Abstract

Abstract Introduction Resting energy expenditure (EE) follows a circadian rhythm in healthy lean participants, with a nadir in the early morning hours. We determined: (1) whether this pattern persists (or how substrate utilization may change), when challenged with exercise, and; (2) whether obesity affects these responses. Methods Fourteen participants (aged 48.5±12.8y; 6-female; 5-obese, BMI 31.9±1.4kg/m2 [avg±SD]) underwent a 5-day inpatient forced desynchrony protocol, comprised of ten 5h 20min ‘days’ in dim-lighting and free of time cues. Resting EE was measured immediately prior to a 15-minute cycle ergometer exercise bout at 50% of estimated heart rate maximum. Substrate utilization was determined from the respiratory quotient (RQ). Circadian phase was calculated using the salivary dim-light melatonin onset (>3pg/mL threshold). EE data were analyzed using a mixed-effect model with group (lean vs. obese) and circadian phase as fixed factors; subject was a random factor. RQ was analyzed using t-tests to determine day/night differences in groups at rest and in response to exercise. Results Resting and exercising EE both displayed endogenous circadian rhythms (p<0.05) with nadirs in the early morning (~5:30am), without any differences between groups (p>0.22). Resting RQ was similar between the day and night in the lean group (p=0.66), but decreased (suggesting lower carbohydrate utilization) at night within the obese group (-2.5±1.6%, p=0.02). The lean group increased RQ in response to exercise both during the day (+8.9±2.8%) and night (+8.0±2.8%) (both p<0.001), but there was no increase in RQ in the obese group during either day or night exercise (p>0.16). Conclusion These data demonstrate that EE during rest and exercise follows a circadian pattern, with limited influence of obesity. Circadian differences in substrate utilization between lean and obese in the resting state and in response to exercise may play a role in expression and maintenance of unwanted weight gain and impaired metabolic health. Support R01HL125893, R01HL140577, KL2TR002370, K01HL146992, F32HL131308, Medical Research Foundation of Oregon, Ford Foundation, and CTSA grant (UL1TR000128)

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call