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Purpose : This study examined the effect of whey protein consumption following high-intensity interval swimming (HIIS) on muscle damage, inflammatory cytokines and performance in adolescent swimmers. Methods : Fifty-four swimmers (11-17 years-old) were stratified by age, sex and body mass to a whey protein (PRO), isoenergetic carbohydrate (CHO) or a water/placebo (H 2 O) group. Following baseline blood samples (06:00 h) and a standardised breakfast, participants performed a maximal 200 m swim, followed by HIIS. A total of two post-exercise boluses were consumed following HIIS and ~5 h post-baseline. Blood and 200 m performance measurements were repeated at 5 h, 8 h and 24 h from baseline. Muscle soreness was assessed at 24 h. Creatine kinase (CK), interleukin-6 (IL-6), interleukin-10 (IL-10) and tumor necrosis factor-alpha (TNF-α) were measured in plasma. Results : No difference in 200 m swim performance was observed between groups. CK activity was elevated at 5 h compared to baseline and 24 h and at 8 h compared to all other timepoints, with no differences between groups. Muscle soreness was lower in PRO compared to H 2 O ( p = 0.04). Anti-inflammatory IL-10 increased at 8 h in PRO, while it decreased in CHO and H 2 O. Conclusions : Post-exercise consumption of whey protein appears to have no additional benefit on recovery indices following HIIS compared to isoenergetic amounts of carbohydrate in adolescent swimmers. However, it may assist with the acute-inflammatory response.

Glycogen synthase kinase 3 (GSK3) slows myogenic differentiation and myoblast fusion partly by inhibiting the Wnt/β-catenin signaling pathway. Lithium, a common medication for bipolar disorder, inhibits GSK3 via Mg + competition and increased Ser21 (GSK3α) or Ser9 (GSK3β) phosphorylation, leading to enhanced myoblast fusion and myogenic differentiation. However, previous studies demonstrating the effect of lithium on GSK3 have used concentrations up to 10 mM, which greatly exceeds concentrations measured in the serum of patients being treated for bipolar disorder (0.5-1.2 mM). Here, we determined whether a low-therapeutic (0.5 mM) dose of lithium could promote myoblast fusion and myogenic differentiation in C2C12 cells. C2C12 myotubes differentiated for three days in media containing 0.5 mM lithium chloride (LiCl) had significantly higher GSK3β (ser9) and GSK3α (ser21) phosphorylation compared with control myotubes differentiated in the same media without LiCl (+2-2.5 fold, p < 0.05), a result associated with an increase in total β-catenin. To further demonstrate that 0.5 mM LiCl inhibited GSK3 activity, we also developed a novel GSK3-specific activity assay. Using this enzyme-linked spectrophotometric assay, we showed that 0.5 mM LiCl-treated myotubes had significantly reduced GSK3 activity (-86%, p < 0.001). Correspondingly, 0.5 mM LiCl treated myotubes had a higher myoblast fusion index compared with control ( p < 0.001) and significantly higher levels of markers of myogenesis (myogenin, +3-fold, p < 0.001) and myogenic differentiation (myosin heavy chain, +10-fold, p < 0.001). These results indicate that a low-therapeutic dose of LiCl is sufficient to promote myoblast fusion and myogenic differentiation in muscle cells, which has implications for the treatment of several myopathic conditions., Competing Interests: The authors declare no conflict of interest.

Non-small cell lung cancer (NSCLC) accounts for 85% of all lung cancer cases, and for the most cancer-related deaths. The survival pathway of Akt, its downstream effectors, the mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase (p70 S6K), and the Ras-extracellular signal-regulated kinase (Erk1/2) pathways are activated in cancer leading to cell survival and growth. Thus, approaches that inhibit these signaling molecules may prove useful in the fight against lung cancer. Exercise is associated with health benefits and a limited number of studies indicate that serum from physically active individuals inhibit mammary and prostate cancer cell growth. In this study, we examined the effects of post exercise serum on proliferation, survival, and signaling cascades of human NSCLC cells. Blood was collected from male subjects prior to, 5 min, 1 h, and 24 h after a single bout of high intensity interval exercise on a cycle ergometer. Exposure of NSCLC cells to post exercise serum resulted in the inhibition of cell proliferation and survival, as well as significant reduction of phosphorylated/activated Akt, mTOR, p70 S6K, and Erk1/2 levels compared to cells treated with serum taken pre-exercise. Our data suggest that post exercise serum has anti-cancer properties in lung cancer and deserves further systematic investigation in animal models.