Impact of adrenaline and metabolic stress on exercise-induced intracellular signaling and PGC-1α mRNA response in human skeletal muscle

This study tested the hypothesis that elevated plasma adrenaline or metabolic stress enhances exercise‐induced PGC‐1α mRNA and intracellular signaling in human muscle. Trained (VO (2)‐max: 53.8 ± 1.8 mL min(−1) kg(−1)) male subjects completed four different exercise protocols (work load of the legs was matched): C – cycling at 171 ± 6 W for 60 min (control); A – cycling at 171 ± 6 W for 60 min, with addition of intermittent arm exercise (98 ± 4 W). DS – cycling at 171 ± 6 W interspersed by 30 sec sprints (513 ± 19 W) every 10 min (distributed sprints); and CS – cycling at 171 ± 6 W for 40 min followed by 20 min of six 30 sec sprints (clustered sprints). Sprints were followed by 3:24 min:sec at 111 ± 4 W. A biopsy was obtained from m. vastus lateralis at rest and immediately, and 2 and 5 h after exercise. Muscle PGC‐1α mRNA content was elevated (P < 0.05) three‐ to sixfold 2 h after exercise relative to rest in C, A, and DS, with no differences between protocols. AMPK and p38 phosphorylation was higher (P < 0.05) immediately after exercise than at rest in all protocols, and 1.3‐ to 2‐fold higher (P < 0.05) in CS than in the other protocols. CREB phosphorylation was higher (P < 0.05) 2 and 5 h after exercise than at rest in all protocols, and higher (P < 0.05) in DS than CS 2 h after exercise. This suggests that neither plasma adrenaline nor muscle metabolic stress determines the magnitude of PGC‐1α mRNA response in human muscle. Furthermore, higher exercise‐induced changes in AMPK, p38, and CREB phosphorylation are not associated with differences in the PGC‐1α mRNA response