Influence of Acute and Chronic Exercise on Glucose Uptake

Table 1

Effect of acute and chronic exercise on molecular signaling pathways.

Metabolic factor	Acute training	Chronic training	Exercise characteristics (intensity, modality)	References
Proximal insulin signaling (IRS-1, PI3-K, PDK, αPKC)		↑↑	Moderate-to-intensive exercise for untrained and high-intensity exercise for trained individuals, independent of modality	[12–22]
AMPK	↑↑	↑↑	Dose-response pattern, independent of modality	[8, 23–31]
Ca^2+-calmodulin axis	↑↑	↑↑	Dose-response pattern, independent of modality	[8, 27, 31–35]
mTOR/S6K	↑↑	↑↑	Dose-response pattern, independent of modality	[29, 36–46]
Downstream targets: AS160, TBC1D1, Rac1	↑	↑	Dose-response pattern for AS160 and Rac1, independent of modality	[16, 47–60]
IKK/NF-κB pathway	↑↕	↓↓	Dose-response pattern, independent of modality	[2, 61–77]
Inflammasome pathway	—	↓↓	Dose-response pattern, independent of modality	[2, 78–80]
JNK/MAPK pathway	↑↑	↓↓	Dose-response pattern, independent of modality	[67–69, 81–85]
Adiponectin	↑	↑	Intense exercise, independent of modality	[3, 5, 53, 86–94]

↑↑/↓↓, consistent findings in animal models and humans; ↑/↓, preliminary evidence from animal models and/or humans; —, no impact; animal studies showed no effects; increase in skeletal muscle and increase/decrease in adipose tissue; αPKC, atypical PKC; AMPK, AMP-activated protein kinase; AS160, Akt substrate of 160 kDa; Ca, calcium; CaMKII, Ca²⁺/calmodulin-dependent protein kinase 2; IRS-1, insulin receptor substrate 1; IKK/NF-κB, IκB kinase/nuclear factor kappa B; JNK, C-Jun N-terminal kinase; MAPK, mitogen-activated protein kinases; mTOR/S6K, mammalian target of rapamycin/ribosomal S6 kinase; PDK, phosphoinositide-dependent kinase; PI3-K, phosphoinositide 3-kinase; Rac1, ras-related C3 botulinum toxin substrate 1; TBC1D1, TBC1 domain family member 1.