Introduction In recent years, a mounting amount of evidence have suggested that contracting muscle can act as a cytokine producingorgan that may influence metabolism (Pedersen 2010). Myostatin (MSTN) relationship with body fat amount, training status and nutritionhas been widely investigated but with conflicting results. Although MSTN inhibits the Akt/mTor pathway some studies have shown alsoan counterintuitive positive correlation between MSTN and muscle mass (myostatin paradox). Moreover MSTN has been shown to reduceIGF-1 stimulated AKT phosphorylation in a dose-dependent manner. We investigated the influence of two months of resistance training(RT) and high protein diet on plasma myostatin, IL1, IL6, TNF-• and IGF-1. Methods Eighteen healthy volunteers participated in a upperlimbs progressive resistance training. Subjects were divided in two groups: an high protein group (HP; 1.8 g/Kg bw/day, n. 9) and normalprotein group (NP 0.9 g/Kg bw-1/day, n. 9). MSTN, IGF-1, IL1, IL6 and TNF-• were analyzed before and after the first training session andbefore and after the last training session (after 8 weeks). Lean body mass and muscle mass were analyzed through skinfolds methods,arm muscle area with MNR, strength with 1 RM test and an isometric pullgrip. ANOVA statistical analysis and linear regression wereperformed. Results MSTN showed an unexpected significant increase (p<0.001) after the last training in the HP group ( ng/ml) comparedto NP group (ng/ml) and to the samples taken after the first training (ng/ml). There were no significant differences (time x treatment) in IGF-1, IL1, IL6 and TNF-•. Interestingly IGF-1 showed a positive correlation with MSTN in HP after the last training (r2=0.6456; p=0.0295). No correlation were found with other blood parameters nor with muscle mass and muscle strength changes. Moreover no significant differenceswere found between treatment group in strength performance and muscle mass. Conclusions Taken together this findings indicatea “paradoxical” response of plasma myostatin to high protein diet after 8 weeks of RT. It is noteworthy that IGF-1 which activity isdown regulated by MSNT is increased in HP group after the last training and it correlates significantly with MSNT increase. This doubleincrease of opposite mediators could explain the substantial overlapping of muscle mass increases in the two groups. We can argue thathigh protein diet influence metabolic regulation of IGF-1 and MSNT upstream the same pathway. Our findings are not in agreement withthose of Hulmi et al (2009) that found a decrease in MSNT with protein ingestion whilst instead are in line with those of Dalbo et al (2011)that found a paradoxical MSNT response to RT in older individuals compared to younger individuals. Taken together this data show acomplex and not yet well understood MSNT release mechanism. More studies are needed to explain this paradoxical response to nutritionand RT exploring also muscle signalling molecules as mTor and Akt.
|Numero di pagine||2|
|Stato di pubblicazione||Published - 2012|