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    Home » News » How caffeine changes the human brain’s electrical braking system
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    How caffeine changes the human brain’s electrical braking system

    healthadminBy healthadminMay 8, 2026No Comments7 Mins Read
    How caffeine changes the human brain’s electrical braking system
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    A new study shows that consuming the equivalent of two cups of coffee increases the brain’s ability to temporarily quiet motor signals in response to sensory input. The results show that daily habits can alter the results of neurological tests, which can influence the diagnosis of certain cognitive conditions. The study was published in the journal Clinical Neurophysiology.

    Measuring electrical activity in the living human brain presents unique challenges. Neurologists often rely on non-invasive techniques to safely investigate how different brain regions communicate. One common tool is transcranial magnetic stimulation, which involves placing electromagnetic coils on a person’s scalp. The coil sends short magnetic pulses through the skull to the underlying nerve tissue.

    When these magnetic pulses are located above the primary motor cortex, they generate a weak electrical current that triggers a downward signal to the body. This nerve pathway travels through the spinal cord to the peripheral nerves. If the stimulation is strong enough, certain muscles, such as those at the base of the thumb, will spasm. Neurologists measure the physical size of this muscle twitch to gauge the baseline excitability of the brain’s motor networks.

    Researchers will also use this technology to study how the brain processes incoming sensory information along with outgoing motor commands. They employ a special testing protocol called short-latency afferent inhibition. In this protocol, the examiner delivers a mild electrical shock to the nerves in the wrist just before sending magnetic pulses to the brain.

    Sensory signals from the wrist travel up the arm and into the somatosensory areas of the brain. After a few milliseconds, a magnetic pulse reaches the nearby motor cortex and causes the thumb to twitch. The arrival of sensory signals acts like a temporary brake on the motor cortex. The resulting muscle spasm will be much smaller than it would have been if there had been no prior wrist impact.

    This temporary suppression requires a coordinated effort between specific chemical messengers in the brain. Researchers believe that acetylcholine and gamma-aminobutyric acid, commonly known as GABA, may control this inhibitory braking system. By measuring the strength of this inhibition, doctors can assess the overall health of the brain’s neurochemical networks.

    Lead author Camila Carozzo, a researcher at the Campus Biomedico University in Rome, wanted to understand how common dietary stimulants affect these sensitive measurements. Millions of people consume caffeine every day to increase alertness and reduce fatigue. In typical doses, caffeine changes brain function by blocking receptors for adenosine, a chemical that normally promotes sleepiness.

    Blocking adenosine starts a chain reaction in the central nervous system. It increases the release of other neurotransmitters such as acetylcholine and glutamate, increasing overall neural excitability. Carozzo and her team sought to determine whether the rise in acetylcholine caused by caffeine intake could alter the brain’s short-term braking system during neurological examinations.

    The research team recruited 20 healthy adults between the ages of 20 and 42 for the control experiment. Participants agreed to abstain from all caffeinated beverages 12 hours before the test session. The researchers tested each participant on two separate days, scheduling the experiment at the same time of day to avoid natural fluctuations in daily brain activity.

    One day, participants chewed military energy gum containing 200 milligrams of caffeine. This amount is roughly equivalent to one cup of strong coffee or a standard energy drink. On another day, they chewed identical placebo gum without the active ingredient. The study used a double-blind design, meaning neither the participants nor the examiner knew which gum they were chewing that day.

    Participants chewed gum for 10 minutes, and the chemicals were rapidly absorbed through the lining of their mouths and stomachs. The brain stimulation experiment began 30 minutes after starting chewing to ensure that the stimulant had reached its peak concentration in the bloodstream.

    During the sessions, the researchers measured the brain’s sensorimotor braking system using two different technical approaches. The first approach relies on constant magnetic stimulation. The examiner utilizes a fixed magnetic force and records how much the muscle spasm decreases in size when preceded by a sensory shock.

    A second approach reverses this logic and relies on variable magnetic stimulation. Instead of monitoring muscle twitch size changes, the tracking software dynamically adjusts the magnetic force to cause the muscle to twitch at a consistent target size every time. Researchers calculate inhibition by noting how much extra magnetic force is needed to overcome the sensory damping effect.

    Results varied depending on the measurement technique used to record brain signals. When researchers analyzed data from a constant stimulation approach, they observed an increase in the brain’s braking force. Caffeine gum enhanced the sensory system’s ability to suppress the motor cortex compared to placebo gum.

    This enhanced suppression was most pronounced for very specific timing parameters. The enhanced braking effect peaked when the sensory pulse preceded the magnetic pulse by exactly 19–21 ms. The results showed that caffeine consumption changed the way the participants’ brains integrated emotion and movement.

    The second measurement technique yielded different results. When the device adjusted the magnetic force to keep the size of the muscle spasms constant, the researchers found no measurable difference between the days people took the caffeine and the days they took the placebo. For this particular protocol, the calculated inhibition differences were not statistically significant.

    The scientific team also noticed changes in the brain’s overall baseline excitability. Caffeine intake lowered the minimum magnetic force required to cause large muscle twitches. This suggests that the motor cortex has become more responsive overall to external stimuli. However, the threshold required to produce much smaller baseline muscle twitches did not change.

    Researchers believe the conflicting results between the two testing methods are due to differences in the underlying brain physiology. The constant stimulation method required a higher baseline magnetic force to generate the first muscle twitch. Higher intensity recruits a larger population of neurons deep in the motor cortex.

    The authors propose that caffeine may selectively affect these deeper, slower-responsive neural circuits. Tracking methods using weaker magnetic pulses may not have activated these particular cell phone networks. The different results may simply reflect the fact that the two protocols are investigating slightly different functional pathways in the brain.

    The researchers note several caveats to the current study that warrant future investigation. The experiment relied on a single, fixed dose of the stimulant, meaning it remains unclear how higher or lower doses affect the results. The sample size was also relatively small and limited to healthy young adults without neurological complaints.

    Because even moderate caffeine intake alters certain measures of brain function, physicians may need to advise patients to avoid coffee before undergoing these specific diagnostic tests. Testing on a brain altered by caffeine may mask underlying abnormalities or provide an inaccurate clinical assessment. Controlling your eating habits helps ensure data accuracy.

    In the future, the researchers hope to assess these dynamics in populations dealing with cognitive decline. People with Alzheimer’s or Parkinson’s disease often have a reduced brain’s ability to suppress motor signals after sensory input. This decrease reflects the gradual loss of the brain’s cholinergic signaling network under these specific conditions.

    Caffeine naturally increases some of the same chemical messengers that these neurodegenerative diseases slow down or destroy. Studying how the brains of Alzheimer’s patients respond to stimuli containing caffeine could help researchers improve diagnostic tools. This information could ultimately improve how doctors track the physical progression of cognitive impairment over time.

    The study, “Effects of caffeine on short-latency afferent inhibition measured with conventional paired-pulse TMS 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.



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