Both acute and chronic caffeine consumption affect cardiovascular responses to total sleep deprivation

Sleep deprivation is known to induce cardiovascular responses. Several studies have shown the beneficial effect of caffeine on neurobehavioral performance during sleep deprivation, but less is known about its influence on the cardiovascular and inflammatory responses associated with sleep deprivation. The aim of this study is to evaluate the impact of acute caffeine intake on (1) peripheral blood pressures, and (2) heart rate, and cutaneous vascular conductance (CVC) and related biomarkers of endothelial activation, during total sleep deprivation (TSD), considering habitual caffeine consumption.

41 subjects followed a randomized, placebo-controlled, cross-over study and underwent 2 conditions of TSD (38 h), one with caffeine intake at 09:00 and 14:00 (2.5 mg/kg), and the other with placebo intake.

We confirm that TSD increases systolic and diastolic arterial pressures (p = 0.001 and p = 0.002 for main effects respectively) and heart rate (p = 0.001), and decreases endothelium-dependent and -independent CVC (p = 0.001). Acute caffeine intake inflates the increase in arterial pressures and IL-6 levels, while it does not affect CVC and levels of E-selectin and monocyte chemotaxis protein-1 (MCP-1). Moreover, chronic caffeine consumption had significant main effects on systolic arterial pressure (p = 0.03), heart rate (p = 0.02), IL-6 levels (p = 0.02), and acetylcholine (ACh)-induced CVC (p = 0.02), and interacted with TSD on E-selectin levels and ACh-induced CVC (p = 0.02 respectively).

Acute caffeine intake provokes immuno-inflammatory and cardiovascular responses, and chronic caffeine consumption should be limited to the lowest efficient doses.

https://clinicaltrials.gov/study/NCT03859882, identifier NCT03859882.