Effect of prior moderate exercise on postprandial metabolism in men with type 2 diabetes: Heterogeneity of responses

Abstract

Prior moderate exercise has been shown consistently to reduce postprandial triglyceride (TG) concentrations in non-diabetic adults, but its effects in men with type 2 diabetes are not known. This study aimed to determine the effect of moderate exercise on postprandial metabolism in men with type 2 diabetes. Ten middle-aged men with type 2 diabetes underwent two oral fat tolerance tests (blood taken fasting and for 8 h after a meal containing 80 g fat, 70 g carbohydrate) in random order. On the afternoon before one test, participants performed a 90-min treadmill walk (Exercise); no exercise was performed before the Control test. Exercise significantly reduced fasting glucose (Control: 9.08 ± 0.75 mmol l⁻¹, Exercise: 8.40 ± 0.72 mmol l⁻¹, p = 0.033) and insulin (Control: 8.01 ± 0.98 μU ml⁻¹, Exercise: 6.81 ± 0.93 μU ml⁻¹, p = 0.046) and increased fasting 3-hydroxybutyrate (Control: 87.1 ± 19.2 μmol l⁻¹, Exercise: 134.3 ± 28.4 μmol l⁻¹, p = 0.011); reduced postprandial insulin by 11.0% (p = 0.04) and increased postprandial 3-hydroxybutrate by 31.8% (p = 0.03); but did not significantly change fasting or postprandial triglyceride or NEFA concentrations. However, the exercise-induced change in postprandial triglyceride concentration ranged from −32.3 to +28.3% and the exercise-induced change in fasting 3-hydroxybutyrate concentration (a marker of hepatic fatty acid oxidation) was highly correlated with the exercise-induced changes in fasting and postprandial triglyceride (r = 0.68, p = 0.03 for both).

Thus, inter-individual variation in propensity to increase hepatic fatty acid oxidation following exercise may account for the considerable heterogeneity in triglyceride responses to moderate exercise observed in men with type 2 diabetes.

Introduction

Free-living humans spend 16–18 h of each day in the postprandial state and disturbances to metabolism occurring during the hours following a meal are implicated in the pathogenesis of atherosclerosis by a number of plausible mechanisms. Postprandial lipoproteins and their remnants can directly infiltrate the arterial wall and accumulate in atheromatous plaques [1]; and systemic inflammation is increased [2], [3] and endothelial function is impaired [3], [4] during the hours following ingestion of meals containing fat. Furthermore, high concentrations of triglyceride (TG)-rich lipoproteins facilitate the exchange of neutral lipids between triglyceride-rich and cholesterol-rich lipoproteins, promoting the atherogenic lipoprotein phenotype of small, dense low-density lipoprotein (LDL) and low high-density lipoprotein (HDL) [1].

Exaggerated postprandial lipemia, largely due to hepatic overproduction of very low-density lipoprotein (VLDL) [5], [6] (although impaired lipoprotein lipase (LPL)-mediated clearance of TG-rich lipoproteins is also likely to contribute [7]) is a major feature of the dyslipidemia observed in patients with type 2 diabetes, and is an important determinant of the low concentrations of HDL cholesterol and high concentration of small-dense LDL which characterises this condition [5], [6]. Resistance to insulin-mediated glucose disposal (rather than hyperglycemia or compensatory hyperinsulinemia) is implicated as the major determinant of diabetic dyslipidemia, particularly as postprandial lipoprotein perturbations persist even when hyperglycemia and hyperinsulinemia are corrected during a “clamp” study [8]. Moreover, insulin resistance is strongly associated with postprandial lipoprotein alterations even in non-diabetic subjects [9], [10].

In non-diabetic subjects, a session of moderate exercise performed on the day before an oral fat load has consistently been shown to lower postprandial TG concentrations by 20–25% [11], [12]. In particular, we have recently demonstrated this effect in centrally obese, insulin resistant middle-aged men [3], suggesting that moderate exercise can be effective in normalising the adverse postprandial lipid profile associated with insulin resistance. In contrast, a recent study reported that a 40-min session of prior low intensity exercise did not reduce postprandial TG concentration in a group men with type 2 diabetes [13]. However, as the exercise ‘dose’ used in this study was much lower than that typically used in studies on non-diabetic subjects [11], [12] and the magnitude of the TG-lowering effect of prior exercise is related to the energy expended during the exercise session [11], [12], this study may not have had sufficient power to detect a clear effect of this level of exercise on postprandial TG metabolism. In order to provide effective evidence-based guidelines for the use of exercise in treating diabetic dyslipidemia, it is important to establish whether, in principle, moderate exercise can reduce postprandial lipemia in adults with type 2 diabetes in a similar manner to that observed in non-diabetic people. The purpose of this study was therefore to determine the effects of 90 min of prior brisk walking – a duration and intensity of exercise previously shown to reduce postprandial TG concentrations in a wide range of non-diabetic subjects [11], [12], including centrally obese, insulin-resistant men [3] – on postprandial metabolism in a group of middle-aged men with type 2 diabetes.