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.
Highlights
One of the most pronounced effect of endurance exercise is an increase in skeletal muscle mitochondrial content as well as enzymes involved in energy supply (Saleem et al 2014)
For the same intensity and duration of cycling, and work done, the intermittent exercise-induced repeated metabolic fluctuations and higher phosphorylation of AMPK, calmodulin-dependent protein kinase II (CaMKII), and p38-mitogen-activated protein kinase (MAPK) compared with the continuous exercise
These kinases are three important signaling cascades linked to PGC-1a and the regulation of mitochondrial biogenesis in skeletal muscle
Summary
One of the most pronounced effect of endurance exercise is an increase in skeletal muscle mitochondrial content as well as enzymes involved in energy supply (Saleem et al 2014). The activation of AMP-activated protein kinase (AMPK), p38-mitogen-activated protein kinase (MAPK) and calcium/calmodulin-dependent protein kinase (CaMKII) signaling pathways are well-characterized upstream modulators of PGC-1a expression in skeletal muscle (Coffey and Hawley 2007; Jager et al 2007).
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