The circadian system modulates the rate of recovery of systolic blood pressure after exercise in humans.

STUDY OBJECTIVES: Recovery rates of systolic blood pressure (BP) and heart rate (HR) after exercise have been used to assess cardiovascular fitness, and slower recovery rates are predictors of coronary heart disease and cardiac mortality. The endogenous circadian system is known to modulate BP and HR at rest and during exercise. Here, we examined whether the post-exercise recovery rates of BP and HR are also under circadian control. METHODS: Twelve healthy adults (mean age = 26 ± 6 (SD) years; 6 female) participated in a 240 h forced desynchrony protocol in dim light where all behaviors, including 15 min cycle exercise tests at 60% maximal HR, were uniformly distributed across the circadian cycle. Circadian phases were assigned based on the rhythm of core body temperature. For each session, HR was measured continuously, and BP every 3-5 min throughout baseline, exercise, and recovery. Recovery was quantified as the proportional return to pre-exercise baseline levels following exercise ([peak exercise-recovery]/[peak exercise-baseline) × 100%], whereby 100% represents full recovery to baseline). RESULTS: There was a significant circadian rhythm in systolic BP recovery, with fastest recovery at the circadian phase corresponding to late afternoon (equivalent to ~5 pm) and slower recovery across the early morning (~8:30 am; p = 0.029, peak-to-trough: 9.2%). There were no significant circadian variations in post-exercise recovery rates of diastolic BP or HR. CONCLUSIONS: The circadian system modulates the rate of recovery of systolic BP after exercise with fastest recovery in the biological afternoon. These data could have implications for exercise prescription and interpretation of clinical tests of stress recovery.

Later circadian timing of food intake is associated with increased body fat.

Background: Weight gain and obesity have reached alarming levels. Eating at a later clock hour is a newly described risk factor for adverse metabolic health; yet, how eating at a later circadian time influences body composition is unknown. Using clock hour to document eating times may be misleading owing to individual differences in circadian timing relative to clock hour.Objective: This study examined the relations between the timing of food consumption relative to clock hour and endogenous circadian time, content of food intake, and body composition.Design: We enrolled 110 participants, aged 18-22 y, in a 30-d cross-sectional study to document sleep and circadian behaviors within their regular daily routines. We used a time-stamped-picture mobile phone application to record all food intake across 7 consecutive days during a participant's regular daily routines and assessed their body composition and timing of melatonin release during an in-laboratory assessment.Results: Nonlean individuals (high body fat) consumed most of their calories 1.1 h closer to melatonin onset, which heralds the beginning of the biological night, than did lean individuals (low body fat) (log-rank P = 0.009). In contrast, there were no differences between lean and nonlean individuals in the clock hour of food consumption (P = 0.72). Multiple regression analysis showed that the timing of food intake relative to melatonin onset was significantly associated with the percentage of body fat and body mass index (both P < 0.05) while controlling for sex, whereas no relations were found between the clock hour of food intake, caloric amount, meal macronutrient composition, activity or exercise level, or sleep duration and either of these body composition measures (all P > 0.72).Conclusions: These results provide evidence that the consumption of food during the circadian evening and/or night, independent of more traditional risk factors such as amount or content of food intake and activity level, plays an important role in body composition. This trial was registered at clinicaltrials.gov as NCT02846077.

Short sleep duration and dietary intake: epidemiologic evidence, mechanisms, and health implications.

Links between short sleep duration and obesity, type 2 diabetes, hypertension, and cardiovascular disease may be mediated through changes in dietary intake. This review provides an overview of recent epidemiologic studies on the relations between habitual short sleep duration and dietary intake in adults from 16 cross-sectional studies. The studies have observed consistent associations between short sleep duration and higher total energy intake and higher total fat intake, and limited evidence for lower fruit intake, and lower quality diets. Evidence also suggests that short sleepers may have irregular eating behavior deviating from the traditional 3 meals/d to fewer main meals and more frequent, smaller, energy-dense, and highly palatable snacks at night. Although the impact of short sleep duration on dietary intake tends to be small, if chronic, it may contribute to an increased risk of obesity and related chronic disease. Mechanisms mediating the associations between sleep duration and dietary intake are likely to be multifactorial and include differences in the appetite-related hormones leptin and ghrelin, hedonic pathways, extended hours for intake, and altered time of intake. Taking into account these epidemiologic relations and the evidence for causal relations between sleep loss and metabolism and cardiovascular function, health promotion strategies should emphasize improved sleep as an additional factor in health and weight management. Moreover, future sleep interventions in controlled studies and sleep extension trials in chronic short sleepers are imperative for establishing whether there is a causal relation between short sleep duration and changes in dietary intake.

Influence of the Circadian System on Disease Severity.

The severity of many diseases varies across the day and night. For example, adverse cardiovascular incidents peak in the morning, asthma is often worse at night and temporal lobe epileptic seizures are most prevalent in the afternoon. These patterns may be due to the day/night rhythm in environment and behavior, and/or endogenous circadian rhythms in physiology. Furthermore, chronic misalignment between the endogenous circadian timing system and the behavioral cycles could be a cause of increased risk of diabetes, obesity, cardiovascular disease and certain cancers in shift workers. Here we describe the magnitude, relevance and potential biological basis of such daily changes in disease severity and of circadian/behavioral misalignment, and present how these insights may help in the development of appropriate chronotherapy.