Prolonged Exercise-Induced Stimulation of Skeletal Muscle Glucose Uptake Is due to Sustained Increases in Tissue Perfusion and Fractional Glucose Extraction

Abstract

The prolonged stimulatory effect of physical exercise on skeletal muscle glucose uptake was mediated via vascular effects combined with an increase in basal glucose transport independent of enhancement of insulin responses.

Treadmill Exercise Inducing Mild to Moderate Ischemia Has No Significant Effect on Skeletal Muscle or Cardiac 18F-FDG Uptake and Image Quality on Subsequent Whole-Body PET Scan

“…First, the duration of exercise stress testing in our patients was relatively short and the intensity relatively low. By comparison, studies in healthy volunteers involved much more demanding regimens (6,9,15,16). Although our patients achieved a reasonable work load, the exercise capacity in a predominantly elderly group of oncology patients is probably lower than that of healthy (and mostly younger) volunteers in applied physiology protocols.…”

“…The latter involves adenosine monophosphate-activated kinase (2,4), which increases substrate delivery to muscle, fatty acid uptake, b-oxidation, and glucose uptake via GLUT4. Exercise also increases nitric oxide synthase activity, and thereby muscle perfusion and substrate delivery (5), which may persist for 12 h after heavy exercise (6). Finally, exercise stimulates secretion of calcium ions from T tubules, thereby augmenting GLUT4 transcription (7).…”

Effect of H1- and H2-histamine receptor blockade on postexercise insulin sensitivity

“…Similarly, Hamrin and colleagues (Hamrin et al. ) demonstrated increased tissue perfusion and skeletal muscle glucose uptake 12 h after the completion of a 2‐h bout of one‐legged cycling. Interestingly, this response was independent of enhancement of insulin responses, as they found similar increases in skeletal muscle glucose uptake in the postexercising and postresting legs in response to a hyperinsulinemic euglycemic clamp.…”

“…Pellinger et al (2010) found that when postexercise skeletal muscle vasodilatation was blunted in humans via local H 1and H 2 -receptor blockade, interstitial glucose concentrations were attenuated. Similarly, Hamrin and colleagues (Hamrin et al 2011) demonstrated increased tissue perfusion and skeletal muscle glucose uptake 12 h after the completion of a 2-h bout of one-legged cycling. Interestingly, this response was independent of enhancement of insulin responses, as they found similar increases in skeletal muscle glucose uptake in the postexercising and postresting legs in response to a hyperinsulinemic euglycemic clamp.…”

Thermodynamic Function of Glycogen in Brain and Muscle

“…It is generally presumed that muscle glycogen is metabolized to augment circulating glucose to fuel the energy demand during very brief periods (10 -40 milliseconds) of high ATP demand associated with individual contractions (Chin and Allen, 1997;). However, glucose concentrations in muscle are in the millimolar range, far too high to be consumed in sub-second intervals, and with onset of exercise muscle glucose content increases rather than decreases, as a result of greater blood flow (Berger et al, 1975;Hamrin and Henriksson, 2008;Hamrin et al, 2011;Henriksson and Knol, 2005;MacLean et al, 1999;Rosdahl et al, 1993;Sahlin, 1990). Even in the absence of glucose, the 20-25 mM concentrations of phosphocreatine (PCr) in muscle are sufficient to maintain muscle ATP levels for at least several seconds (Baker et al, 2010;Bogdanis et al, 1996;Funk et al, 1989;Meyer, 1988) (see Box).…”