A recent study published in the journal Nutrition describes the impact of caffeine intake on cerebral blood flow in young, healthy individuals.
Caffeine is the most commonly consumed pharmacologically active substance worldwide and is present in variable amounts in coffee, tea, soft drinks, chocolates, and energy drinks. At moderate doses, caffeine acts as a stimulant to the central nervous system (CNS) and, as a result, is associated with increased alertness, cognitive enhancement, and energy levels.
Nevertheless, the long-term consumption of caffeine at high doses can cause adverse health effects, including increased blood pressure and vascular resistance, as well as cause arterial stiffness and cerebral vasoconstriction. Regular consumption of two to four cups of caffeine each day is known to reduce cerebral blood flow by 22-30%.
Due to its structural similarities with adenosine, caffeine can bind and subsequently block adenosine receptors in the brain. This leads to increased release of neurotransmitters responsible for mood improvement, increased energy levels, and concentration enhancement. Caffeine can also inhibit the activity of phosphodiesterase, which subsequently leads to increased cellular concentrations of cyclic adenosine monophosphate (cAMP) and blood pressure levels.
In the current study, scientists investigate whether caffeine consumption can affect the blood flow velocity in the middle cerebral artery in clinically healthy young individuals. A total of 45 university students between 18 and 22 years of age were included in the study, none of whom were regular coffee drinkers. Notably, most study participants reported consuming one to two cups of coffee daily in unusual situations, such as during exam season.
The participants were randomly categorized into three groups, with each group comprising 15 participants. In the low- and high-caffeine groups, participants were administered 45 mg and 120 mg caffeine in capsulated forms, respectively. In the control no-caffeine group, participants were given flour capsules as a placebo.
Transcranial Doppler ultrasonography was performed to measure the flow velocity in the middle cerebral artery at baseline before caffeine consumption and 30 minutes after caffeine consumption. While obtaining the velocity measurements, participants were asked to perform functional tests that assessed hypo- and hyper-ventilation, as well as three cognitive activities measuring short-term memory, vocabulary problem-solving, and math problem-solving.
The comparison between baseline and post-intervention measurements in the low-caffeine group revealed a significant reduction in mean and peak systolic velocities during hypoventilation, as well as the short-term memory and vocabulary problem-solving tests. A substantial reduction in end-diastolic velocity was also observed during hypoventilation, hyperventilation, and the short-term memory test. Regarding heart rate, a significant reduction was observed during hypoventilation and hyperventilation, as well as the short-term memory and math problem-solving tests.
The same comparison in the high-caffeine group revealed a significant reduction in all tested parameters of mean velocity, peak systolic velocity, end-diastolic velocity, and heart rate in all evaluations. Comparatively, no significant differences in the velocities were observed between baseline and post-intervention conditions in the control group
Changes during cognitive tests
A significant induction in end-diastolic velocity and heart rate was observed in the high-caffeine group during the short-term memory test. In the control group, a significant induction in end-diastolic velocity was observed during the math problem-solving test.
No significant changes in velocities and heart rate were observed in the low-caffeine group during cognitive tests.
Caffeine intake acutely influences the cardiovascular system and interferes with blood flow velocities of the middle cerebral artery in a dose-dependent manner. The study findings suggest that caffeine-mediated reduction in cerebral arterial velocities could be due to vasodilation of cerebral arteries caused by the acute effect.