Abstract

Active breaks in prolonged sitting has beneficial impacts on cardiometabolic risk biomarkers. The molecular mechanisms include regulation of skeletal muscle gene and protein expression controlling metabolic, inflammatory and cell development pathways. An active communication network exists between adipose and muscle tissue, but the effect of active breaks in prolonged sitting on adipose tissue have not been investigated. This study characterized the acute transcriptional events induced in adipose tissue by regular active breaks during prolonged sitting. We studied 8 overweight/obese adults participating in an acute randomized three-intervention crossover trial. Interventions were performed in the postprandial state and included: (i) prolonged uninterrupted sitting; or prolonged sitting interrupted with 2-minute bouts of (ii) light- or (iii) moderate-intensity treadmill walking every 20 minutes. Subcutaneous adipose tissue biopsies were obtained after each condition. Microarrays identified 36 differentially expressed genes between the three conditions (fold change ≥0.5 in either direction; p < 0.05). Pathway analysis indicated that breaking up of prolonged sitting led to differential regulation of adipose tissue metabolic networks and inflammatory pathways, increased insulin signaling, modulation of adipocyte cell cycle, and facilitated cross-talk between adipose tissue and other organs. This study provides preliminary insight into the adipose tissue regulatory systems that may contribute to the physiological effects of interrupting prolonged sitting.

Highlights

  • Prolonged uninterrupted sitting is positively associated with cardiometabolic risk biomarkers and premature mortality, independent of moderate-to-vigorous intensity physical activity[1]

  • Our group has observed favourable changes in skeletal muscle gene and protein expression that likely contribute to the improved glucose control associated with breaking up of prolonged sitting via light- or moderate-intensity activities

  • 7/36 genes were upregulated and 2/36 genes were downregulated in the light-intensity breaks condition, compared to uninterrupted sitting; 1/36 genes was upregulated and none were downregulated in the moderate-intensity breaks condition compared to uninterrupted sitting; and, 29/36 genes were upregulated and none were downregulated in the moderate-intensity breaks condition compared to the light-intensity breaks (Table 1)

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Summary

Introduction

Prolonged uninterrupted sitting is positively associated with cardiometabolic risk biomarkers and premature mortality, independent of moderate-to-vigorous intensity physical activity[1]. Our group has observed favourable changes in skeletal muscle gene and protein expression that likely contribute to the improved glucose control associated with breaking up of prolonged sitting via light- or moderate-intensity activities. These changes include some which align with, and others which may be distinct from, the effects of continuous acute exercise[12,13]. In a previous study we showed that, compared to uninterrupted sitting, frequent brief bouts of either light- or moderate-intensity walking lowered acute postprandial glucose and insulin responses[2]. An ancillary analysis of vastus lateralis muscle collected from 8 participants in the main study showed that those brief interruptions to sitting time resulted in upregulation of genes involved in cell development, glucose uptake, and anti-inflammatory pathways; and, downregulation of genes associated with protein degradation and muscle atrophy[13]

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