In the present study, we also showed that after 28 days of heavy resistance training and supplementation NO underwent increases in myofibrillar protein of 70.39% that were significantly greater than the 26.34% increase in PL (p < 0.001), and that the increases for NO were significantly different than PL (p = 0.014). This is a similar pattern of response from longer-term studies where creatine supplementation, in conjunction with 12 wk of resistance training, resulted in a 57.92% increase in myofibrillar protein content when
compared to a maltodextrose placebo group, which only increased 11.62% [24]. In addition, 10 wk of heavy resistance training combined with a protein and amino acid supplement resulted in a 25.03% increase in myofibrillar protein compared to 10.54% for a carbohydrate placebo [34]. We have Nutlin-3a research buy demonstrated 28 days of heavy resistance training to increase serum IGF-1 by 9.34% Wortmannin and 8.58%, respectively for NO and PL; however, AZD0156 order there
was no difference between groups. Treating C2C12 myoblasts with creatine has been shown to increase the expression of the IGF-1 peptide [40]. A positive relationship has been reported between IGF-1 peptide and total DNA content in muscle during resistance exercise due to satellite cell proliferation stimulated by the locally produced IGF-1 [7]. However, while the IGF-I peptide expressed in skeletal muscleincreases muscular protein synthesis and stimulates differentiation of proliferating satellite cells [14, 41], it is unclear whether increases in hepatically-derived circulating IGF-1 has any direct effect on muscle hypertrophy. We have previously shown that 10 wk of heavy resistance training combined with a daily supplement containing whey/casein protein and free amino acids increased circulating IGF-1 levels, while also increasing muscle strength and mass [34]. Additionally, 16 wk of resistance training has been shown to increase circulating IGF-1 levels [42]. However, 12 wk of heavy resistance training has been shown to increase muscle strength and mass without any corresponding
increases in circulating IGF-1 [43]. Increases in muscle hypertrophy independent of increases in circulating IGF-1 can possibly be explained by a recent study using a liver IGF-1 deficient mouse model, which selleck kinase inhibitor involves a reduction in serum IGF-1 of approximately 80% [44]. After 16 wk of resistance training, the IGF-1-deficient mice and control mice exhibited equivalent gains in muscle strength, suggesting that performance and recovery in response to resistance training is normal even when there is a severe deficiency in circulating IGF-1. HGF is a growth factor bound to an extracellular matrix in skeletal muscle [45] that is capable of activating quiescent satellite cells [46]. Serum HGF levels have been shown to increase 24 hr following a single bout of eccentric exercise [47].