Exercise-induced metabolic fluctuations influence AMPK, p38-MAPK and CaMKII phosphorylation in human skeletal muscle

Abstract

During transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of this study was to determine whether metabolic fluctuations per se affect the signaling cascades known to regulate peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). On two separate occasions, nine men performed a continuous (30-min) and an intermittent exercise (30 × 1-min intervals separated by 1-min of recovery) at 70% of . Skeletal muscle biopsies from the vastus lateralis were taken at rest and at +0 h and +3 h after each exercise. Metabolic fluctuations that correspond to exercise-induced variation in metabolic rates were determined by analysis of VO2 responses. During intermittent exercise metabolic fluctuations were 2.8-fold higher despite identical total work done to continuous exercise (317 ± 41 vs. 312 ± 56 kJ after intermittent and continuous exercise, respectively). Increased phosphorylation of AMP-activated protein kinase (AMPK) (˜2.9-fold, P < 0.01), calcium/calmodulin-dependent protein kinase II (CaMKII) (˜2.7-fold, P < 0.01) and p38-mitogen-activated protein kinase (MAPK) (˜4.2-fold, P < 0.01) occurred immediately in both exercises and to a greater extent after the intermittent exercise (condition x time interaction, P < 0.05). A single bout of intermittent exercise induces a greater activation of these signaling pathways regulating PGC-1α when compared to a single bout of continuous exercise of matched work and intensity. Chronic adaptations to exercise on mitochondria biogenesis are yet to be investigated.

The impact of high‐intensity interval training on the cTnT response to acute exercise in sedentary obese young women

“…This phenomenon also has been noted in our prior and another study . Of note, it has been suggested that the use of intermittent effort instead of continuous could have independent physiological effects such as metabolic fluctuations, which per se induces a greater activation of mitochondrial biogenesis . Whether this is related to a gradual decrease in exercise HR during the progression of interval training or an alternative explanation of the gradual blunting of the cTnT response to acute interval exercise in the present study is unclear but worth exploring in further research.…”

Exercise, oxidants, and antioxidants change the shape of the bell-shaped hormesis curve

“…The contribution of signaling pathways to mitochondrial biogenesis, as an example, which could be driven by Ca ++ , CaMK, ROS, AMPK, PKD1, p38a [63], would be the same at different exercise intensities? In all likelihood, this is not the case [14], [34]. Hence, the same amount of antioxidant would affect the exercise-induced adaptation in a different fashion.…”

Metabolic stress‐dependent regulation of the mitochondrial biogenic molecular response to high‐intensity exercise in human skeletal muscle

“…The intermittent pattern of interval exercise per se may also play a key role in evoking the signalling cascade towards mitochondrial biogenesis (Combes et al . 2015).…”