Glutamine supplementation accelerates functional recovery of EDL muscles after injury by modulating the expression of S100 calcium-binding proteins.

The aim of the current study was to investigate the effect of glutamine supplementation on the expression of HSP70 and the calcium-binding proteins from the S100 superfamily in the recovering extensor digitorum longus (EDL) muscle after injury. Two-month-old Wistar rats were subjected to cryolesion of the EDL muscle and then randomly divided into two groups (with or without glutamine supplementation). Starting immediately after the injury, the supplemented group received daily doses of glutamine (1 g/kg/day, via gavage) for 3 and 10 days orally. Then, muscles were subjected to histological, molecular, and functional analysis. Glutamine supplementation induced an increase in myofiber size of regenerating EDL muscles and prevented the decline in maximum tetanic strength of these muscles evaluated 10 days after injury. An accelerated upregulation of myogenin mRNA levels was detected in glutamine-supplemented injured muscles on day 3 post-cryolesion. The HSP70 expression increased only in the injured group supplemented with glutamine for 3 days. The increase in mRNA levels of NF-κB, the pro-inflammatory cytokines IL-1ß and TNF-α, and the calcium-binding proteins S100A8 and S100A9 on day 3 post-cryolesion in EDL muscles was attenuated by glutamine supplementation. In contrast, the decrease in S100A1 mRNA levels in the 3-day-injured EDL muscles was minimized by glutamine supplementation. Overall, our results suggest that glutamine supplementation accelerates the recovery of myofiber size and contractile function after injury by modulating the expression of myogenin, HSP70, NF-κB, pro-inflammatory cytokines, and S100 calcium-binding proteins.

Glutamine supplementation improves contractile function of regenerating soleus muscles from rats.

This study evaluated the effects of glutamine supplementation immediately after freezing injury on morphological and contractile function of regenerating soleus muscles from rats. Young male Wistar rats were subjected to cryolesion of soleus muscles, and immediately after received a daily supplementation of glutamine (1 g/kg/day). The muscles were evaluated on post-injury days 3 and 10. Glutamine-supplemented injured muscles had a lower number of CD11b positive immune cells and higher mRNA levels of IL-4 compared to those from the cryolesioned muscles analyzed on post-injury day 3. The mRNA and protein expression levels of the myogenic transcription factor MyoD were also higher in glutamine-supplemented injured muscles than in injured muscles examined on post-cryolesion day 3. In addition, glutamine-supplemented injured muscles had a higher size of their regenerating myofibers, attenuated decline in maximum tetanic strength and improved fatigue resistance compared to those from injured muscles evaluated on post-cryolesion day 10. No effect was observed in uninjured muscles supplemented with glutamine. Our results suggest that glutamine supplementation improves the resolution of inflammation, as well as the size and functional recovery of regenerating myofibers from soleus muscles by accelerating the up-regulation of IL-4 and MyoD expression. Future non-pharmacological rehabilitation studies are warranted to investigate the effect of glutamine supplementation on the outcome of injured skeletal muscles.