0126 CVD biomarker profiling reveals distinct responses to acute exercise under conditions of recurrent sleep loss in healthy humans

Abstract

Abstract Introduction Physical exercise impacts a plethora of signaling pathways, which mediate the acute and long-term benefits of exercise. Whereas the acute effects of exercise on overall metabolism and cardiovascular disease (CVD) risk factors have been extensively studied in humans, little is known about how a wider range of CVD biomarkers change in response to acute exercise under conditions of sleep loss. Thus, here we examined whether a few nights of short sleep alter the diurnal and exercise-induced levels of a range of CVD biomarkers. Methods In a randomized two-condition crossover study, 16 men partook in two sessions, comprising three consecutive nights of full-night sleep (NS, 8.5 hours sleep/night) and three nights of partial sleep restriction (SR, 4.25 hours/night). In both conditions, blood was repeatedly sampled in the evening and about 12 hours later (for evening-to-morning analysis) as well as repeatedly before and after a 30-min bout of high-intensity exercise (at 75% VO2maxReserve). Olink's CVD II panel and ELISAs were used to measure 92 CVD protein biomarkers. Results Under pre-exercise sedentary conditions, the diurnal changes of several CVD biomarkers differed in response to SR compared with NS. However, several proteins exhibited diurnal changes regardless of sleep condition (as also confirmed in a separate a cohort with overnight wakefulness). In response to exercise, we observed that most proteins increased vs. decreased in their relative levels, including inflammatory markers. Furthermore, some proteins exhibited an early vs. more delayed increase. However, following SR, the exercise-induced induction of CVD biomarkers was markedly dampened, compared with the NS condition, and SR resulted in an altered exercise-induced response for several inflammatory-related CVD biomarkers. Conclusion Recurrent sleep restriction impacts the evening-to-morning dynamics of several CVD biomarkers, and the extent to which blood-based CVD biomarkers are induced by acute, high-intensity exercise. This may indicate that some of the cardiometabolic responses to vigorous exercise differ under conditions of sleep loss. Whether such changes alter the long-term benefits of aerobic exercise under conditions of chronic sleep loss, and whether these changes differ in e.g. older subjects or CVD, remains to be investigated. Support (if any) Swedish Society for Medical Research, Swedish Cancer Foundation, Diabetesfonden, Göran Gustafsson, Hjärnfonden