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Abstract
The effect of a short-term creatine supplementation on hindlimb suspension (HS)-induced muscle atrophy was investigated. Creatine monohydrate (5 g/kg b.w. per day) or placebo, divided in 2 daily doses, was given by oral gavage for 5 days. Rats were maintained in HS with dietary supplementation concomitantly for 5 days. Body weight, soleus and EDL muscle masses, and cross-sectional areas (CSA) of the muscle fibers were measured. Signaling pathways associated with skeletal muscle mass regulation (FST, MSTN, FAK, IGF-1, MGF, Akt, mTOR, atrogin-1, and MuRF1 expressions, and Akt, S6, GSK3B, and 4EBP1 proteins) were evaluated in the muscles. Soleus muscle exhibited more atrophy than the EDL muscle due to HS. Creatine supplementation attenuated the decrease of wet weight and increased p-4EBP1 protein in the EDL muscle of HS rats. Also, creatine increased mTOR and atrogin-1 expressions in the same muscle and condition. In the absence of HS, creatine supplementation increased FAK and decreased MGF expressions in the EDL muscle. Creatine attenuated the increase in FST expression due to HS in the soleus muscle. MuRF1 expression increased in the soleus muscle due to creatine supplementation in HS animals whereas atrogin-1 expression increased still further in this group compared with untreated HS rats. In conclusion, short-term creatine supplementation changed protein metabolism signaling in soleus and EDL muscles. However, creatine supplementation only slightly attenuated the mass loss of both muscles and did not prevent the CSA reduction and muscle strength decrease induced by HS for 5 days.
Highlights
Skeletal muscle disuse atrophy is characterized by a decrease in activity of protein synthesis and/or an increase in protein degradation pathways leading to a reduction of muscle mass and strength and in the crosssectional area (CSA) of muscle fibers [1,2]
In the extensor digitorum longus (EDL) muscle, the wet weight was significantly decreased by 16% (Po0.05) by hindlimb suspension (HS), while the dry weight was decreased by 12% (Po0.05)
Creatine supplementation had an effect on preventing muscle mass loss that was more notable in the EDL muscle, in the rats submitted to HS (Table 1)
Summary
Skeletal muscle disuse atrophy is characterized by a decrease in activity of protein synthesis and/or an increase in protein degradation pathways leading to a reduction of muscle mass and strength and in the crosssectional area (CSA) of muscle fibers [1,2]. Several strategies have been tested to attenuate muscle wasting such as electrical stimulation [3], physical exercise [4], and dietary supplementation; e.g., fish oil, leucine, isoleucine, valine, creatine, and L-carnitine [2,5,6]. Creatine may act as an attenuating agent of skeletal muscle atrophy [6] and leads to an increase of physical exercise capacity [7]. A consensus about the beneficial effects of creatine dietary supplementation in skeletal muscle atrophy is still lacking. Creatine supplementation has been reported to act on skeletal muscle atrophy through an increase in strength, resistance to fatigue, intramuscular phosphocreatine content, and protein synthesis markers. Creatine supplementation decreases cytoplasmic Ca2+ levels, production of reactive oxygen species, contents of proinflammatory cytokines, satellite cell activation, and muscle cell apoptosis [11,12,13]
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