Concurrent training is the combination of endurance and resistance training. This form of training is thought to decrease strength gains compared to resistance training alone. However, for swimming, resistance training alone is not plausible.
Peroxisome proliferation receptor-gamma coactivator-1 alpha (PGC-1 alpha) has been recognized as the main transcriptional cofactor mediating mitochondrial biogenesis and improved oxidative capacity in skeletal muscle.
Resistance exercise is known to activate mammalian target of rapamycin (mTOR) signaling pathway. This cascade results in protein synthesis and muscle growth. Recent studies suggest mTOR interacts with the signaling of mitochondrial biogenesis.
This study looked to see if resistance training can alter the molecular signaling response to endurance exercise in skeletal muscle.
What was done
Ten healthy untrained subjects performed VO2max and one-repetition maximum on the leg press. Then two trials were performed:
- Endurance exercise of 60 minutes at 65% of VO2max.
- Endurance exercise of 65% VO2max followed by six sets of leg press at workloads ranging from 70 – 85% 1-RM with 3 minutes rest in between until volitional fatigue.
Blood samples, muscle biopsies of the vastus lateralis muscle were taken before and after exercise.
Plasma glucose concentration decreased over time, and plasma free fatty acid was increased threefold without difference between exercise training. Plasma lactate concentration increased in resistance training (1 h Post) but was unchanged endurance
training. Muscle glycogen content was reduced to 42% in the endurance trial and 34% endurance and resistance training trial of the initial level at 1 h Post and remained reduced at 3 h Post. There was no significant difference between exercise models in muscle glycogen depletion.
The mRNA marker for mitochondrial biogenesis was higher after the resistance exercise compared to only endurance exercise. There was a significant difference in protein phosphorylation, most notably with mTOR.
The genes (Rheb, cMyc) influencing protein regulation of mTOR significantly increased as well.
This is the first study looking at the genes associated with concurrent training which resulted in a novel finding of an increase in gene expression of genes involved in the signaling cascade of mitochondrial biogenesis.
This suggests beneficial genetic alterations in concurrent training in untrained people. Future studies must look at trained and athletic populations before practical implications are applicable.
- Wang L, Mascher H, Psilander N, Blomstrand E, Sahlin K. Resistance exercise enhances the
molecular signaling of mitochondrial biogenesis induced by endurance exercise in human
skeletal muscle.J Appl Physiol. 2011 Nov;111(5):1335-44. Epub 2011 Aug 11.
Originally Posted July 2012