Sleep duration, sample timing, and physical exercise could affect the blood levels of proteins commonly used to assess cardiovascular risk, according to a controlled study involving healthy young men.
Investigators found that even short-term changes in sleep and activity can shift proteomic profiles in ways previously linked to increased risks of heart failure, coronary artery disease, and atrial fibrillation.
Sixteen men participated in two in-lab sleep conditions: 3 nights of normal sleep (8.5 hours per night) and 3 nights of sleep restriction (4.25 hours per night). During each condition, 88 cardiovascular-related proteins were measured using proteomic assays. Blood samples were collected in the morning, evening, as well as prior to and following 30 minutes of high-intensity exercise.
Time of day influenced biomarker levels. Proteins such as leptin and lipoprotein lipase showed clear morning-to-evening variation. These changes were more frequent after sleep restriction, with 33% of proteins affected compared with 18% during normal sleep. Early morning shifts (between 8:30 AM and 10:30 AM) were only observed after normal sleep, when approximately 40% of proteins decreased.
Exercise also modified biomarker levels. After 30 minutes of cycling, 46 proteins increased under normal sleep compared with just 18 following sleep restriction. Levels of interleukin (IL)-6 and brain-derived neurotrophic factor, known for their cardiovascular relevance, rose following exercise regardless of sleep condition, but the magnitude of change was smaller during sleep restriction.
The investigators stressed that their results indicated that sleep history and sampling time must be considered when interpreting cardiovascular biomarkers.
When comparing baseline biomarker levels between sleep conditions—regardless of exercise—the investigators identified 16 proteins with higher levels and nine with lower levels during sleep restriction. Many of these were associated with inflammation and stress pathways. The overall proteomic pattern under sleep restriction resembled profiles previously linked to higher cardiovascular risk in large-scale cohorts.
Specifically, levels of IL-27 and galectin-9—both associated with adverse cardiac outcomes—were elevated following restricted sleep. A comparison with data from three large cardiovascular cohorts (n > 44,000) revealed a significant overlap between proteins altered by sleep restriction and those predictive of future heart failure and other cardiac events (P = .006).
The findings suggested that short-term physiological states—such as recent sleep loss, physical activity, and blood draw timing—can influence biomarker results in ways that may misrepresent long-term cardiovascular risk.
The investigators recommended recording sleep duration, recent physical activity, and sample timing in both clinical and research settings to improve accuracy when interpreting cardiovascular biomarkers. Additional studies are needed in women, older adults, and patients with cardiovascular disease.
Full disclosures are available in the study.
Source: Biomarker Research