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How quickly a minute seems to pass, and how consistently a person can judge its length, may be tied to the body’s resting metabolism, hormone levels, and working memory, according to an exploratory study published in Psychophysiology. Comparing healthy adults with individuals who have rare genetic disorders that impair cellular energy production, the researchers found that both groups judged time with similar overall speed and consistency. Yet the underlying biological and cognitive factors linked to time perception differed between the two groups, suggesting that cellular energy constraints may alter how the brain and body coordinate to track time.
Even though physical clocks tick at a uniform rate, the subjective experience of time varies widely from person to person and from moment to moment. Researchers who study time perception often separate this internal sense into two distinct dimensions: clock speed and variation. Clock speed refers to the average pace of a person’s internal timer, where a faster clock causes a given span of time to feel longer, while variation measures how much a person’s duration estimates fluctuate from one attempt to the next.
Early psychological models treated timekeeping as the work of a standalone neural pacemaker inside the brain, operating largely independently of the rest of the body. Newer frameworks propose that our sense of duration emerges across multiple brain networks that continuously monitor internal bodily states, including heart rate, body temperature, and physical exertion. Consistent with this view, an experiment with adults performing physical exercise found that participants perceived time as passing more slowly while working out than when they were resting before or afterward.
Comparisons across animal species and studies of human fatigue also point to a role for metabolism, the chemical processes through which the body converts food into energy. Higher metabolic rates and elevated body temperatures tend to go hand in hand with faster internal timing, whereas low oxygen or mental exhaustion can dull temporal processing.
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Chemical messengers involved in the body’s stress and alertness responses, known as catecholamines, are implicated in time perception as well. When the nervous system releases catecholamines such as norepinephrine or dopamine, it can shift both the perceived speed and the consistency of duration judgments. For instance, an animal study of mice given amphetamine indicated that artificially boosting these chemical signals made the animals’ timing more erratic by disrupting how neurons in the prefrontal cortex coordinated their firing.
At the cellular level, energy supply depends heavily on mitochondria, tiny structures inside cells that combine oxygen and nutrients to generate chemical fuel through a process called oxidative phosphorylation. When cells cannot efficiently adapt this energy production to meet shifting demands, it may limit the brain’s ability to maintain the synchronized neural rhythms needed to track time and space, as the authors of a 2026 review on schizophrenia in Neuroscience and Biobehavioral Reviews proposed as a hypothesis for future testing.
People who carry rare mutations in their mitochondrial DNA, a condition known as mitochondrial disease, often experience both reduced cellular energy capacity and chronically elevated norepinephrine levels, offering a natural way to examine whether long-term energetic constraints change how the body regulates its sense of time.
To explore these connections in humans, a research team led by Darshana Kapri and Professor Martin Picard of the Mitochondrial Psychobiology Lab at Columbia University Irving Medical Center analyzed data collected as part of their broader Mitochondrial Stress, Brain Imaging, and Epigenetics study. The researchers wanted to test whether whole-body energy expenditure, baseline norepinephrine levels, and working memory relate to internal clock speed and timing stability, and whether mitochondrial disease disrupts those relationships.
“We wanted to better understand the everyday problems that people with mitochondrial disease might face,” Kapri and Picard told PsyPost. “Our sense of time is part of so many daily mental tasks, from following a conversation to doing simple math in your head. Very little research had looked at whether the body’s energy systems, including mitochondria, shape how we experience time. That was the gap we wanted to start filling.”
The study included 95 adults between the ages of 18 and 60, comprising 59 healthy control participants and 36 individuals diagnosed with genetic mitochondrial disease caused by either a specific point mutation or a single large deletion in their mitochondrial DNA. The broader project is listed in a clinical trials registry. For this analysis, the authors specified four hypotheses in advance and corrected those tests for multiple comparisons, while treating all other analyses as exploratory and hypothesis-generating. Data from the study were not posted to a public repository but are available from the authors upon request.
To measure prospective time perception, meaning how people track durations when they know in advance that time is being tested, participants removed all watches and digital devices and completed two 10-minute behavioral tasks in a quiet room. In the verbal time estimation task, an experimenter ran a hidden timer for 12 randomized intervals ranging from 8 to 55 seconds, and participants stated how much time they felt had passed after hearing an audio cue. In the verbal time production task, the experimenter named a target duration of 10, 30, or 60 seconds, and participants indicated when they believed that exact interval had elapsed.
If a person’s internal clock runs fast, a 30-second wait feels longer than it really is, leading them to overestimate elapsed intervals in the first task and stop the timer too early in the second task. The researchers combined each participant’s ratios across both tasks into a single clock speed score, and they calculated the trial-to-trial consistency of those ratios to measure timing variation.
Alongside the timing tasks, participants underwent a wide battery of biological assessments. The scientists measured resting energy expenditure, the rate at which the body burns calories while at rest, and adjusted the values for each person’s lean body mass. They also collected fasted blood and urine samples to measure baseline levels of signaling chemicals including norepinephrine, epinephrine, dopamine, and serotonin, and they isolated specific types of white blood cells and platelets to calculate a mitochondrial health index reflecting cellular energy-producing enzyme activity relative to mitochondrial abundance.
Participants also completed cognitive tests of working memory, which is the ability to temporarily hold and manipulate information in mind, using number-recall and letter-tracking tasks. They filled out standardized questionnaires assessing stress, anxiety, depression, burnout, and fatigue, and performed a 30-second sit-to-stand physical test. Finally, participants underwent structural MRI scans to measure the volume and thickness of the brain’s outer gray matter layer, as well as resting-state functional MRI scans to measure regional homogeneity, an index of how closely neighboring areas within seven major brain networks synchronize their spontaneous activity.
Across the entire sample, performance on the two timing tasks aligned as expected: individuals who overestimated elapsed durations also tended to produce shorter intervals, consistent with both tasks capturing a shared internal clock rate. Participants whose clock speeds were at either extreme, running unusually fast or unusually slow, tended to show greater trial-to-trial variation in their estimates. When the researchers compared the 36 participants with mitochondrial disease directly against the 59 healthy controls, they found no statistically significant differences between the two groups in average clock speed or timing variation.
“We expected people with mitochondrial disease to have a noticeably different sense of time, but on average they didn’t,” the researchers said. “Their time perception looked about the same as everyone else’s.”
Even though overall timing behavior looked similar between the two groups, the physiological factors associated with time perception differed. Among healthy controls, burning more energy at rest relative to lean body mass was moderately associated with lower timing variation, while higher urinary norepinephrine levels were moderately associated with greater timing variation; both of these relationships with timing stability survived statistical correction for multiple comparisons. Healthy participants with higher resting energy expenditure and lower blood norepinephrine also tended to have a faster clock speed, though those clock speed associations weakened to suggestive trends and were not statistically significant after adjusting for multiple tests.
In participants with mitochondrial disease, the links between resting energy expenditure, norepinephrine, and time perception were either absent or trended in the opposite direction, although the group differences in these relationships did not remain statistically significant after correction. A similar pattern emerged in exploratory analyses of other chemical messengers in urine: higher levels of dopamine, serotonin, and epinephrine corresponded to greater timing variation in healthy adults, whereas those links were weaker or absent in the mitochondrial disease group.
The sharpest divergence between the two groups involved working memory. In healthy adults, stronger performance on a backward number-recall working memory task was modestly associated with a faster internal clock speed. In adults with mitochondrial disease, that relationship reversed direction, with higher working memory scores tending to correspond to a slower clock speed, though this reversed link was weak and not statistically significant on its own. The difference in direction between the two groups held up after statistical correction for multiple comparisons, whereas for timing variation, stronger working memory was consistently tied to more stable timing across both groups.
“This was the strongest finding in the study,” Kapri and Picard noted. “It suggests their brains may reach a normal sense of time by a different route.”
In the researchers’ exploratory analyses, mitochondrial enzyme efficiency in one class of white blood cells called monocytes showed a modest positive link with clock speed across the cohort, while relationships between timing variation and mitochondrial markers in several blood cell types differed between healthy participants and those with mitochondrial disease. Psychological questionnaires showed no statistically significant links between stress, anxiety, or fatigue and clock speed, but higher timing variation was modestly linked to greater burnout, specifically lower self-reported work efficiency, across both groups.
In the brain imaging data, local synchronization within resting brain networks and structural measures such as cortical thickness and gray matter volume showed modest associations with time perception in healthy controls, accounting for a small fraction of individual differences, whereas several of these brain-behavior relationships were altered or absent in participants with mitochondrial disease.
Because individuals with mitochondrial disease judged time much like healthy controls on average, despite lacking the usual physiological and cognitive correlations, the authors suggest that cellular energy defects do not directly speed up or slow down the internal clock. Instead, the researchers propose that mitochondrial dysfunction alters how metabolic and neurochemical signals are integrated, and that patients may rely on alternative neural or cognitive strategies to keep their sense of time stable.
The authors also offer a preliminary explanation for why higher baseline blood norepinephrine trended toward a slower clock speed in healthy adults, even though acute stress typically makes time feel stretched. In the researchers’ reading, baseline norepinephrine in the bloodstream reflects a chronic regulatory set-point that may act like a physiological brake on the internal pacemaker, whereas sudden spikes of norepinephrine during an immediate threat temporarily accelerate it.
“Time perception is complicated,” the researchers explained. “How fast time seems to pass for you depends partly on your body’s metabolism, how much energy it uses at rest, and partly on your thinking skills. In our healthy participants, people with better working memory (the ability to hold and juggle information in your mind for a short time) tended to have a faster ‘inner clock.'”
They added that “our sense of time isn’t only in the head. It is tied to both the brain and the body.”
As with all research, there are several caveats to keep in mind when interpreting these results. Because the study measured variables at a single point in time and many of the broader analyses were exploratory, the findings cannot establish cause and effect, and several of the initial associations weakened to statistical trends once adjusted for multiple comparisons. In addition, the timing tasks spanned intervals of 8 to 60 seconds without a distraction task to prevent participants from silently counting seconds in their heads, meaning that individual differences in counting habits, attention, and memory likely contributed to the timing scores. That may be especially relevant to the working memory findings.
“This was an exploratory study,” Kapri and Picard told PsyPost. “It was meant to open up questions, not settle them. The links we found were modest, and the study was not large enough to detect small effects with confidence. Readers should see these results as early clues that point to where future research should look.”
Another limitation involves how cellular energy capacity was measured. The researchers assessed mitochondrial enzyme activity in circulating immune cells and platelets, which turn over rapidly in the bloodstream and often eliminate mutated mitochondrial DNA, so those blood markers may not reflect the true energy constraints inside long-lived brain cells. At the same time, the participants with mitochondrial disease carried two different types of genetic mutations and varied widely in symptom severity, which may have masked subtler group-wide effects that future, larger studies designed to test specific mechanisms could help resolve.
“These findings need to be tested in larger groups before we can say anything for certain,” the authors added.
The study, “Psychobiological and Metabolic Correlates of Time Perception in Humans: An Exploratory Study,” was authored by Darshana Kapri, Gabriel Sturm, Catherine Kelly, Ke Bo, Cynthia C. Liu, Tor D. Wager, Michio Hirano, Caroline Trumpff, and Martin Picard.
