Interrupting Prolonged Sitting With Intermittent Walking Increases Postprandial Gut Hormone Responses

Yung-Chih Chen; Jean-Philippe Walhin; Aaron Hengist; Javier T. Gonzalez; James A. Betts; Dylan Thompson


Med Sci Sports Exerc. 2022;54(7):1183-1189. 

In This Article

Abstract and Introduction


Introduction: Continuous exercise can increase postprandial gut hormone such as glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) responses, but it is unknown whether interrupting prolonged sitting with intermittent walking elicits this effect.

Method: Ten participants with central overweight/obesity (7 men and 3 postmenopausal women, 51 ± 5 yr; mean ± SD) completed a randomized crossover study in which they consumed breakfast and lunch in the laboratory while either sitting continuously for the entire 5.5-h period (SIT) or the prolonged sitting interrupted every 20 min by walking briskly (6.4 km·h−1) for 2 min (BREAKS). Blood samples were collected at regular intervals to examine postprandial plasma GLP-1, PYY, and glucose-dependent insulinotropic polypeptide concentrations. Adipose tissue samples were collected at baseline and at the end of the trials to examine changes in net dipeptidyl peptidase 4 secretion from primary explants.

Results: Mean (95% confidence interval) postprandial GLP-1 and PYY incremental area under curve values were elevated by 26% and 31% in the BREAKS trial versus SIT (8.4 [0.7, 16.1] vs 6.7 [−0.8, 14.2], P = 0.001, and 26.9 [8.1, 45.6] vs 20.4 [5.1, 35.8] nmol·330 min·L−1, P = 0.024, respectively) but without any such effect on glucose-dependent insulinotropic polypeptide (P = 0.076) or net adipose tissue dipeptidyl peptidase 4 secretion (P > 0.05).

Conclusions: Interrupting prolonged sitting with regular short bouts of brisk walking increases postprandial GLP-1 and PYY concentrations in healthy middle-age men and women with central adiposity.


Prolonged sitting contributes to increased adiposity (i.e., overweight/obesity), impaired appetite control (e.g., gut hormones dysfunction), reduced insulin sensitivity and glucose tolerance, and greater likelihood of experiencing metabolic-related diseases.[1,2] Studies have shown that gut hormones such as glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and glucose-dependent insulinotropic polypeptide (GIP) can regulate appetite, glycemic control and insulin secretion, gut motility, and/or nutrient digestion/absorption.[3–6] For example, elevated GLP-1 and PYY concentrations have been shown to inhibit gastric emptying and suppress energy consumption.[7] Within the context of obesity, these responses are considered beneficial by contributing to a negative energy balance. However, individuals with greater adiposity often exhibit abnormal circulating gut hormone concentrations compared with lean individuals.[8,9] This typically manifests as lower postprandial GLP-1 and PYY concentrations[8] but higher GIP concentrations in those with overweight/obesity.[10] Because gut hormones play important roles in metabolism and energy balance regulation, normalizing gut hormone concentrations may contribute to better metabolic control and/or weight management.

Clinical strategies, such as medication (e.g., GLP-1 analogues and dipeptidyl peptidase 4 [DPP-4] inhibitor) and surgery (e.g., bariatric surgery), have been shown to enhance gut hormones concentrations (e.g., GLP-1 and PYY).[11,12] However, these approaches have potential side effects, highlighting the need for less invasive and/or nonpharmacological strategies. Studies have revealed that continuous exercise at moderate-intensity[13,14] and low-volume high-intensity/sprint interval training[15] elevates gut hormone concentrations in individuals with overweight/obesity. However, the effect of less strenuous or prolonged modalities of physical activity on gut hormone concentrations in people with obesity is not known. This is particularly relevant in people with overweight/obesity as lower-intensity physical activity may be better tolerated than more strenuous exercise.

At present, only two studies have investigated the responses of any gut hormones in response to breaking sitting, and these have only determined PYY responses.[16,17] These studies found that breaking prolonged sitting does not alter PYY concentrations in young individuals with and without obesity.[16,17] GLP-1 and GIP are two key gut hormones with therapeutic potential in relation to glucose and weight control,[18,19] but neither were measured in those studies. Moreover, the meals provided during trials had low external validity (e.g., liquid diet with only carbohydrate and fat, and small meals every 2 h).[16,17] Thus, the purpose of current study was to investigate whether breaking up prolonged sitting can affect gut hormones responses (GLP-1, PYY, and GIP) to feeding in middle-age people with central overweight/obesity.