Introduction: Exercise improves glucose disposal and insulin sensitivity of tissues both acutely and chronically but the dose which elicits this response, and the persistence of this effect is yet to be determined.
Aim: To explore the dose-response relationship between exercise and glycaemic control.
Methods: Participants (n=10) (age 23 ± 4, BMI = 26 ± 5 kg/m2) attended the lab and cycled at 60% V̇O2 max for a time commensurate with expending 0kcal, 175kcal, 350kcal or 700kcal (randomised). Participants were fitted with a continuous glucose monitor (CGM) for the next 72 hours. The evening of these exercise visits, subjects consumed a control meal (772kcal, carbohydrate=66%, fat=18%, and protein=16%). Following a 12 hour overnight fast, subjects undertook an oral glucose tolerance test (OGTT). Bloods were taken from an arterialised dorsal hand vein at baseline (before ingestion of 75g dextrose in 300ml water), and every 30 minutes for two-hours. Indirect calorimetry was taken 20 mins before the test and during the last 20 mins of the OGTT.
Results: The area under the curve (AUC) of glucose during the OGTT was highest for 350kcal of exercise (0kcal = 12.3 ± 1.2 mmol/L * hour; 175kcal = 12.7 ± 2.0 mmol/L * hour; 350kcal = 14.1 ± 2.6 mmol/L * hour; 700kcal = 13.0 ± 1.8 mmol/L * hour, p = 0.04). There were no differences in the range or average glucose concentrations recorded from the CGM for 72hours (p >0.05). Insulin AUC concentration was highest after 700kcal of exercise (0kcal = 137.9 ± 41.7 μUI/mL*hour, 175kcal = 128.1 ± 36.0 μUI/mL*hour, 350kcal = 142.9 ± 54.7 μUI/mL*hour, 700kcal = 169.7 ± 37.6 μUI/mL*hour, p = 0.03). FFA concentrations significantly decreased with 700kcal of exercise (0kcal = 5.3 ± 0.4 mmol/L * hour, 175kcal = 4.5 ± 0.8 mmol/L * hour, 350kcal = 4.6 ± 0.9 mmol/L * hour, 700kcal = 4.3 ± 0.8 mmol/L * hour, p = 0.006), suggesting exercise increased triglyceride synthesis and lipid storage. The respiratory exchange ratio (RER) was significantly greater at the end of the OGTT (p<0.001) but there were no differences between exercise doses (p>0.05). The AUC for GLP-1 (total) was significantly increased in larger doses of exercise (350kcal and 700kcal) (0kcal = 20.9 ± 9.5 pg/mL * hour, 175kcal = 24.9 ± 12.4 pg/mL * hour, 350kcal = 34.0 ± 11.7 pg/mL * hour, 700kcal = 35.3 ± 8.5 pg/mL * hour, p = 0.02). This further suggests greater insulin resistance with greater doses of exercise. IL-1β AUC concentrations were highest after 700kcal of exercise (0kcal = 2.3 ± 1.0 pg/mL * hour, 175kcal = 1.6 ± 1.0 pg/mL * hour, 350kcal = 3.0 ± 1.9 pg/mL * hour, 700kcal = 3.6 ± 1.2 pg/mL * hour, p = 0.01) suggesting that inflammation may be causing this increase in insulin resistance.
Conclusion: Collectively, these data suggest that greater exercise doses cause a greater level of inflammation post-exercise which can acutely impair insulin sensitivity. Further investigations are warranted to better understand the inflammatory mechanisms regulating post-exercise changes in glycaemic control.