# Independent effects of exercise intensity on hepatic fat reduction in adults with metabolic dysfunction–associated steatotic liver disease: a randomized controlled trial protocol

**Authors:** Wei Huang, Yifei He, Rong Chen, Cuilan Huo, Yijun Xie, Yanyu Lin, Tian Wang, Xiangdi Dai, Junyu Wang, Weiqi Ruan, Haonan Zhai, Jie Zhuang, Jin Lu

PMC · DOI: 10.3389/fendo.2026.1711420 · Frontiers in Endocrinology · 2026-02-10

## TL;DR

This study tests if high-intensity exercise can reduce liver fat as effectively as moderate-intensity exercise in people with liver disease.

## Contribution

It is the first randomized trial comparing high-intensity and moderate-intensity exercise under energy-matched conditions for hepatic fat reduction in MASLD.

## Key findings

- Evaluates the independent effect of exercise intensity on hepatic fat content in MASLD patients.
- Investigates whether low-volume high-intensity exercise can match moderate-intensity exercise in reducing liver fat.

## Abstract

Exercise is considered a cornerstone of Metabolic dysfunction–associated steatotic liver disease (MASLD) management, but the independent role of exercise intensity in hepatic fat reduction has not been fully elucidated in clinical practice. The primary objective in this study is to evaluate the difference in exercise-induced reduction of hepatic fat content (HFC) between energy-matched high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT). Furthermore, this study aims to investigate whether high-intensity exercise with lower exercise volume can yield comparable HFC reductions to moderate-intensity continuous training.

This single-center, three-arm, open-label randomized controlled trial will recruit 105 adults aged 18–45 years with MASLD. Participants will be randomized in a 1:1:1 ratio to HIIT, MICT, or a low-volume HIIT (LHIIT). The sample size of 35 participants per group was calculated to provide 90% power to detect a significant difference in HFC reduction between the HIIT and MICT groups (two-sided α = 0.05, accounting for 20% dropout). The supervised exercise training will be conducted at a community fitness center for 12 weeks. The primary outcome is the absolute change in HFC, measured by magnetic resonance imaging–proton density fat fraction. Secondary outcomes include anthropometric parameters, abdominal adipose tissue, body composition, cardiometabolic biomarkers, and cardiorespiratory fitness. The analysis of the primary and secondary outcomes will be conducted according to the intention-to-treat principle.

This trial rigorously evaluates the independent effect of exercise intensity on HFC under energy-matched conditions, while simultaneously exploring the therapeutic efficiency of low-volume interventions. The findings of this study are expected to provide a theoretical and practical basis for precise exercise prescriptions for the MASLD population. The results will be disseminated through a peer-reviewed journal.

https://www.chictr.org.cn/showprojEN.html?proj=279678, identifier ChiCTR2500107821.

## Linked entities

- **Diseases:** Metabolic dysfunction–associated steatotic liver disease (MONDO:0013209), MASLD (MONDO:0013209)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, KRT18 (keratin 18) [NCBI Gene 3875] {aka CK-18, CYK18, K18}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1) [NCBI Gene 5562] {aka AMPK, AMPK alpha 1, AMPKa1}, FGF21 (fibroblast growth factor 21) [NCBI Gene 26291], TIMP1 (TIMP metallopeptidase inhibitor 1) [NCBI Gene 7076] {aka CLGI, EPA, EPO, HCI, TIMP, TIMP-1}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}
- **Diseases:** NAFLD (MESH:D065626), dyspnea (MESH:D004417), angina (MESH:D000787), hepatic fibrosis (MESH:D008103), liver inflammation (MESH:D007249), MASLD (MESH:D008107), Fibrosis (MESH:D005355), syncope (MESH:D013575), fat (MESH:D004620), Metabolic dysfunction (MESH:D008659), hepatic steatosis (MESH:D005234), Obesity (MESH:D009765), CVDs (MESH:D002318), weight loss (MESH:D015431), Insulin resistance (MESH:D007333), dizziness (MESH:D004244), HFC (MESH:D063466), type 2 diabetes (MESH:D003924), hepatic fat (MESH:D005218), musculoskeletal injuries (MESH:D009140), liver fat accumulation (MESH:D017093)
- **Chemicals:** TG (MESH:D014280), ADP (MESH:D000244), oxygen (MESH:D010100), cholesterol (MESH:D002784), blood glucose (MESH:D001786), glycogen (MESH:D006003), fatty acid (MESH:D005227), HFC (-), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12929106/full.md

## References

33 references — full list in the complete paper: https://tomesphere.com/paper/PMC12929106/full.md

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Source: https://tomesphere.com/paper/PMC12929106