In addition to the anabolic hormones, glucocorticoids, mainly cortisol have a profound influence on human skeletal muscle (165). Further studies have shown MGF acts independently and is expressed earlier than other IGF-I isoforms in response to resistance exercise training, and therefore may have greater anabolic potency (159). Furthermore, IGF-I and MGF mRNA have increased 2 h post exercise (but not 6 h) after a single bout of moderate (65% of 1RM; 18–20 repetitions) and moderately-high (85% of 1RM; 8–10 repetitions) intensity resistance exercise training (158). AR protein content explains a large amount of variance in muscle hypertrophy seen during RT (84), and its role may be potentiated with interaction of other hormones such as growth hormone and IGF-I. Spillane et al. (45) reported significant up-regulation of VL muscle β-catenin following upper and lower body RT at 3 and 24 h PE and increased AR-DNA binding capacity and suggested the increased binding capacity was linked to greater β-catenin pathway signaling. Wnt binds to frizzled/lipoprotein receptor protein 6 receptors and activates disheveled and inhibits glycogen synthase kinase-3 (GSK-3) reducing β-catenin dephosphorylation and increases its activity.
If daily carbohydrate intake is insufficient to fully replace the glycogen metabolized during hard labor or training, muscle glycogen concentration in active muscles will fall progressively over a period of days, a circumstance that is well established in the scientific literature.75–77 If postexercise carbohydrate supplementation is not maintained, GLUT4 transporters are removed from the membrane after 30–60 minutes.41 In short, the reduction in muscle glycogen stores that occurs during exercise is a major driving factor for subsequent glycogenesis.69 That binding sparks a cascade of intracellular responses that result in the movement of GLUT4 glucose transporters from the interior of the muscle cell into the sarcolemma, allowing for glucose to move into the cell.
However, increasing fat intake beyond moderate levels does not necessarily lead to higher muscle growth. Since training intensity is a key driver of hypertrophy, lower performance can slow muscle growth over time. The ideal carbohydrate intake for muscle gain depends on your body weight, activity level, and total calorie intake.
In turn, only a small subset of these exercise studies considered the issue and importance of GH assay choice employed and the large difference it can make in interpreting experimental data. The AR mRNA and protein up-regulation correlated to TT and FT concentrations in the blood (19, 79). Notable up-regulation of AR mRNA and protein is seen ~28 h PE (89) while is most pronounced 48 h PE (74, 75). Initially, AR protein content may not change or be down-regulated within the first 2 h PE in the fasted state (73). The most expected pattern of change is acute up-regulation of AR mRNA and protein content within 1–2 days of RT followed by a return to baseline unless another workout is performed.
There is also some evidence that creatine supplementation along with adequate calorie and protein intake can hasten muscle recovery after strenuous exercise. The reason could be related to the association of creatine supplementation and increased glycogen storage in muscle. NSAIDs (ibuprofen, naproxen) reduce pain but also impair the adaptive inflammatory response that drives muscle growth, tendon strengthening, and bone remodeling. Growth hormone and testosterone — released during sleep — drive the anabolic response. During rest, muscle protein synthesis peaks at hours post-exercise (requiring adequate protein and amino acids). Macronutrient distribution matters, but calories and protein intake are the primary drivers of muscle growth.