A new study reveals that consuming an amount of caffeine equivalent to two cups of coffee enhances the brain’s ability to temporarily quiet its own motor signals in response to sensory input. The results indicate that everyday habits can alter neurological test readouts, which has implications for diagnosing certain cognitive conditions. The research was published in the journal Clinical Neurophysiology.
Measuring the electrical activity of the living human brain presents unique challenges. Neurologists often rely on noninvasive techniques to safely probe how different brain regions communicate. One common tool is transcranial magnetic stimulation, which involves placing an electromagnetic coil against a person’s scalp. The coil delivers brief magnetic pulses through the skull and into the underlying nervous tissue.
When positioned over the primary motor cortex, these magnetic pulses generate weak electrical currents that trigger downward signals to the body. This neural pathway travels down the spinal cord and out to the peripheral nerves. If the stimulation is strong enough, it forces a specific muscle to twitch, such as the muscle located at the base of the thumb. Neurologists measure the physical size of this muscle twitch to gauge the baseline excitability of the brain’s motor networks.
Researchers also use this technique to study how the brain processes incoming sensory information alongside outgoing movement commands. They employ a specific testing protocol called short-latency afferent inhibition. In this protocol, an examiner delivers a mild electrical shock to a nerve at the wrist shortly before sending the magnetic pulse into the brain.
The sensory signal from the wrist travels up the arm and enters the brain’s somatosensory area. Milliseconds later, the magnetic pulse hits the nearby motor cortex to trigger the thumb twitch. The arrival of the sensory signal acts like a temporary brake on the motor cortex. The resulting muscle twitch ends up being much smaller than it would have been without the preceding wrist shock.
This fleeting suppression requires a coordinated effort among specific chemical messengers in the brain. Researchers suspect that acetylcholine and gamma-aminobutyric acid, widely known as GABA, manage this inhibitory braking system. By measuring the strength of this suppression, doctors can evaluate the overall health of the brain’s neurochemical networks.
Lead author Camilla Carrozzo, a researcher affiliated with the Campus Bio-Medico University of Rome, wanted to understand how common dietary stimulants affect these delicate measurements. Millions of people consume caffeine daily to improve alertness and alleviate fatigue. At typical doses, caffeine alters brain function by blocking receptors for adenosine, a chemical that normally promotes sleepiness.
Blocking adenosine sets off a chain reaction in the central nervous system. It increases the release of other neurotransmitters, including acetylcholine and glutamate, which elevate overall neural excitability. Carrozzo and her team sought to determine if elevated acetylcholine from consuming caffeine might alter the brain’s short-term braking system during neurological testing.
The research team recruited twenty healthy adults ranging in age from 20 to 42 for a controlled experiment. The participants agreed to abstain from all caffeinated beverages for 12 hours before the testing sessions. The researchers tested each participant on two separate days, scheduling the experiments at the same time of day to avoid natural fluctuations in daily brain activity.
On one day, participants chewed a piece of military-grade energy gum containing 200 milligrams of caffeine. This amount is roughly equivalent to a strong cup of brewed coffee or a standard energy drink. On the other day, they chewed an identical placebo gum containing no active ingredients. The trial used a double-blind design, meaning neither the participants nor the examiners knew which gum was being chewed on any given day.
The participants chewed the gum for ten minutes, which allowed the chemical to absorb rapidly through the lining of the mouth and the stomach. The brain stimulation experiments began 30 minutes after chewing started, to ensure the stimulant had reached peak concentrations in the bloodstream.
During the sessions, the investigators measured the brain’s sensory-motor braking system using two distinct technical approaches. The first approach relies on a constant magnetic stimulus. The examiner utilizes a fixed magnetic strength and records how much the muscle twitch shrinks in size when the sensory shock precedes it.
The second approach flips this logic and relies on a variable magnetic stimulus. Instead of watching the muscle twitch change in size, the tracking software dynamically adjusts the magnetic power to force the muscle to twitch at a consistent target size every time. The researchers calculate inhibition by noting how much extra magnetic power is required to overcome the sensory braking effect.
The findings varied depending on the measurement technique used to record the brain signals. When the researchers analyzed the data from the constant-stimulus approach, they observed an enhancement in the brain’s braking power. The caffeine gum strengthened the sensory system’s ability to suppress the motor cortex compared to the placebo gum.
This heightened suppression was most obvious at very specific timing parameters. The enhanced braking effect peaked when the sensory pulse preceded the magnetic pulse by exactly 19 to 21 milliseconds. The results indicated that the dose of caffeine altered how the participants’ brains integrated feeling and movement.
The second measurement technique yielded different results. When the equipment adjusted the magnetic intensity to maintain a constant muscle twitch size, the researchers did not find any measurable differences between the caffeinated days and the placebo days. For this specific protocol, the calculated differences in inhibition were not statistically significant.
The scientific team also noticed a shift in the brain’s general baseline excitability. Following caffeine consumption, the minimum magnetic strength required to produce a large muscle twitch dropped. This suggests the motor cortex became more responsive to external stimulation overall. However, the threshold required to produce a much smaller baseline muscle twitch did not change.
The researchers attribute the conflicting results between the two testing methods to differences in underlying brain physiology. The constant-stimulus method required a higher baseline magnetic power to generate the initial muscle twitches. Higher intensities recruit larger populations of nerve cells deep within the motor cortex.
The authors propose that caffeine might selectively influence these deeper, late-responding neural circuits. The tracking method, which used weaker magnetic pulses, might not have activated those specific cellular networks. The divergent results could simply reflect the fact that the two protocols probe slightly different functional pathways within the brain.
The investigators note a few caveats to their current work that require future exploration. The experiment relied on a single fixed dose of the stimulant, meaning it remains unknown how a larger or smaller amount might influence the results. The sample size was also relatively small and limited exclusively to healthy young adults with no neurological complaints.
Because even moderate caffeine consumption alters certain readouts of brain function, doctors should likely advise patients to abstain from coffee before undergoing these specific diagnostic tests. Taking the tests with a caffeine-altered brain could mask underlying abnormalities or produce inaccurate clinical assessments. Controlling for dietary habits helps ensure the accuracy of the data.
Moving forward, the research team hopes to evaluate these dynamics in populations dealing with cognitive decline. In individuals with Alzheimer’s disease or Parkinson’s disease, the brain’s ability to suppress motor signals after sensory input is often reduced. This reduction mirrors the gradual loss of the brain’s cholinergic signaling networks in these specific conditions.
Caffeine naturally boosts some of the same chemical transmitters that these neurodegenerative diseases slow down or destroy. Investigating how the brains of patients with Alzheimer’s respond to caffeinated stimulation could help researchers refine diagnostic tools. This information might eventually improve how doctors track the physical progression of cognitive disorders over time.
The study, “The effects of caffeine on short-latency afferent inhibition measured with paired-pulse conventional and threshold-tracking TMS,” was authored by Camilla Carrozzo, Martina Cannazza, Diletta Fratini, Gaia Fanella, Bulent Cengiz, Vincenzo Di Lazzaro, Gintaute Samusyte, and Hatice Tankisi.