News · Fitness & Exercise
Atrial fibrillation sped up muscle loss over 12 years
A Swedish study of 2,048 older adults found people with the common heart rhythm disorder lost strength faster, and lost it fastest when inflammation markers were high.
Based on a peer-reviewed 12-year cohort study in GeroScience
- Researchers followed 2,048 people aged 60 and over in the Swedish National Study on Aging and Care in Kungsholmen for 12 years, publishing in GeroScience.
- Muscle was tracked three ways: calf circumference, handgrip strength and how long it took to stand from a chair repeatedly.
- People with atrial fibrillation got slower at the chair stand test faster than those without it (beta = 1.49; 95% CI, 0.82 to 2.16).
- Two inflammation markers, interleukin-6 and growth differentiation factor-15, were measured once at the start.
- High growth differentiation factor-15 amplified the decline in both muscle mass (beta = -0.12; 95% CI, -0.20 to -0.05) and chair stand performance (beta = 2.48; 95% CI, 1.66 to 3.30) among people with the arrhythmia.
- High interleukin-6 did the same, accelerating loss of calf circumference and chair stand performance.
- Observational. Inflammation was measured only at baseline, and nobody was randomly assigned to anything.
- The cohort is one district of Stockholm, which limits how far the numbers generalize.
Atrial fibrillation is treated as a stroke problem. A study in GeroScience followed 2,048 older Swedes for 12 years and found it is also, quietly, a strength problem.
The authors open by naming the gap: the long-term impact of atrial fibrillation (AF) and systemic inflammation on muscle health and, hence, functional decline remains unclear.
Twelve years of measurements
The data came from a cohort built for exactly this kind of question. Participants were drawn from 2,048 participants (60 and over) in the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), followed for 12 years.
Muscle was not assessed once but repeatedly, and in three different ways: muscle mass and strength were assessed using calf circumference, handgrip strength, and chair stand test. Calf circumference stands in for muscle bulk, grip for upper-body strength, and the chair stand for the lower-body function that determines whether someone can get off a sofa unaided at 85.
Two blood markers were taken at the start: inflammatory marker interleukin-6 (IL-6) and the stress-response mediator growth differentiation factor-15 (GDF-15).
Losing function faster
The core comparison was between people with and without the arrhythmia, tracked over the full 12 years.
Participants with AF experienced a steeper increase in the duration of the chair stand test. Longer is worse here: the test measures time, so a rising number means getting up from a chair became harder.
The estimate was 1.49 with a range from 0.82 to 2.16, comfortably clear of no effect. It is a difference in trajectory rather than a difference at any one moment, which is what makes 12 years of repeated measurement worth the trouble.
Where inflammation came in
The paper’s real contribution is what happened when the researchers combined the arrhythmia with the blood markers.
High levels of GDF-15 amplified declines in muscle mass and chair stand test performance in individuals with AF. Both measures worsened, and the chair stand estimate rose to 2.48, well above the 1.49 seen for the condition alone.
Interleukin-6 behaved the same way. Participants with AF and high IL-6 levels also experienced an accelerated decline of calf circumference and chair stand test performance.
So the arrhythmia alone predicted a steeper slide, and the arrhythmia alongside a high inflammatory state predicted a steeper one still. That layering is the finding.
What it does not establish
Both markers were measured once, at baseline, and inflammation is not static across 12 years. A single reading is a snapshot standing in for a long trajectory.
Nothing here shows direction either. Inflammation may drive muscle loss in people with the arrhythmia. Or declining muscle, reduced activity and accumulating illness may drive inflammation. Or a third process may be producing all of it. The design cannot separate those, and the authors do not claim it can.
There is also the activity question. People whose hearts beat irregularly often move less, from breathlessness or from caution, and reduced activity costs muscle on its own. Whether the association here reflects biology, behavior, or both is not resolved.
And the cohort is one district of central Stockholm, well-off and predominantly white. The trajectories may differ elsewhere.
Why it is worth knowing
The conclusion is direct: AF is associated with a steeper decline in muscle mass and strength over time, exacerbated by elevated inflammatory biomarkers, underscoring the importance of systemic inflammation in AF-related functional decline.
Care for this condition is organized around rhythm and stroke prevention, which is appropriate, because strokes are what kill and disable people. What this study adds is that the same patients are on a faster path to being unable to rise from a chair, and that decline gets measured by nobody unless someone thinks to look.
A chair and a stopwatch would do it.
People also ask
What is atrial fibrillation?
The most common sustained heart rhythm disorder, in which the upper chambers of the heart quiver instead of beating in an organized rhythm. It becomes markedly more common with age, affecting a substantial share of people over 65. It is best known for raising stroke risk, which is why treatment focuses on rhythm control and preventing clots. Its effects on muscle and physical function have had far less attention.
Why would a heart rhythm problem affect muscle?
Several plausible routes exist and this study cannot separate them. An irregular rhythm reduces how efficiently the heart pumps, which limits blood and oxygen reaching muscle during exertion. People with the condition often reduce activity, through breathlessness or caution, and disuse costs muscle quickly. And the condition travels with chronic inflammation, which is the mechanism this paper specifically examined.
What is the chair stand test?
A standard measure of lower-body strength and function: how long it takes to stand up from a seated position and sit back down a set number of times, usually five. It is simple, needs no equipment, and predicts falls and disability well. A rising time means declining function, which is why the positive numbers in this study represent worsening rather than improvement.
What are interleukin-6 and growth differentiation factor-15?
Both are blood markers of the body's stress and inflammatory state. Interleukin-6 is a signaling molecule central to inflammation and has been tied to frailty and muscle loss for years. Growth differentiation factor-15 rises with cellular stress and is one of the strongest single blood predictors of mortality in older adults. Neither is routinely measured in ordinary care.
What should someone with atrial fibrillation take from this?
This is general information rather than medical advice. The finding does not change treatment for the arrhythmia itself, but it does suggest that physical function is worth watching, not just rhythm and stroke risk. Resistance training and staying active preserve muscle in older adults generally, and anyone with a heart condition should agree an exercise approach with their clinician before starting.
References
- Celik D, Ornago AM, Triolo F, et al. Association between atrial fibrillation and systemic inflammation with muscle mass and strength trajectories in old age. GeroScience (2026).
- National Heart, Lung, and Blood Institute. Atrial Fibrillation.
- National Institute on Aging. How Can Strength Training Build Healthier Bodies as We Age?