenças cardiovasculares e a primeira causa de internação em idosos no Brasil, apresentam deterioração do tecido muscular esquelético. Além disso, as lesões na musculatura têm relação direta com a qualidade de vida e a autonomia dos pacientes, por meio do nível de tolerância aos esforços físicos, além de constituírem um preditor independente de mortalidade na síndrome. Ao longo da presente revisão de literatura serão discutidos em relação à insuficiência cardíaca: seu conceito e um breve histórico; a importância da musculatura esquelética; as anormalidades funcionais, estruturais, bioquímicos e moleculares que acometem esse tecido; as potenciais causas dessas alterações (hiperatividade simpática, redução na ingestão alimentar, espécies reativas de oxigênio, citocinas pró-inflamatórias e diminuição do nível de atividade física e do fluxo sanguíneo); e os efeitos da principal terapia direcionada para combater essa disfunção, o treinamento físico aeróbio de intensidade moderada. Reconhecida a importância do tecido muscular esquelético na síndrome, essa é uma área da investigação científica com muitos temas ainda não estudados, como o efeito de terapias farmacológicas utilizadas pelos pacientes, de exercícios físicos aeróbios de maior intensidade e intervalados, de exercícios físicos de força, de intervenções nutricionais e de terapias celulares e gênicas. No futuro, os resultados desses estudos que serão desenvolvidos certamente contribuirão para uma menor degeneração da musculatura esquelética na doença, o que, consequentemente, vai melhorar a ualidade de vida, a autonomia e o prognóstico dos pacientes.

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Effect of continuous and intermittent clenbuterol feeding on rat growth rate and muscle

Cited by 37 publications

References 12 publications

Sympathetic hyperactivity differentially affects skeletal muscle mass in developing heart failure: role of exercise training

Sympathetic hyperactivity differentially affects skeletal muscle mass in developing heart failure: role of exercise training

Role of Masseter Muscle β2-Adrenergic Signaling in Regulation of Muscle Activity, Myosin Heavy Chain Transition, and Hypertrophy

Relevância e tratamento das lesões características da insuficiência cardíaca na musculatura esquelética

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