Exercise Snacking before meals as a novel approach to glycaemic control in pre diabetes

Abstract

Introduction: An acute bout of exercise increases glucose uptake into skeletal muscle, an effect that persists for several hours and which is insulin-independent. Contraction-stimulated skeletal muscle glucose uptake is unimpaired in individuals with insulin resistance (i.e., pre diabetes). Meal times elicit large perturbations in glucose concentrations in individuals with pre diabetes. These postprandial glucose excursions, the so-called ‘hyperglycaemic spikes’ that are an early and often undetected feature of the insulin resistant state are more predictive for the onset of CVD complications than elevated fasting plasma glucose and are strongly associated with HbA1c content in individuals with pre diabetes. Therefore, pre-meal exercise bouts may be an effective strategy to control blood glucose throughout the day. Such ‘exercise snacking’ might also be effective in lowering blood pressure (BP) and oxidative stress and improving insulin sensitivity. The aims of this study were to examine whether (i) Exercise Snacking would be more effective than traditional exercise guidelines for blood glucose homeostasis and other risk factors of type 2 diabetes, and (ii) the combination of aerobic and resistance intervals (Composite Exercise Snacking, CES) would be as effective as an aerobic interval Exercise Snacking (ES) regime. Methods: Nine participants (7 M & 2 F; 48 ± 6 y; BMI 36 ± 8 kg.m-2, OGTT: FG 6.3 ± 1.2 mmol.L-1 & 2-h GT 9.3 ± 2.6 mmol.L-1) completed three experimental trials, in a randomised order. Trials were conducted over 5 days, under free-living conditions, with exercise performed on the third day, as either: i) Exercise Feasting (EF), comprising 30 min of moderate (60% HRmax) intensity incline walking; ii) Exercise Snacking (ES), 3*(6 x 1-min @ 90% HRmax) incline walking with 1-min min rests (which matched the energy use of EF), or iii) Composite Exercise Snacking (CES), 3*(6 x 1-min -min intervals alternating aerobic (90% HRmax incline walking) and resistance (resistance band exercises). ES and CES were completed 30 min before breakfast, lunch and dinner, whilst EF was prior to dinner only. Blood [glucose] was measured continuously across the 5 days (Medtronic iPro2 CGM), and ambulatory blood pressure was measured hourly across 4 days (Oscar 2 SunTech Medical). Plasma samples (fasting and 1-h postprandial evening meal) provided measures of insulin sensitivity ([glucose]/[insulin]), oxidative stress ([MDA] & [AOPP]) and antioxidant capacity (ORAC) the days before, of and following exercise. Effects of exercise and type were examined using two-way, repeated measures ANOVA (Bonferroni corrected). Results: ES reduced mean 24-h [glucose] on the exercise day and the day following, by 0.6 ± 0.4 mmol.L-1 (p = 0.01) and 0.6 ± 0.6 mmol.L-1 (p = 0.03), respectively compared to EF, relative to the control day before. ES reduced glycaemic variability (SD) by 35% (p = 0.05), postprandial glucose (sum of 3 h: by 0.85 mmol.L-1, p = 0.03), and consequently hyperglycaemia (Area above 6.1 mmol.L-1 by 28%, p = 0.06) on the exercise day compared to EF. Insulin sensitivity ([glucose/insulin]) was unaffected 1 h after dinner on the exercise day for ES, but tended to be higher when fasted the morning next morning (p = 0.07). MAP was reduced by 7 ± 4 mm Hg (p = 0.01) across the exercise day with ES relative to the control day before, and by 9 ± 8 mm Hg compared to EF (p = 0.03). ES increased [AOPP] at 1 h postprandial, whereas ORAC had decreased, relative to EF (p < 0.04); all measures had returned to baseline by next morning. CES was as effective as ES (i.e., no interactions; p >0.65) at reducing [glucose] (by 0.7 ± 0.1 mmol.L-1) and MAP (by 2 ± 9 mm Hg) on the exercise day relative to baseline, with no interaction for [glucose] or MAP). Conclusion: Dosing exercise as high-intensity ‘snacks’ before main meals appears to be an efficient and effective approach to glycaemic and blood pressure control in pre diabetes (in this acute setting).