Abstract
We investigated glucose tolerance and postprandial glucose fluxes immediately after a single bout of aerobic exercise in subjects representing the entire glucose tolerance continuum. Twenty‐four men with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or type 2 diabetes (T2D; age: 56 ± 1 years; body mass index: 27.8 ± 0.7 kg/m2, P > 0.05) underwent a 180‐min oral glucose tolerance test (OGTT) combined with constant intravenous infusion of [6,6‐2H2]glucose and ingestion of [U‐13C]glucose, following 1 h of exercise (50% of peak aerobic power) or rest. In both trials, plasma glucose concentrations and kinetics, insulin, C‐peptide, and glucagon were measured. Rates (mg kg−1 min−1) of glucose appearance from endogenous (RaEndo) and exogenous (oral glucose; RaOGTT) sources, and glucose disappearance (Rd) were determined. We found that exercise increased RaEndo, RaOGTT, and Rd (all P < 0.0001) in all groups with a tendency for a greater (~20%) peak RaOGTT value in NGT subjects when compared to IGT and T2D subjects. Accordingly, following exercise, the plasma glucose concentration during the OGTT was increased in NGT subjects (P < 0.05), while unchanged in subjects with IGT and T2D. In conclusion, while a single bout of moderate‐intensity exercise increased the postprandial glucose response in NGT subjects, glucose tolerance following exercise was preserved in the two hyperglycemic groups. Thus, postprandial plasma glucose responses immediately following exercise are dependent on the underlying degree of glycemic control.
Highlights
Glycemic control is key in the management of type 2 diabetes (T2D), with postprandial glucose proposed as a better predictor of diabetes-related complications than fasting blood glucose or HbA1c (Cavalot et al 2011)
Subjects with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and T2D were not significantly different with respect to age and body mass index (BMI); fat-free mass was higher in NGT subjects compared to IGT (P = 0.05)
Fasting glucose levels were highest in subjects with T2D (P < 0.05), and 2-h oral glucose tolerance test (OGTT) glucose values were progressively higher across the groups (NGT < IGT < T2D, P < 0.05, ÀP < 0.0001)
Summary
Glycemic control is key in the management of type 2 diabetes (T2D), with postprandial glucose proposed as a better predictor of diabetes-related complications than fasting blood glucose or HbA1c (Cavalot et al 2011). Aerobic exercise is prescribed clinically to prevent and treat T2D because it improves glycemic control (Church et al 2010) and insulin sensitivity (Coker et al 2009; Slentz et al 2011) in obese and hyperglycemic individuals. Exercise training is commonly accompanied by improvements in aerobic fitness and weight loss which independently influence glucose metabolism (Ivy 1997; Coker et al 2009). A single bout of aerobic exercise, that does not alter fitness or body composition, is sufficient to increase insulin sensitivity both in healthy (Richter et al 1989), prediabetic (Devlin and Horton 1985), and T2D subjects (Burstein et al 1990; Bordenave et al 2008). The specific effect of a single exercise bout on postprandial glycemic control is far less consistent (Nazar et al 1987; Rogers et al 1988; Pestell et al 1993; King et al 1995; Larsen et al 1997; Bonen et al 1998; Baynard et al 2005; Venables et al 2007; van Dijk et al 2013; Gonzalez et al 2013; Roberts et al 2013; Oberlin et al 2014; Rynders et al 2014) likely due to between-study differences in the subject populations studied, the pre-exercise nutritional state, the exercise modality, and/or the method and timing of the postprandial measure following exercise
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