Impact of pre-exercise feeding status on metabolic adaptations to endurance-type exercise training.

Abstract

KEY POINTS\nSkeletal muscle adaptations relating to glucose uptake (e.g. GLUT4 protein levels) and energy sensing (e.g. AMPK) can be augmented with exercise training before versus after nutrient provision in healthy individuals and in individuals classified as overweight or obese. Performing exercise training sessions before versus after nutrient provision can increase oral glucose insulin sensitivity in healthy individuals and in individuals classified as overweight or obese. In individuals with type 2 diabetes, metabolic inflexibility may attenuate, or abolish the effects of nutrient-exercise timing on skeletal muscle adaptations to exercise training.\n\n\nABSTRACT\nNutrition and exercise metabolism are vibrant physiological fields, yet at times it feels as if greater progress could be made by better integrating these disciplines. Exercise is advocated for improving metabolic health, in part by increasing peripheral insulin sensitivity and glycaemic control. However, when a modest-to-high carbohydrate load is consumed before and/or during each exercise bout within a training program, increases in oral glucose insulin sensitivity can be blunted in both men of a healthy weight and those with overweight/obesity. Exercise training induced adaptation in the energy sensing AMP-activated protein kinase (AMPK) and the insulin-sensitive glucose transporter GLUT4 protein levels are sensitive to pre-exercise feeding status in both healthy individuals and in individuals classified as overweight or obese. Increased lipid oxidation may, in part, explain the enhanced adaptive responses to exercise training performed before (i.e. fasted-state exercise) versus after nutrient ingestion. Evidence in individuals with type 2 diabetes currently shows no effect of altering nutrient-exercise timing for measured markers of metabolic health, or greater reductions in glycated haemoglobin (HbA1c) concentrations with exercise performed after versus before nutrient provision. Since the metabolic inflexibility associated with type 2 diabetes diminishes differences in lipid oxidation between the fasted- and fed-states, it is plausible that pre-exercise feeding status does not alter adaptations to exercise when metabolic flexibility is already compromised. Current evidence suggests restricting carbohydrate intake before and during exercise can enhance some health benefits of exercise, but in order to establish clinical guidelines, further research is needed with hard outcomes and different populations. Abstract Figure legend Candidate mechanisms linking nutrient-exercise timing to insulin sensitivity. Exercise performed in an overnight-fasted state (before nutrient intake), increases fatty acid availability for skeletal muscle, and also increases intramuscular triglyceride utilisation. An increase in skeletal muscle lipid turnover may result in phospholipid remodelling, with a relative reduction in saturated fatty acids within skeletal muscle phospholipids. Increased fatty acid availability can also increase AMPK activity and this increase PGC-1α levels. Exercise before versus after nutrient intake can also result in an increase in skeletal muscle GLUT4 and CHC22 levels, which are involved in insulin-stimulated glucose transport. AkT, Protein kinase B; AMPK, adenosine monophosphate-activated protein kinase; CD36, fatty acid translocase; CHC22, clathrin heavy chain 22; CPT1, carnitine palmitoyltransferase 1; GLUT4, glucose transporter 4; IMTG, intramuscular triglyceride; MUFA, monounsaturated fatty acid; OXPHOS, oxidative phosphorylation proteins; PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; PUFA, polyunsaturated fatty acid; SFA, saturated fatty acid; TBC1D1/D4, TBC1 domain family member 1/family member 4 (AS160). This article is protected by copyright. All rights reserved.