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Endogenous erythropoietin signaling facilitates skeletal muscle repair and recovery following pharmacologically induced damage.

ABSTRACT: Erythropoietin acts by binding to its cell surface receptor on erythroid progenitor cells to stimulate erythrocyte production. Erythropoietin receptor expression in nonhematopoietic tissue, including skeletal muscle progenitor cells, raises the possibility of a role for erythropoietin beyond erythropoiesis. Mice with erythropoietin receptor restricted to hematopoietic tissue were used to assess contributions of endogenous erythropoietin to promote skeletal myoblast proliferation and survival and wound healing in a mouse model of cardiotoxin induced muscle injury. Compared with wild-type controls, these mice had fewer skeletal muscle Pax-7(+) satellite cells and myoblasts that do not proliferate in culture, were more susceptible to skeletal muscle injury and reduced maximum load tolerated by isolated muscle. In contrast, mice with chronic elevated circulating erythropoietin had more Pax-7(+) satellite cells and myoblasts with increased proliferation and survival in culture, decreased muscle injury, and accelerated recovery of maximum load tolerated by isolated muscle. Skeletal muscle myoblasts also produced endogenous erythropoietin that increased at low O(2). Erythropoietin promoted proliferation, survival, and wound recovery in myoblasts via the phosphoinositide 3-kinase/AKT pathway. Therefore, endogenous and exogenous erythropoietin contribute to increasing satellite cell number following muscle injury, improve myoblast proliferation and survival, and promote repair and regeneration in this mouse induced muscle injury model independent of its effect on erythrocyte production.

SUBMITTER: Jia Y

PROVIDER: S-EPMC3382092 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ContextThe early events regulating the remodeling program following skeletal muscle damage are poorly understood.ObjectiveThe objective of this study was to determine the association between myofibrillar protein synthesis (myoPS) and nuclear factor-kappa B (NF-κB) signaling by nutritionally accelerating the recovery of muscle function following damage.Design, setting, participants, and interventionsHealthy males and females consumed daily postexercise and prebed protein-polyphenol (PP; n = 9; 4 females) or isocaloric maltodextrin placebo (PLA; n = 9; 3 females) drinks (parallel design) 6 days before and 3 days after 300 unilateral eccentric contractions of the quadriceps during complete dietary control.Main outcome measuresMuscle function was assessed daily, and skeletal muscle biopsies were taken after 24, 27, and 36 hours for measurements of myoPS rates using deuterated water, and gene ontology and NF-κB signaling analysis using a quantitative reverse transcription PCR (RT-qPCR) gene array.ResultsEccentric contractions impaired muscle function for 48 hours in PLA intervention, but just for 24 hours in PP intervention (P = 0.047). Eccentric quadricep contractions increased myoPS compared with the control leg during postexercise (24-27 hours; 0.14 ± 0.01 vs 0.11 ± 0.01%·h-1, respectively; P = 0.075) and overnight periods (27-36 hours; 0.10 ± 0.01 vs 0.07 ± 0.01%·h-1, respectively; P = 0.020), but was not further increased by PP drinks (P > 0.05). Protein-polyphenol drinks decreased postexercise and overnight muscle IL1R1 (PLA = 2.8 ± 0.4, PP = 1.1 ± 0.4 and PLA = 1.9 ± 0.4, PP = 0.3 ± 0.4 log2 fold-change, respectively) and IL1RL1 (PLA = 4.9 ± 0.7, PP = 1.6 ± 0.8 and PLA = 3.7 ± 0.6, PP = 0.7 ± 0.7 log2 fold-change, respectively) messenger RNA expression (P < 0.05) and downstream NF-κB signaling compared with PLA.ConclusionProtein-polyphenol drink ingestion likely accelerates recovery of muscle function by attenuating inflammatory NF-κB transcriptional signaling, possibly to reduce aberrant tissue degradation rather than increase myoPS rates.

Project description:Plyometric exercise (PE) is an effective training method to increase muscle mass and strength. However, excessive or inappropriate conditions might cause exercise-induced muscle damage (EIMD). Resveratrol (RES) is a natural polyphenol plant antitoxin, which improves exercise performance, and exhibits anti-oxidation, anti-inflammatory, and anti-cancer effects. Therefore, this study investigated the effect of RES supplementation on the recovery of muscle damage, inflammation, soreness, muscle power, and anaerobic performance following plyometric-exercise-induced muscle damage (PEIMD). The present study was a double-blind, placebo-controlled research trial. Thirty-six young, untrained males were enrolled into the placebo (n = 12), RES-500 (500 mg RES/day, n = 12), or RES-1000 (1000 mg RES/day, n = 12) group by a jumping height-counterbalanced grouping design. At baseline, to pre-PEIMD, supplements were pre-loaded 7 days before they conducted PEIMD, and the exercise performance, delayed-onset muscle soreness (DOMS) and muscle damage biomarkers were measured over the experimental period at baseline, pre-PEIMD, and post-PEIMD at 2, 24, 48, and 72 h. As a result, we found that, at 72 h post-EIMD, the force peak (FP) and rate of force development (RFD) of the counter movement jump (CMJ) in RES groups showed no significant difference compared to that at baseline but was significantly greater than the placebo group. In the Wingate anaerobic test (WAnT), supplementation in the RES group had a better recovery effect on the relative peak power (RPP), relative mean power (RMP) and fatigue index (FI) (p < 0.05), especially in the high-dose group. For the detection of muscle pain after PEIMD, the RES supplement group was significantly better than the placebo group (p < 0.05). In addition, for muscle damage indexes, such as creatine kinase (CK) and lactate dehydrogenase (LDH), after PEIMD, supplementation with RES could significantly reduce and accelerate recovery (p < 0.05). In addition, the blood biochemical indicators of blood count, liver function, and kidney function showed that RES will not cause adverse risks to the human body. Our results suggest that replenishing RES in advance could effectively reduce muscle pain, increase exercise performance, and decrease muscle damage indicators caused by PEIMD, and the recovery was faster. Therefore, plyometric exercises combined with suitable RES supplementation could be an effective candidate for controlling muscle damage, improving physical adaption, and recovering anaerobic capacity.

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Endogenous erythropoietin signaling facilitates skeletal muscle repair and recovery following pharmacologically induced damage.

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