The impact of daily caffeine intake on nighttime sleep in young adult men

Abstract

Acute caffeine intake can delay sleep initiation and reduce sleep intensity, particularly when consumed in the evening. However, it is not clear whether these sleep disturbances disappear when caffeine is continuously consumed during daytime, which is common for most coffee drinkers. To address this question, we investigated the sleep of twenty male young habitual caffeine consumers during a double-blind, randomized, crossover study including three 10-day conditions: caffeine (3 × 150 mg caffeine daily), withdrawal (3 × 150 mg caffeine for 8 days, then switch to placebo), and placebo (3 × placebo daily). After 9 days of continuous treatment, electroencephalographically (EEG)-derived sleep structure and intensity were recorded during a scheduled 8-h nighttime sleep episode starting 8 (caffeine condition) and 15 h (withdrawal condition) after the last caffeine intake. Upon scheduled wake-up time, subjective sleep quality and caffeine withdrawal symptoms were assessed. Unexpectedly, neither polysomnography-derived total sleep time, sleep latency, sleep architecture nor subjective sleep quality differed among placebo, caffeine, and withdrawal conditions. Nevertheless, EEG power density in the sigma frequencies (12-16 Hz) during non-rapid eye movement sleep was reduced in both caffeine and withdrawal conditions when compared to placebo. These results indicate that daily caffeine intake in the morning and afternoon hours does not strongly impair nighttime sleep structure nor subjective sleep quality in healthy good sleepers who regularly consume caffeine. The reduced EEG power density in the sigma range might represent early signs of overnight withdrawal from the continuous presence of the stimulant during the day.

Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1

Average caffeine levels collected prior to and after nighttime sleep (grey bar) in the placebo (black open circles), caffeine (blue filled circles), and withdrawal (red semi-filled circles) condition (mean values ± standard errors). The x-axis indicates the mean time of day of sample collection and color-coded asterisks represent significant (p < 0.05) post-hoc comparisons of the interaction effect condition × time.

Figure 2

Temporal dynamics of SWA (top) and sigma activity (bottom) during the first four sleep cycles in the placebo (black open circles), caffeine (blue filled circles), and the withdrawal (red semi-filled circles) condition (mean values). The x-axis indicates the mean time of day. While SWA (0.75–4.5 Hz) was not significantly affected by the treatment, sigma activity (12–16 Hz) showed reduced activity during both caffeine and withdrawal compared to the placebo condition (pall < 0.05). The inset in each right upper corner represents the mean values ± standard errors of the all-night SWA and sigma activity respectively during NREM sleep in the placebo, caffeine, and withdrawal condition. While all-night SWA (0.75–4.5 Hz) did not differ among the conditions, sigma activity (12–16 Hz) was lower in the caffeine and withdrawal condition compared to placebo (p < 0.05). All analyses are based on log-transformed data.

Figure 3

Relative withdrawal symptoms in the caffeine and withdrawal condition (i.e. withdrawal score of the caffeine and withdrawal condition respectively minus the score of the placebo condition) assessed 35 min, 4 h, and 8 h after wake-up on day ten of treatment. Depicted are mean values and standard errors of the relative values (i.e. difference to placebo). Overall, volunteers reported more withdrawal symptoms in the withdrawal condition compared to the caffeine condition (p < 0.05). This difference was particularly present 8 h after wake-up during withdrawal compared to caffeine (p < 0.001).

Figure 4

Illustration of the study design. Twenty volunteers participated in a placebo, a caffeine, and a withdrawal condition during which they ingested either caffeine or placebo capsules three times daily (wake-up + 45 min, + 255 min, and + 475 min). Each condition started with an ambulatory part of 9 days and was followed by a laboratory part of 43 h. After 9 days of continuous treatment, we recorded 8 h of polysomnography (PSG), indicated as arrows, during nighttime sleep under controlled laboratory conditions. The sleep episode was scheduled to volunteers’ habitual bedtime.