{"id":941,"date":"2026-06-16T23:25:00","date_gmt":"2026-06-16T20:25:00","guid":{"rendered":"https:\/\/www.life-on.com.ua\/?p=941"},"modified":"2026-06-16T23:25:03","modified_gmt":"2026-06-16T20:25:03","slug":"circadian-rhythm-physical-activity-mortality","status":"publish","type":"post","link":"https:\/\/www.life-on.com.ua\/en\/circadian-rhythm-physical-activity-mortality\/","title":{"rendered":"Circadian rhythm and movement: why the \u221265% mortality figure is not about the clock, but about the two together."},"content":{"rendered":"

The circadian rhythm \u2014 the daily cycle of sleep and activity \u2014 has made the headlines following a new study of 6,621 adults from the NHANES, which found a \u221265% association with all-cause mortality. However, this figure does not relate to the circadian rhythm in isolation, but rather to the combination of a \u00abstrong rhythm plus sufficient activity\u00bb compared with the worst-performing group. Let\u2019s examine where the science lies and where there is some licence in the reporting, and what lessons we can take from this for real life.<\/p>\n\n\n\n

What the study actually showed about the circadian rhythm<\/h2>\n\n\n\n

A team from Capital Medical University used data from 6621 NHANES participants between 2011\u20132014. The daily mobility profile was calculated not from a questionnaire but from a wrist-worn ActiGraph GT3X+ accelerometer. This is an objective measure of daily movement, rather than a subjective \u00abhow did you sleep this week\u00bb.<\/p>\n\n\n\n

The median observation period was 6.75 years. During this time, 518 deaths from all causes and 165 cardiovascular deaths were recorded. Researchers divided the sample into four combinations: strong or weak rhythm, sufficient or insufficient activity. They then compared the extreme groups to each other.<\/p>\n\n\n\n

The key finding is as follows. In the \u00abstrong circadian rhythm plus sufficient physical activity\u00bb group, the risk of all-cause mortality was 65% lower. The reference group was \u00abweak circadian rhythm plus low physical activity\u00bb. The hazard ratio was 0.35, with a confidence interval of 0.24\u20130.51. For cardiovascular mortality, the effect is even greater: HR 0.25, i.e. a reduction of 75%. This is precisely where the eye-catching figure in the headlines comes from.<\/p>\n\n\n\n

It is worth noting the limitations of the sample size straight away. 165 cardiovascular deaths is not a large number for this kind of analysis. The fewer events there are, the wider the confidence interval and the less robust the estimate. Therefore, the \u221275% effect on cardiac mortality sounds impressive, but is based on a shakier foundation than overall mortality.<\/p>\n\n\n\n

Why the number \u221265% cannot be read as \u00abrhythm saves lives\u00bb<\/h2>\n\n\n\n

Here is the first simplification that any brief summary makes. Minus 65% is not about the circadian rhythm in and of itself. It is about two things combined, measured against the worst-case scenario.<\/p>\n\n\n\n

Imagine a simple analogy. Let's compare a person who both gets enough sleep and exercises, with a person who does neither. The difference will be enormous. But it doesn't tell you how much was contributed by sleep alone, and how much by exercise. It's precisely this \u00abblended\u00bb difference that the headline figure of the digest shows.<\/p>\n\n\n\n

The second caveat relates to the type of study. It is an observational cohort, not a randomised experiment. It shows a link, but does not prove causation. People with a strong circadian rhythm are often younger, healthier, and have higher incomes. Part of the effect is driven by these accompanying factors, not by the rhythm itself. Statistics attempt to account for them, but it is impossible to completely remove such an influence.<\/p>\n\n\n\n

What does the larger cohort say about a disrupted circadian rhythm<\/h2>\n\n\n\n

Here it is useful to go beyond a single study and look at broader data. The UK's UK Biobank measured the daily profile of 92,614 adults using an accelerometer. This is a fourteen times larger sample than NHANES and an independent population.<\/p>\n\n\n\n

The results from Feng et al. (2023) are as follows: A low amplitude of the diurnal rhythm is associated with an all-cause mortality risk of HR 1.54 with a confidence interval of 1.40\u20131.70. For cardiovascular mortality, the figure is 1.73. This means that a disrupted circadian rhythm is indeed correlated with a higher risk. The link has been confirmed on a large independent group, not just a single sample.<\/p>\n\n\n\n

The same study revealed something else important. A weak rhythm amplitude was linked not only to mortality but also to higher morbidity. Specifically, risks of infectious, respiratory, and cardiovascular diagnoses increased. This suggests that the daily profile is not just a narrow sleep marker, but a reflection of the body's overall condition.<\/p>\n\n\n\n

But take note of the scale. Here, the difference is roughly one and a half times, not three times. The high figures of \u221265% are due precisely to the fact that movement was added to the rhythm and it was compared with the worst-performing group on two parameters at once. The rhythm itself, in its pure form, makes a more modest, albeit genuine, contribution. The wrist-worn accelerometer is the very same tool that is increasingly being tested as a screening marker for risk. For more details on this, see Activity Tracker Explained<\/a>.<\/p>\n\n\n\n

Is it true that movement \u00abneutralises\u00bb a disrupted rhythm<\/h2>\n\n\n\n

This is the most interesting part of the NHANES work, and at the same time the most fragile. The authors suggest that sufficient activity mitigates the harm from a disrupted circadian rhythm. It sounds encouraging: you work night shifts, compensate for it with regular gym sessions, and the risk is partially offset.<\/p>\n\n\n\n

The authors sought to test the mechanism using markers of accelerated biological ageing. According to their assessment, the PhenoAgeAccel index explains 13.55% of the association between circadian rhythm and all-cause mortality, and 21.67% for cardiovascular mortality. The second marker, BioAgeAccel, explains only 5.06% and 8.06% respectively.<\/p>\n\n\n\n

Let\u2019s put these figures into plain language. Even the strongest marker accounts for barely a fifth of the effect. The remaining 78\u201387% remain completely unexplained. The authors themselves state quite clearly: this is an exploratory analysis of a hypothesis; further research is needed. Therefore, the claim that \u00abmovement neutralises a disrupted rhythm\u00bb is, for the time being, a cautious assumption rather than a proven fact. It should not be presented as a ready-made guide.<\/p>\n\n\n\n

When the \u00abright time\u00bb to move stops being obvious<\/h2>\n\n\n\n

This leads to temptation. If rhythm is so important, then surely there's a \u00abcorrect\u00bb time for training. Here the data becomes truly contradictory, and it's important to address this honestly.<\/p>\n\n\n\n

In a separate study involving 92,139 participants from the UK Biobank, the same Feng group looked at when people are most active. Compared to morning activity, afternoon activity between 11:00\u201317:00 and mixed activity both showed lower mortality \u2013 HR 0.89 in both cases. Evening activity did not statistically differ from morning activity.<\/p>\n\n\n\n

And now for a counter-argument that shatters this simplistic picture. Another cohort, looking at obese adults, found the opposite: it was evening activity that carried the lowest risk. The reason for the discrepancy lies in the methodology, different comparison groups, and different populations. The honest conclusion is that the data so far do not provide a universal \u00abbest time.\u00bb This means that the regularity of exercise matters more than hunting for the ideal hour.<\/p>\n\n\n\n

A disrupted circadian rhythm can harm the body in several ways. It regulates sleep-wake cycles, hormone release, and other vital bodily functions. When this natural rhythm is thrown off, it can lead to:\n\n* **Sleep problems:** Difficulty falling asleep, staying asleep, or experiencing poor quality sleep.\n* **Hormonal imbalances:** Affecting hormones like cortisol, melatonin, and growth hormone, which can impact mood, metabolism, and immune function.\n* **Metabolic issues:** Increased risk of weight gain, obesity, and type 2 diabetes due to changes in appetite, insulin sensitivity, and energy expenditure.\n* **Cardiovascular problems:** A disrupted rhythm is linked to higher blood pressure, an increased risk of heart disease, and stroke.\n* **Mental health issues:** Contributing to mood disorders like depression, anxiety, and irritability.\n* **Weakened immune system:** Making the body more susceptible to infections and illness.\n* **Cognitive impairment:** Affecting concentration, memory, learning, and overall cognitive performance.\n* **Digestive problems:** Leading to issues such as indigestion, irritable bowel syndrome (IBS), and changes in gut bacteria.<\/h2>\n\n\n\n

This leaves the question that rings out in the headline: why does a disrupted rhythm fundamentally increase the risk. Here, it is worth separating the reliably known from speculation.<\/p>\n\n\n\n

The diurnal rhythm doesn't just dictate sleep. Arterial pressure, cortisol levels, insulin sensitivity, body temperature, and vascular tone also fluctuate in a near 24-hour cycle. When activity and rest are \u00abspread out\u00bb over the day without a clear peak, these systems lose synchrony. The body more often operates in a mode it's not calibrated for at that particular hour.<\/p>\n\n\n\n

What exactly does \u00abstrong\u00bb or \u00abweak\u00bb circadian rhythm mean in these studies? It refers to amplitude \u2013 how pronounced is the difference between the most active hours of the day and the quietest hours of the night. High amplitude: the person is clearly active during the day and genuinely rests at night. Low amplitude: the boundary between day and night is blurred, with nighttime awakenings and daytime drowsiness. It is precisely this blurred boundary that the accelerometer registers as a weak rhythm.<\/p>\n\n\n\n

This provides a plausible bridge to cardiovascular mortality, where the effect was greatest. A weak pulse rhythm often accompanies hypertension, impaired glucose metabolism, and chronic inflammation. Here, it remains an open question as to what is cause and what is effect. The NHANES study honestly leaves it open, not mistaking correlation for a proven mechanism.<\/p>\n\n\n\n

How are physical activity and the circadian rhythm linked at the genetic level?<\/h2>\n\n\n\n

The most interesting thing is that the daily clock ticks not only in the brain. It is present in almost every cell, including skeletal muscle itself. This is the level where the circadian rhythm ceases to be an abstraction about \u00abowls and larks\u00bb and becomes biochemistry.<\/p>\n\n\n\n

At the heart of the cellular clock is the protein Bmal1. Together with its partner Clock, it switches hundreds of genes on and off on a daily schedule. In muscle, Bmal1 controls insulin sensitivity and glucose metabolism. Studies in mice have shown that when Bmal1 is switched off in muscle, glucose metabolism drops and excess fat accumulates in the tissue. The muscle clock is not a passenger, but a driver of metabolism.<\/p>\n\n\n\n

Here, movement and rhythm converge at a single point. Work on rats showed that heavy exercise temporarily disrupts the Bmal1 circadian rhythm in muscle. At the same time, it triggers the NAMPT\/NAD\u207a\/SIRT1 pathway \u2013 the same cascade through which the cell controls energy and mitochondria. In other words, exercise \u00abspeaks\u00bb to the clock directly, in the language of the same molecules.<\/p>\n\n\n\n

This is important for understanding the big picture. The molecular level suggests why movement and a strong circadian rhythm act synergistically, rather than simply adding up. They affect shared gears: rhythm tunes metabolic genes, movement activates them. But I must stress \u2013 this is a mechanism from animals and cells. It explains the direction, but does not prove that it is enough for humans to \u00abtrain correctly\u00bb to rewrite a broken clock.<\/p>\n\n\n\n

What to do with this in practice<\/h2>\n\n\n\n

If you strip away the hype, there are a few claims left that stand on solid ground. They aren\u2019t as sensational as \u00ab\u221265%\u00bb, but they won\u2019t fall apart in six months\u2019 time when new research comes to light.<\/p>\n\n\n\n