A new exploratory study suggests that how quickly a minute feels may be tied to the body’s resting metabolism, hormone levels and working memory. Researchers compared healthy adults with individuals who have rare mitochondrial disorders affecting cellular energy production and found that both groups judged time with similar average speed and consistency. Yet the biological and cognitive factors linked to time perception differed markedly between the groups, implying energy constraints can shape how the brain and body coordinate our sense of time.
Time perception is often described in two dimensions: clock speed, which reflects the baseline pace of our internal timer, and variation, which measures how much estimates fluctuate from moment to moment. While the brain has long been imagined as a self-contained timekeeper, newer theories propose that perception of duration emerges from multiple brain networks continually monitoring bodily states such as heart rate, temperature and effort.
Past work has tied subjective timing to metabolic processes. When people exercise, for instance, time can feel like it passes more slowly. Across species and fatigue studies, metabolism appears linked to how we perceive durations, with higher energy use and warmth often associated with faster internal timing, and conditions like low oxygen or cognitive fatigue dulling temporal processing.
The study, led by Darshana Kapri and Professor Martin Picard of the Mitochondrial Psychobiology Lab at Columbia University Irving Medical Center, set out to test how whole-body energy expenditure, baseline norepinephrine levels and working memory relate to clock speed and timing stability—and whether mitochondrial disease disrupts these 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 involved 95 adults aged 18 to 60, including 59 healthy controls and 36 individuals with genetic mitochondrial disease caused by point mutations or a large mitochondrial DNA deletion. The broader project is registered as a clinical trial, though the current analysis followed four pre-specified hypotheses with corrections for multiple comparisons and treated other findings as exploratory.
To probe prospective time perception, participants underwent two 10-minute timing tasks in a quiet room, after removing watches and devices. In the verbal time estimation task, a hidden timer produced 12 random intervals between 8 and 55 seconds, and participants reported how much time they thought had passed. In the verbal time production task, a target duration of 10, 30 or 60 seconds was given, and participants indicated when that interval had elapsed.
From these tasks the researchers derived a clock speed score for each participant by combining the two measures, and calculated trial-to-trial timing variation. In addition to timing tests, they gathered a broad range of biological data: resting energy expenditure adjusted for lean body mass, fasting blood and urine markers of signaling chemicals including norepinephrine, epinephrine, dopamine and serotonin, and a mitochondrial health index based on enzyme activity relative to mitochondrial abundance in white blood cells and platelets. Participants also completed working memory tests, psychological questionnaires, a 30-second sit-to-stand test, and underwent brain scans to assess gray matter and network activity at rest.
Across all participants, timing performance followed expected patterns: those who overestimated durations tended to produce shorter intervals, consistent with a shared internal clock rate. Extreme clock speeds—very fast or very slow—were associated with greater trial-to-trial variation, supporting the link between clock speed and consistency.
When comparing the two groups, the researchers found no statistically significant differences 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 noted. “Their time perception looked about the same as everyone else’s.”
Yet the two groups diverged in how physiological factors related to time perception. Among healthy controls, higher resting energy expenditure relative to lean body mass correlated with lower timing variation, while higher urinary norepinephrine corresponded with greater variation. There were also hints that higher resting energy expenditure combined with lower norepinephrine related to a faster clock, though these latter associations did not survive correction for multiple comparisons.
In contrast, the links between energy expenditure, norepinephrine and time perception in those with mitochondrial disease were absent or oriented in the opposite direction, and the study notes these patterns were not statistically significant after adjustment. Similar trends emerged with other urine chemicals, with dopamine, serotonin and epinephrine showing stronger variation effects in healthy adults than in the mitochondrial-disease group.
The most striking contrast lay in working memory. In healthy participants, stronger backward digit recall tended to accompany a faster internal clock. In adults with mitochondrial disease, the direction of this relationship appeared reversed, though the trend was weak and not statistically significant on its own. Importantly, despite this divergence, stronger working memory remained associated with more stable timing across both groups, a finding Kapri and Picard described as the strongest of the study.
“This was the strongest finding in the study,” Kapri and Picard said. “It suggests their brains may reach a normal sense of time by a different route.”
Exploratory analyses hinted at further differentiation between groups. In healthy individuals, mitochondrial enzyme efficiency in a type of white blood cell called monocytes showed a modest positive link with clock speed, while relationships between timing variation and mitochondrial markers varied across cell types and between groups. Psychological measures found no robust links between stress, anxiety or fatigue and clock speed, but higher timing variation correlated modestly with greater burnout-related work inefficiency across both groups.
Brain imaging offered additional clues. In healthy controls, local network synchrony and structural measures such as cortical thickness and gray matter volume showed modest associations with time perception, accounting for only a small portion of individual differences. Several of these brain-behaviour relationships were diminished or absent in participants with mitochondrial disease.
The authors concluded that because individuals with mitochondrial disease judged time similarly to healthy controls despite a lack of typical physiological and cognitive correlations, cellular energy defects do not simply speed up or slow the internal clock. They propose instead that mitochondrial dysfunction alters how metabolic and neurochemical signals are integrated, prompting patients to rely on alternative neural or cognitive strategies to keep time stable.
They also offered a preliminary interpretation for why higher baseline norepinephrine in healthy adults tended to align with a slower clock speed, even though acute stress is known to stretch time. Baseline norepinephrine may reflect a chronic regulatory set-point that acts like a brake on the internal pacemaker, while sudden spikes during immediate danger can accelerate it.
Time perception, the researchers caution, remains a complex phenomenon. “Time perception is complicated,” they 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 tended to have a faster ‘inner clock.’” They added: “our sense of time isn’t only in the head. It is tied to both the brain and the body.”
As with all such research, several caveats apply. The study measured variables at a single point in time and many analyses were exploratory, so causation cannot be established. The timing tasks also spanned 8 to 60 seconds and did not include a distraction task to prevent silent counting, meaning individual differences in counting, attention and memory may have influenced scores. The authors emphasised that the findings should be viewed as early clues for future work rather than definitive conclusions.
“These findings need to be tested in larger groups before we can say anything for certain,” the authors added. The study is titled Psychobiological and Metabolic Correlates of Time Perception in Humans: An Exploratory Study and was authored by Kapri, Sturm, Kelly, Bo, Liu, Wager, Hirano, Trumpff and Picard.
