The impact of resistance training in patients diagnosed... : European Journal of Gastroenterology & Hepatology (original) (raw)

Key points:

• Resistance training contributes to the reduction of hepatic fat in adults diagnosed with nonalcoholic fatty liver disease.
• Resistance training improves insulin sensitivity and reduces insulin resistance in adults diagnosed with nonalcoholic fatty liver disease.
• The practice of resistance training is easily accepted and maintained by individuals with nonalcoholic fatty liver disease.

Background

Metabolic dysfunction-associated steatotic liver disease (MASLD) impacts about one-third of the global population [1–3], leading to varied liver diseases [4,5]. Its progression is tied to critical factors such as a sedentary lifestyle, insulin resistance, and metabolic syndrome [2,3,6]. Nonpharmacological approaches, particularly resistance training, are gaining traction for treating and preventing MASLD [3,7]. Muscle strength loss, as a risk factor, makes resistance training vital [8].

Resistance training focuses on resistance to boost muscle strength, easily executed, especially for those with low cardiorespiratory fitness, common in most MASLD patients [7]. Regular exercise is linked to a reduced MASLD risk [7,9], improved liver parameters, insulin sensitivity, and reduced hepatic fat [10,11]. Resistance training significantly improves insulin resistance and triglyceride levels in metabolic syndrome patients, crucial MASLD risk factors [12].

Recent reviews and meta-analysis [9,13–16] focus on aerobic training, neglecting results from isolated resistance training. Given the MASLD-muscle strength link and scarce reviews on resistance training, a systematic review is justified to analyze the effects on hepatic fat, liver enzymes, and insulin resistance in individuals with MASLD. The aim of this study is to provide evidence for healthcare professionals in choosing the best approach for MASLD patients.

Methods

Protocol registration

This study is a systematic review of randomized controlled trials (RCTs), designed following the recommendations of the Cochrane Collaboration To Intervention Systematic Reviews Book [17] and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement [18]. Also, this study is registered in the International Prospective Register of Systematic Reviews (PROSPERO) 2022, under the code CRD4202236638.

Search strategies and studies selection

We systematically searched the Medline database (accessed through PubMed), Lilacs, Embase, Cochrane, SciELO, and Pedro and conducted a manual search to identify randomized clinical trials (published between January 2011 to December 2022) evaluating the effect of isolated resistance training in patients with MASLD. We compared these with patients diagnosed with MASLD belonging to the control group, as well as patients diagnosed with MASLD undergoing other types of interventions than resistance training exercises. The detailed search strategy is provided in Supplementary Material 1, Supplemental digital content 1, https://links.lww.com/EJGH/B89 and the PRISMA checklist can be found in Supplementary Material 2, Supplemental digital content 1, https://links.lww.com/EJGH/B89. Our searches included only human studies, with no restrictions based on gender, ethnicity, language, or geographical area.

We included studies that met the following inclusion criteria: (1) randomized clinical trials (RCTs); (2) study subjects previously diagnosed with MASLD through biopsy or imaging; (3) use of isolated resistance training protocols in patients diagnosed with nonalcoholic fatty liver disease; and (4) studies with a control group or groups with intervention protocols different from resistance training. Excluded were abstracts, case reports, theses, observational studies, reviews, meta-analyses, comments, editorials, protocols, and cross-sectional studies. Also excluded were studies involving individuals with evidence of viral and autoimmune hepatitis or other drug-induced liver diseases or alcoholic liver disease (>20 g of alcohol/day). Additionally, studies with patients with type 2 diabetes who did not remain stable for >6 months or required an increase in their medication doses were excluded.

Data extraction

Two authors independently selected titles and abstracts. Full texts of potentially relevant articles were reviewed and included if they met the predefined criteria. Discrepancies were resolved by a third reviewer. For all eligible studies, we extracted: (1) study characteristics (first author, study design, year, study location); (2) studied population (specifying the instrument used to diagnose nonalcoholic fatty liver disease); (3) experimental design (studied groups, intervention arms, sample size, gender, average age); and (4) intervention characteristics [specifying the exercise protocol used, exercise methods, frequency, time (min), and intervention duration].

The measures used to assess the primary and secondary outcomes of this review were (1) fat liver: hepatic fat assessed through proton magnetic resonance spectroscopy (MRS), ultrasonography, transient elastography (FibroScan, Echosens, Paris, France); (2) levels of liver enzymes [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)] were quantified through biochemical tests after a 12-hour fast, before, and at the end of the resistance training program or by spectrophotometry; (3) insulin resistance was determined using the homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity was assessed by the clamp test; and (4) measurement of attendance of participants in the resistance training group was analyzed by comparing the initial ‘_n_’ preintervention with the final ‘_n_’ postintervention.

Quality and risk of bias assessment

The quality assessment and risk of bias for the included studies were independently conducted by two authors using the ROB 2.0 tool: a revised tool for assessing the risk of bias in randomized trials [19] to judge the risk of bias in eligible studies. Discrepancies were resolved in a meeting with a third researcher. Bias risk for each criterion was classified as low risk, high risk, or uncertain risk. Five criteria were considered for evaluating RCTs: (1) randomization bias; (2) bias due to deviations from intended interventions; (3) risk of bias due to missing outcome data; (4) bias due to outcome measurement; and (5) bias due to selection of the reported result and other sources of biases.

Synthesis and data analysis

Due to the significant heterogeneity in studies concerning multiple outcome measurements and different intervention comparators, a meta-analysis may not always be appropriate. Therefore, the data were summarized using a synthesis without meta-analysis [20] approach for the outcomes related to the effect of resistance training on hepatic fat, liver enzyme behavior, and insulin resistance in patients diagnosed with MASLD, as described in Supplementary Material 3, Supplemental digital content 1, https://links.lww.com/EJGH/B89.

Each study was summarized based on the outcome measure, and P values and confidence intervals (CIs) were analyzed to determine the significant effects of the intervention. A two-tailed P value <0.05 was considered statistically significant, and the 95% CIs presented in some of the eligible studies were used to calculate the overall effect size estimate.

Results

Studies characteristics

The literature search yielded 4089 studies from the mentioned databases. We identified 202 studies for title reading. Consequently, we found 29 potentially eligible studies that were fully analyzed, with 23 studies being excluded due to unsatisfactory study design or results. Ultimately, six studies were included in this systematic review [21–26], as presented in PRISMA 2020 flowchart (Fig. 1):

Fig. 1.:

PRISMA 2020 flowchart (flow diagram of study screening and selection). PRISMA, Preferred Reporting Items for Systematic Reviews and Meta-Analyses.

A total of 232 sedentary adults with MASLD, with an average age ranging from 37.4 to 62.4 years, were included in the final analysis. Among these individuals, 132 (59%) were men, 75 (33%) were women, and 19 (8%) did not have gender identification. Four eligible studies were conducted in Asia (Japan, Israel, Iran, Thailand) [23–26], and two studies were conducted in Europe (Italy and the UK) [21,22]. The 232 participants were concurrently subjected to intervention or control groups, with 119 individuals in isolated resistance training protocols, 42 individuals in isolated aerobic training protocols, and 81 individuals in control groups. Three eligible studies enrolled patients with confirmed MASLD through ultrasonography [24–26]; two studies enrolled patients with MASLD diagnosed by MRS [21,22]; and one study included patients with MASLD diagnosed by transient elastography (FibroScan) [23]. The main characteristics of the six eligible studies are summarized in Table 1.

Table 1. - Characteristics of the randomized clinical trials included

C, control group; NI, not informed; TA, aerobic training; TR, resistance training.

aValues presented as means ± SD; n: sample.

The summary of the proposed interventions in each eligible study can be found in Supplementary Table 1, Supplemental digital content 1, https://links.lww.com/EJGH/B89. Additionally, Supplementary Table 2, Supplemental digital content 1, https://links.lww.com/EJGH/B89 outlines the objectives and outcomes of each randomized clinical trial included in this systematic review.

According to Supplementary Table 3, Supplemental digital content 1, https://links.lww.com/EJGH/B89, which presents the summary of the risk of bias assessment of eligible studies, all randomized clinical trials revealed some considerations in criterion 2 due to the nonblinding of participants and researchers, given the nature of exercise interventions. No study, however, was assigned a high risk of bias, suggesting a low risk of bias with some considerations for all randomized clinical trials included in this systematic review.

Hepatic fat and resistance training

Hepatic fat was assessed differently at the beginning and end of the studies due to variations in assessment instruments. At the end of the resistance training program, two studies [22,25] reported a significant reduction in hepatic fat (P < 0.01 and P < 0.05, respectively) within the same resistance training group. Additionally, studies by Hallsworth et al. [22], Shamsoddini et al. [24], Takahashi et al. [25], and Zelber-Sagi et al. [26] showed a significant reduction in hepatic fat (P < 0.05) when comparing the resistance training group with the control group from baseline to the end of the intervention.

According to Charatcharoenwitthaya et al. [23], there was a significant reduction in hepatic steatosis value (P < 0.001) when comparing the start and end of the 12-week training within the same resistance training group. Moreover, during the same intervention period, it was observed that the resistance training group showed a relative reduction of 12.6% with a 95% CI, compared within the same group, while the aerobic training group showed a relative reduction of 10.3% with a 95% CI, in the comparison within the same group [23].

According to Bacchi et al. [21], hepatic fat measured by MRI with a cutoff point of hepatic fat fraction of 5.56% showed a significant (P < 0.001) and relative reduction of 13% in hepatic fat content, comparing from baseline to the end of the 16-week training within the same resistance training group.

Insulin resistance and resistance training

RCTs provided consistent evidence of the positive impact of resistance training on insulin resistance. Hallsworth et al. [22] reported a significant decrease in insulin resistance (P < 0.05), as measured by HOMA-IR, comparing baseline and the end of 8 weeks of intervention within the resistance training group. Similarly, Takahashi et al. [25] showed a significant reduction in insulin resistance (P < 0.001) when comparing the resistance training group to the control group after 12 weeks of intervention.

Charatcharoenwitthaya et al. [23] demonstrated a significant reduction in HOMA-IR (P < 0.05) within the resistance training group, comparing the start and the 12th week of intervention. Likewise, the aerobic training group showed a significant reduction in HOMA-IR (P < 0.05) between the beginning and the end of the 12th week of intervention. Bacchi et al. [21] observed a significant increase in insulin sensitivity, measured by the clamp test (P < 0.025), comparing the baseline to the end of 16 weeks of intervention within the resistance training group.

In Shamsoddini et al.’s RCT [24], there was a significant decrease (P < 0.05) in the HOMA-IR index when comparing the aerobic training group to the control group over 8 weeks. The resistance training group, however, exhibited a reduction in the HOMA-IR index, which was NS when comparing the baseline to the end of the 8-week intervention within the same resistance training group, as well as in the comparison between resistance training and the control group.

In Zelber-Sagi et al.’s RCT [26], there was no significant decrease in the HOMA-IR index when comparing baseline to the end of 12 weeks of intervention within the same resistance training group. Similarly, no significant differences were observed when comparing the control group to the resistance training group.

Behavior of liver enzymes and resistance training

Takahashi et al. [25] reported a significant reduction (P < 0.001) in the concentration of ALT within the same resistance training group when comparing the baseline to the end of the intervention. Additionally, Zelber-Sagi et al.’s RCT [26] showed a significant reduction (P < 0.05 for AST, P < 0.01 for ALT) in AST and ALT between baseline and the end of the intervention within the same resistance training group. In the comparison between the control group and the resistance training group, there, however, was no significant difference in the reduction of liver enzymes.

Shamsoddini et al. [24] demonstrated significant differences in ALT and AST liver enzymes (P < 0.003 and P < 0.04, respectively) when comparing resistance training to the control group from baseline to the end of the 8-week intervention. Likewise, ALT and AST liver enzymes showed a significant reduction (P < 0.002 and P < 0.02, respectively) within the same resistance training group when comparing the start and end of the training intervention.

In the RCTs conducted by Bacchi et al. [21], Hallsworth et al. [22], and Charatcharoenwitthaya et al. [23], the concentrations of ALT and AST liver enzymes, however, did not exhibit significant reductions when comparing baseline to the end of the intervention within the same resistance training group. Moreover, there was no significant reduction in liver enzymes when comparing the resistance training group to the control or aerobic group during the same period.

Participants’ adherence to the resistance training group

It was observed that participants in the strength training groups showed 100% attendance at the end of 8 weeks [22,24], 12 weeks of intervention [23,25], and 16 weeks of intervention [21]. In the study by Zelber-Sagi et al. [26], there, however, was a reduction in attendance among participants in the strength training group (83%), as well as in the control group (87%) at the end of the 12 weeks of intervention. In the study by Bacchi et al. [21], 93% of participants in the aerobic training group completed the program, in contrast, 100% of study participants who underwent the strength training group completed the intervention.

Summary of intervention data in each group and participant attendance are presented in Tables 2 and 3.

Table 2. - Resistance training intervention data vs. control group and aerobic training (part 1 of 2)

| | Liver fat | Insulin resistance(HOMA-IR/clamp testa) | BMI | | | | | | | | | ------------------------------------- | --------------------------------------- | --------------------------------------- | ----------------------------------------- | ----------------------------------------- | ----------------------------------------------- | ------------------------------------- | ---------------------------------------------- | ------------------------------------------------------- | ------------------------- | | Preintervention | Postintervention | P value | Preintervention | Postintervention | P value | Preintervention | Postintervention | P value | | | Hallsworth et al. [22] | TR: 14.0%C: 11.2% | TR: 12.2%C: 11.5% | TR: P < 0.05↔** C: 0.80 | TR: 5.9 ± 5.9b C: 4.7 ± 2.1b | TR: 4.6 ± 4.6b C: 5.1 ± 2.5b | TR**: _P_ < 0.05↔** C: 0.57 | TR: 32.3 (4.9)c C: 32.3 (4.8)c | TF: 32.3 (4.5)c C: 32.5 (4.2)c | TF: 0.89C: 0.42 | | Shamsoddini _et al_. [24] | TR: 1.7b TA: 1.8b C: 1.4b | TR: 1.1b TA: 0.9b C: 1.6b | TR × C: **_P_ > 0.05↕ | TR: 3.5b TA: 3.2b C: 3.1b | TR: 3.3b TA: 2.3b C: 3.2b | TR × C: P > 0.05↕ TR × TA: 0.6 | TR: 30.6 ± 2.6b TA: 28.1 ± 3.1b C: 28.2 ± 3.7b | TF: 29.9 ± 2.6b TA: 27.5 ± 3.5b C: 27.5 ± 3.9b | TF: P < 0.05↔** | | Takahashi _et al_. [25] | TR: 1.77 ± 0.80b C: 2.00 ± 0.60b | TR: 1.53 ± 0.64b C: 2.05 ± 0.58b | TR: **_P_ < 0.05↔** C: 0.427 | TR: 3.8 ± 2.8b C: 3.1 ± 1.4b | TR: 3.1 ± 1.5b C: 3.1 ± 1.7b | TR: **_P_ < 0.05↔** C: 0.888 | TR: 28.5 ± 3.1b C: 28.2 ± 4.2b | TR: 28.4 ± 2.9b C: 28.1 ± 3.9b | TF: 0.254C: 0.406 | | Zelber-Sagietal. [26] | TR: 2.11 ± 0.44b C: 1.96 ± 0.46b | TR: 1.86 ± 0.37b C: 1.91 ± 0.28b | TR × C: **_P_ < 0.05↕** | TF: 5.65 ± 2.41b C: 5.97 ± 2.72b | TF: 5.28 ± 2.04b C: 5.73 ± 1.75b | TR × C: 0.209 | TR: 30.75 ± 4.52b C: 31.30 ± 4.14b | TR: 30,62 ± 0.49b C: 0.12 ± 0.41b | TF × C: **_P_ < 0.05 ↕** | | Bacchi E _et al_. [21] | TR: 31.3%TA: 25.7% | TR: 19.5%TA: 16% | TR: **_P_ < 0.001↔** TA: **_P_ < 0.001↔** | TR: 4.64 (0.56)a , d TA: 3.72 (0.61)a , d | TR: 4.12 (0.52)a , d TA: 2.75 (0.97)a , d | TR × TA: **_P_ > 0.05↕ | TR: 28.8 (1.1)d TA: 31.8 (1.0)d | TR: −0.55 (−0.90 to −0.19)e TA: −0.70 (−1.11 to −0.28)e | TF × TA: P < 0.001↕** | | Charatcharoenwitthaya _et al_. [23] | TR: 296.1 ± 9.1b TA: 284.2 ± 8.3b | TR: 258.79 ± 23.42b TA: 254.92 ± 22.45b | TR: **_P_ < 0.05↔** TA: **_P_ < 0.05↔** | NI | TR: 20.61(21.34–0.13)e TA: 21.21 (22.35–20.08)e | TA × TR: **_P_ > 0.05↕ | TR: 27.3 ± 0.9b TA: 26.8 ± 0.7b | TR: −1.24 (−2.19 to −0.29)b TA: −1.46 (−2.29 to −0.64)e | TR × TA: 0.637 |

↔ indicates comparison between the same group, intragroup; ↕ indicates comparison between two different groups, intergroup.

Bold indicates statistically significant differences.

C, control group; NI, not informed; TA, aerobic training; TR, resistance training.

aClamp test.

bValues are as means ± SD.

cValues are means (SD).

dValues are mean (SE).

eData are mean (95% confidence interval).

Table 3. - Strength training intervention data vs. control group and aerobic training (part 2 of 2)

| | AST enzyme | ALT enzyme | | | | | | | | ------------------------------------- | -------------------------------------------- | ----------------------------------------------------- | ------------------------ | ----------------------------------------------- | ----------------------------------------------------- | ----------------------------- | -------------------------------------------------------------------------------------------- | | Preintervention | Postintervention | P value | Preintervention | Postintervention | P value | Treatment attendance (%) | | | Hallsworth et al. [22] | NI | NI | NI | TR: 59.6 (38.6)a C: 61.6 (41.4)a | TR: 59.6 (39.0)a C: 61.4 (44.0)a | TR: 0.99C: 0.92 | TF (n = 11) = 100% completedC (n = 8) = 100% completed | | Shamsoddini et al. [24] | TR: 39.8 ± 21.19b TA: 29.7 ± 9b C: 32 ± 7.1b | TR: 34.7 ± 18.1b TA: 20.9 ± 4.4b C: 31.6 ± 7.6b | TR × C: P > 0.05↕ | TR: 56 ± 23.7b TA: 36.9 ± 16.4b C: 48.3 ± 17.6b | TR: 41.3 ± 19.5b TA: 24.4 ± 7.2b C: 49.6 ± 17.6b | TR × C: P < 0.05↕ | TF (n = 10) = 100% completedTA (n = 10) = 100% completedC (n = 10) = 100% completed | | Takahashi et al. [25] | TR: 45.2 ± 25.1b C: 48.0 ± 25.4b | TR: 38.1 ± 18.4b C: 42.5 ± 14.9b | TR: P < 0.05↔ | TR: 75.1 ± 61.3b C: 78.5 ± 47.6b | TR: 56.3 ± 49.7b C: 71.0 ± 38.4b | TR: P < 0.001↔ C: 0.243 | TF (n = 31) = 100% completedC (n = 22) = 100% completed | | Zelber-Sagi et al. [26] | TR: 34.30 ± 17.49b C: 32.00 ± 14.76b | TR: −2.76 ± 7.75b C: −2.68 ± 6.95b | TR: P < 0.01↔ | TR: 53.00 ± 35.61b C: 50.13 ± 37.20b | TR: −5.30 ± 9.65b C: −5.10 ± 14.43b | TR: P < 0.05↔ | TF (n = 44) = 82% (n = 36) completedC (n = 38) = 87% (n = 33) completed | | Bacchi et al. [21] | TR: 20.5 (2.5)TA: 17.7 (1.1) | TR: −1 (−3.82 to 1.82)c TA: 0.15 (−2.61 to 2.92)c | TR × TA:0.612 | TR: 32.4 (6.2)TA: 24.7 (3.1) | TR: −5.33 (−10.77 to 0.10)c TA: 0.38 (−4.35 to 5.12)c | TR × TA: 0.721 | TF (n = 17) = 100% completedTA (n = 14) = 93% (n = 13) completed | | Charatcharoenwitthaya et al. [23] | TR: 19.9 ± 2.5b TA: 22.4 ± 2.1b | TR: 20.76 (−4.37 to 2.84)c TA: 20.70 (−0.70 to 9.48)c | TR × TA: 0.797 | TR: 17.6 ± 2.3b TA: 31.6 ± 7.8b | TR: −0.29 (25.44–4.85)c TA: 0.94 (28.45–10.3)c | TR × TA: 0.999 | TF (n = 17) = 100% completedTA (n = 18) = 100% completed |

↔ indicates comparison between the same group, intragroup; ↕ indicates comparison between two different groups, intergroup.

Bold indicates statistically significant differences.

C, control group; NI, not informed; TA, aerobic training; TR, resistance training.

aValues are means (SD).

bValues are as means ± SD.

cData are mean (95% confidence interval)

Discussion

To the best of our knowledge, this is the first systematic review of RCTs investigating the isolated effects of resistance training on hepatic fat, liver enzymes, and insulin resistance in MASLD patients. Evidence suggests that resistance training, performed at least three times weekly for 8–16 weeks, significantly reduces hepatic fat. This reduction was observed in both baseline-to-postintervention comparisons within resistance training groups and between the resistance training and control groups over the intervention period.

Our findings align with recent studies [14,27,28] highlighting the positive effects of resistance training, aerobic exercise, or combined dietary therapy on hepatic fat reduction in obese MASLD patients. A nationwide study of 1897 men aged ≥50 years and 2206 postmenopausal women found an inverse relationship between muscle strength and hepatic steatosis, stressing the importance of resistance training [29]. Additionally, low muscle strength is linked to higher long-term mortality in MASLD [30], while low hand grip strength is associated with developing the disease [31]. Higher skeletal muscle mass may help prevent MASLD, reinforcing the role of resistance training in treatment [32].

Systematic reviews by Smart et al. [9] and Fu et al. [13] show that both aerobic and resistance exercises modulate hepatic lipid metabolism, reducing hepatic fat. Oh et al. [33] found that exercise reduces liver fat and stiffness, independent of weight loss, and these improvements are linked to reduced adipose tissue, preserved muscle mass, and increased muscle strength. A recent meta-analysis also provided strong evidence that exercise-based lifestyle interventions reduce intrahepatic fat and aminotransferase levels [34]. These findings align with our results on the positive effects of resistance training on liver fat in MASLD patients.

Hepatic enzymes, ALT and AST, and insulin resistance are linked to the severity of hepatic steatosis [34,35], highlighting the relationship between liver fat and MASLD clinical markers. Resistance training has been shown to significantly reduce cholesterol, triglycerides, and serum AST in MASLD patients [16,36]. In our review, ALT and AST levels significantly decreased both in resistance training groups compared with controls postintervention and from baseline to postintervention within the same group [24–26]. These results may be influenced by the intervention frequency (at least three times per week) and the participants’ average age of 45–55 years.

Gao et al. [37] found that long-term exercise, at least three times per week, significantly improves ALT and AST levels in MASLD patients. Similarly, Hong et al.’s meta-analysis [38] identified age as a key factor in the exercise-induced reduction of liver enzymes. Other studies [21–23], however, did not show significant reductions in ALT and AST within resistance training groups or compared with control and aerobic groups over the intervention. Wang et al. [39] confirmed this, noting that short-term exercise (<4 months) did not improve ALT and AST levels in individuals with metabolic syndrome, a risk factor for MASLD.

On the other hand, insulin resistance and excess triglycerides, especially from visceral fat, are key factors in the development and progression of MASLD [35]. Silva et al. [40] suggest that diabetes and insulin resistance assessments, like HOMA-IR, are useful screening tools for steatosis in severely obese MASLD patients. Physical activity, as a nonpharmacological intervention, improves insulin resistance by enhancing insulin receptor phosphorylation and reducing inflammation, making exercise a viable treatment option for MASLD patients [41].

Our systematic review found a significant improvement in insulin sensitivity and resistance (HOMA-IR) in three studies [21–23] comparing pre- and postintervention within the same resistance training group. Similarly, a significant improvement in insulin resistance was noted when comparing resistance training with control groups [25], though one study [24] showed nonsignificant improvements. These findings align with Son and Park [42], who observed improved insulin, blood glucose, and HOMA-IR in obese women with metabolic syndrome, highlighting the potential benefits of resistance training in reducing MASLD severity and progression to steatohepatitis [39].

A key finding of this systematic review was the 100% adherence of participants aged 38 to 56 years in the resistance training groups [21–26]. This may be linked to Wang et al. [43], who suggest that a simple, convenient, and structured exercise program enhances adherence in MASLD patients. Resistance exercise is a suitable option for those lacking motivation for aerobic exercise or with cardiovascular limitations [8,14]. The American Association for the Study of Liver Diseases practical guide [3] highlights that personalized exercise plans can improve sustainability and provide benefits beyond weight loss. Moreover, higher strength training activity is linked to a lower risk of developing MASLD [8].

The articles in this systematic review showed heterogeneity in intervention protocols and MASLD diagnostic criteria, limiting the study’s conclusions. Jin [44] emphasizes that controlling bias related to exercise intensity, frequency, and type across studies is crucial but challenging. Another limitation was the small sample sizes in the RCTs, which may reduce the practical application of strength training and its impact on the clinical management of MASLD patients.

In summary, resistance training may be an effective approach for managing MASLD [34]. Our systematic review concludes that resistance training can significantly improve clinical and liver markers, serving as a well-accepted and consistent option for adults with MASLD. Further research, however, is needed to explore resistance training effects and models in these patients, particularly studies focusing on interventions that assess hepatic steatosis and muscle strength.

Acknowledgements

This study was financed in part, L.F.F. is currently receiving a fellowship grant from Coordenação de Aperfeiçoamento de Pessoal de Nível Superior – Brazil (CAPES) – Finance Code 001.

All relevant data to the results of this study can be found in the tables and results of this manuscript. If any researcher is interested in the original datasets and spreadsheets, they are available upon request to the corresponding author.

Conflicts of interest

There are no conflicts of interest.

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Keywords:

fatty liver; insulin resistance; metabolic dysfunction-associated steatotic liver disease; muscle strength; resistance training; physical activity

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