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What is Clenbuterol?

clenbuterolgraph The change in muscle tension as a result of a 5-minute fatigue protocol, showing the differences in maximal force and 50% initial force (black dotted lines), as well as the resistance to fatigue (Tlim) between rat extensor digitorum longus (EDL) muscle treated with clenbuterol and that of controls. From Sirvent et al., Effects of chronic administration of clenbuterol on contractile properties and calcium homeostasis in rat extensor digitorum longus muscle. PloS one. 2014;9(6):e100281.


What is Clenbuterol? 

Clenbuterol is an adrenergic beta-2 receptor agonist associated with increases in skeletal muscle growth1. It is associated with the increase of fast-twitch glycolytic muscle fibers as opposed to slow-twitch oxidative fibers2. This results in rapid changes (or 'remodeling') in the structure of skeletal muscle. Recent animal studies have shown that chronic subcutaneous clenbuterol administration may not increase relevant characteristics of muscular activity such as specific maximal tetanic force and contractile efficiency3. Another study demonstrated that chronic administration did not change relative force in the muscles of male Wistar rats2. However, it was associated with an increase in absolute force2.

Clenbuterol increases calpain (a serine protease) activity2. Chronic clenbuterol intake was also found to be associated with an imbalance in calcium (Ca2+) signaling and concentration in muscle fibers2. A study using rat soleus muscle fibers showed inhibitory effects on intracellular Ca2+ and action potential4. The latter was not reversed in the presence of a beta-2 antagonist, indicating clenbuterol may also have activity at alternative receptors4. Therefore, clenbuterol may change the kinetics of muscle contraction via indirect pathways based on the disruption of cellular Ca2+ homeostasis3.

Clenbuterol may be associated with the increased risk of muscle fatigue2. The switch to fast-twitch fiber activity results in varying levels of hypertrophy (rapid growth) in different muscle types5. This may be due to the responses of different subtypes of calpain to this drug5. Some researchers argue that clenbuterol administration results in myotoxicity at high doses (approximately 1mg/kg per day)6. Clenbuterol is also associated with damage to cardiac muscle4.

Other Functions and Applications of Clenbuterol 

Adrenergic beta-receptors are also present in the central nervous system. Their specific roles in the brain may be elicited through the experimental application of clenbuterol. Intraperitoneal clenbuterol (at three different doses) reduced visuospatial learning discrepancies in a rat model of impaired cortical function (elicited by significantly reduced beta-receptor expression in the neocortex)7.

The injection of clenbuterol into a brain region (the ventral bed nucleus of the stria terminalis) implicated in the stress-related use of cocaine reinstated this behavior in rats8. This indicates that beta-receptors may regulate the activation of the ventral tegmental area (another brain region) associated with cocaine-seeking8. The infusion of clenbuterol into the basolateral complex of the amygdala enhanced 'emotional' and 'aversive' memory in rats9.

Some studies have indicated that beta-2 receptors are associated with the breakdown of glycogen in astrocytes, which supplies energy to neurons in the absence of dietary glucose10. A study using a mouse model of this found that clenbuterol administration did not influence this, but that beta-2 activation was associated with the protection of axons10.

Clenbuterol may also have a therapeutic role in developmental disorders. The administration of clenbuterol resulted in the reduction of respiratory and motor co-ordination deficits in a mouse model of Rett syndrome (knockout of the Mecp2 gene)11. It was also associated with improvements in the survival and social recognition abilities of young male mice with this mutation11. Clenbuterol also improved cognition and anxiety in older female heterozygous mice11.


1. Emery PW, Rothwell NJ, Stock MJ, Winter PD. Chronic effects of beta 2-adrenergic agonists on body composition and protein synthesis in the rat. Bioscience reports. 1984;4(1):83-91.

2. Sirvent P, Douillard A, Galbes O, et al. Effects of chronic administration of clenbuterol on contractile properties and calcium homeostasis in rat extensor digitorum longus muscle. PloS one. 2014;9(6):e100281.

3. Py G, Ramonatxo C, Sirvent P, et al. Chronic clenbuterol treatment compromises force production without directly altering skeletal muscle contractile machinery. The Journal of physiology. 2015.

4. Head SI, Ha TN. Acute inhibitory effects of clenbuterol on force, Ca(2)(+) transients and action potentials in rat soleus may not involve the beta(2)-adrenoceptor pathway. Clinical and experimental pharmacology & physiology. 2011;38(9):638-646.

5. Douillard A, Galbes O, Rossano B, et al. Time course in calpain activity and autolysis in slow and fast skeletal muscle during clenbuterol treatment. Canadian journal of physiology and pharmacology. 2011;89(2):117-125.

6. Burniston JG, McLean L, Beynon RJ, Goldspink DF. Anabolic effects of a non-myotoxic dose of the beta2-adrenergic receptor agonist clenbuterol on rat plantaris muscle. Muscle & nerve. 2007;35(2):217-223.

7. Saez-Briones P, Soto-Moyano R, Burgos H, et al. beta-Adrenoceptor stimulation restores frontal cortex plasticity and improves visuospatial performance in hidden-prenatally-malnourished young-adult rats. Neurobiology of learning and memory. 2014;119c:1-9.

8. Vranjkovic O, Gasser PJ, Gerndt CH, Baker DA, Mantsch JR. Stress-induced cocaine seeking requires a beta-2 adrenergic receptor-regulated pathway from the ventral bed nucleus of the stria terminalis that regulates CRF actions in the ventral tegmental area. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2014;34(37):12504-12514.

9. McReynolds JR, Anderson KM, Donowho KM, McIntyre CK. Noradrenergic actions in the basolateral complex of the amygdala modulate Arc expression in hippocampal synapses and consolidation of aversive and non-aversive memory. Neurobiology of learning and memory. 2014;115:49-57.

10. Laureys G, Valentino M, Demol F, et al. beta(2)-adrenergic receptors protect axons during energetic stress but do not influence basal glio-axonal lactate shuttling in mouse white matter. Neuroscience. 2014;277:367-374.

11. Mellios N, Woodson J, Garcia RI, et al. beta2-Adrenergic receptor agonist ameliorates phenotypes and corrects microRNA-mediated IGF1 deficits in a mouse model of Rett syndrome. Proceedings of the National Academy of Sciences of the United States of America. 2014;111(27):9947-9952.

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