FormalPara Key Points

Metabolic-associated fatty liver disease (MAFLD) affects one in four adults globally and is linked with type 2 diabetes, cardiovascular disease and lifestyle-related cancers, as well as progressive liver disease and liver cancer.

This position statement collates evidence on the role of exercise in the management of MAFLD including referral pathways, assessment and management priorities, exercise prescription recommendations, action planning and considerations for clinicians working with people with MAFLD. 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.

The majority of research evidence indicates that 150–240 min per week of at least moderate-intensity aerobic exercise can reduce liver fat by ~ 2–4%, but as little as 135 min/week has been shown to be effective. This dose of exercise is likely to improve central adiposity, cardiorespiratory fitness and cardiometabolic health, irrespective of weight loss.

1 Background

Metabolic-associated fatty liver disease (MAFLD), historically known as non-alcoholic fatty liver disease (NAFLD), represents the hepatic manifestation of a multi-system metabolic dysfunction-driven disorder [1]. MAFLD affects at least 25% of people globally and within Australia [2,3,4]. In addition to increasing the risk of end-stage liver disease and primary liver cancer, MAFLD plays a central role in the development of type 2 diabetes (T2D), cardiovascular disease (CVD) and extrahepatic lifestyle-related cancers [5], reducing life expectancy by 4 years and increasing time spent living with high metabolic burden [6]. In Australia, it is expected that MAFLD cases will increase by 25% between 2019 and 2030 to over 7 million cases [4], considerably elevating the related disease burden. Globally, from 1991 to 2019, MAFLD increased from 22 to 37%, with an annual increase of 0.7% [7].

Given its strong association with obesity, and in the absence of pharmacological agents approved for the long-term management of MAFLD, lifestyle modifications with dietary changes and increased physical activity/exercise remain the cornerstone of MAFLD management. Allied health professionals (e.g. dietitians, exercise physiologists, physiotherapists, health psychologists) play an integral role in managing the burden of MAFLD. The aim of this position statement was to synthesise the literature on the role of exercise for the management of MAFLD and to produce evidence-based statements to be used to develop recommendations for exercise prescription. Evidence to facilitate the translation, implementation and uptake of these recommendations was also reviewed.

1.1 Definitions of Metabolic-Associated Fatty Liver Disease (MAFLD)

Until recently, MAFLD was known as non-alcoholic fatty liver disease (NAFLD) and was diagnosed if there was evidence of steatosis in ≥ 5% of hepatocytes and the exclusion of other chronic liver diseases and ‘excess’ alcohol intake. NAFLD was further dichotomised into NAFL (referring to simple steatosis) and non-alcoholic steatohepatitis (NASH, referring to the more progressive condition characterised by hepatocyte ballooning, inflammation and varying degrees of fibrosis). Concerns with this terminology included stigma relating to the term ‘alcohol’ and the reprioritisation of disease significance with the term ‘non’. Given the metabolic dysfunction underlying the pathophysiology the term ‘MAFLD’ has been proposed and increasingly used, although a global consensus has not been reached at the time of this publication. MAFLD is defined by the presence of hepatic steatosis in the setting of metabolic dysfunction characterised by having overweight/obesity or T2D, or specific features of metabolic dysregulation [1] (Fig. 1).

Fig. 1
figure 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%

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MAFLD can coexist with any liver disease (including alcohol related liver disease) and disease severity is further categorised by grade of activity and stage of fibrosis. Importantly for this position statement, many of the citations and reported studies have used the term NAFLD. There is marked overlap between NAFLD as previously defined and MAFLD [1, 8] with high overall concordance of the two definitions (Cohen’s kappa of up to 0.92) [9]. For consistency throughout the statement, we have used the term MAFLD with appropriate clarifications where necessary.

1.2 Development and Clinical Impacts of MAFLD

1.2.1 Development

MAFLD develops when there is dysfunction in hepatic fuel utilisation resulting in excess storage of fat (as intrahepatic triglyceride) in the liver (hepatic steatosis) and reduced clearance [via oxidation or repackaging as very low-density lipoprotein (VLDL)-cholesterol]. Hepatic steatosis is a cause and a consequence of insulin resistance [10,11,12]. Increased free fatty acid (FFA) delivery to the liver primarily arises (59%) from insulin-resistant adipose tissue [13] [especially visceral adipose tissue (VAT) that delivers FFAs directly to the liver via the portal vein [10]]. Additionally, de novo lipogenesis, accounting for a further 26% of FFA flux, uses excess substrate from glucose metabolism (glycerol 3 phosphate), exacerbated by insulin resistance in skeletal muscles, to form intrahepatic triglyceride. Dietary fats, which deliver FFA from the gut via chylomicrons, account for the remaining 15% [13]. Within the liver, these FFAs are excreted by VLDL, oxidised through hepatic β-oxidation, or are synthesised to triglyceride for storage.

1.2.2 Clinical Impacts

MAFLD leads to a range of liver-related and extra-hepatic clinical consequences. Obesity and insulin resistance are the key pathophysiological drivers for both liver-related and extra-hepatic disease severity, underpinned by genetic predisposition and/or disruption to the microbiome [14]. People with MAFLD have increased overall mortality, with a 34% higher death rate observed over 7.5 years compared with age- and sex-matched individuals in the general population [15]. The primary causes of death in MAFLD are non-liver related, with CVD and lifestyle-related extra-hepatic cancers accounting for 37% and 21% of deaths, respectively [16]. Approximately 30% of people with MAFLD will develop metabolic-associated steatohepatitis (characterised by hepatocyte injury and death with associated inflammation and varying degrees of fibrosis, historically called non-alcoholic steatohepatitis/NASH); a burgeoning indication for liver transplantation [17, 18]. However, unlike the high incidence of progression from MAFLD to metabolic-associated steatohepatitis, the onset of cirrhosis is relatively low with slow progression (~ 3% in 15 years) [19]. People with histological evidence of steatohepatitis have an increased liver-related mortality rate that is dose-dependent based on the severity of liver fibrosis [20].

1.3 Definitions of Physical Activity, Exercise and Sedentary Behaviour

Physical activity is defined as bodily movement that increases the metabolic rate and can be categorised in relation to the metabolic demands of the activity termed ‘metabolic equivalents’ or METs. Exercise is considered as planned and structured physical activity, generally with a goal to improve or maintain health, wellbeing and/or performance. Exercise prescription centres on the manipulation of programming variables which include the mode of exercise, the frequency (number of sessions per week) of the exercise bouts, the duration (time of the individual exercise bout) and the intensity (the physiological effort/ energy demands of activity). The volume of exercise encompasses the total energy expended in kilojoules per exercise bout or per week, and is a function of the intensity, frequency and duration of weekly exercise. While there are different intensity domain cut points across different professional bodies, intensity is generally framed as ‘light’, ‘moderate’ and ‘vigorous’, and described by approach (e.g. continuous, interval) and modality (e.g. aerobic, anaerobic, resistance). Additionally, sedentary behaviour is classified as activities involving sitting or lying/reclined that have a low energy requirement and little additional movement [21]. Further guidance on exercise prescription variables for both aerobic and resistance training and definitions of intensity domains can be sought elsewhere [21, 22]. The focus of this position paper is on the health effects of exercise on the pathophysiological features of MAFLD, with a specific lens on those that are pertinent to the exercise professional.

1.4 Objectives of the Management of People with MAFLD

1.4.1 Clinical Presentation

Most people with MAFLD do not present with specific symptoms; MAFLD is often identified incidentally through routine assessment of blood biochemistry [e.g. abnormal liver enzymes: alanine aminotransferase (ALT) and aspartate aminotransferase (AST)] or on imaging performed for another health reason. MAFLD may be suspected based on an individual’s medical history or the presence of central obesity, or on investigations including abdominal imaging (ultrasound or computed tomography) showing features of hepatic steatosis. There are established criteria to diagnose MAFLD (see Fig. 1) [8, 23], but in addition physicians may consider the following:

  1. (i)

    An assessment of the severity of liver injury including the degree of liver fibrosis. This is most often undertaken with multi-modal non-invasive approaches using bloodwork that relies on routine tests (such as a full blood count and standard biochemistry panels for the NAFLD fibrosis score and Fibrosis-4 (FIB-4) algorithms) and/or serum biomarkers [as used for the enhanced liver fibrosis (ELF) test], or assessments of liver stiffness based on ultrasound [such as vibration-controlled transient elastography (Fibroscan™)], shear wave elastography or acoustic radiation force imaging, or other imaging modalities (e.g. magnetic resonance elastography). Where these non-invasive tests suggest a patient has advanced disease, they may be referred to hepatology services for further evaluation including possible liver biopsy.

  2. (ii)

    Other co-morbid contributors to liver disease including hepatitis C and hepatitis B viruses, and hazardous alcohol consumption as these may require management in conjunction with MAFLD.

  3. (iii)

    Medication and over the counter preparations (including herbal remedies and traditional medicines), as well as surgical and general health history.

  4. (iv)

    Screening for cardiometabolic health risk and common comorbidities including personal and family history of CVD and T2D, metabolic syndrome, hyperglycaemia [e.g. elevated glycosylated haemoglobin (HbA1c), impaired fasting glucose], atherogenic dyslipidaemia, hypertension, smoking status, alcohol intake and anthropometry [including body mass index (BMI), weight history and waist circumference].

It is common for people to present to exercise services with a chief complaint of T2D, obesity or metabolic syndrome but without a formal specialist review or diagnosis of MAFLD. In these instances, MAFLD may be suspected based on clinical presentation. Given the common underlying pathophysiology, if MAFLD is suspected based on the individual’s clinical history and risk factors (e.g. high waist circumference, T2D, low physical activity), depending on the scope and standards of the local healthcare systems, the exercise professional may facilitate referral to the individual’s primary care physician to establish a diagnosis and determine appropriate care pathways. Potential referral pathways and clinical care team partners are illustrated in Fig. 2.

Fig. 2
figure 2

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

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1.4.2 Clinical Assessment and Management Priorities for the Exercise Professional

The management of MAFLD requires a multi-disciplinary approach. From the medical perspective, the overall management priorities for people with MAFLD are centred around two primary goals:

  1. (i)

    The resolution of MAFLD and/or prevention of liver disease progression

  2. (ii)

    The prevention of cardiovascular related morbidity and mortality

The forefront of management for most people with MAFLD is lifestyle therapy, including both dietary modification and regular exercise, with a primary goal of reducing hepatic steatosis, achieving adiposity reduction, managing cardiometabolic comorbidities and preventing lifestyle-related extra-hepatic cancers. Weight loss of 5–10% will result in clinically meaningful health improvements [24]; however, a number of health benefits are likely to be achieved irrespective of significant weight loss. Beyond body weight, a 30% reduction in hepatic steatosis as measured by magnetic-resonance imaging (MRI) is associated with histological improvement and resolution of steatohepatitis [25]. One challenge in assessing the efficacy of therapeutic interventions to improve liver histology is the limited availability of robust measures that can reliably and non-invasively identify clinically meaningful improvements in these parameters. Tools to quantify and monitor liver fat and liver fibro-inflammation are presently available in research settings only. A suite of tools based on common biochemical and anthropometric measures have been proposed as surrogates to imaging methods and liver biopsy [26]. However, these are validated as screening tools only and are not used routinely for assessing change in liver health status, meaning assessing waist and body weight change remains the primary strategy for longitudinal monitoring in response to treatment.

People with MAFLD have lower levels of cardiorespiratory fitness than the general population [27, 28]. Low cardiorespiratory fitness has been reported to be a potent risk factor for MAFLD and is inversely associated with steatohepatitis [29] and liver fibrosis [28], and may predict the degree of steatosis reduction possible with lifestyle intervention [30]. This may explain in part why people with MAFLD frequently report high levels of fatigue, low levels of energy and low exercise-related self-efficacy [31].

Dietary targets include improving diet quality with a focus on heart healthy eating patterns, that are predominantly plant based with abundant daily vegetables, fruit consumption, use of extra virgin olive oil, fish, seafood, legumes and nuts as preferred protein sources and selecting reduced fat dairy and wholegrain bread and cereal options. Reducing intake of alcohol, sugar-sweetened beverages, highly processed foods and processed red meats is also recommended. Practical resources are available elsewhere [32].

Regardless of the presentation or referral pathway, a risk assessment should be undertaken by an appropriately trained exercise professional [e.g. using the Australian Pre-Exercise Screening System (APSS) screening tool].

For the clinical exercise professional, assessment and management priorities for people with known or suspected MAFLD are suggested to include:

  1. (i)

    Cardiometabolic risk factors: Practitioners should assess waist circumference, BMI, blood pressure, family history of heart disease and diabetes, smoking status, alcohol use and physical inactivity. Further clinical assessment, requested by the treating physician, may also include blood lipids and lipoproteins, blood glucose and HbA1c. Scores such as the Atherosclerotic Cardiovascular Disease (ASCVD) score (score calculator freely available online https://www.mdcalc.com/calc/3398/ascvd-atherosclerotic-cardiovascular-disease-2013-risk-calculator-aha-acc) may be used to inform 10 year risk of heart disease or stroke. Management priorities should include reduction in central obesity (as waist circumference), blood pressure and sedentary time, and increasing physical activity. Reducing excess adiposity remains an important part of the clinical management of MAFLD, irrespective of BMI. However, weight loss and/or additional components of metabolic syndrome may also be targets for management depending on clinical presentation. Reductions of 3–5% body weight can improve the cardiometabolic profile [33], reduce liver steatosis [8] and achieve MAFLD remission in people with BMI < 25 kg/m2 [34]. Body weight reductions of ≥ 7–10% are recommended for improvements in histological features of MAFLD, especially in people with comorbid MAFLD and overweight/obesity [8, 35]. In people who achieved ≥ 10% weight loss, 90% had steatohepatitis resolution, 81% had fibrosis regression and all improved hepatic steatosis [36].

  2. (ii)

    Physical capacity: Assessment may include physical activity levels and sedentary behaviour, cardiorespiratory fitness, neuromuscular fitness and assessment of any musculoskeletal or orthopaedic limitations (including sarcopenia) that may impact physical and functional capacity. Whilst not necessarily a focus of research to date in MAFLD, it is highly likely that consideration of musculoskeletal health, its assessment and prescription are relevant for many people with MAFLD, when functional capacity and avoidance of muscle loss/sarcopenia are key considerations. Further clinical assessment to establish sarcopenia [37] and frailty via imaging and/or relevant clinical measures such as the short physical performance battery (SPPB) [38] may be clinically appropriate to consider based on individual presentation. While all these outcomes are important for people with MAFLD, priority for assessment and targets for management will depend on individual presentation and intervention targets. Identifying barriers to the uptake and maintenance of physical activity/exercise may also enable personalised exercise programmes (see Sect. 3.3).

  3. (iii)

    Comorbidities: Comorbidities such as metabolic syndrome, pre-diabetes, T2D, obesity, polycystic ovarian syndrome (PCOS), hypertension and depression/mental ill health should be identified, and the broader management of these conditions should be considered in the context of MAFLD management.

  4. (iv)

    Patient-important outcome measures: Practitioners should assess issues particularly relevant to MAFLD such as rating levels of fatigue, energy and exercise-related self-efficacy (e.g. via the Self-Efficacy for Exercise Scale [39]). This may also include sleep quality (e.g. via the Pittsburgh Sleep Quality Index [40]), low-mood, ability to undertake activities of daily living and health-related quality of life (e.g. via the Chronic Liver Disease Questionnaire – Non-Alcoholic Fatty Liver Disease version [41]) or other goals specific to the patient that exercise may address. Patient-important outcome measures could be monitored and assessed using visual analogue scales or the goal attainment scale[42].

  5. (v)

    Identification of need for referral onwards based on clinical opinion. Practitioners should ask about:

  6. -

    Diet (in accordance with national healthy eating guidelines) with referral to a dietitian if indicated. Referral is indicated if the patient’s needs extend beyond general healthy eating advice, if they have complications due to MAFLD (notably liver cirrhosis, see Sect. 4.3), have additional comorbidities, have specific nutritional composition questions and/or request extra specialist support.

  7. -

    Emotional, social and cognitive functioning with referral to a psychologist or behavioural counsellor if indicated.

  8. -

    Medication use to determine whether the individual is taking medication (e.g. for blood pressure, T2D, cholesterol) and if not, referring to their primary care physician for medical review if indicated based on clinical assessment. Medications may also need modifying by the primary care physician as the patient starts regular exercise or significantly changes their exercise programme (e.g. to reduce antihypertensives, oral hypoglycaemics or insulin).

  9. -

    If MAFLD is suspected, referral back to the primary care physician to establish a pathway for diagnosis, assessment of disease severity and additional care pathways if required.

2 Section 2: Evidence for the Role of Exercise in the Management of MAFLD

There is clear and consistent evidence that regular exercise is cardioprotective and has multiple benefits on musculoskeletal function and mental health, irrespective of weight loss [43]. The mechanisms by which exercise modulates hepatic steatosis have been detailed elsewhere [14, 44,45,46]. Briefly, putative mechanisms centre on altering the flux of free fatty acids (FFA) to and from the liver via changes to substrate metabolism within the muscle, adipose tissue and liver [11, 47, 48]. These may be mediated, in part, by improvements in peripheral insulin sensitivity and glucose uptake which alter liver signalling pathways [i.e. sterol regulatory element binding protein-1c (SREBP-1c) and carbohydrate response element binding protein (ChREBP)] and gene expression [e.g. lipogenic proteins fatty acid synthase (FAS) and acetyl-coenzyme A carboxylase (ACC)]. In rodents, exercise-mediated increases in mitochondrial enzymes (e.g. cytochrome c oxidase, citrate synthase and β-hydroxyacyldehydrogenase) and increases in mitochondrial content and oxidative capacity have been shown [49]. These improvements in liver mitochondrial content and function have been associated with increased β-oxidation, which may prevent the accumulation of metabolic by-products such as ceramides and diacylglycerides that contribute to insulin resistance (Fig. 3). A key signalling pathway for direct liver benefit may be the activation of the metabolic energy sensor adenosine monophosphate-activated protein kinase (AMPK). This pathway plays an important role in regulating metabolism (i.e. increasing fatty acid oxidation and glucose uptake). AMPK activity is reduced in obesity, diabetes and inflammatory states [50] and is increased acutely during and after exercise in mice [51], with indirect evidence suggesting that exercise modulates the AMPK/mTORC1 pathway in people with MAFLD [52]. A recent phase 2a pharmacological trial targeting AMPK activation observed reduction in liver fat and metabolic parameters in some people with MAFLD [53]. Extra-hepatic adaptations to exercise, notably exercise-mediated reductions in VAT, may also reduce the delivery of FFA and to the liver [11].

Fig. 3
figure 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

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2.1 Literature Search

A systematic online literature search for systematic reviews with meta-analyses was conducted (by SK) from database inception to June 2023 across seven electronic databases [PubMed, Cochrane Library, Embase (Ovid), CINAHL (Ebsco host), Web of Science and SPORTDiscus]. Search terms included keywords and Medical Subject Headings (MeSH) to find literature involving exercise and liver fat and/or MAFLD populations (see Online Resource 1 for the full list of search terms and specific database strategies). Included reviews were systematic reviews with meta-analyses that were in a MAFLD cohort and/or reported on a liver outcome (e.g. hepatic steatosis or liver biochemistries). The evidence generated by extraction (by SK and AS) and collation of literature via these searches was reviewed and evidence was graded (all authors). Consensus on the content and recommendations of the position statement was reached through an iterative process involving the multi-disciplinary authorship team. Decisions on how evidence-based guidelines could be best translated into clinical practice were developed via evidence review and authors’ professional experiences.

The majority of evidence was from early stage MAFLD, with limited data from people with metabolic-associated steatohepatitis and/or cirrhosis. Five overarching evidence statements were defined, and the strength of each evidence statement was graded based on the National Health and Medical Research Centre (NHMRC) guidelines (Table 1). The evidence grade reflects the degree of certainty based on the overall body of evidence that an effect or association is correct.

Table 1 Evidence Statements
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2.2 Evidence for the Benefits of Exercise on Hepatic Steatosis

As at June 2023, 25 systematic reviews with meta-analyses had examined the efficacy of exercise for reducing hepatic steatosis [54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77]. Reviews predominantly included randomised controlled trials (RCTs) in adults [54, 55, 58, 59, 61, 62, 64, 67, 68, 70,71,72,73,74, 76,77,78,79,80,81], children or adolescents [59, 63], or both [66], with overweight or obesity [58, 66, 71] and/or confirmed MAFLD [54, 64, 65, 69, 72,73,74,75,76,77, 79,80,81,179]. Maintaining functional status and improving quality of life are key treatment goals in this patient group.

Data from people with broad-aetiology cirrhosis indicate that exercise training is safe and effective for lowering portal pressures [180, 181], with further exercise prescription guidance published (see Tandon et al. [158] for prescription recommendations). However, there is a dearth of evidence for the efficacy of exercise specifically in people with metabolic steatohepatitis-related cirrhosis. Data from small studies of patients with early stage or well-compensated cirrhosis (mixed aetiologies) have shown that supervised and home exercise programmes, combining aerobic and resistance exercise, are safe, with no apparent increased risk of variceal haemorrhage or encephalopathy; these programmes also led to increases in lean body mass, reduction in overall adiposity, improved mobility and a marginal reduction in hepatic venous pressure gradient [182,183,184,185].

Evidence to inform exercise interventions for people with decompensated cirrhosis is lacking. Low-intensity activity is likely safe and feasible for those with decompensated cirrhosis, but it is important to liaise closely with other members of the multi-disciplinary team (including physician evaluation) before initiating an exercise programme for all patients with cirrhosis. This is to ensure complications of end-stage liver disease are being appropriately managed for safety reasons. For example, if the patient is at high risk of varices or has had a previous variceal bleed, relevant prophylaxis must be in place before exercise is prescribed. For further information on clinical considerations regarding these complications and recommendations for exercise assessment and prescription for people with cirrhosis (see Tandon et al. [158].

People with cirrhosis are hypercatabolic and may experience decreased appetite, early satiety and nutritional malabsorption. Nutritional assessment and optimisation should occur alongside the initiation of exercise to identify malnutrition, ensure that patients are meeting the appropriate protein and calorie requirements, and determine whether an increased energy intake is required due to becoming more physically active. Continued communication with the dietetic team should be maintained throughout [186].

5 Conclusions

MAFLD is a highly prevalent chronic liver condition characterised by hepatic steatosis that is strongly linked with both cardiometabolic and liver-related sequalea. MAFLD management centres on lifestyle therapy (exercise and diet) driven by a patient-centred multi-disciplinary team. The broader management goals should target preventing liver disease progression and reversing MAFLD and reducing cardiovascular morbidity and mortality. The exercise professional plays a central care role in MAFLD management. There is strong evidence that aerobic exercise reduces hepatic steatosis with modest benefits (2–4%) and can be demonstrated irrespective of weight loss. At least 135 min/week and up to 240 min/week of moderate intensity aerobic activity is recommended for hepatic steatosis reduction, with no further benefit from completing higher intensity exercise (including HIIT approaches) so long as this volume of aerobic activity is achieved. This exercise dose is likely to result in broader health benefits. There is no clear evidence for a benefit of resistance training on outcomes for MAFLD beyond its established effects on lean mass maintenance, blood glucose control and neuromuscular strength. Resistance training should be considered in addition to, and not instead of, aerobic exercise targets. Exercise management should encompass shared decision making and engage practical behavioural strategies that are cognisant of an individual’s local, cultural and socioeconomic circumstances, along with personal preferences, comorbidities and physical capacity.