Effects of low- and high-intensity single-leg resistance exercise on the mitogen-activated protein kinase ERK1/2 family signal transduction response in skeletal muscle of untrained males.

Acute resistance exercise signals responses in the body to promote adaptations to the exercise stimulus. One key response during and following exercise is the role of signal transduction in the skeletal muscle (MAPK family) and its downstream effects on muscular adaptation. Therefore, the purpose of this study was to determine the differential response of a prominent signal transduction pathway following a high-(HI) and a low-intensity (LI) bout of acute resistance exercise. Participants completed a single-legged bout of HI (8-10 reps at 85% of 1-RM) and LI (18-20 reps at 65% of 1-RM) resistance exercise designed to reach muscular fatigue in a randomized, crossover design. Venous blood and muscle biopsies were taken at PRE, 30PST, 2HRPST, and 6HRPST for the two resistance exercise sessions (RES), with an additional blood draw occurring at POST time point. Serum analyses included cortisol, insulin, GH, IGF-1, and IGFBP-3. Muscle analyses included phosphorylated IGF-1R, MEK1, ERK1/2, and activated Elk-1. Statistical analyses utilized a 2X4 MANOVA for muscle and a 2X5 MANOVA for serum variables on delta responses (p>0.05). RES resulted significant increases in cortisol (p<0.001), GH (p<0.001), insulin (p<0.01), and IGFBP-3 (p<0.001) in serum, with the peak elevations occurring by 30MPST, with no significant differences observed between exercise intensities. RES resulted in significant increases in pIGF-1R (p<0.05), pMEK1 (p<0.001), pERK1/2 (p<0.001), and Elk-1(p<0.001) from baseline levels in muscle, with the peak activation by the 2HRPST time point. The LI RES resulted in a significant difference in pIGF-1R (p<0.05) and Elk-1 (p<0.05) activation. The results of this study indicate that acute RES of both HI and LI results in similar responses in the serum markers cortisol, insulin, GH, and IGFBP-3. The RES also up-regulated various levels of the ERK1/2 signal transduction pathway in skeletal muscle, with some beneficial responses observed in the LI group. Thus, these findings suggest that exercise intensity is not as important in up-regulating these anabolic and signaling mechanisms as once thought and that exercising to muscular fatigue may be a more important aspect of an acute exercise bout. Additionally, the effect of higher exercise volume may also have a positive effect on these responses.