Modest sleep restriction does not influence steps, physical activity intensity or glucose tolerance in obese adults.

Sleep restriction (SR) (<6 h) and physical activity (PA) are risk factors for obesity, but little work has examined the inter‐related influences of both risk factors. In a free‐living environment, 13 overweight/obese adults were sleep restricted for five nights to 6 h time‐in‐bed each night, with and without regular exercise (45 min/65% VO2max; counterbalanced design). Two days of recovery sleep followed SR. Subjects were measured during a mixed meal tolerance test (MMT), resting metabolic rate, cognitive testing and fat biopsy (n=8). SR increased peak glucose response (+7.3 mg/dl, p =.04), elevated fasting non‐esterified fatty acid (NEFA) concentrations (+0.1 mmol/L, p =.001) and enhanced fat oxidation (p <.001) without modifying step counts or PA intensity. Inclusion of daily exercise increased step count (+4,700 steps/day, p <.001) and decreased the insulin response to a meal (p =.01) but did not prevent the increased peak glucose response or elevated NEFA levels. The weekend recovery period improved fasting glucose (p =.02), insulin (p =.02), NEFA concentrations (p =.001) and HOMA‐IR (p <.01) despite reduced steps (p <.01) and increased sedentary time (p <.01). Abdominal adipose tissue (AT) samples, obtained after baseline, SR and exercise, did not differ in lipolytic capacity following SR. Fatty acid synthase protein content tended to increase following SR (p =.07), but not following exercise. In a free‐living setting, SR adversely affected circulating NEFAs, fuel oxidation and peak glucose response but did not directly affect glucose tolerance or AT lipolysis. SR‐associated metabolic impairments were not mitigated by exercise, yet recovery sleep completely rescued its adverse effects on glucose metabolism. [ABSTRACT FROM AUTHOR]