anzctr.org.au ACTRN12613000576729 FUNDING: : This research was supported by a National Health and Medical Research Council (NHMRC) project grant (no. 1081734) and the Victorian Government Operational Infrastructure Support scheme.

Breaking up sitting with light physical activity (PA) is effective in reducing hyperglycemia in the laboratory. Whether the same effects are observed in the free-living environment remains unknown. We evaluated how daily and postprandial glycemia is impacted by 20, 40, or 60 min of activity performed as either breaks from sitting after each meal (BR) or as one continuous walk after breakfast (WALK). Thirty individuals with type 2 diabetes completed three experimental conditions [BR, WALK, and control (CON)] in a randomized crossover design. Conditions were performed in a free-living environment with strict dietary control over 7 days. Participants increased PA in BR and WALK by 20, 40, or 60 min ( n = 10 in each group) and maintained habitual levels of PA during CON. A continuous glucose monitor (iPro2) and activPAL activity monitor were worn to quantify glycemic control and PA. Using linear mixed models with repeated measures, we 1) compared postprandial glucose (PPG) across conditions and 2) assessed the relationship between activity volume and glucose responses. Whereas WALK tended to shorten the daily duration of hyperglycemia compared with CON ( P = 0.0875), BR was not different from CON. BR and WALK significantly attenuated the breakfast PPG versus CON ( P ≤ 0.05), but lunch and dinner PPG were unaffected by BR and WALK. In conclusion, continuous walking was more effective than breaks from sitting in lowering daily hyperglycemia for the group, but both conditions lowered breakfast PPG. In contrast to tightly controlled laboratory studies, breaks from sitting did not lower hyperglycemia in the free-living environment. NEW & NOTEWORTHY Our “ecolabical” approach is new and noteworthy. This approach combines the external validity of the free-living environment (ecological) with the control of key confounding variables in the laboratory and allows for highly translatable findings by minimizing confounding variables. We found that both postmeal continuous walking and short breaks from sitting similarly attenuated the postprandial glucose (PPG) response to breakfast. Unlike previous laboratory studies, neither condition (walk after breakfast or postmeal breaks) significantly impacted PPG at lunch or dinner.

The extent and duration of serum lipid and lipoprotein changes were examined in 12 mildly obese women who walked 45 minutes at 60% VO2max in a laboratory setting. A two-factor, 2 x 6 design with repeated measures on both factors was utilized. The first factor was condition (exercise and rest) and the second factor was time (six times of measurement over a 24-hour period) with treatment counterbalanced. The patterns of change in total high-density lipoprotein-cholesterol (HDL-C) [F(5,55) = 5.75, p less than 0.001] and HDL3-C [F(5,55) = 2.62, p = 0.034], but not HDL2-C [F(5,55) = 1.15, p = 0.346], were significantly different between conditions. Relative to baseline and the rest condition, total HDL-C tended to rise due to a significant 11.6% increase in HDL3-C immediately post-exercise, with values returning to baseline 1.5 hours post-exercise. The interaction statistic for triglycerides was significant with trends for a decrease in triglycerides at 1.5 and 23 hours post-exercise relative to baseline and the rest condition. No significant differences were seen between the exercise and rest conditions for total cholesterol, low-density lipoprotein cholesterol, glucose, or plasma volume. These data indicate that an exercise intensity achievable by brisk walking (7.4 kph) is sufficient to evoke significant but short-term changes in serum HDL3-C concentrations in women.

We determined the effects of altering meal timing and diet composition on temporal glucose homeostasis and physical activity measures. Eight sedentary, overweight/obese men (mean ± SD, age: 36 ± 4 years; BMI: 29.8 ± 1.8 kg/m2) completed two × 12-day (12-d) measurement periods, including a 7-d habitual period, and then 5 d of each diet (high-fat diet [HFD]: 67:15:18% fat:carbohydrate:protein versus high-carbohydrate diet [HCD]: 67:15:18% carbohydrate:fat:protein) of three meals/d at ±30 min of 0800 h, 1230 h, and 1800 h, in a randomised order with an 8-d washout. Energy intake (EI), the timing of meal consumption, blood glucose regulation (continuous glucose monitor system (CGMS)), and activity patterns (accelerometer and inclinometer) were assessed across each 12-d period. Meal provision did not alter the patterns of reduced physical activity, and increased sedentary behaviour following dinner, compared with following breakfast and lunch. The HCD increased peak (+1.6 mmol/L, p < 0.001), mean (+0.5 mmol/L, p = 0.001), and total area under the curve (+670 mmol/L/min, p = 0.001), as well as 3-h postprandial meal glucose concentrations (all p < 0.001) compared with the HFD. In overweight/obese males, the provision of meals did not alter physical activity patterns, but did affect glycaemic control. Greater emphasis on meal timing and composition is required in diet and/or behaviour intervention studies to ensure relevance to real-world behaviours.