Exercise as a Therapeutic Intervention for Fatty Liver Disease

1. Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), affects approximately 30% of the global population and continues to rise in prevalence. This condition encompasses a spectrum ranging from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, and cirrhosis. Without approved pharmacotherapy until recently, lifestyle modification, particularly structured exercise, remains the cornerstone of treatment across all disease stages.

The evidence for exercise as a therapeutic intervention has grown substantially over the past decade, with numerous meta-analyses and randomized controlled trials demonstrating clinically meaningful improvements in liver fat, inflammation, and fibrosis markers. Importantly, these benefits occur even in the absence of significant weight loss, highlighting exercise’s direct effects on hepatic metabolism.

This chapter synthesizes the current evidence on exercise interventions for fatty liver disease, providing actionable protocols based on rigorous research. We’ll explore the mechanisms by which exercise improves liver health, examine specific exercise modalities, and provide practical guidance for implementation across the disease spectrum, including patients with compensated cirrhosis.

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1.1 What is Standardized Mean Difference (SMD)

SMD stands for Standardized Mean Difference. It’s a way researchers compare the size of an effect (for example, how much exercise lowers liver fat) across different studies; even when those studies used different measurement scales.

For example:

One trial might measure liver fat with MRI (in %),
Another might measure it using ultrasound scores (in points),
Another might use liver enzyme changes (U/L).

Because the units differ, we can’t directly compare raw numbers.

So researchers standardize them by dividing the difference between the treatment group and control group by the amount of variability in each study (the standard deviation).

The resulting number, known as the SMD, has no units. It just shows how big the change was relative to the natural variation in that measurement.

Mathematically:

SMD = (Mean of treatment group – Mean of control group)/Pooled standard deviation

1.1.1 Interpreting SMD Values

A widely accepted guideline (from statistician Jacob Cohen) is:

SMD (Cohen’s d)	Interpretation	Layperson Meaning
0.2	Small effect	Noticeable only if you look closely or use precise tools
0.5	Medium effect	Clear, visible change that most people would feel or observe
0.8 or higher	Large effect	Big and meaningful change; obvious in real life

Let’s say a meta-analysis reports:

SMD = −0.4 for reduction in liver fat → That’s a medium effect: exercise makes a clinically visible improvement compared with doing nothing.
SMD = −0.6 for lowering ALT levels → That’s moving toward large, meaning many patients see significant lab improvements.

The minus sign (−) just means “reduction,” which is good in the context of liver fat or enzyme levels.

1.1.2 Why We Even Bother With SMD

Because studies often use different measurement tools, SMD lets us:

Combine apples and oranges: MRI, ultrasound, or lab tests into one comparable scale.
Judge importance, not just significance.: A result might be “statistically significant” but tiny in real-world impact. SMD tells us if the effect size actually matters.
Compare interventions.: We can see if exercise, diet, or medication produces a bigger average benefit.

In Lay Terms:

Think of SMD like a “universal yardstick” for measuring improvement:

An SMD of 0.2 is like taking a small but measurable step forward.
An SMD of 0.5 is like noticeably feeling better or seeing your test results move in the right direction.
An SMD of 0.8+ is like a major visible change: your energy, blood work, or imaging results clearly improve.

It helps researchers say, “This treatment worked moderately well across all studies, regardless of how they measured success.”

1.1.3 Effect Size vs. Standardized Mean Difference (SMD)

Effect size is the general concept, a broad term meaning “how big the effect is”.

It tells you how much difference or change a treatment makes compared to a control.

SMD (Standardized Mean Difference) is one specific type of effect size.

SMD is one type of effect size, but not all effect sizes are SMDs. If every study measures the outcome in the same unit, for example, “ALT levels in U/L”, they can just report the mean difference directly (like “ALT fell by 12 U/L”). That’s still an effect size, just not standardized.

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2. The Evidence Base: Meta-Analyses and Systematic Reviews

2.1 Exercise Reduces Liver Fat Independent of Weight Loss

A landmark 2023 systematic review and meta-analysis by Stine and colleagues analyzed 14 randomized controlled trials with 551 participants. The findings were striking: exercise training was 3.5 times more likely to achieve a clinically meaningful response (≥30% relative reduction in MRI-measured liver fat) compared to standard clinical care. This benefit occurred with an average weight loss of only 2.8%, far below the 5-10% threshold previously thought necessary for histologic improvement.

The dose-response analysis revealed that 39% of patients prescribed ≥750 metabolic equivalents of task (MET-minutes) per week, equivalent to 150 minutes of brisk walking, achieved significant treatment response, compared to only 26% of those prescribed lesser doses. This finding established the minimum effective dose for clinically meaningful improvement.

METs are an objective way to calculate your body’s energy expenditure when performing different types of excersises or activities. MET minutes gets us a quantitative way to compare two different excersises such as a walking on 3 incline of a treadmill vs cycling on a stationary bike at 10mph or even rowing on a concept 2 machine. If you visit any neighborhood gym, you will see METs listed on cardio equipment’s digital display, in addition to other metrics.

Instead of going into the weeds on MET, the main thing is that 750 MET-minutes per week that they mentioned simply equals to around 150 minutes of brisk walking per week or about 30 minutes, five days a week. That’s the minimum amount of activity linked with measurable improvement in liver fat. Doing less still helps overall health, but hitting this level gives your liver a clear advantage.

2.2 Comprehensive Benefits Across Multiple Outcomes

A 2025 meta-analysis by Chen and colleagues examining exercise effects on body composition and cardiometabolic parameters in MASLD patients included 26 articles with 1,123 participants. Exercise interventions produced significant reductions in:

Body mass index (BMI): SMD = -0.28, p < 0.001
Waist circumference: SMD = -0.41, p < 0.001
Maximal oxygen uptake (VO2 max): marked improvement
Diastolic blood pressure: significant reduction

These findings demonstrate that exercise provides multisystem benefits beyond liver-specific improvements, addressing the cardiometabolic dysfunction that characterizes MASLD.

In plain language: Regular exercise not only targets the liver but rather it helps the whole body. People in these studies saw smaller waistlines, lower blood pressure, and stronger heart and lung fitness. Because fatty liver is part of a broader “metabolic” problem, these improvements reduce the risk of diabetes and heart disease too.

2.3 Long-Term Studies and Prevention

Sung et al (2016) conducted a very large 5-year study of over 233,000 people, and found that those who exercised at least five times a week were less likely to develop fatty liver and more likely to have existing fatty liver go away. Even people with normal weight (BMI under 25) who were regularly active had a lower risk, roughly an 11% reduction compared with inactive people.

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3. How Exercise Improves Liver Health: Molecular Mechanisms

Understanding the mechanisms by which exercise improves MASLD provides insight into why it works even without significant weight loss and helps optimize exercise prescriptions. Exercise affects liver health through multiple interconnected pathways:

3.1 Enhanced Insulin Sensitivity

Insulin resistance is central to MASLD pathogenesis. In peripheral tissues, insulin resistance leads to incomplete suppression of lipase activity, resulting in enhanced lipolysis and increased delivery of free fatty acids to the liver. Simultaneously, insulin resistance in skeletal muscle diverts glucose to the liver, providing substrate for de novo lipogenesis.

Exercise improves insulin sensitivity in both skeletal muscle and liver through multiple mechanisms, including increased glucose transporter-4 (GLUT-4) translocation, enhanced AMP-activated protein kinase (AMPK) activity, and improved mitochondrial function. These changes reduce hepatic glucose and fatty acid influx while improving glucose disposal in muscle.

3.2 Modulation of Lipid Metabolism

Exercise directly affects hepatic lipid metabolism by:

Increasing β-oxidation of fatty acids: Exercise upregulates peroxisome proliferator-activated receptor-α (PPARα) and carnitine palmitoyltransferase-1 (CPT-1), enhancing fatty acid oxidation in hepatocytes and reducing triglyceride accumulation.
Decreasing de novo lipogenesis: Both aerobic and resistance exercise reduce expression of sterol regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FAS), and stearoyl-CoA desaturase-1 (SCD1), key enzymes in hepatic fat synthesis.

Studies demonstrate that 12-week aerobic exercise or resistance training can decrease SREBP-1c through increased AMPK activity, leading to substantial reductions in de novo lipogenesis.

3.3 Anti-Inflammatory and Antioxidant Effects

Oxidative stress and inflammation drive progression from simple steatosis to steatohepatitis. Exercise produces powerful anti-inflammatory effects through:

Upregulation of antioxidant enzymes: Exercise increases expression of superoxide dismutase (SOD), catalase, and glutathione peroxidase, enhancing cellular defense against reactive oxygen species (ROS).
Reduction of pro-inflammatory cytokines: Regular exercise decreases chronic elevation of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). While acute exercise transiently increases IL-6 release from muscle (where it acts as a beneficial myokine), chronic training reduces baseline inflammatory IL-6 levels.
Myokine secretion: Contracting skeletal muscle releases myokines like irisin that exert anti-inflammatory effects systemically and in the liver. Irisin reduces inflammation by inhibiting the MD2-TLR4 pathway and improving mitochondrial function.

These effects reduce hepatocyte injury, attenuate stellate cell activation, and may slow fibrosis progression.

3.4 Mitochondrial Function and Autophagy

Mitochondrial dysfunction contributes to MASLD through impaired fatty acid oxidation and increased ROS production. Exercise induces mitochondrial biogenesis through activation of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), improving mitochondrial function and increasing oxidative capacity.

Additionally, exercise induces hepatoprotective autophagy, a cellular quality control mechanism that removes damaged organelles and protein aggregates. This process helps maintain hepatocyte health and may prevent progression to more severe disease.

3.5 Gut-Liver Axis Modulation

Emerging evidence demonstrates that exercise modifies gut microbiota composition, increasing beneficial bacteria and short-chain fatty acid production. Exercise also improves intestinal barrier function, reducing bacterial translocation and endotoxemia. These changes reduce hepatic exposure to pathogen-associated molecular patterns (PAMPs), decreasing liver inflammation. Studies comparing high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) show both modalities improve gut microbiota structure, enhance bile acid metabolism, and restore gut-liver axis homeostasis.

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4. Exercise Modalities: Evidence and Protocols

4.1 Aerobic Exercise

Evidence Base

Aerobic exercise has the most extensive evidence base for MASLD treatment. Keating et al (2012) meta-analysis of exercise interventions found that aerobic exercise produces significant reductions in hepatic steatosis compared to control groups, with pooled effect sizes of -0.37 (95% CI: -0.69 to -0.06, p=0.02) which equates to a “medium” effect; not tiny, not huge, but clearly meaningful in real life.

Multiple studies have demonstrated that aerobic exercise reduces liver fat regardless of intensity or volume, with no significant differences between moderate-intensity (50% VO2 peak) and vigorous-intensity (70% VO2 peak) protocols when matched for duration. The apparent minimum effective dose is 135 minutes of moderate-intensity aerobic activity per week, with no additional benefit on hepatic steatosis from increasing volume or intensity.

Practical Protocols

Recommended Prescription:

Duration: 150-200 minutes per week of moderate-intensity exercise
Frequency: 3-5 sessions per week
Intensity: Moderate (can talk but not sing; 50-70% VO₂peak; RPE 5-⁶⁄₁₀)
Session duration: 30-60 minutes per session (can accumulate in 10-minute bouts)
Modalities: Brisk walking, cycling, swimming, elliptical, jogging
Minimum Effective Dose: ≥750 MET-minutes per week (equivalent to 150 minutes of brisk walking)

4.2 Resistance Training

Evidence Base

While aerobic exercise has been more extensively studied, resistance training shows comparable efficacy for reducing liver fat. de Oliveira Silva et. al (2024) systematic review of resistance training in MASLD demonstrated significant reductions in:

Liver fat (p < 0.001)
Liver enzymes (ALT/AST) (p < 0.05)
Insulin resistance (HOMA-IR) (p < 0.05)

Importantly, resistance training showed greater adherence rates (>90%) compared to aerobic training in several studies, suggesting it may be more sustainable for some patients.

A landmark 2011 study by Hallsworth and colleagues demonstrated that 8 weeks of resistance exercise elicited a 13% relative reduction in liver lipid content (p<0.05) without any change in body weight, proving resistance training’s direct effects on hepatic fat independent of weight loss. The study also showed improvements in lipid oxidation and glucose control.

The RAED2 trial (Bacchi et al 2013) compared aerobic and resistance training in type 2 diabetics with MASLD, finding both modalities equally effective at reducing hepatic fat content over 12 weeks (-10.3% vs -12.6% relative reduction), though resistance exercise required significantly lower energy expenditure.

Practical Protocols

Recommended Prescription:

Frequency: 2-3 sessions per week on non-consecutive days
Exercises: 8-10 exercises targeting major muscle groups (chest, back, legs, shoulders, arms, core)
Sets and repetitions: 2-3 sets of 10-15 repetitions per exercise
Intensity: Moderate to high (60-80% of 1-repetition maximum; RPE 5 - 7 / 10)
Rest: 60-90 seconds between sets
Progression: Increase weight by 2-5% when able to complete target repetitions with good form

Sample Exercise Selection:

Lower body: squats, lunges, leg press, leg curls
Upper body push: chest press, shoulder press, tricep extensions
Upper body pull: rows, lat pulldowns, bicep curls
Core: planks, bird dogs, dead bugs

Resistance training is particularly valuable for patients with cardiorespiratory limitations or osteoarticular issues that make sustained aerobic exercise difficult. It also addresses sarcopenia, which commonly coexists with MASLD.

4.3 High-Intensity Interval Training (HIIT)

Evidence Base

HIIT has emerged as a time-efficient alternative to traditional continuous aerobic exercise. A 2025 meta-analysis (Fu et al 2025) examining HIIT effects on MASLD found significant reductions in:

Intrahepatic lipids: SMD -0.56%, p=0.01
BMI: SMD -0.31, p=0.04
ALT: SMD -0.61, p=0.0006
AST: SMD -0.43, p=0.03

A 2015 randomized controlled trial by Hallsworth and colleagues demonstrated that 12 weeks of HIIT (30-40 minutes, 3 times weekly) reduced liver fat from 11% to 8% (p=0.019) while improving cardiac function, whole-body fat mass, and liver enzymes. Importantly, these benefits occurred without significant changes in body weight.

Mechanistic studies comparing HIIT to moderate-intensity continuous training show HIIT may be more effective at improving mitochondrial function, with greater improvements in citrate synthase activity, PGC-1α expression, and mitochondrial fusion protein levels (p<0.001 vs MICT). A 2025 study showed that both HIIT and MICT improved lipid metabolism and restored gut-liver axis homeostasis, but HIIT’s superior effects on mitochondrial dynamics may provide additional benefits.

HIIT also modulates cortisol levels, reducing this stress hormone that contributes to hepatic fat deposition and insulin resistance. Studies show HIIT combined with Mediterranean diet produces significant reductions in cortisol alongside improvements in liver health.

Practical Protocols

Beginner Protocol (Weeks 1-4):

Frequency: 2-3 sessions per week
Warm-up: 5 minutes moderate intensity
Work intervals: 30 seconds at 80-85% peak heart rate
Recovery intervals: 90 seconds at 60% peak heart rate
Repetitions: 6-8 intervals
Cool-down: 5 minutes easy pace

Advanced Protocol (Weeks 5+):

Frequency: 3 sessions per week
Work intervals: 60 seconds at 85-90% peak heart rate
Recovery intervals: 60 seconds at 60% peak heart rate
Repetitions: 8-10 intervals
Total session: 20-30 minutes including warm-up/cool-down

HIIT is particularly attractive for patients with time constraints, as it can achieve similar or superior results to longer-duration moderate-intensity exercise in significantly less time. However, it requires adequate cardiovascular fitness and should be progressed gradually.

4.4 Combined Training Approaches

Several studies have examined combined aerobic and resistance training programs. While combined protocols show benefits, they don’t appear superior to either modality alone when matched for total exercise time. However, combined training may optimize both cardiovascular fitness and muscle mass, addressing multiple aspects of the MASLD phenotype. A practical combined approach might include 3 sessions of aerobic exercise (90-120 minutes total) plus 2 sessions of resistance training per week.

Table 1. Comparison of Exercise Modalities for MASLD

Modality	Key Benefits	Time Commitment	Best For
Aerobic	Most evidence, cardiovascular fitness, accessible	150-200 min/week	All patients, first-line
Resistance	High adherence, addresses sarcopenia, lower energy cost	2-3 sessions/week, 45 min each	Cardiorespiratory limitations, sarcopenia
HIIT	Time-efficient, superior mitochondrial effects	60-90 min/week total	Time-constrained, higher baseline fitness

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5. Exercise Dosage: Finding the Minimum Effective Dose

Establishing the minimum effective dose of exercise is crucial for clinical implementation and patient adherence. Recent research has provided clearer guidance on this critical question.

5.1 The 150-Minute Threshold

Converging evidence from multiple studies establishes ≥750 MET-minutes per week as the threshold for clinically meaningful improvement in liver fat. This translates to:

150 minutes of moderate-intensity activity (e.g., brisk walking at 3 mph)
75 minutes of vigorous-intensity activity (e.g., jogging at 6 mph)
Equivalent combinations (e.g., 100 minutes moderate + 25 minutes vigorous)

This recommendation aligns with guidelines from the American Gastroenterological Association, European Association for the Study of the Liver, and Exercise and Sport Science Australia. Importantly, this dose can be accumulated throughout the week and broken into bouts as short as 10 minutes, improving feasibility.

5.2 Dose-Response Relationship

The relationship between exercise dose and liver fat reduction appears curvilinear rather than linear. The largest benefits occur when moving from sedentary to minimally active, with diminishing returns at higher volumes.

In lean individuals with MASLD/NAFLD, studies suggest that even intermediate levels of physical activity may lower risk compared with inactivity, though exact risk-reduction percentages vary by study.

5.3 Progressive Exercise Prescription

For deconditioned patients, gradual progression is essential. A recommended 12-week progression might be:

Weeks 1-2: Start with 10-15 minutes per session, 3 days per week (30-45 min/week total)
Weeks 3-4: Increase to 15-20 minutes per session, 3-4 days per week (45-80 min/week total)
Weeks 5-6: Increase to 20-25 minutes per session, 4 days per week (80-100 min/week total)
Weeks 7-8: Increase to 25-30 minutes per session, 4-5 days per week (100-150 min/week total)
Weeks 9-12: Achieve target of 30-40 minutes per session, 5 days per week (150-200 min/week total)

This gradual progression allows physiological adaptation, reduces injury risk, and improves long-term adherence.

6. Exercise in Cirrhosis: Evidence and Safety

Exercise prescription for patients with cirrhosis requires special consideration, but mounting evidence demonstrates that appropriately dosed exercise is not only safe but beneficial across the disease spectrum.

6.1 The SportDiet Study: Landmark Evidence

The SportDiet study, published in Hepatology in 2017 by Berzigotti and colleagues, provided groundbreaking evidence for exercise safety and efficacy in cirrhosis. This prospective, multicenter study enrolled 60 patients with compensated cirrhosis, portal hypertension (HVPG ≥6 mm Hg), and obesity (BMI ≥26) in an intensive 16-week lifestyle intervention:

Personalized hypocaloric normoproteic diet
60 minutes per week of supervised physical activity
Protein supplementation (9 g/day)

Results were remarkable:

Average body weight loss: -5.0 ± 4.0 kg (p<0.0001)
≥5% weight loss achieved in 52% of participants
HVPG significantly decreased from 13.9 ± 5.6 to 12.3 ± 5.2 mm Hg (p<0.0001)
≥10% HVPG reduction in 42% of participants
≥20% HVPG reduction in 24% of participants
No episodes of clinical decompensation occurred

Importantly, ≥10% body weight loss was associated with greater decreases in portal pressure (-23.7% vs -8.2%, p=0.024). Weight loss achieved at 16 weeks was maintained at 6-month follow-up, and Child-Pugh and MELD scores remained stable. This study definitively demonstrated that moderate exercise combined with diet is safe and can reduce portal pressure in compensated cirrhosis with portal hypertension.

6.2 Mechanisms of Benefit in Cirrhosis

Exercise provides multiple benefits in cirrhosis:

Reverses sarcopenia: Skeletal muscle loss affects nearly all patients with cirrhosis and predicts mortality. Exercise stimulates muscle protein synthesis and increases muscle mass even in advanced disease.
Improves functional capacity: Exercise increases VO2 max and improves performance on functional tests like the 6-minute walk test and Liver Frailty Index.
Reduces portal pressure: Weight loss through exercise can reduce HVPG, potentially slowing decompensation.
Mitigates frailty: Exercise addresses the components of frailty (weakness, exhaustion, low activity, slowness) that predict poor outcomes.
Improves transplant outcomes: Pre-transplant exercise capacity predicts post-transplant survival. Prehabilitation programs can maintain patients above the deconditioning threshold that would contraindicate transplantation.

Importantly, these benefits occur even in the setting of hyperammonemia and the unique metabolic derangements of cirrhosis, though the mechanisms may differ from those in patients without cirrhosis.

6.3 Safety Considerations and Contraindications

Current Evidence on Safety: Most evidence focuses on patients with compensated cirrhosis (Child-Pugh A/B). Endurance exercise for up to 12 weeks is clinically well-tolerated in this population. Data on decompensated cirrhosis remains limited.

Relative Contraindications:

Active variceal bleeding (avoid exercise until stabilized)
Severe or refractory ascites (may limit exercise tolerance)
Grade 3-4 hepatic encephalopathy (impairs safety awareness)
Recent spontaneous bacterial peritonitis (delay until resolved)
Hepatorenal syndrome
Hepatopulmonary syndrome with severe hypoxemia

Special Precautions:

Avoid straining/Valsalva maneuvers (may increase portal pressure acutely)
Avoid abdominal exercises that increase intra-abdominal pressure
Monitor for signs of decompensation (worsening ascites, encephalopathy)
Ensure adequate protein intake (1.2-1.5 g/kg/day) to support muscle synthesis
Consider supervised sessions initially to assess tolerance

While exercise can acutely increase portal pressure during the activity itself, long-term exercise training appears to reduce resting portal pressure, particularly when combined with weight loss.

6.4 Recommended Protocols for Cirrhosis

For Compensated Cirrhosis (Child-Pugh A/B):

Type: Aerobic exercise (walking, cycling, swimming) with or without resistance training
Duration: Progress toward 150+ minutes per week of moderate intensity
Frequency: 4-5 sessions per week
Intensity: Moderate (RPE 5 - ⁶⁄₁₀; able to talk comfortably)
Progression: Start with 15-20 minutes per session, increase by 5 minutes every 1-2 weeks
Additional: Add balance exercises if fall risk present; include flexibility work

Resistance training 2-3 times per week can be added once aerobic base is established, using moderate loads and avoiding straining. Focus on functional movements that improve activities of daily living.

Cirrhosis patients should take the contents here as general guidance only, and they need approve their training plans by their doctors before starting an exercise regimen.

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7. Practical Implementation for coaches/doctors/physiotherapists: From Evidence to Action

Translating research evidence into sustainable behavior change requires attention to barriers, facilitators, and practical strategies for long-term adherence.

7.1 Initial Assessment

Before prescribing exercise, assess:

Current activity level: Use standardized questionnaires (IPAQ, GPAQ) to establish baseline
Medical clearance: Screen for contraindications; consider exercise stress test if cardiovascular risk factors
Functional capacity: Use 6-minute walk test or similar to gauge starting point
Barriers and preferences: Discuss time constraints, access to facilities, exercise history, preferences
Comorbidities: Consider diabetes, cardiovascular disease, arthritis that may affect exercise prescription

For cirrhosis patients, additional assessment should include Child-Pugh score, presence of varices, ascites grade, and history of encephalopathy.

7.2 Overcoming Common Barriers

Time Constraints:

Emphasize that 10-minute bouts count toward weekly total
Consider HIIT protocols that achieve results in 60-90 minutes weekly
Integrate activity into daily routine (walking meetings, active commuting, exercise during lunch)

Fatigue:

Start with very low doses and progress gradually
Schedule exercise when energy levels are highest (often morning)
Emphasize that regular exercise improves energy levels over time
Consider splitting sessions (e.g., 15 minutes AM + 15 minutes PM)

Lack of Access/Resources:

Walking requires no equipment and can be done anywhere
Bodyweight exercises for resistance training (squats, push-ups, lunges)
Online video resources for home exercise guidance
Community centers often have low-cost facilities

Physical Limitations: Adapt exercise type to individual capabilities. For arthritis, use low-impact activities (swimming, cycling, water aerobics). For balance issues, use supported exercises initially. For severe obesity, start with seated exercises or water-based activity.

7.3 Enhancing Long-Term Adherence

Adherence rates in lifestyle interventions typically decline after 6-12 months. Strategies to enhance sustainability include:

Set specific, achievable goals: Use SMART goal framework (Specific, Measurable, Achievable, Relevant, Time-bound)
Self-monitoring: Activity trackers, exercise logs, or smartphone apps increase accountability
Find enjoyable activities: Adherence is highest when exercise is perceived as enjoyable rather than obligatory
Social support: Exercise with family/friends, join groups/classes, or connect with online communities
Variety: Rotate activities to prevent boredom and maintain motivation
Regular follow-up: Schedule check-ins to troubleshoot barriers, celebrate progress, and adjust prescription
Link to outcomes: Periodically measure liver fat (if feasible), liver enzymes, metabolic parameters to demonstrate impact

Consider referral to exercise physiologists or physical therapists, particularly for complex cases or patients with multiple barriers. The American College of Sports Medicine’s ProFinder tool can help locate qualified professionals.

7.4 Counseling Framework

When counseling patients about exercise, structure discussions using the 5 A’s framework:

Ask: Assess current activity, readiness to change, barriers, preferences
Advise: Provide clear, personalized recommendation based on evidence
Assess: Determine patient’s willingness and confidence to make changes
Assist: Help develop action plan, problem-solve barriers, connect to resources
Arrange: Schedule follow-up, provide written prescription, arrange referrals if needed

Emphasize that the 10-minute minimum per exercise bout makes the goal much more achievable than patients may initially perceive. Frame exercise as a treatment equivalent to medication, prescribe it with the same specificity and follow-up as pharmaceutical interventions.

7.5 Sample Exercise Prescription for MASLD

Patient: Adult with MASLD, no cirrhosis, minimal prior exercise

Exercise Type: Moderate-intensity aerobic exercise
Activities: Brisk walking, cycling, swimming, or combination
Target Dose: 150 minutes per week (≥750 MET-minutes)
Frequency: 5 days per week, 30 minutes per session
Intensity: Moderate (able to talk but not sing; RPE 5 - 6 / 10)
Progression: Start with 15 min/session for 2 weeks, increase by 5 min every 2 weeks
Note: Each session may be broken into 10-minute bouts if needed
Follow-up: Return in 4 weeks to assess tolerance and adjust prescription
Safety: Stop if chest pain, severe shortness of breath, or dizziness occurs

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8. Monitoring Progress and Expected Outcomes

8.1 Timeline of Changes

Patients should be counseled on realistic timelines for improvements:

Weeks 1-4: Improved energy, mood, sleep quality. Initial improvements in insulin sensitivity.
Weeks 4-12: Improvements in cardiorespiratory fitness (VO2 max). Reductions in liver enzymes (ALT/AST) may be detectable.
Months 3-6: Clinically meaningful reductions in liver fat (≥30% relative reduction) achievable, fibrosis markers may begin to improve. Body composition changes become more apparent. Improvements in metabolic parameters (glucose, lipids, blood pressure).
Beyond 6 months: Sustained improvements with continued exercise. Some studies show histologic improvement (inflammation, fibrosis) at 12 months. Cardiovascular risk reduction continues to accrue.

8.2 Assessment Tools

Monitor progress using:

Liver enzymes (ALT, AST): Expect reductions within 4-12 weeks. Declining ALT is a good indicator of improving hepatocyte injury.
Metabolic parameters: Fasting glucose, HbA1c, lipid panel, blood pressure. Improvements in insulin resistance and lipid profile occur early.
Anthropometrics: Body weight, waist circumference, BMI. Note that liver fat can decrease independent of weight loss, but weight reduction enhances benefits.
Imaging: Repeat ultrasound, FibroScan (CAP score for steatosis, liver stiffness for fibrosis), or MRI-PDFF if baseline imaging was performed. Typically reassessed at 6-12 months.
Fibrosis scores: Non-invasive scores (FIB-4, NAFLD fibrosis score) can track progression risk over time.
Functional capacity: 6-minute walk test, VO2 max testing if available. Demonstrates improvements in physical fitness.
Quality of life: Validated questionnaires (SF-36, CLDQ) show improvements in patient-reported outcomes.

For patients with cirrhosis, additional monitoring might include Child-Pugh score, MELD score, markers of muscle mass, kidneys (creatinine/eGFR, body composition analysis), and fibroscan apart from regular HCC screening (USG abdomen etc.).

8.3 When to Adjust the Prescription

Increase exercise dose if:

Patient tolerates current prescription well and wants to progress
Minimal improvements in outcomes after 3 months at current dose
Cardiorespiratory fitness has improved substantially (can increase intensity)

Decrease or modify exercise if:

Signs of overtraining (persistent fatigue, declining performance, increased illness)
New injury or medical condition emerges
For cirrhosis: signs of decompensation, worsening encephalopathy, new variceal bleeding
Patient struggling with adherence (consider reducing dose temporarily rather than abandoning exercise entirely)

Remember that some improvements (particularly fibrosis reduction) may take 12 months or longer to detect. Encourage patients to maintain exercise even if liver-specific outcomes show slower improvement than hoped, the cardiovascular, metabolic, and quality-of-life benefits occur throughout the journey.

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9. Conclusion: Exercise as Core Therapy

The evidence is clear and compelling: exercise is a cornerstone therapeutic intervention for metabolic dysfunction-associated steatotic liver disease across the entire disease spectrum. Multiple meta-analyses and randomized controlled trials demonstrate that structured exercise, at a dose of 150 minutes per week of moderate-intensity activity, produces clinically meaningful reductions in liver fat, inflammation, and cardiometabolic risk factors.

Critically, these benefits occur independent of significant weight loss, challenging previous assumptions about the necessity of substantial weight reduction for hepatic improvement. Exercise works through multiple interconnected mechanisms: enhancing insulin sensitivity, increasing fatty acid oxidation, decreasing de novo lipogenesis, reducing oxidative stress and inflammation, improving mitochondrial function, and modulating the gut-liver axis.

Both aerobic exercise and resistance training are effective, as is high-intensity interval training for those with time constraints. The choice of modality should be individualized based on patient preference, comorbidities, baseline fitness, and likelihood of sustained adherence. Critically, even patients with compensated cirrhosis can safely exercise and derive substantial benefits, including reductions in portal pressure, improvements in sarcopenia, and enhanced functional capacity.

The key to success lies in implementation: setting specific, achievable goals; starting where the patient is and progressing gradually; addressing barriers proactively; using monitoring and feedback to demonstrate progress; and maintaining long-term engagement through variety, social support, and connection to meaningful outcomes.

Exercise should be prescribed with the same specificity and rigor as pharmacological interventions. Provide written prescriptions, schedule follow-up, adjust based on response, and recognize adherence challenges as opportunities for problem-solving rather than patient failure. Consider collaboration with exercise professionals, particularly for complex cases.

While pharmacological treatments continue to evolve, lifestyle modification, with exercise as a central pillar, will remain fundamental to MASLD/MASH management. The evidence supports an urgent shift from simply recommending exercise to actively prescribing, supporting, and monitoring structured exercise programs as first-line therapy for this increasingly prevalent condition.

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10. Key Takeaways for Clinical Practice

Minimum effective dose: ≥150 minutes per week of moderate-intensity exercise (≥750 MET-minutes)
Benefits occur independent of significant weight loss (average 2.8% weight loss in studies showing liver fat reduction)
Exercise is 3.5x more likely to achieve ≥30% liver fat reduction vs standard care
All modalities work: aerobic, resistance, HIIT, choose based on patient preference and adherence likelihood
Exercise can be safely prescribed in compensated cirrhosis and reduces portal pressure
10-minute bouts count—accumulation throughout the day is valid
Benefits appear within 4-12 weeks; maximal effects at 6-12 months
Prescribe exercise as specifically as medication: written prescription, specific dose, follow-up scheduled
Address barriers proactively; refer to exercise professionals when appropriate

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11. References

The following references represent key meta-analyses and landmark studies cited throughout this chapter:

Stine JG, DiJoseph K, Pattison Z, Harrington A, Chinchilli VM, Schmitz KH, Loomba R. Exercise training is associated with treatment response in liver fat content by magnetic resonance imaging independent of clinically significant body weight loss in patients with nonalcoholic fatty liver disease: A systematic review and meta-analysis. Am J Gastroenterol. 2023;118(7):1204-1213. [Established 150-minute minimum effective dose]. link

Chen J, Gong P, Xie J. Effects of exercise on body composition, fitness, and blood pressure in overweight or obese patients with MASLD: A systematic review and meta-analysis. Dig Liver Dis. 2025;S1590-8658(25)01078-3. [26 studies, 1123 participants showing comprehensive cardiometabolic benefits]. Link

Sung KC, Ryu S, Lee JY, Kim JY, Wild SH, Byrne CD. Effect of exercise on the development of new fatty liver and the resolution of existing fatty liver. J Hepatol. (2016) 65:791–7. Link

Berzigotti A, Albillos A, Villanueva C, Genescá J, Ardevol A, Augustín S, Calleja JL, Bañares R, García-Pagán JC, Mesonero F, Bosch J; Ciberehd SportDiet Collaborative Group. Effects of an intensive lifestyle intervention program on portal hypertension in patients with cirrhosis and obesity: The SportDiet study. Hepatology. 2017;65(4):1293-1305. [Landmark trial showing exercise safety and portal pressure reduction in cirrhosis].Link

Keating SE, Hackett DA, George J, Johnson NA. Exercise and non-alcoholic fatty liver disease: a systematic review and meta-analysis. J Hepatol. 2012;57(1):157-166. [Foundational meta-analysis demonstrating exercise efficacy].Link

de Oliveira Silva Junior G, Aguiar SS, Soares V, Mota MPGD, Stone W, Amorim PRS, Dantas EHM. The impact of resistance training in patients diagnosed with metabolic dysfunction-associated steatotic liver disease: a systematic review. Front Physiol. 2024;15:1455071. [Comprehensive review of resistance training evidence],Link

Hallsworth K, Thoma C, Moore S, Ploetz T, Anstee QM, Taylor R, Day CP, Trenell MI. Modified high-intensity interval training reduces liver fat and improves cardiac function in non-alcoholic fatty liver disease: a randomized controlled trial. Clin Sci (Lond). 2015;129(12):1097-1105. [HIIT efficacy in NAFLD].Link

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. [One of the first studies showing resistance training reduces liver fat independent of weight loss].link

Bacchi E, Negri C, Targher G, Faccioli N, Lanza M, Zoppini G, Bonora E, Schena F, Moghetti P. Both resistance training and aerobic training reduce hepatic fat content in type 2 diabetic subjects with nonalcoholic fatty liver disease (RAED2 randomized trial). Hepatology. 2013;58(4):1287–1295. link

Sabag A, Barr L, Armour M, Armstrong A, Baker CJ, Twigg SM, Chang D, Hackett DA, Keating SE, George J, Johnson NA. The effect of high-intensity interval training vs moderate-intensity continuous training on liver fat: A systematic review and meta-analysis. J Clin Endocrinol Metab. 2022;107(3):862-881. [HIIT vs MICT comparison].link

Fu et al Effect of high-intensity interval training on clinical parameters in patients with metabolic dysfunction-associated steatotic liver disease: A systematic review and meta-analysis. Eur J Gastroenterol Hepatol. 37(7):p 789-798, July 2025. link

Orci LA, Gariani K, Oldani G, Delaune V, Morel P, Toso C. Exercise-based interventions for nonalcoholic fatty liver disease: a meta-analysis and meta-regression. Clin Gastroenterol Hepatol. 2016;14(10):1398-1411. [Important dose-response analysis].link

Keating SE, Sabag A, Hallsworth K, Hickman IJ, Macdonald GA, Stine JG, George J, Johnson NA. Exercise in the management of metabolic-associated fatty liver disease (MAFLD) in adults: A position statement from Exercise and Sport Science Australia. Sports Med. 2023;53(12):2347-2371. [Comprehensive practice guidelines].Link

Tandon P, Raman M, Mourtzakis M, Merli M. A practical approach to nutritional screening and assessment in cirrhosis. Hepatology. 2017;65(3):1044-1057. [Guidelines for cirrhosis management].Link

Cigrovski Berkovic M, Bilic-Curcic I, Mrzljak A, Cigrovski V. NAFLD and physical exercise: Ready, steady, go! Front Nutr. 2021;8:734859. [Excellent practical review of exercise recommendations].Link

Farzanegi P, Dana A, Ebrahimpoor Z, Asadi M, Azarbayjani MA. Mechanisms of beneficial effects of exercise training on non-alcoholic fatty liver disease (NAFLD): Roles of oxidative stress and inflammation. Eur J Sport Sci. 2019;19(7):994-1003. [Comprehensive mechanistic review].Link

Alabdul Razzak I, Fares A, Stine JG, Trivedi HD. The Role of Exercise in Steatotic Liver Diseases: An Updated Perspective. Liver Int. 2025 Jan;45(1):e16220. doi: 10.1111/liv.16220. PMID: 39720849; PMCID: PMC12536350. [Recent comprehensive review on exercise benefits across all stages].Link

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This chapter provides evidence-based guidance for exercise prescription in fatty liver disease and is for information purpose only. You need to consult a doctor for any specific treatment plans. Always individualize recommendations based on patient characteristics, comorbidities, and preferences and consult a doctor.