Measurement of postprandial glucose fluxes in response to acute and chronic endurance exercise in healthy humans

Abstract

The effect of endurance exercise on enhancing insulin sensitivity and glucose flux has been well established with techniques such as the hyperinsulinemic clamp. Although informative, such techniques do not emulate the physiological postprandial state, and it remains unclear how exercise improves postprandial glycaemia. Accordingly, combining mixed-meal tolerance testing and the triple-stable isotope glucose tracer approach, glucose fluxes [rates of meal glucose appearance (Ra), disposal (Rd), and endogenous glucose production (EGP)] were determined following acute endurance exercise (1 h cycling; ~70% V̇o) and 4 wk of endurance training (cycling 5 days/wk). Training was associated with a modest increase in V̇o (~7%, P < 0.001). Postprandial glucose and insulin responses were reduced to the same extent following acute and chronic training. Interestingly, this was not accompanied by changes to rates of meal Ra, Rd, or degree of EGP suppression. Glucose clearance (Rd relative to prevailing glucose) was, however, enhanced with acute and chronic exercise. Furthermore, the duration of EGP suppression was shorter with acute and chronic exercise, with EGP returning toward fasting levels more rapidly than pretraining conditions. These findings suggest that endurance exercise influences the efficiency of the glucoregulatory system, where pretraining rates of glucose disposal and production were achieved at lower glucose and insulin levels. Notably, there was no influence of chronic training over and above that of a single exercise bout, providing further evidence that glucoregulatory benefits of endurance exercise are largely attributed to the residual effects of the last exercise bout.

Prior exercise enhances skeletal muscle microvascular blood flow and mitigates microvascular flow impairments induced by a high‐glucose mixed meal in healthy young men

“…Postprandial blood glucose and insulin were similar between the 24 h post-exercise and no-exercise control conditions. This contradicts previous reports of improved insulin sensitivity in the days following acute exercise in healthy individuals (Mikines et al 1988;Brestoff et al 2009;Ortega et al 2015;Morrison et al 2018). However, Bogardus et al (1983) reported a similar finding where the insulin-sensitizing effects the day after exercise are absent when participants are fed 100 g of glucose 3 h post-exercise.…”

“…However, Bogardus et al (1983) reported a similar finding where the insulin-sensitizing effects the day after exercise are absent when participants are fed 100 g of glucose 3 h post-exercise. In light of previous findings (Bogardus et al 1983), the high-glucose ingested 3 h post-exercise in the current study may have led to faster and more complete glycogen replenishment compared to other studies where habitual meal regimes are resumed after exercise (Morrison et al 2018). Additionally, and in contrast to others (Ortega et al 2015;Morrison et al 2018), we also observed an elevation in postprandial NEFAs and fat oxidation 24 h post-exercise, a possible result of the preceding 3 h post-exercise trial which may have also precluded improvements in 24 h postprandial glucose and insulin.…”

“…Here we show for the first time that compared to a no-exercise control meal, muscle microvascular blood flow is elevated at 0 min (pre-meal), and 60 and 120 min postprandially when a high-glucose mixed-nutrient meal is ingested 3 h post-exercise, and elevated at 120 min postprandially when the meal is ingested 24 h post-exercise. These findings are important, as the insulin sensitizing effects of acute exercise are well-known to be observed for up to 24-48 h post-exercise (Mikines et al 1988;Brestoff et al 2009;Ortega et al 2015;Parker et al 2016aParker et al , 2017Morrison et al 2018). In addition to the well-characterized increase in distal insulin signalling in skeletal muscle after exercise (Parker et al 2016b(Parker et al , 2019Sjoberg et al 2017), research by Sjoberg et al (2017) established the importance of muscle microvascular blood flow for enhancing post-exercise insulin-mediated glucose disposal when measured by euglycaemic-hyperinsulinaemic clamp.…”

“…Skeletal muscle contraction and exercise are potent stimuli for increasing muscle microvascular blood flow (Vincent et al 2006;Durham et al 2010;St-Pierre et al 2012), and are well known to enhance insulin sensitivity and glycaemic control throughout the 24 h post-exercise recovery period (Mikines et al 1988;Brestoff et al 2009;Ortega et al 2015;Parker et al 2016a;Morrison et al 2018). Research by Sjoberg et al (2017) established that 1 h of single-legged knee extensor exercise in healthy young adults enhances insulin-mediated leg glucose uptake and microvascular blood flow 4 h later during euglycaemic-hyperinsulinaemic clamp conditions.…”

Short-term dietary reduction of branched-chain amino acids reduces meal-induced insulin secretion and modifies microbiome composition in type 2 diabetes: a randomized controlled crossover trial

“…Indeed, postprandial insulin sensitivity as calculated from the OGIS and PREDIM, which have been validated and correlate with clamp-derived measures of whole-body insulin sensitivity (33), was >20% higher than after the BCAA + diet. This improvement could have resulted from increased insulin-mediated glucose disposal, which mainly occurs in skeletal muscle under these conditions (46). Alternatively, EGP could have been decreased under BCAA-depleted conditions owing to lower substrate supply for hepatic gluconeogenesis (47).…”