Fig. 1.

Proposed mechanisms mediating increases in skeletal muscle glucose uptake and insulin sensitivity following HIIT and SIT. A) During an acute bout of HIIT/SIT, increases in skeletal muscle blood flow promote glucose delivery to active muscle. Increases in glucose delivery coupled with increased intracellular glucose utilization via contraction-mediated mechanisms promotes an increased glucose diffusion gradient across the muscle sarcolemma. Glucose uptake is facilitated by the activation of contraction-mediated signaling proteins that promote GLUT4 translocation to the muscle membrane though direct evidence demonstrating an increase in GLUT4 translocation with HIIT/SIT is currently lacking (as indicated by the dashed arrow). In the hours to days following exercise when contraction-mediated mechanisms have subsided, insulin-mediated glucose uptake is enhanced for up to ∼24–48 h. Increased insulin sensitivity post-exercise has been attributed to increased activity of distal (but not proximal; in grey) proteins in the insulin signaling cascade (TBC1D4) and glycogen synthase activity to facilitate glycogen resynthesis. B) HIIT/SIT training interventions (weeks to months) promote numerous metabolic adaptations in skeletal muscle that are implicated in improved insulin sensitivity following training. This includes increased mitochondrial content and function, capillary density, and the expression of proteins involved in glucose uptake, utilization, and storage within muscle, as well as reductions in lipid intermediates. Glycogen utilization and re-synthesis with acute exercise bouts, including the final training session, may also contribute to improved insulin sensitivity observed in the days following HIIT/SIT training. Note: HIIT: high-intensity interval training; SIT: sprint interval training; Akt: Protein kinase B; AMP: adenosine monophosphate; AMPK: AMP-activated protein kinase; Ca²⁺: calcium; CaMKII: calcium calmodulin-dependent protein kinase II; G6P: glucose-6-phosphate; GLUT4: glucose transporter 4; GS: glycogen synthase; HK: hexokinase; IRS-1: insulin receptor substrate-1; PI3K: phosphatidylinositol 3 kinase; TBC1D1/4: TBC1 domain family member 1/4.