After reading “The Molecular Bases of Training Adaptation” review by Vernon G. Coffey and John A Hawley. I realized that this slightly older review did not mention another method the PGC-1a “master switch” was activated to create local aerobic adaptations. Those adaptations being the following …
↑ Type I Fibers
↑ Mitochondrial Biogenesis
↑ Fat Oxidative Capacity
↑ Glut4, Glycogen stores
↑ Angiogenesis and capillary formation
In a more recent review (May 2010) by Hùkan Wcsrerb1ud”, Joseph D. Biuton and Abram Katz named “Skeletal muscle: Energy metabolism, fiber types, fatigue and adaptability” the authors mentioned that hypoxic conditions actually activated PGC-1a to initiate those aerobic adaptations. From my understanding PGC-1a can be activated by the following methods.
| Activity Type | Cellular Changes | Cellular Signals |
| Mechanical Load Resulting in hypoxia | Hypoxic conditions | HIF-1a |
| High Volume Training | ↑ Ca2+ Repeated contractions | CaMKII Calcineurin |
| High Intensity Training | Change ATP/AMP levels Changes in high energy phosphates | AMPK
|
| High Intensity Training (through Glycolysis) | ↑ ROS | MAPK |
I think this clearly shows the importance of aerobic energy system. If all of these different types of exercise can trigger aerobic adaptations, one must realize the importance of properly developing the aerobic system.
Jordan Webb
Thanks for the PDF guys!
Also don’t forget that moderate volume, low intensity training in a “fasted” state, ideally on waking also seems to induce a much larger activation of PGC1 alpha than the same training stimulus in a “feed” state!