scholarly journals Hyperinsulinaemia and hyperglycaemia promote glucose utilization and storage during low- and high-intensity exercise

2019 ◽  
Vol 120 (1) ◽  
pp. 127-135 ◽  
Author(s):  
Hamid Mohebbi ◽  
Iain T. Campbell ◽  
Marie A. Keegan ◽  
James J. Malone ◽  
Andrew T. Hulton ◽  
...  

Abstract Purpose The effect of hyperglycaemia with and without additional insulin was explored at a low and high intensity of exercise (40% vs 70% VO2peak) on glucose utilization (GUR), carbohydrate oxidation, non-oxidative glucose disposal (NOGD), and muscle glycogen. Methods Eight healthy trained males were exercised for 120 min in four trials, twice at 40% VO2peak and twice at 70% VO2peak, while glucose was infused intravenously (40%G; 70%G) at rates to “clamp” blood glucose at 10 mM. On one occasion at each exercise intensity, insulin was also infused at 40 mU/m2/per min (i.e. 40%GI and 70%GI). The glucose and insulin infusion began 30 min prior to exercise and throughout exercise. A muscle biopsy was taken at the end of exercise for glycogen analysis. Results Hyperglycaemia significantly elevated plasma insulin concentration (p < 0.001), although no difference was observed between the exercise intensities. Insulin infusion during both mild and severe exercise resulted in increased insulin concentrations (p < 0.01) and GUR (p < 0.01) compared with glucose (40%GI by 25.2%; 70%GI by 26.2%), but failed to significantly affect carbohydrate, fat and protein oxidation. NOGD was significantly higher for GI trials at both intensities (p < 0.05) with storage occurring during both lower intensities (62.7 ± 19.6 g 40%GI; 127 ± 20.7 g 40%GI) and 70%GI (29.0 ± 20.0 g). Muscle glycogen concentrations were significantly depleted from rest (p < 0.01) after all four trials. Conclusion Hyperinsulinaemia in the presence of hyperglycaemia during both low- and high-intensity exercise promotes GUR and NOGD, but does not significantly affect substrate oxidation.

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Corey A Rynders ◽  
Alice Chan ◽  
Judy Y Weltman ◽  
Eugene J Barrett ◽  
Arthur Weltman

2021 ◽  
Author(s):  
Jeppe F. Vigh-Larsen ◽  
Niels Ørtenblad ◽  
Lawrence L. Spriet ◽  
Kristian Overgaard ◽  
Magni Mohr

1999 ◽  
Vol 165 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Balsom ◽  
Gaitanos ◽  
Söderlund ◽  
Ekblom

1987 ◽  
Vol 63 (6) ◽  
pp. 2195-2200 ◽  
Author(s):  
A. R. Poso ◽  
T. Soveri ◽  
M. Alaviuhkola ◽  
L. Lindqvist ◽  
L. Alakuijala ◽  
...  

Previous studies in humans have shown that alanine is released from the skeletal muscle in proportion to the work load. We have measured plasma alanine and urea concentrations in well-trained Standardbred and Finnish-bred (cold-blooded) trotters after a graded-intensity exercise and during recovery to study metabolic responses to exercise in this animal model. As controls we measured blood lactate, pyruvate, and glucose concentrations as well as hematocrit values. Metabolic responses to exercise were closely reflected in all these parameters. Plasma alanine increased relatively more than plasma lactate at moderate-intensity exercise near anaerobic threshold. The linear correlation between the intensity of exercise and plasma alanine was similar to that observed earlier in humans. Interestingly, plasma alanine concentrations remained elevated long after the submaximal exercise, whereas the concentration of lactate, pyruvate, and glucose decreased more rapidly. No significant changes were found in plasma urea concentration under these conditions. The most significant differences in the metabolic responses to exercise of the two breeds studied were the higher lactate-to-pyruvate ratios achieved during the high-intensity exercise and the more sensitive increases of plasma alanine even during low-intensity exercise in the Finnish-bred horses. These differences probably reflect different compositions of muscle fiber types in the two breeds. The findings together indicate that plasma alanine is greatly increased in the racehorse during and after a high-intensity exercise and thus is an important vehicle in transporting ammonia and carbon skeletons of products of anaerobic glycolysis out of the muscle tissue.


1995 ◽  
Vol 78 (3) ◽  
pp. 1203-1207 ◽  
Author(s):  
A. R. Coggan ◽  
C. A. Raguso ◽  
B. D. Williams ◽  
L. S. Sidossis ◽  
A. Gastaldelli

In humans, endurance training reduces the rates of glucose production and utilization during moderate-intensity exercise. It is uncertain, however, whether this is also true during high-intensity exercise. Accordingly, we studied eight endurance-trained cyclists and eight untrained subjects during 30 min of cycling at approximately 80% of maximal oxygen uptake (VO2max). Rates of glucose appearance (Ra) and disappearance (Rd) were determined using a primed, continuous infusion of [6,6–2H]glucose. Average glucose Ra during exercise did not differ in the trained and untrained subjects (34.3 +/- 3.6 vs. 36.0 +/- 1.7 mumol.min-1.kg-1; mean +/- SE; P, not significant). Plasma insulin, glucagon, norepinephrine, and epinephrine concentrations were also similar in the two groups. In contrast, glucose Rd during exercise was 19% lower in the trained compared with the untrained subjects (27.0 +/- 2.6 vs. 33.2 +/- 1.5 mumol.min-1.kg-1; P < 0.001). Consequently, during exercise, plasma glucose concentration rose significantly (P < 0.05) in the trained subjects but did not change in the untrained subjects. We conclude that utilization of plasma glucose is lower in trained subjects during high-intensity exercise, even when the exercise is performed at the same relative (and therefore a higher absolute) intensity as in the untrained state. Hyperglycemia in trained subjects during intense exercise appears to be due to this lower rate of glucose utilization rather than a higher rate of glucose production.


2000 ◽  
Vol 88 (1) ◽  
pp. 219-225 ◽  
Author(s):  
Jeffrey F. Horowitz ◽  
Ricardo Mora-Rodriguez ◽  
Lauri O. Byerley ◽  
Edward F. Coyle

This investigation determined whether ingestion of a tolerable amount of medium-chain triglycerides (MCT; ∼25 g) reduces the rate of muscle glycogen use during high-intensity exercise. On two occasions, seven well-trained men cycled for 30 min at 84% maximal O2 uptake. Exactly 1 h before exercise, they ingested either 1) carbohydrate (CHO; 0.72 g sucrose/kg) or 2) MCT+CHO [0.36 g tricaprin (C10:0)/kg plus 0.72 g sucrose/kg]. The change in glycogen concentration was measured in biopsies taken from the vastus lateralis before and after exercise. Additionally, glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the rate of glucose disappearance from plasma (Rd glucose), as measured by stable isotope dilution techniques. The change in muscle glycogen concentration was not different during MCT+CHO and CHO (42.0 ± 4.6 vs. 38.8 ± 4.0 μmol glucosyl units/g wet wt). Furthermore, calculated glycogen oxidation was also similar (331 ± 18 vs. 329 ± 15 μmol ⋅ kg− 1 ⋅ min− 1). The coingestion of MCT+CHO did increase ( P < 0.05) Rd glucose at rest compared with CHO (26.9 ± 1.5 vs. 20.7 ± 0.7 μmol ⋅kg− 1 ⋅ min− 1), yet during exercise Rd glucose was not different during the two trials. Therefore, the addition of a small amount of MCT to a preexercise CHO meal did not reduce muscle glycogen oxidation during high-intensity exercise, but it did increase glucose uptake at rest.


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