Exercise in the Management of Metabolic-Associated Fatty Liver Disease (MAFLD) in Adults: A Position Statement from Exercise and Sport Science Australia

Abstract

Metabolic-associated fatty liver disease (MAFLD) is the most prevalent chronic liver disease worldwide, affecting 25% of people globally and up to 80% of people with obesity. MAFLD is characterised by fat accumulation in the liver (hepatic steatosis) with varying degrees of inflammation and fibrosis. MAFLD is strongly linked with cardiometabolic disease and lifestyle-related cancers, in addition to heightened liver-related morbidity and mortality. This position statement examines evidence for exercise in the management of MAFLD and describes the role of the exercise professional in the context of the multi-disciplinary care team. The purpose of these guidelines is to equip the exercise professional with a broad understanding of the pathophysiological underpinnings of MAFLD, how it is diagnosed and managed in clinical practice, and to provide evidence- and consensus-based recommendations for exercise therapy in MAFLD management. The majority of research evidence indicates that 150-240 min per week of at least moderate-intensity aerobic exercise can reduce hepatic steatosis by ~ 2-4% (absolute reduction), but as little as 135 min/week has been shown to be effective. While emerging evidence shows that high-intensity interval training (HIIT) approaches may provide comparable benefit on hepatic steatosis, there does not appear to be an intensity-dependent benefit, as long as the recommended exercise volume is achieved. This dose of exercise is likely to also reduce central adiposity, increase cardiorespiratory fitness and improve cardiometabolic health, irrespective of weight loss. Resistance training should be considered in addition to, and not instead of, aerobic exercise targets. The information in this statement is relevant and appropriate for people living with the condition historically termed non-alcoholic fatty liver disease (NAFLD), regardless of terminology.

Conflict of interest statement

SEK has received funding for unrelated work by Diabetes Australia, Exercise and Sports Science Australia and NHMRC. JGS receives or has received research support from Astra Zeneca, Galectin, Noom, Inc., Novo Nordisk and Zydus. AS, KH, IJH, GAM, JG and NAJ have nil to disclose.

© 2023. The Author(s).

Figures

Fig. 1

Schematic definition of MAFLD. Adapted from Eslam 2020 [1], with permission. BMI body mass index, HDL-cholesterol high-density lipoprotein-cholesterol, HbA1c glycated haemoglobin, HOMA homeostatic model assessment, hs-CRP high-sensitivity C-reactive protein. *Relates to liver histology from liver biopsy, with ≥ 5% referring to the proportion of hepatocytes containing visible intracellular lipid droplets. Other modalities (imaging, blood biomarkers/scores) have assigned thresholds to detect steatosis at ≥ 5%

Fig. 2

Potential referral and clinical care pathways. MAFLD metabolic-associated fatty liver disease

Fig. 3

Putative mechanisms for the effects of exercise on reducing hepatic steatosis Solid lines indicate enhanced mechanisms (e.g. insulin sensitisation). Dashed lines indicate reduced mechanisms (e.g. reduced concentrations of plasma insulin and glucose, reduced de novo lipogenesis). VAT visceral adipose tissue, SAT subcutaneous adipose tissue, FFA free fatty acid, TG triglyceride, SREBP- 1c sterol regulatory element binding protein, ChREBP carbohydrate responsive element binding protein, DNL de novo lipogenesis, FAS fatty acid synthase, ACC acetyl-coenzyme A carboxylase, VLDL very low-density lipoprotein-cholesterol, AMPK adenosine monophosphate-activated protein kinase, SIRT1 sirtuin 1, IRS-1 insulin receptor substrate 1, PI3K phosphatidylinositol-3-kinase, GLUT4 glucose transporter type 4, G6P glucose 6-phosphate. Created with BioRender.com

Fig. 4

Patient-centred multi-disciplinary approach to MAFLD management

Fig. 5

Framework for the implementation of exercise recommendations