Regular activity breaks improve postprandial triglyceride response

Background

Although physical activity (PA) and sedentary behavior affect the risk of all-cause mortality, cardiovascular disease and type 2 diabetes [1,2], the pattern of PA versus sedentary behavior to achieve this is not completely elucidated yet. Thus far, focus had been laid on their effects on the postprandial metabolism. In this context, it seems that regularly performed, short bouts of activity exert immediate effects on glucose and insulin, but the effects on postprandial triglyceride concentrations may be delayed [3-5].

As many studies measured the postprandial response immediately after PA, a study was performed to compare the effects of prolonged sitting and regular activity breaks for 2 minutes every 30 minutes, with or without an additional 30 min of continuous PA of the afternoon of day 1, on delayed postprandial metabolism measured on the morning of day 2. This study followed a randomized, crossover design and was performed in New Zealand between 2014 and 2016. Individuals were healthy and between 18 and 40 years, had a predominantly sedentary occupation and did not report more than 150 minutes of moderate to vigorous PA per week. Thirty-six participants completed all four intervention sessions.

The study comprised four intervention programs: 1) SIT: prolonged sitting (continuous sitting), 2) SIT+PA: prolonged sitting except for 30 min of continuous walking at the end of day 1, 3) RAB: sitting on both days was interrupted every 30 minutes by 2 minutes of walking and 4) RAB+PA: sitting on both days was interrupted every 30 minutes by 2 minutes of walking and additionally, 30 minutes of continuous walking at the end of day 1. Comparisons between intervention programs were made using mixed models including correction for fasting values at day 1.

Main results

• Whereas fasting concentrations on day 2 for non-esterified fatty acid (NEFA), glucose, and insulin were not significantly different between interventions, these of triglycerides were (SIT: 87.22 mg/dL, SIT+PA: 83.66 mg/dL, RAB: 85.44 mg/dL, RAB+PA: 79.21 mg/dL, P=0.005).
• More specifically, RAB+PA resulted in lower fasting triglycerides compared to all other 3 interventions (mean difference compared to SIT -8.9, SD -16.02 to -2.67, P=0.008, compared to SIT+PA -6.23, SD -13.35 to 0.00, P=0.054, compared to RAB -10.68, SD -17.80 to -4.45, P=0.002).
• Looking at the total AUCs the overall effect of intervention at day 2 was significant for triglycerides (P=0.008), NEFA (P<0.001) and insulin (P<0.001), but not for glucose (P=0.290).
• More specifically, RAB and RAB+PA reduced triglyceride response with 7% and 11% respectively, when compared to SIT and RAB+PA reduced it by 10% when compared to SIT+PA. Moreover, RAB and RAB+PA attenuated the postprandial suppression of NEFA by 23% and 15% respectively, when compared to SIT. Regarding insulin, both interventions with PA reduced the response with 13-15%, compared to SIT.
• Looking at the incremental AUCs, the overall effect of intervention was not significant for NEFA, glucose or insulin, but was for triglycerides (SIT: 175.33 mg/dL, SIT+PA: 184.23 mg/dL, RAB: 141.51 mg/dL and RAB+PA: 150.41 mg/dL, P=0.002).

Conclusion

References

Find this article online at J Clin Lipidol