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Can You Train With Fatty Liver? The Marbled-Liver Barbell Audit: Where 8 Weeks of Resistance Training Cut Liver Lipid 13% With Body Weight, Visceral Fat and Whole-Body Fat Mass All Statistically Unmoved, 16 Weeks of Guideline-Dose Aerobic Work Cut Intrahepatic Triglyceride 10.3% While the Scale Read 103.1 and Then 102.9 kg, 12 Weeks of Supervised Cycling-Plus-Barbell in Biopsy-Proven NASH Cut Liver Fat 16% Against a 9% Gain in Untreated Controls With Fibrosis Markers Honestly Unmoved, the Pooled Dose Threshold Sits Above 10,000 kcal of Total Program Workload, the Global File Reads 30.05% of Adults Rising 50.4% in Two Decades With Latin America the World's Highest Region at 44.37%, and EASL's 2024 Guideline Prescribes Lifestyle First — Train for the Organ the Bathroom Scale Can't See

By RightRep AI Assistant · · 24 min read

Fatty liver is the condition this library has already opened from the treatment side — does exercise help fatty liver is the general file, and the type 2 diabetes and high blood pressure doors cover the two conditions it travels with. This file answers the diagnosed lifter's version: what happens to a training program when the liver is marbled — a condition whose global file reads 30.05% of adults pooled across 92 studies and 9,361,716 people [2], whose fresh MASLD-era burden review prices at 30–40% of adults worldwide [3], and whose curve is the steepest in this library: prevalence climbed +50.4% in two decades, from 25.26% in 1990–2006 to 38.00% in 2016–2019 [2], with Latin America the highest region on Earth at 44.37% [2]. The default scripts fail in opposite directions. The scared script reads "liver disease" as a fragility verdict — training is quit "until the liver heals," the diagnosis is hidden from the gym, and the deconditioning spiral feeds the exact metabolic machinery that marbled the liver in the first place. The reckless script reads the diagnosis as a fat joke — "it's just gordura no fígado, keep the bulk, the beer and the blood-work denial" — and never learns that steatosis is staging information, not a cosmetic note. The reframe that carries the whole file is one line: the bathroom scale cannot see the organ the barbell fixes — in the founding resistance-training trial, liver lipid fell 13% while body weight, visceral fat volume and whole-body fat mass all stood statistically still [5], and that weight-independent lever is the one this library exists to teach. Which puts the fences in order. First: the hepatologist names it and stages it. This file assumes MASLD — metabolic dysfunction-associated steatotic liver disease, the 2023 rename of NAFLD — diagnosed and staged by a hepatology or metabolic team, with the FIB-4 blood score and, where indicated, transient elastography doing the staging work the 2024 EASL-EASD-EASO guideline assigns them [4]. Second: the staging outranks every training question. Plain steatosis and early fibrosis are exercise-tolerant territory; cirrhosis, portal hypertension and the hepatocellular-carcinoma screening era are a different program built with the hepatology team — the guideline is explicit that advanced fibrosis changes the management conversation [4]. Third: the drug, diet and alcohol shelf is the prescriber's. No session, set or "liver detox protocol" edits a resmetirom prescription, an incretin chart or the alcohol conversation the guideline has — and the alcohol question is definitional here: MASLD is steatosis without harmful drinking, and the guideline's lifestyle line includes discouraging alcohol outright [4]. With the fences standing, the operational file is unusually barbell-shaped for a liver condition: the permission question has its own resistance-training randomized controlled trial [5], the modality question has an aerobic-versus-barbell systematic review [6], the dose question has a pooled energy threshold from 21 randomized trials [9], and the honesty question — what training does not do — has a biopsy-proven meta-analysis that answers it flatly [11].

The short answer: yes — it is first-line, not a concession

Strip the file to its spine. The condition's own review literature frames exercise as first-line therapy: the aerobic-versus-resistance systematic review opens with the premise that "exercise is a first-line therapy for patients with non-alcoholic fatty liver disease" and then asks only which modality delivers it best [6]. The founding barbell trial: 8 weeks of resistance training in sedentary adults with clinically defined NAFLD (n=11 against n=8 continued normal treatment) produced a 13% relative reduction in liver lipid (14.0±9.1 to 12.2±9.0; p<0.05) — with lipid oxidation, glucose control (−12% versus +12% change in glucose AUC; p<0.01) and insulin resistance (HOMA-IR 5.9±5.9 to 4.6±4.6; p<0.05) all improving alongside, and body weight, visceral adipose tissue volume and whole-body fat mass all statistically unmoved (p>0.05) — the first study to demonstrate that resistance exercise specifically improves NAFLD independent of any change in body weight [5]. The aerobic replication at guideline dose: 18 obese adults with NAFLD randomized to 16 weeks of exactly the physical-activity amounts governments recommend (45–55% VO₂peak, 30–60 minutes, five days a week) saw intrahepatic triglyceride fall 10.3%±4.6% (p<0.05) while total body weight read 103.1±4.2 kg before and 102.9±4.2 kg after [7]. The biopsy-proven trial: 24 patients with biopsy-proven NASH — the inflamed stage, not just steatosis — completed 12 weeks of supervised cycling-plus-resistance training three times a week on a weight-maintaining protocol: hepatic triglyceride content fell 16%±24% against a 9%±15% gain in the untreated controls (p<0.05), visceral fat fell 22±33 cm² while controls gained 14±48 cm², plasma triglycerides fell 0.5±1.0 mmol/L while controls rose — and the circulating markers of inflammation and fibrosis did not move, the trial's own verdict being that weight-free exercise "affects some but not all factors associated with NASH" [8]. What the file does not promise: exercise alone has not yet moved liver histology in the small biopsy-proven meta-analysis [11], the pooled liver-enzyme response to exercise is statistically null [9], and the weight-loss ladder — where the truly dramatic histology numbers live — is a diet-plus-training project, not a barbell-only one [12]. The honest split, named: the hepatology team owns the staging, the drug shelf, the alcohol conversation and the cirrhosis door; the program owns the dose, the engine, the strength column and the fat-ledger trend [4][5][6][12].

The reframe: the scale is the wrong ruler

Everything operational in this file hangs on one measured fact the fitness industry keeps failing to absorb: in trial after trial, the liver's fat content moved while the bathroom scale did not. Hallsworth's lifters: liver lipid −13%, body weight p>0.05 [5]. Sullivan's walkers-and-cyclists: intrahepatic triglyceride −10.3%, body weight 103.1→102.9 kg, body fat percentage 38.9%→39.2% [7]. Houghton's NASH patients: hepatic triglyceride −16% on an explicitly weight-maintaining design [8]. Three independent research groups, three modalities, one pattern — the organ and the scale are different ledgers [5][7][8]. That single fact retires both broken scripts at once. The lifter who quits training "until the liver heals" is abandoning the one lever that edits the liver's ledger without waiting for the diet war to be won — and hands the liver to the same sedentary metabolism that marbled it, in a population where the condition's co-travelers read obesity 51.34%, hyperlipidemia 69.16%, metabolic syndrome 42.54%, hypertension 39.34%, type 2 diabetes 22.51% [1]. The lifter who treats the diagnosis as cosmetic is ignoring that steatosis is the first entry in a staging ledger — steatosis, steatohepatitis, fibrosis, cirrhosis, hepatocellular carcinoma — whose later chapters the hepatology team manages and whose early chapters respond to exactly the levers the gym owns [3][4]. The ruler note matters too: the trials measured liver fat with magnetic resonance spectroscopy and computed tomography — instruments that see the organ directly — which is why the reframe is not a motivational slogan but a measurement statement. Your program's job is to keep the training log dense enough that the next hepatology visit has a real "what have you been doing" to read, and this library's tracking file explains why that log beats memory every time. The scale still counts — for the weight-loss ladder below, it counts enormously [12] — but it is the wrong primary endpoint for the training column, and the audit's most quotable sentence is that you train for the organ the bathroom scale can't see [5][7][8].

The mechanism file: the muscle-liver axis

The honest mechanistic sentence first: the full causal chain from a counted rep to a hepatocyte's lipid droplet is not closed, and this file will not pretend otherwise. What the literature does hold is a two-way street between muscle and liver that the barbell audience should read twice. The liver-to-muscle direction: across 24 studies and 88,609 participants, NAFLD pooled against sarcopenia at OR 1.74 (95% CI 1.39–2.17) — the fatty liver and the shrinking muscle travel together, with the association strongest in Asian populations at OR 1.97 (1.54–2.51) [13]. The reading for the diagnosed lifter: this is a condition that eats the very tissue that disposes of glucose — the less muscle you carry, the harder the liver works as a metabolic organ, and the marbled liver in turn accelerates the muscle loss [13]. The muscle-to-liver direction: the exercise trials that measured the mediators show training improving the machinery the liver's lipid ledger runs on — Hallsworth's 8 weeks of barbell work improved HOMA-IR (5.9±5.9 to 4.6±4.6) and flipped the glucose-AUC change from +12% in controls to −12% in lifters [5]; the pooled analysis of exercise-only trials shows fasting free fatty acids falling −74.15 µmol/L (95% CI −118.47 to −29.84) with a large effect size (SMD −0.94) and insulin falling −1.88 U/L (−3.43 to −0.34) [9]. Free fatty acids are the raw material the liver packages into the triglyceride droplets that marble it — a training effect that drains the feedstock is a mechanism file, not a coincidence [9]. And the honest null: Sullivan's team measured VLDL-triglyceride secretion directly with stable-isotope tracers and found exercise did not change hepatic VLDL-TG or apolipoprotein B-100 secretion — the liver's export machinery ran at the same speed while its fat store shrank anyway, meaning the improvement works through the intake-and-oxidation side of the ledger rather than the export side [7]. That null is carried here rather than laundered: the mechanism file is strong where it is strong (glucose, fatty acids, insulin) and openly unfinished where it is unfinished (lipoprotein kinetics, histology) [7][11].

The barbell file: the crown RCT and the modality verdict

Now the sentence this library exists to write: for the lifter with a marbled liver, the permission has its own resistance-training randomized controlled trial — and its design is the gym's native language. The Hallsworth trial: sedentary adults with clinically defined NAFLD, assigned to 8 weeks of resistance exercise (n=11) or continued normal treatment (n=8) [5]. The result, in the trial's own instruments: liver lipid down 13% relatively (14.0±9.1 vs 12.2±9.0; p<0.05), submaximal respiratory quotient shifted toward fat oxidation (−0.020±0.010 vs −0.004±0.003; p<0.05), glucose tolerance improved (−12% vs +12% AUC change; p<0.01), HOMA-IR improved (p<0.05) — and no effect whatsoever on body weight, visceral adipose tissue volume or whole-body fat mass (p>0.05), under the trial's own closing verdict that this was "the first study to demonstrate that resistance exercise specifically improves NAFLD independent of any change in body weight" [5]. The modality verdict: the systematic review that compared the two shelves — 23 studies and 24 aerobic against 7 resistance protocols — concluded both improve hepatic steatosis, with the median effective aerobic prescription at 4.8 METs, 40 minutes a session, 3 times a week, 12 weeks and the median effective resistance prescription at 3.5 METs, 45 minutes a session, 3 times a week, 12 weeks — but the resistance protocols achieved it at significantly lower cardiovascular intensity (%VO₂max 28% vs 50%, p=0.0034) and lower total energy consumption (6,470 vs 11,064 kcal over the total period, p=0.0475), under the reviewers' verdict that resistance exercise "may be more feasible than aerobic exercise for NAFLD patients with poor cardiorespiratory fitness or for those who cannot tolerate or participate in aerobic exercise" [6]. Read that as the lane's quietest crown: for the deconditioned, obese, joint-beaten lifter this condition recruits — BMI 38.1 in Sullivan's trial [7] — the barbell is not the compromise modality; it is the efficient one, delivering the liver effect at roughly half the energy bill [6]. The translation for the diagnosed lifter: this is a both-columns file — the barbell carries the strength column and the muscle the condition eats [13], the aerobic base carries the engine and the splanchnic ledger — and the two share a program exactly the way this library has always taught them to [5][6][9].

The dose file: the 10,000-kcal threshold and the weekly template

The pooled analysis gives the dose question its number. Across 21 randomized controlled trials and 1,530 participants, exercise programs whose total workload exceeded 10,000 kcal produced significant intrahepatic fat reduction — −3.46% (95% CI −5.20 to −1.73; p<0.0001) absolute, with a huge effect size (SMD −1.77, −3.11 to −0.42) — while programs under the threshold did not, under the reviewers' verdict that "an aggregate exercise programme energy expenditure (>10,000 kcal) may be required to promote reductions in intrahepatic fat" [9]. Translate the threshold into gym units and it lands almost exactly on the review median protocols [6]: a combined program at roughly 3 sessions a week, 40–45 minutes each, for 12 weeks burns through 10,000 kcal of cumulative work right on schedule — which is why the practical file below prescribes exactly that shape. Two more dose notes, both honest. The pooled free-fatty-acid and insulin moves came from the exercise-only trials (FFAs −74.15 µmol/L, SMD −0.94; insulin −1.88 U/L) — the training column earns its line items even without the diet column attached [9]. And the enzyme null: alanine aminotransferase, aspartate aminotransferase and γ-glutamyltransferase did not significantly change with exercise in the pooled analysis [9] — blood work may lag the organ's improvement, which is exactly why the staging conversation belongs to the hepatologist with the right instruments, not to a panic-read ALT printout the morning after a hard session [4][9]. For programming, the template the evidence supports is boring on purpose: training frequency at 3 non-consecutive days, sustainable weekly set budgets, loads climbed by progressive overload, plus the zone 2 base for the engine column — the dose is cumulative work, and cumulative work survives boring [6][9].

The honest counterfile: what training does not do

The lane's honesty policy demands this section, and this condition's biopsy literature makes it unusually sharp. The Chen meta-analysis: three controlled clinical trials of exercise alone in biopsy-proven NAFLD — 72 total participants, 40 exercising against 32 comparing — pooled under random-effects models, and the verdict is flat: exercise did not significantly improve Brunt grade, NAFLD activity score, or fibrosis [11]. The companion systematic review of six biopsy-proven studies found the same shape: the two randomized trials detected no significant histological improvement, while non-randomized interventional studies showed exercise reducing hepatocyte ballooning and liver fibrosis — and across five studies of non-invasive tests, exercise improved steatosis measured by MRI-based techniques but not serum biomarkers for steatohepatitis and fibrosis [10]. Houghton's NASH trial had already said it from inside an RCT: liver fat −16%, visceral fat −22 cm², triglycerides −0.5 mmol/L — and interleukin 6, tumor necrosis factor-α, C-reactive protein and the fibrosis markers unmoved [8]. Put the whole ledger side by side and the honest reading is precise, not deflating: training's weight-independent effect is real, repeatable and measured on the organ itself — in fat fraction, lipid content and the metabolic mediators — while the histology endpoints at current trial sizes and durations remain unmoved [8][9][10][11]. Two cautions ride with that sentence. The trials are small (72 participants is the entire biopsy-proven exercise-alone meta [11]) and short (8–16 weeks [5][7][8]) against a condition measured in decades — absence of evidence at 12 weeks is not evidence of absence at year three. And the histology column that does move dramatically belongs to the weight-loss ladder, which is why the next section is not optional reading for this condition the way it isn't for most [12]. The audit's verdict: the barbell is a first-line column, not a stand-alone cure — and the difference between those two sentences is the difference between a program and a fantasy.

The weight-loss ladder: the numbers that made the guidelines

The therapeutic frame the EASL guideline builds its lifestyle line around has a dose-response spine, and it comes from the 293-patient Havana cohort: 52 weeks of lifestyle modification, paired liver biopsies in 261 patients, and the histology ladder set by weight lost [12]. The numbers that made the guidelines: overall, 25% achieved resolution of steatohepatitis and 19% regression of fibrosis; among the 88 patients (30%) who lost ≥5% of body weight, 58% achieved NASH resolution and 82% a 2-point NAS reduction; among those who lost ≥10%, all had NAS reduction and 90% achieved NASH resolution — with the degree of weight loss independently associated with improvement in every NASH-related histologic parameter [12]. Two translations, both honest. For the reader whose program includes weight loss — and at a comorbidity profile of 51% obesity [1], many will — the ladder reframes training's role: exercise is the delivery vehicle that makes the diet's weight loss actually happen and actually stick, the column that protects muscle while the scale falls, and the why am I not losing weight file is the companion audit. For the reader who cannot lose weight — the majority in real clinics, which is precisely why the weight-independent RCTs matter — the audit's spine still stands: 13% [5], 10.3% [7], 16% [8] of liver-fat reduction on stable body weight is a real, organ-measured column, and the guideline's lifestyle line runs on weight loss, diet, exercise and alcohol — a four-part conjunction, not a one-part sentence [4]. The MASH-era drug shelf (incretins for the diabetes and obesity indications, resmetirom for non-cirrhotic F2+ disease) sits on top of that lifestyle base, prescribed by the team that staged you — never instead of the base the guideline ordered first [4].

The fences, in order

  1. The staging fence — FIB-4 and elastography before programming assumptions. The 2024 EASL-EASD-EASO guideline's case-finding architecture is explicit: adults with cardiometabolic risk factors, abnormal enzymes or imaging-confirmed steatosis get stepped staging — the FIB-4 blood score first, transient elastography where the score is indeterminate — because advanced fibrosis predicts the liver-related outcomes and changes the management conversation [4]. Your first training-relevant question to the hepatology team is not "can I train?" but "what stage am I, and does it change the program?"
  2. The cirrhosis door. This file's permission is written for the steatosis-to-early-fibrosis majority. Compensated cirrhosis is trainable territory with medical co-sign; decompensation, portal hypertension and the HCC-screening era are hepatology-led programs with their own rules — the guideline reserves its treatment pathways for exactly that stratum [4].
  3. The alcohol fence is definitional. MASLD is steatosis plus cardiometabolic risk minus harmful drinking — the drinker's overlap gets its own name, MetALD, priced at 2–8% of adults [3][4]. The guideline's lifestyle sentence includes "discouraging alcohol consumption" alongside weight loss, diet and exercise [4]. No training column buys back a drinking column here.
  4. The supplement fence. The liver processes everything on the shelf, and "liver detox" products are the industry's most backwards invention — the detox organ does not need detoxing, it needs fewer insults. Nothing in this file licenses an unvetted supplement stack; the hepatology team vets the shelf.
  5. The red-flag list outranks every training decision. Jaundice, ascites, confusion, vomiting blood, unexplained bruising — same-day medicine, program paused without apology, re-entry through the sick rules this library already teaches.

The Brazil anchors

The pt-BR lane's reader holds a specific position in this condition, and the numbers are unusually direct. Latin America is the highest-prevalence region in the world — 44.37% (95% CI 30.66–59.00) in the 92-study global pooled analysis, ahead of the Middle East and North Africa at 36.53%, South Asia at 33.83%, North America at 31.20% and Western Europe at 25.10% [2] — and the 2016 meta-analysis had already flagged South America among the highest-prevalence geographies at 25.24% global pooled [1]. The Brazilian cohort file: ELSA-Brasil — 15,105 civil servants aged 35–74 across six capital cities — carries the steatosis ledger: in 8,166 adults without diabetes at baseline followed a mean 3.8 years, incident diabetes struck 7.83% of those with ultrasound-detected steatosis against 3.88% of those without (p<0.001), with steatosis predicting diabetes at HR 1.31 (95% CI 1.09–1.56) after adjustment for body mass index [14] — the fatty liver is a metabolic alarm clock, not a cosmetic note. The same cohort's vascular file: in 7,196 cardiovascular-disease-free participants, NAFLD presence and severity tracked aortic stiffness (carotid-femoral pulse wave velocity) beyond abdominal obesity — the marbled liver reads on the arteries, adjusted for waist and pressure [15]. And the global file has Brazilian fingerprints: the 2026 global burden review pricing MASLD at 30–40% of adults worldwide — rising fastest in lower-sociodemographic-index regions, with cardiovascular disease a major cause of death across the steatotic-liver spectrum — counts a Federal University of Rio de Janeiro first author on its byline [3]. The Brazilian gym conversation this file retires has the same two scripts as the English one: "doença no fígado é frágil, descansa" from the scared side and "gordura no fígado é brincadeira de gordo, treina e bebe" from the dismissive side. The priced line the pt-BR twin delivers instead: a régua do banheiro não vê o órgão que a barra conserta — 8 semanas de treino de força cortaram a gordura do fígado em 13% com o peso parado [5], e a América Latina é a região de maior prevalência do planeta [2].

So what do you actually do? The practical file

Six rules, every one sourced from the files above:

  1. Get staged, then program. Ask the hepatology team for the FIB-4 → elastography answer before you assume anything about limits [4]; the staging decides which program-shape conversation you're having.
  2. Lift 3 non-consecutive days a week, 40–45 minutes, for at least 12 weeks — the median effective resistance protocol [6] — and let the cumulative work cross the 10,000-kcal threshold [9]. Ordinary frequency, sustainable set budgets, loads climbing by progressive overload; machines welcome on heavy days via the machines vs free weights audit, rest between sets generous, warm-up unhurried [5][6].
  3. Add the aerobic column — and if the engine is the weak link, start with the barbell anyway. The review's verdict: resistance training delivers the liver effect at roughly half the energy cost of aerobic work, which matters precisely for the deconditioned lifter this condition recruits [6]. Build the zone 2 base alongside.
  4. Stop reading the scale as the liver's ruler. The trials moved the organ while the weight stood still [5][7][8]; the scale is the ruler for the weight-loss ladder [12], the training log is the ruler for this column. Log the tracking file's way — dated, dosed, complete.
  5. If weight loss is on your program, climb the ladder on purpose. ≥5% buys 58% NASH resolution, ≥10% buys 90% [12] — training is the delivery vehicle and the muscle-protection column, not a bystander; pair this file with the type 2 diabetes audit if that door is also yours.
  6. The fences outrank the session. Staging questions to hepatology, the alcohol conversation the guideline already had, the supplement shelf vetted, red flags same-day — the program runs with the treatment plan, never instead of it [4].

How RightRep fits into this

The MASLD program runs on one currency this app counts better than any notebook — the dated, dosed, camera-verified session:

  • The fat-ledger trend needs dated evidence, not memory. The liver's ruler moves in 8-to-16-week trial windows [5][7][8] — a session-by-session log is how a 12-week dose actually gets delivered and how the next hepatology visit reads the trend.
  • The 10,000-kcal threshold needs counting. The dose is cumulative work [9] — reps, sets and load counted per session is the difference between crossing the threshold and assuming you did.
  • The muscle column, defended. The condition pools against sarcopenia at OR 1.74 [13] — the camera-counted strength log is the column that proves the muscle is still there while the diet runs.
  • Progressive overload honesty at moderate entry doses. The file says build — but only if the load actually climbs [5][6]; the camera keeps the climb honest without the guesswork.
  • The hepatology-visit artifact. "What have you been doing since the last visit?" — the question every staging consult asks is answered by the camera-counted log you hand over [4].

The bottom line

  • The barbell file: 8 weeks of resistance training, liver lipid −13% relative, glucose AUC −12% vs +12% in controls, HOMA-IR improved — with body weight, visceral fat and fat mass all statistically unmoved [5].
  • The replication file: 16 weeks of guideline-dose aerobic work, intrahepatic triglyceride −10.3% at a body weight of 103.1→102.9 kg [7]; the biopsy-proven NASH file: cycling-plus-resistance −16% hepatic triglyceride against +9% in untreated controls, with inflammation and fibrosis markers honestly unmoved [8].
  • The modality verdict: both shelves work; the barbell delivers at 28% vs 50% VO₂max and 6,470 vs 11,064 kcal total energy — the efficient prescription for the deconditioned [6].
  • The dose threshold: >10,000 kcal of cumulative program workload — −3.46% absolute intrahepatic fat, SMD −1.77, across 21 RCTs and 1,530 participants — with the enzyme null carried [9].
  • The honest counterfile: exercise alone did not move Brunt grade, NAS or fibrosis in the 3-trial, 72-participant biopsy-proven meta [10][11] — first-line column, not stand-alone cure.
  • The weight-loss ladder: ≥5% lost → 58% NASH resolution, ≥10% → 90%, across 293 patients with paired biopsies [12] — the frame the EASL 2024 lifestyle-first guideline builds on [4].
  • The scale file: 30.05% of adults globally, +50.4% in two decades, Latin America the world's highest region at 44.37% [1][2][3]; the muscle-liver axis at OR 1.74 [13]; ELSA-Brasil: steatosis predicting incident diabetes at HR 1.31 beyond BMI [14] and tracking aortic stiffness beyond abdominal obesity [15].

Train for the organ the bathroom scale can't see — the staging is the hepatologist's, the dose is yours, and the modality the trials used is the one you already own: the barbell, at rightrep.app.

This post was written by the RightRep AI Assistant — the same AI that counts and scores your reps at rightrep.app.

Sources

  1. Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M. Global epidemiology of nonalcoholic fatty liver disease — meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology, 2016;64(1):73–84. pubmed.ncbi.nlm.nih.gov
  2. Younossi ZM, Golabi P, Paik JM, Henry A, Van Dongen C, Henry L. The global epidemiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH): a systematic review. Hepatology, 2023;77(4):1335–1347. pubmed.ncbi.nlm.nih.gov
  3. Danpanichkul P, Souza M, Tothanarungroj P, Ahmed A, Kim D. Global epidemiological patterns and disease burden of metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction and alcohol-associated liver disease, and alcohol-associated liver disease. Clinical and Molecular Hepatology, 2026;32(Suppl):e2026.0444. pubmed.ncbi.nlm.nih.gov
  4. European Association for the Study of the Liver; European Association for the Study of Diabetes; European Association for the Study of Obesity. EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD): Executive Summary. Diabetologia, 2024;67(11):2375–2392. pubmed.ncbi.nlm.nih.gov
  5. Hallsworth K, Fattakhova G, Hollingsworth KG, Thoma C, Moore S, Taylor R, Day CP, Trenell MI. Resistance exercise reduces liver fat and its mediators in non-alcoholic fatty liver disease independent of weight loss. Gut, 2011;60(9):1278–1283. pubmed.ncbi.nlm.nih.gov
  6. Hashida R, Kawaguchi T, Bekki M, et al. Aerobic vs. resistance exercise in non-alcoholic fatty liver disease: a systematic review. Journal of Hepatology, 2017;66(1):142–152. pubmed.ncbi.nlm.nih.gov
  7. Sullivan S, Kirk EP, Mittendorfer B, Patterson BW, Klein S. Randomized trial of exercise effect on intrahepatic triglyceride content and lipid kinetics in nonalcoholic fatty liver disease. Hepatology, 2012;55(6):1738–1745. pubmed.ncbi.nlm.nih.gov
  8. Houghton D, Thoma C, Hallsworth K, et al. Exercise reduces liver lipids and visceral adiposity in patients with nonalcoholic steatohepatitis in a randomized controlled trial. Clinical Gastroenterology and Hepatology, 2017;15(1):96–102.e3. pubmed.ncbi.nlm.nih.gov
  9. Smart NA, King N, McFarlane JR, Graham PL, Dieberg G. Effect of exercise training on liver function in adults who are overweight or exhibit fatty liver disease: a systematic review and meta-analysis. British Journal of Sports Medicine, 2018;52(13):834–843. pubmed.ncbi.nlm.nih.gov
  10. Chen G, Banini B, Do A, Lim JK. The independent effect of exercise on biopsy-proven non-alcoholic fatty liver disease: a systematic review. Clinical and Molecular Hepatology, 2023;29(Suppl):S319–S332. pubmed.ncbi.nlm.nih.gov
  11. Chen G, Banini BA, Do A, Gunderson C, Zaman S, Lim JK. Exercise does not independently improve histological outcomes in biopsy-proven non-alcoholic fatty liver disease: a systematic review and meta-analysis. Genes (Basel), 2023;14(9):1811. pubmed.ncbi.nlm.nih.gov
  12. Vilar-Gomez E, Martinez-Perez Y, Calzadilla-Bertot L, et al. Weight loss through lifestyle modification significantly reduces features of nonalcoholic steatohepatitis. Gastroenterology, 2015;149(2):367–378.e5. pubmed.ncbi.nlm.nih.gov
  13. Deng C, Ou Q, Ou X, Pan D. Association between non-alcoholic fatty liver disease and risk of sarcopenia: a systematic review and meta-analysis. BMJ Open, 2024;14(5):e078933. pubmed.ncbi.nlm.nih.gov
  14. Faria LC, Diniz MFHS, Giatti L, Schmidt MI, Goulart AC, Duncan BB, Barreto SM. Liver steatosis as a predictor of incident diabetes in adults: a prospective evaluation in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Cadernos de Saúde Pública, 2023;39(3):e00090522. pubmed.ncbi.nlm.nih.gov
  15. Harada PH, Bensenõr IJM, Drager LF, Goulart AC, Mill JG, Lotufo PA. Non-alcoholic fatty liver disease presence and severity are associated with aortic stiffness beyond abdominal obesity: the ELSA-Brasil. Atherosclerosis, 2019;284:59–65. pubmed.ncbi.nlm.nih.gov