Biology subjects

Garbazza, C.

Publications and source records attributed to Garbazza, C..

5 recordsLinked to original sources

bioRxiv2026

A single day of natural daylight exposure and physical activity does not conclusively change circadian phase: A Bayesian crossover experiment

Among the environmental signals that shape human physiology, the daily light-dark cycle is the primary zeitgeber of the human circadian system. Physical activity may provide an additional non-photic time cue and frequently co-occurs with daylight in everyday life. However, their independent and combined effects on circadian phase have rarely been disentangled under naturalistic daylight conditions. In a counterbalanced mixed-design experiment, 41 healthy adults (24 women; mean age = 23.7 years, SD = 4.3) participated in up to three 40-h visits on fixed individual sleep-wake schedules. Each visit comprised an 8-h exposure beginning 1.5 h after wake to natural daylight, daylight attenuated by amber-tinted glasses, or indoor electric light (within subjects; mean photopic illuminances: 1196, 460, and 75 lx), with otherwise dim-light conditions. Participants hiked for approximately 4 h or remained sedentary (between subjects; activity indexed by median heart rate reserve [HRR]; group means: 32.7% and 2.7%). Bayesian hierarchical models used individual photopic illuminance (ActTrust 2) and median HRR to predict change in dim-light melatonin onset (DLMO; primary outcome) and exploratory outcomes (daytime and evening sleepiness, mood, and wellbeing, daytime perceived exertion, and evening psychomotor vigilance). Per standard-deviation increase in log-transformed illuminance and median HRR, estimated DLMO changes were -4.22 min (95% HDI [-10.93, 2.22]; BF = 0.70) and -6.48 min (95% HDI [-13.79, 1.27], BF = 1.56), respectively. Evidence remained inconclusive for both predictors and their interaction. Exploratory findings were largely inconclusive, practically negligible, or favoured the absence of effects. The circadian effects of a single day of natural daylight exposure, with or without physical activity, therefore remain unclear. Resolving this question may require larger samples and brighter, repeated, or habitual exposure timed to phases of greater circadian light sensitivity.

neuroscience↗

bioRxiv2021

Time to recover from daily caffeine intake.

Caffeine elicits widespread effects in the central nervous system and is the most frequently consumed psychostimulant worldwide. First evidence indicates that, during daily intake, the elimination of caffeine may slow down and the primary metabolite, paraxanthine, may accumulate. The neural impact of such adaptions is virtually unexplored. In this report, we leveraged the data of a laboratory study with N= 20 participants and three within-subject conditions: caffeine (150 mg caffeine x 3/day x 10 days), placebo (150 mg mannitol x 3/day x 10 days), and withdrawal (caffeine x 9 days, afterwards placebo x 1 day). Using liquid chromatography-mass spectrometry coupled with tandem mass spectrometry, we determined the course of salivary caffeine and paraxanthine, measured regularly at day 10. We assessed grey matter (GM) intensity and cerebral blood flow (CBF) in the withdrawal condition as compared to their changes in caffeine in our previous report. The results indicate high remaining levels of paraxanthine and of caffeine carried overnight during daily intake, and the levels of paraxanthine remained higher than in placebo during withdrawal. After 36 h of withdrawal, the previously reported caffeine-induced GM reduction was partially mitigated, while CBF was elevated compared to placebo. Our findings unveil that conventional daily caffeine intake does not provide sufficient time to clear up psychoactive compounds and restore cerebral responses, even after 36 hours of abstinence. They also suggest investigating consequences of a paraxanthine accumulation during daily caffeine intake.

pharmacology and toxicology↗

bioRxiv2020

Rest-activity cycles and melatonin phase angle of circadian entrainment in people without cone-mediated vision

BackgroundLight exposure entrains the circadian clock through the intrinsically photosensitive retinal ganglion cells, which sense light in addition to the cones and rods. In congenital achromatopsia (ACHM; prevalence 1:30-50,000), the cone system is non-functional, resulting in severe light avoidance and photophobia at daytime light levels. How this condition affects circadian and neuroendocrine responses to light is not known. MethodsIn genetically confirmed ACHM patients (n=7; age 30-72 years; 6 women, 1 male), we examined survey-assessed sleep/circadian phenotype (PSQI, ESS, MEQ, MCTQ), self-reported visual function (NEI-VFQ-25), sensitivity to light (VLSQ-8) and use of spectral filters that modify chronic light exposure. In all but one patient, we measured rest-activity cycles using actigraphy over 3 weeks and measured the melatonin phase angle of entrainment using the dim-light melatonin onset (DLMO). ResultsACHM patients experience a severely attenuated light-dark cycle due to severe light sensitivity and habitual use of filters to reduce retinal illumination. In aggregate, both MEQ and MCTQ indicated a tendency to late chronotype. We found regular rest-activity patterns in all patients and normal phase angles of entrainment in participants with a measurable DLMO. ConclusionsOur results reveal that a functional cone system and exposure to daytime light intensities are not necessary for regular behavioural and hormonal entrainment, even when survey-assessed sleep and circadian phenotype indicated a tendency for a late chronotype and sleep problems in our ACHM cohort. Our results can be explained by an adaptation mechanism in circadian photoreception which adjusts to the range of habitual light exposures.

neuroscience↗

bioRxiv2020

Wide awake at bedtime? The effects of caffeine on sleep and circadian timing in teenagers - a randomized crossover trial

BackgroundAdolescents frequently consume caffeine with unknown consequences on sleep and circadian rhythms. In adults, the evidence indicates that caffeine acutely reduces homeostatic sleep pressure and delays the circadian timing system. ObjectiveHere, we investigated the acute effects of caffeine intake on the developing sleep-wake regulatory system of teenagers. DesignIn a double-blind randomized crossover laboratory study, 18 teenagers (16.1 {+/-} 1 years old, pubertal development scale [PDS]: 2.76 {+/-} 0.35) ingested 80 mg caffeine (vs placebo) four hours prior to bedtime. Until bedtime, participants regularly filled in the Karolinska Sleepiness Scale and gave saliva samples to measure melatonin secretion. During nighttime, we quantified homeostatic sleep need by the electroencephalographically derived amount of slow wave sleep duration (SWS). After sleep, participants rated sleep quality by the Leeds Sleep Evaluation Questionnaire. ResultsWhile participants felt less sleepy after caffeine vs. placebo (P=0.038), their ratings of sleep quality were not strongly affected by the treatment. However, objectively, SWS was on average reduced by [~]20 min after caffeine vs. placebo (P=0.026). This caffeine-induced reduction was more pronounced in those individuals with more SWS under placebo (regression: P=0.042; standardized beta=0.622, P=0.011), even if controlling for habitual caffeine intake or pubertal stage (PDS). In melatonin onsets we observed both delays and advances in response to caffeine. This variance could partly be explained by differences in relative dose (i.e., mg caffeine/kg of bodyweight): the higher the relative dose, the more likely were delays (regression: P=0.01; standardized beta=0.592, P=0.01). ConclusionsIn teenagers, evening caffeine intake of already 80 mg (i.e. [~]8fl oz of common energy drinks) is sufficient to promote alertness at the costs of subsequent sleep. These costs might be more pronounced in adolescents with a higher need for SWS. Moreover, caffeine might disturb the circadian timing system, consequently hampering the balanced interplay of sleep-wake regulatory components. Sources of SupportMarie-Heim-Voegtlin Grant of the Swiss National Science Foundation (SNSF) PMPDP1_171364

neuroscience↗

bioRxiv2019

Caffeine-dependent changes of sleep-wake regulation: evidence for adaptation after repeated intake

To enhance wakefulness, daily consumption of caffeine in the morning and afternoon is highly common. However, it is unknown whether such a regular intake pattern affects timing and quality of wakefulness, as regulated by an interplay of circadian and sleep-homeostatic mechanisms. Thus, we investigated the effects of daily caffeine intake and its withdrawal on circadian rhythms and wake-promotion in 20 male young habitual caffeine consumers. We applied a double-blind, within-subject design with a caffeine (150 mg, 3 x daily), a placebo, and a withdrawal condition each lasting ten days. Starting on day nine of treatment, salivary melatonin and cortisol, evening nap sleep, as well as sleepiness and vigilance performance throughout day and night were quantified during 43 h under controlled laboratory conditions. Neither the time course of melatonin (i.e., onset, amplitude, or area under the curve) nor the time course of cortisol were significantly affected by caffeine intake or its withdrawal. During withdrawal, however, volunteers reported increased sleepiness, showed more attentional lapses, as well as polysomnography-derived markers of elevated sleep propensity in the late evening compared to both, placebo and caffeine conditions. Thus, the typical timing of habitual caffeine intake in humans may not necessarily shift circadian phase nor lead to clear-cut benefits in alertness. The time-of-day independent effects of caffeine withdrawal suggest an adaptation to the substance, presumably in the homeostatic aspect of sleep-wake regulation.

neuroscience↗