Effects of exercise training alone vs a combined exercise and nutritional lifestyle intervention on glucose homeostasis in prediabetic individuals: a randomised controlled trial

Abstract

Aims/hypothesis Although the Diabetes Prevention Program (DPP) established lifestyle changes (diet, exercise and weight loss) as the ‘gold standard’ preventive therapy for diabetes, the relative contribution of exercise alone to the overall utility of the combined diet and exercise effect of DPP is unknown; furthermore, the optimal intensity of exercise for preventing progression to diabetes remains very controversial. To establish clinical efficacy, we undertook a study (2009 to 2013) to determine: how much of the effect on measures of glucose homeostasis of a 6 month programme modelled after the first 6 months of the DPP is due to exercise alone; whether moderate- or vigorous-intensity exercise is better for improving glucose homeostasis; and to what extent amount of exercise is a contributor to improving glucose control. The primary outcome was improvement in fasting plasma glucose, with improvement in plasma glucose AUC response to an OGTT as the major secondary outcome. Methods The trial was a parallel clinical trial. Sedentary, non smokers who were 45–75 year old adults (n=195) with elevated fasting glucose (5.28–6.94 mmol/l) but without cardiovascular disease, uncontrolled hypertension, or diabetes, from the Durham area, were studied at Duke University. They were randomised into one of four 6 month interventions: (1) low amount (42 kJ kg body weight−1 week−1 [KKW])/moderate intensity: equivalent of expending 42 KKW (e.g. walking ~16 km [8.6 miles] per week) with moderate-intensity (50% peak V̇O2reserve) exercise; (2) high amount (67 KKW)/moderate intensity: equivalent of expending 67 KKW (~22.3 km [13.8 miles] per week) with moderate-intensity exercise; (3) high amount (67 KKW)/vigorous intensity: equivalent to group 2, but with vigorous-intensity exercise (75% peak V̇O2reserve); and (4) diet + 42 KKW moderate intensity: same as group 1 but with diet and weight loss (7%) to mimic the first 6 months of the DPP. Computer-generated randomisation lists were provided by our statistician (GPS). The randomisation list was maintained by LHW and CAS with no knowledge of or input into the scheduling, whereas all scheduling was done by LAB, with no knowledge of the randomisation list. Subjects were automatically assigned to the next group listed on the randomisation sheet (with no ability to manipulate the list order) on the day that they came in for the OGTT, by LHW. All plasma analysis was done blinded by the individuals doing the measurements (i.e. lipids, glucose, insulin). Subjects and research staff (other than individuals analysing the blood) were not blinded to the group assignments. Results Number randomised, completers and number analysed with complete OGTT data for each group were: low-amount/moderate-intensity (61, 43, 35); high-amount/moderate-intensity (61, 44, 40); high-amount/vigorous-intensity (61, 43, 38); diet/exercise (54, 45, 37), respectively. Only the diet and exercise group experienced a decrease in fasting glucose ( p<0.001). The means and 95% CIs for changes in fasting glucose (mmol/l)...

Glycemic and Metabolic Effects of Two Long Bouts of Moderate-Intensity Exercise in Men with Normal Glucose Tolerance or Type 2 Diabetes

“…Although other studies have suggested a dose–response relationship between exercise duration and improvements in glucose tolerance or insulin sensitivity (36–38), we did not observe any improvements in glucose tolerance following 3 h of exercise.…”

Autophagy activation, not peroxisome proliferator‐activated receptor γ coactivator 1α, may mediate exercise‐induced improvements in glucose handling during diet‐induced obesity

“…; Slentz et al . ). The major regulator of mitochondrial quality control is the transcriptional coactivator, peroxisome proliferator‐activated receptor γ coactivator 1α (PGC‐1α), which is increased with endurance exercise (Yan et al .…”

“…Mitochondria, the predominant energy suppliers to the cell, have been implicated in the deterioration of myocyte health during insulin resistance (Kelley et al 2002;Mogensen et al 2007;Koves et al 2008). Mitochondrial function and quality can be dramatically improved by exercise, subsequently leading to improvements in glucose handling Gong et al 2015;Kim et al 2015;Slentz et al 2016). The major regulator of mitochondrial quality control is the transcriptional coactivator, peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), which is increased with endurance exercise Greene et al 2015).…”

Effects of regular endurance exercise on GlycA: Combined analysis of 14 exercise interventions

“…24 The following studies had only one exercise training group (i.e., prescribed only one dose of exercise): APOE (~13-15 kilocalories per kilogram of body weight per week [KKW]) 18 , HERITAGE (~12-14 KKW) 20 , and GERS (~10-12 KKW). 21 The DREW study was a randomized control trial with three different exercise training groups that expended 4, 8, or 12 KKW at 50% VO 2 peak for six months.…”

“…23 Finally, STRRIDE-PD participants were randomized to one of four groups: low-amount and moderate intensity (10 KKW at 50% VO 2 peak), high amount and moderate intensity (16 KKW at 50% VO 2 peak), high amount and vigorous intensity (16 KKW at 75% VO 2 peak), and Clinical Lifestyle intervention: low amount moderate intensity intervention plus diet (with weight loss goal of 7%). 24 The sample, study design, and exercise training protocol of each study have been described elsewhere and are summarized in the Supplemental Methods.…”