Table 1.

Effects of Exercise in Healthy Individuals

	Result	Mechanism
During exercise
Muscle contraction	Insulin-independent translocation of GLUT4, resulting in increased glucose uptake	• Ca2+/CaMK activation • AMPK activation • PKC activation
Muscle energetic demands	Increases glucose disposal	• Increased glycolytic flux
Endogenous glucose production	Increases blood glucose availability	• Increased glucagon concentration • Increased catecholamine concentration
Muscle blood flow	Increases glucose delivery	• Elevated cardiac output • Increased capillary blood flow • Skeletal muscle vasodilation
After exercise
Insulin sensitivity	Leftward shift of insulin response curve for 24–48 h after cessation of exercise	• Currently unknown, possibly involving phosphorylation by AMPK of TBC1D1 and AS160

Skeletal muscle glucose uptake increases dramatically in response to exercise together with a drop in plasma insulin concentrations in healthy individuals to overnight fasted levels. During exercise, the increase in glucose uptake is the result of muscle contraction that activates the Ca²⁺/calmodulin-activated protein kinase (CaMK) family, 5'-AMP-activated protein kinase (AMPK), and atypical protein kinase C (PKC). Exercise also increases the energetic demands of skeletal muscle, resulting in increased glycolytic flux and demand for glucose as an energy substrate. Endogenous glucose production increases, making blood glucose more available as a result of elevations in circulating glucagon and catecholamine concentrations. Finally, increased skeletal muscle blood flow as a result of elevations in cardiac output and increased capillary blood flow together with local vasodilation increase glucose delivery to active tissues. After exercise, a leftward shift of the insulin dose–response curve persists for 24–48 h after the cessation of exercise through a currently unknown mechanism that increases the sensitivity of skeletal muscle to plasma insulin concentration.

GLUT4, glucose transporter type 4.