Author information
1 K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Sor Trondelag, Norway; School of Human Movement and Nutrition Sciences, University of Queensland, Brisbane, QLD, Australia. Electronic address: ilaria.croci@ntnu.no.
2 School of Human Movement and Nutrition Sciences, University of Queensland, Brisbane, QLD, Australia.
3 K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Sor Trondelag, Norway.
4 K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Sor Trondelag, Norway; Institute of Public Health, College of Medicine and Health Sciences, United Arab Emirates University, Al-Ain, United Arab Emirates.
5 Department of Gastroenterology and Hepatology, Brisbane, QLD, Australia; PA-Southside Clinical School, School of Medicine, The University of Queensland; Princess Alexandra Hospital, Brisbane, QLD, Australia; Translational Research Institute, Brisbane, QLD, Australia.
6 K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Sor Trondelag, Norway; School of Human Movement and Nutrition Sciences, University of Queensland, Brisbane, QLD, Australia.
Abstract
PURPOSE:
Sedentary behaviour (SB) and low physical activity (PA) are independently associated with non-alcoholic fatty liver disease (NAFLD). Compared to PA, high cardiorespiratory fitness (CRF) has been associated with a higher protection against all-cause mortality and a number of specific diseases. However, this relationship has not been investigated in NAFLD. This study examined the roles of SB and CRF on: i) the likelihood of having NAFLD in the general population, and ii) the risk of mortality over 9 years within individuals having NAFLD.
METHODS:
A cross-sectional analysis of 15,781 adults (52% female; age range 19-95 years) was conducted. Self-reported SB was divided into tertiles. CRF was estimated using validated non-exercise models, and the presence of NAFLD from the Fatty LiverIndex. Adjusted Odds Ratios and 95% Confidence Intervals for NAFLD were estimated using logistic regression analyses. Hazard Ratios for all-cause mortality were estimated using Cox proportional hazard regression in individuals with NAFLD.
RESULTS:
For each additional 1h/d of SB, the likelihood of having NAFLD was significantly increased by 4% (CI, 3-6%). In combined analyses, compared with the reference group [high CRF and low (≤4h/d) SB], individuals with low CRF had a markedly higher likelihood of having NAFLD (OR, 16.9; CI 12.9-22.3), even if they had SB≤4h/d. High CRF attenuated the negative role of SB up to 7h/d on NAFLD. Over 9.4±1.3 years of follow-up, individuals with NAFLD and low CRF had the risk of mortality increased by 52% (CI, 10-106%) compared to those with high CRF, regardless of SB or meeting PA guidelines.
CONCLUSIONS:
Low CRF increases the risk of premature death in individuals with NAFLD, and is strongly associated with higher likelihood of having NAFLD, outweighing the influence of SB.