Effect of the β2-agonist clenbuterol on the locomotor activity of rat submitted to a 14-day period of hypodynamia–hypokinesia

Canu, Marie‐Hélène; Stevens, Laurence; Ricart-Firinga, Carole; Picquet, Florence; Falempin, Maurice

doi:10.1016/s0166-4328(01)00178-4

Cited by 15 publications

(5 citation statements)

References 40 publications

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“…The results of the present study demonstrated the anabolic effects of low doses of clenbuterol under conditions of disuse, i.e., prevented loss of soleus weight and cross-sectional area. This correlates with the Canu et al study (20), in which the anabolic action of clenbuterol was observed in both normal and atrophied muscles. Pellegrino et al (21) also observed increased cross-sectional area of mouse soleus muscle in the presence of clenbuterol.…”

Section: Discussionsupporting

confidence: 90%

The effect of a low dose of clenbuterol on rat soleus muscle submitted to joint immobilization

Cancelliero

Durigan

Silva

et al. 2008

Braz J Med Biol Res

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The aim of the present study was to evaluate the effect of joint immobilization on morphometric parameters and glycogen content of soleus muscle treated with clenbuterol. Male Wistar (3-4 months old) rats were divided into 4 groups (N = 6 for each group): control, clenbuterol, immobilized, and immobilized treated with clenbuterol. Immobilization was performed with acrylic resin orthoses and 10 µg/kg body weight clenbuterol was administered subcutaneously for 7 days. The following parameters were measured the next day on soleus muscle: weight, glycogen content, cross-sectional area, and connective tissue content. The clenbuterol group showed an increase in glycogen (81.6%, 0.38 ± 0.09 vs 0.69 ± 0.06 mg/100 g; P < 0.05) without alteration in weight, cross-sectional area or connective tissue compared with the control group. The immobilized group showed a reduction in muscle weight (34.2%, 123.5 ± 5.3 vs 81.3 ± 4.6 mg; P < 0.05), glycogen content (31.6%, 0.38 ± 0.09 vs 0.26 ± 0.05 mg/100 mg; P < 0.05) and cross-sectional area (44.1%, 2574.9 ± 560.2 vs 1438.1 ± 352.2 µm 2 ; P < 0.05) and an increase in connective tissue (216.5%, 8.82 ± 3.55 vs 27.92 ± 5.36%; P < 0.05). However, the immobilized + clenbuterol group showed an increase in weight (15.9%; 81.3 ± 4.6 vs 94.2 ± 4.3 mg; P < 0.05), glycogen content (92.3%, 0.26 ± 0.05 vs 0.50 ± 0.17 mg/100 mg; P < 0.05), and cross-sectional area (19.9%, 1438.1 ± 352.2 vs 1724.8 ± 365.5 µm 2 ; P < 0.05) and a reduction in connective tissue (52.2%, 27.92 ± 5.36 vs 13.34 ± 6.86%; P < 0.05). Statistical analysis was performed using Kolmogorov-Smirnov and homoscedasticity tests. For the muscle weight and muscle glycogen content, two-way ANOVA and the Tukey test were used. For the crosssectional area and connective tissue content, Kruskal-Wallis and Tukey tests were used. This study emphasizes the importance of anabolic pharmacological protection during immobilization to minimize skeletal muscle alterations resulting from disuse.

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Section: Discussionsupporting

confidence: 90%

The effect of a low dose of clenbuterol on rat soleus muscle submitted to joint immobilization

Cancelliero

Durigan

Silva

et al. 2008

Braz J Med Biol Res

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“…Space flight animals and unloaded animals show similar atrophic changes in muscles and bones (Edgerton & Roy, 1996). Moreover, perturbations in posture and gait reported in unloaded rats (Canu, Stevens, Ricart-Firinga, Picquet, & Falempin, 2001;Ohira et al, 2002;Walton, 1998) are very similar to those observed after space flight in rats (Fox, Corcoran, Daunton, & Morey-Holton, 1994) and humans (Kozlovskaya et al, 1981;Layne et al, 1997). However, the behavioral motor activity has been poorly investigated in animal models of microgravity.…”

mentioning

confidence: 83%

Effect of hindlimb unloading on motor activity in adult rats: Impact of prenatal stress.

Canu¹,

Darnaudéry²,

Falempin³

et al. 2007

Behavioral Neuroscience

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Environmental changes that occur in daily life or, in particular, in situations like actual or simulated microgravity require neuronal adaptation of sensory and motor functions. Such conditions can exert long-lasting disturbances on an individual's adaptive ability. Additionally, prenatal stress also leads to behavioral and physiological abnormalities in adulthood. Therefore, the aims of the present study were (a) to evaluate in adult rats the behavioral motor adaptation that follows 14 days of exposure to simulated microgravity (hindlimb unloading) and (b) to determine whether restraint prenatal stress influences this motor adaptation. For this purpose, the authors assessed rats' motor reactivity to novelty, their skilled walking on a ladder, and their swimming performance. Results showed that unloading severely impaired motor activity and skilled walking. By contrast, it had no effect on swimming performance. Moreover, results demonstrated for the first time that restraint prenatal stress exacerbates the effects of unloading. These results are consistent with the role of a steady prenatal environment in allowing an adequate development and maturation of sensorimotor systems to generate adapted responses to environmental challenges during adulthood.

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“…When comparing the effects of ␤-agonists on skeletal muscle size and strength in different animal models, it is also important to consider the mode of ␤-agonist administration, i.e., whether administered orally via the drinking water (70,181,337,351,376,423,482), via the feed (76), via a slow-release pellet (85), oral gavage (57), mini-osmotic pump (74), or via intraperitoneal or subcutaneous injection (21,117,208,209,367,411). While administration of ␤-agonists via the food or drinking water is convenient, there is uncertainty as to whether every treated animal will receive an identical dose.…”

Section: Growth-promoting Effects Of ␤-Agonistsmentioning

confidence: 99%

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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Effect of the β2-agonist clenbuterol on the locomotor activity of rat submitted to a 14-day period of hypodynamia–hypokinesia

Cited by 15 publications

References 40 publications

The effect of a low dose of clenbuterol on rat soleus muscle submitted to joint immobilization

The effect of a low dose of clenbuterol on rat soleus muscle submitted to joint immobilization

Effect of hindlimb unloading on motor activity in adult rats: Impact of prenatal stress.

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

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