Introduction: 

It is well known that mitochondrial biogenesis in human skeletal muscle is affected by moderate endurance training. The peroxisome proliferator-activated receptor-g coactivator (PGC)-1a is one of the most important regulators of mitochondrial biogenesis. Previous studies determined the changes of the mitochondrial biogenesis primarily in response to moderate endurance exercise. The aim of this study was to analyse the molecular signalling of mitochondrial biogenesis in response to prolonged, intense endurance exercise in junior cyclists during a typical competitive-season (CS).

Methods: 

Before and after CS 10 competitive cyclists (17.3 ± 0.5yr) underwent an incremental bicycle exercise test to determine the VO_2peak. Muscle biopsies were obtained from the vastus lateralis muscle. The molecular factors PGC-1a, mitochondrial transcription factor A (Tfam), AMP-activated protein kinase (AMPK), phosphorylated AMPK (pAMPK), nuclear respiratory factor (NRF)-1 and NRF-2 were analysed immunohistochemically.

Results: 

In the CS the VO_2peak increased by 7.8% (P < 0.05). Protein levels of the molecular markers PGC-1a, Tfam, pAMPK and NRF-2 increased by 23.6%, 16.7%, 46% and 16.6%, respectively (P < 0.05). The protein levels of the nuclear factor AMPK and NRF-1 remained unchanged (P > 0.05).

Conclusion: 

Following the pre-season in CS the change of exercise regimen by an increase of exercise intensity accompanied by a reduction of total exercise volume leads to a significant increase of the oxidative capacity VO_2peak. The elevation of the analysed nuclear factors indicates, that prolonged, intense endurance exercise enhances the molecular signalling of mitochondrial biogenesis in human skeletal muscle.