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)
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