Enhancement of hybrid-fiber types in rat soleus muscle after clenbuterol administration during hindlimb unloading

Abstract

Our objective was to determine the effects of a clenbuterol (CB) treatment orally administered (2 mg per kg) to rats submitted to 14 days of hindlimb unloading (HU). The morphological and the contractile properties as well as the myosin heavy chain isoforms contained in each fiber type were determined in whole soleus muscles. As classically described after HU, a decrease in muscle wet weight and in body mass associated with a loss of muscular force, an evolution of the contractile parameters towards those of a fast muscle type, and the emergence of fast myosin heavy chain isoforms were observed. The CB treatment in the HU rats helped reduce the decrease in 1) muscle and body weights, 2) force and 3) the proportion of slow fibers, without preventing the emergence of fast myosin isoforms. Clenbuterol induced a complex remodelling of the muscle typing promoting the combination of both slow and fast myosin isoforms within one fiber. To conclude, our data demonstrate that CB administration partially counteracts the effects produced by HU, and they allow us to anticipate advances in the treatment of muscular atrophy.

Effects of Co-Administration of Clenbuterol and Testosterone Propionate on Skeletal Muscle in Paraplegic Mice

“…In contrast, hybrid fibers were increased in proportion, suggesting a phase shift from type I towards type I þ II fibers. This is supported by previous studies, showing that clenbuterol can promote a slow-to-fast fiber transition in the soleus of normal or hindlimb-unloaded rats (Criswell et al, 1996;Oishi et al, 2002;Picquet et al, 2004). On the other hand in EDL, where type I fibers do not exist in rodents, a different but comparable conversion was found: fewer hybrid fibers and more type II fibers in treated and control Tx animals.…”

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

“…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.…”

Icaritin requires Phosphatidylinositol 3 kinase (PI3K)/Akt signaling to counteract skeletal muscle atrophy following mechanical unloading

“…However, low compliance of patients limits their use of physical therapies. Recently, pharmacological agents, such as insulin-like growth factor-I (IGF-I) 12 , anabolic androgenic steroids 13 , myostatin inhibitors 14 , and β2-adrenergic agonists 15 , have been also tested to counteract muscle atrophy. But, it should be pointed out that potential risks of drug resistance, cardiovascular and prostate cancer and cardiac hypertrophy/dysfunction 16 17 , are the bottleneck for their clinical translation.…”