Metabolic adaptations in post‐exercise recovery

Abstract

To investigate further the hormonal and metabolic adaptations occurring when carbohydrates are ingested after prolonged exercise, we have compared the fate of a 100-g oral glucose load (using 'naturally labelled' 13C-glucose) in healthy volunteers after an overnight fast at rest either without previous exercise or after a 3-h exercise performed on a treadmill at about 50% of the individual VO2 max. In comparison to the control conditions, the oral glucose tolerance test (OGTT) performed in the post-exercise recovery period was characterized by a greater rise in peripheral blood glucose levels and delayed insulin response. Plasma glucagon values were significantly elevated at the time glucose was given (+48 +/- 13 pg ml-1) and at the end of the OGTT. Plasma-free fatty acid (FFA) levels were 1675 +/- 103 microEq 1-1 when glucose was given, and subsequently reduced to values similar to those observed in the control conditions. Indirect calorimetry indicated that OGTT in post-exercise recovery was associated with decreased carbohydrate and increased lipid oxidation when compared to control conditions. Exogenous glucose oxidation was also significantly reduced: 21.1 +/- 2.6 vs. 35.9 +/- 1.9 g per 7 h. We suggest that the higher plasma glucagon levels and the delayed insulin response played a role in the decreased hepatic glucose retention previously described by others in post-exercise recovery. Our data also suggest that the higher lipid oxidation rate observed at the time glucose was given in the post-exercise period could explain, according to the Randle 'glucose-fatty acid cycle', the decreased carbohydrate oxidation and the preferential muscle glycogen repletion already well documented. The reason why the lipid oxidation rate remains increased 3-7 h after glucose ingestion in spite of the fact that FAA levels at that time are similar to those observed in control conditions is still unknown; further kinetic studies are needed to clarify this point.

The gastroenteroinsular response to glucose ingestion during postexercise recovery

“…This reduced or delayed insulin response has also been reported by other investigators (21,25,27,32,33,37,Fig. 3.…”

“…These data suggest that VIP may play an important glucoregulatory role when glucose is ingested during the immediate postexercise recovery period. insulin resistance; gut peptides; exercise performance; carbohydrate THE IMMEDIATE POSTEXERCISE PERIOD appears to be associated with mild reversible insulin resistance, which is characterized by an attenuated insulin response and an increased glucose response to oral glucose (10,21,25,27,33,37,39,43). The physiological basis for the increased glucose response has been shown to be partly a function of greater release of glucose from the splanchnic tissues (20,30,39).…”

Exercise prior to a freely requested meal modifies pre and postprandial glucose profile, substrate oxidation and sympathovagal balance

“…The effect on postprandial glucose was observed even after a single bout of exercise [2,3]; however, the delay between the exercise session and the test meal is an important parameter. In the immediate post-exercise period and up to 90 min later, postprandial glucose concentrations have been reported to be increased [4-11] or unchanged [5,12-17]. This is thought to be mainly the consequence of reduced insulin concentrations [5,7,13,14].…”

Sélection des substrats lors de l’exercice prolongé avec ingestion de glucides : études par traçage au 13C

“…Il existe également peu de données systématiques sur l'effet du mode d'administration des glucides exogènes [bolus vs doses (Massicotte et al, 1996a) ; ingestion avant vs pendant l'exercice Caron et al, 2004;Krzentowski et al, 1984a) ; effet de la concentration de la solution ingérée (Jandrain et al, 1989;Jentjens et al, 2004bJentjens et al, , 2006Moodley et al, 1992)] sur leur oxydation. Un certain nombre d'études se sont penchées, par contre, sur l'effet de l'entraînement Jeukendrup et al, 1997;Krzentowski et al, 1984b;Péronnet et al, 2009;van Loon et al, 1999), de l'état nutritionnel (Ravussin et al, 1979), de certains facteurs environnementaux [froid (Galloway et al, 2001), chaud (Jentjens et al, 2006(Jentjens et al, , 2002, hypoxie (Péronnet et al, 2006)] et de certains nutriments ou agents pharmacologiques dont on sait qu'ils interfèrent ou pourraient interférer avec la digestion et l'absorption des glucides et la sélection des substrats [acarbose qui inhibe les glucosidases (Gerard et al, 1986), sodium (Massicotte et al, 1996b) qui pourrait faciliter l'absorption du glucose par le « sodium-glucose transporter 1 » (SLGT1) , métoclopramide qui accélère la vidange gastrique (Massicotte et al, 1996b), acipimox qui bloque la lipolyse (Gautier et al, 1994) ; caféine (Desbrow et al, 2009;Hulston et Jeukendrup, 2008;Yeo et al, 2005)]. …”