Future studies should examine the acute and chronic effects of different dosages of creatine ingestion before and/or after resistance exercise on pathways involved in skeletal muscle growth.
These included the well established exercise response pathways, insulin signalling [ 68], Type II diabetes mellitus [ 72], mTOR signalling [ 73] and MAPK signaling [ 74- 76] as well as focal adhesion and p53 signaling pathway.
It will be interesting to know how intracellular exercise signalling pathways relieve the repression of PGC-1α by FoxO6 and whether these mechanisms can reset the sensitivity of PGC-1α promoter to FoxO6-mediated repression.
For us the exercise of pathway construction has provided a resource for training, pathway modelling, literature/data interpretation, hypothesis generation and as such is now central to our ongoing investigations of macrophage biology.
Notably, these exercise-relevant pathways (cell death, stress response, proliferation) comprise significant number of intersecting mRNAs.
Patients with early-onset type 2 diabetes display abnormalities in the exercise-dependent pathway that regulates the expression of PGC-1α and Mfn2.
Atherosclerosis and CVD are caused by a complex interaction of lifestyle factors (diet, energy balance, smoking, exercise) and inflammatory pathways.
Both cold exposure and exercise trigger transcriptional pathways that lead to increased mitochondrial abundance and oxidative capacity in skeletal muscle and brown adipose tissue [17] [20].
However, they focused on cross-talk due to the effect that pathways exercise on each other for the presence of overlapping genes.
After acute endurance-type exercise, several cellular pathways (Fig. 1), mainly AMP-activated protein kinase, calcium signalling and p38 mitogen-activated protein kinase, stimulate myocellular glucose transport [ 11] and may also increase flux through ATP synthase in vivo, even in relatives of patients with type 2 diabetes [ 12].
