A comprehensive literature search was conducted across eight electronic databases—PubMed, Embase, Cochrane Library, Web of Science, Wanfang Data, Chinese Biomedical Literature Database (CBM), VIP Database, and China National Knowledge Infrastructure (CNKI)—to identify randomized controlled trials (RCTs) published from database inception to October 2025. Both Medical Subject Headings (MeSH) terms and free-text keywords were employed, with no restrictions on language. The core search terms included: “Baduanjin,” “Eight-Section Brocade,” “standing Baduanjin,” “chronic heart failure,” “heart failure,” “cardiac function,” and “quality of life”. Boolean operators (AND, OR, NOT) were applied to refine the search.

To ensure comprehensiveness, manual searches were also performed on the reference lists of all included articles to identify additional eligible studies. Two reviewers (YJ and YX) independently conducted the search and screening processes, and any discrepancies were resolved through discussion or consultation with a third reviewer (LS). Detailed search strategies for each database are provided in Supplementary Material S2.

The inclusion criteria were as follows:

Study design: randomized controlled trials (RCTs).

Two reviewers (YJ and XG) independently extracted data from all eligible studies, including the first author, year of publication, sample size, participant characteristics, intervention protocol (frequency, duration, and training period), control measures, and outcome indicators. Any discrepancies were resolved through discussion or adjudication by a third reviewer (LZ). The methodological quality of the included trials was assessed using the Cochrane Risk of Bias Tool (21), covering seven domains: random sequence generation, allocation concealment, blinding, completeness of outcome data, and selective reporting, among others. Additionally, the modified Jadad scale (total score = 7 points) was applied to evaluate study quality, with scores ≥4 indicating high-quality studies (22).

Meta-analyses were performed using Stata version 18.0. Dichotomous variables were expressed as risk ratios (RRs) with 95% confidence intervals (CIs), while continuous variables were reported as standardized mean differences (SMDs) with 95% CIs. Between-study heterogeneity was assessed using the I² statistic. A random-effects model was applied when I² > 50%, and a fixed-effects model was used otherwise. For continuous outcomes, a positive SMD indicates improvement for outcomes with higher-is-better values (e.g., LVEF and 6-MWD), whereas a negative SMD indicates improvement for outcomes with lower-is-better values (e.g., LVEDD, LVESD, BNP, NT-pro BNP, and MLHFQ).

Sensitivity analyses were conducted by sequentially omitting individual studies to evaluate the robustness of pooled results. Publication bias was assessed using Egger's test, and, when necessary, the trim-and-fill method was employed to adjust for potential bias. Additionally, subgroup analyses were performed according to intervention duration (<12 weeks, 12 weeks, and >12 weeks), based on commonly used exercise rehabilitation cycles, to explore the temporal effects of SBE on cardiac function and QoL outcomes.

A total of 387 records were initially identified, of which 50 RCTs (23–72) met the inclusion criteria, encompassing 3,964 participants (2,219 males and 1,745 females) (Figure 1). All included studies were conducted in China and published between 2016 and 2025. Sample sizes ranged from 22 to 90 participants, with intervention durations varying from 2 to 48 weeks. All patients were classified as NYHA functional class II-III, and no adverse events related to SBE were reported. The control groups received CPT recommended by clinical guidelines, including ARNIs, ACEIs, angiotensin receptor blockers (ARBs), β-blockers, sodium-glucose cotransporter-2 inhibitors (SGLT2i), mineralocorticoid receptor antagonists (MRAs), and diuretics. The intervention groups performed SBEs in addition to these conventional therapies. No statistically significant differences were observed between the two groups at baseline. The main outcome measures included LVEF (39 studies), LVEDD (20 studies), LVESD (15 studies), 6-MWD (32 studies), BNP (11 studies), NT-pro BNP (18 studies), MLHFQ total score (24 studies), and its subdomains—physical (11 studies), psychological (10 studies), and other dimensions (8 studies)—as well as clinical efficacy (20 studies). The baseline characteristics of the included studies are summarized in Table 1.

All 50 included RCTs reported their methods of randomization. Among them, 32 studies (24–31, 33–42, 44, 49, 54, 55, 57, 59, 60, 62–67, 69) used the random number table method, 3 studies (23, 45, 56) used lot-drawing, and 1 study (51) used sealed envelopes, all assessed as having low risk of bias. In contrast, 1 study (57) allocated participants based on order of admission, and 2 studies (43, 53) by treatment type, all considered to have high risk of bias. Eight studies (32, 46, 50, 61, 68, 70–72) did not specify the method of randomization and were rated as unclear. Only one study (31) explicitly reported the use of blinding and was assessed as low risk, whereas the remaining studies did not report details of blinding or allocation concealment and were thus rated as unclear. All studies reported complete outcome data, suggesting a low risk of attrition bias. None of the studies mentioned other potential sources of bias, and these were therefore classified as unclear. Detailed assessments of bias risk are presented in Figure 2 and Supplementary Material S3.

Sensitivity analyses were performed for LVEF (Figure 14A), LVEDD (Figure 14B), LVESD (Figure 14C), 6-MWD (Figure 14D), NT-pro BNP (Figure 14E), and MLHFQ total score (Figure 14F) by sequentially excluding individual studies. The pooled results showed minimal variation in effect size or significance, indicating that the findings were stable and reliable.

Publication bias was assessed for LVEF, LVEDD, LVESD, 6-MWD, NT-pro BNP, and MLHFQ using Egger's test. Egger's test suggested potential publication bias for LVEF (Figure 15A, P = 0.028), 6-MWD (Figure 15D, P = 0.015), and NT-pro BNP (Figure 15E, P = 0.003), while no significant bias was found for LVEDD (Figure 15B, P = 0.101), LVESD (Figure 15C, P = 0.760), or MLHFQ (Figure 15F, P = 0.978). To further verify these results, the trim-and-fill method was applied to the indicators showing bias (Supplementary Material S4). The adjusted pooled effects showed minimal change, indicating that although minor publication bias might exist, the overall findings remained robust and credible.

The results of this systematic review and meta-analysis demonstrate that SBE, as an adjunctive intervention for patients with CHF, exerts significant benefits in improving both cardiac function and QoL. In terms of cardiac function, SBE markedly increased LVEF and 6-MWD, indicating enhanced myocardial contractility and exercise tolerance. Meanwhile, it significantly reduced LVEDD, LVESD, BNP, and NT-pro BNP levels, suggesting attenuation of ventricular remodeling and improvement in cardiac load. Regarding QoL, SBE significantly decreased total and domain scores (physical, psychological, and other) of the MLHFQ, reflecting not only alleviation of physical symptoms and functional impairment but also mitigation of psychological distress and social limitations. Moreover, when combined with CPT, SBE further enhanced overall clinical efficacy, underscoring its potential as a complementary rehabilitation approach.

Sensitivity analyses revealed that the pooled effect sizes for major outcomes remained stable after sequential exclusion of individual studies, indicating the robustness and reliability of the meta-analytic results. Egger's tests suggested minor publication bias for LVEF, 6-MWD, and NT-pro BNP, whereas no significant bias was observed for LVEDD, LVESD, or MLHFQ, implying an overall low risk of publication bias. To explore the potential influence of intervention duration, subgroup analyses were performed based on treatment length. The results indicated that 12 weeks of SBE produced the greatest improvement in cardiac function, whereas interventions lasting more than 12 weeks yielded the most pronounced benefits in QoL. This pattern may reflect the distinct physiological and psychosocial adaptation processes underlying exercise rehabilitation. Moderate-intensity mind-body SBE typically induce significant autonomic remodeling, anti-inflammatory, and antioxidative adaptations within 8–12 weeks, leading to enhanced myocardial contractility and metabolic efficiency. Beyond this period, although further physiological gains may plateau, continued practice helps consolidate behavioral adherence, emotional regulation, and psychosocial well-being, resulting in sustained improvement in QoL. Overall, SBE represents a safe, cost-effective, and sustainable adjunctive therapy that supports both functional recovery and long-term holistic rehabilitation in patients with CHF.

The core pathophysiological mechanisms underlying CHF involve excessive activation of the renin-angiotensin-aldosterone system (RAAS), heightened sympathetic nervous activity, and sustained upregulation of pro-inflammatory cytokines (73). These abnormalities, through neurohormonal imbalance and immune-inflammatory cascades, jointly promote cardiomyocyte hypertrophy, apoptosis, and fibrosis, ultimately resulting in ventricular remodeling and progressive cardiac dysfunction. SBE, characterized by slow, coordinated movements integrated with deep breathing, contributes to autonomic regulation by restoring the balance between the sympathetic and parasympathetic nervous systems (74). It has been shown to reduce circulating norepinephrine levels, enhance vagal tone, and thereby suppress sympathetic overactivation, which in turn decreases cardiac preload and myocardial oxygen consumption (75). Furthermore, SBE exerts potent anti-inflammatory and antioxidative effects, potentially through inhibition of the NF-κB signaling pathway and upregulation of endogenous antioxidant enzymes such as SOD and GSH-Px (18). These effects collectively alleviate myocardial inflammation and fibrotic progression. Improvement in endothelial function represents another crucial cardioprotective mechanism. Evidence suggests that SBE can upregulate NOS expression and increase NO bioavailability, enhancing vasodilation and microcirculatory perfusion (19). Activation of the L-arginine-NO signaling pathway further reduces peripheral vascular resistance and optimizes cardiac loading conditions (76). In addition, the “integration of movement and stillness” and “coordination of body and mind” inherent in SBE can help alleviate anxiety and depression while stabilizing the hypothalamic-pituitary-adrenal (HPA) axis, thereby promoting cardiac recovery from both psychological and physiological dimensions (77, 78). Collectively, SBE provides both evidence-based support and modern physiological rationale for its role as an integrative rehabilitation approach in CHF.

Previous meta-analyses by Mei et al. (79) and Yang et al. (80) investigated the effects of Baduanjin on CHF, the present study provides a more systematic and methodologically refined evaluation. First, this study is the first to distinguish between standing and sitting forms of Baduanjin, including only trials that adopted SBE. This distinction minimized the potential confounding effects caused by variations in exercise intensity, posture, and movement patterns. The results demonstrated that SBE produced more pronounced improvements in both cardiac function and QoL than those reported in earlier mixed-form analyses. Second, through subgroup analyses, this study identified a time-dependent relationship between intervention duration and therapeutic efficacy, showing that a 12-week intervention produced the greatest improvement in cardiac function, while interventions longer than 12 weeks resulted in the most pronounced enhancement in QoL. This finding suggests that the rehabilitative benefits of SBE may depend on the physiological adaptation period required for neurocardiac and behavioral conditioning. Finally, unlike previous studies that primarily focused on cardiac function outcomes, the current meta-analysis incorporated QoL (MLHFQ total and subdomain scores) as co-primary endpoints. This comprehensive approach provided a more holistic understanding of SBE's multidimensional rehabilitation value—encompassing physiological, psychological, and social domains. Overall, this study collectively reinforces the clinical potential of SBE as a safe, feasible, and multidimensionally beneficial exercise-based rehabilitation strategy for patients with CHF.

Impaired cardiac function and reduced quality of life represent two major challenges in the long-term management of CHF. Cardiac pump dysfunction leads to diminished exercise capacity and excessive neurohormonal activation, while sustained declines in QoL are closely associated with depression, anxiety, and increased risk of rehospitalization (81–83). In recent years, exercise-based rehabilitation has been shown to improve cardiac function, exercise tolerance, and overall well-being in patients with CHF (84); however, the optimal modality and duration of intervention remain uncertain. This study comprehensively evaluated the effects of SBE on cardiac function and QoL in patients with CHF, with several notable strengths. First, it is the first meta-analysis to distinguish standing from sitting Baduanjin, including only standing Baduanjin RCTs to minimize confounding from differences in exercise intensity. Second, a subgroup analysis based on intervention duration (<12 weeks, =12 weeks, >12 weeks) revealed the time-dependent characteristics of its cardiorehabilitative effects. Third, by integrating both cardiac function and QoL as co-primary outcomes, the study established a more comprehensive assessment framework, providing systematic evidence for the clinical application of SBE in CHF rehabilitation.

However, several limitations should be acknowledged. First, all included studies were conducted in China, with relatively homogeneous populations, which may limit the generalizability of the findings to other regions and ethnic groups. Second, some trials lacked methodological rigor, particularly regarding allocation concealment and blinding, which may introduce selection or detection bias. Third, the included studies did not distinguish between heart failure subtypes—such as reduced ejection fraction (HFrEF), mildly reduced ejection fraction (HFmrEF), and preserved ejection fraction (HFpEF)—nor did they consistently stratify outcomes according to NYHA functional class II or III, thereby limiting the ability to assess differential effects across CHF phenotypes and disease severity. In addition, the etiology of CHF (e.g., ischemic, hypertensive, or other causes) was not uniformly reported, precluding etiology-specific analyses. Fourth, inconsistencies existed in training frequency, session duration, instructional formats, and supervision quality of SBE, and most studies did not include objective measures of exercise intensity (e.g., heart rate zones or Borg scale), which may affect reproducibility and dose-response analysis. Fifth, standard pharmacological regimens varied across studies, and such heterogeneity could have influenced the observed outcomes. Finally, most trials had short follow-up periods and lacked data on long-term outcomes such as rehospitalization rates, mortality, and adverse events, preventing comprehensive evaluation of long-term safety and sustainability. Future research should therefore focus on multicenter, large-sample, rigorously designed prospective studies with extended follow-up periods. Further refinement of heart failure subtype stratification, etiological classification, and standardized exercise prescription parameters is warranted to clarify the cardioprotective mechanisms and clinical value of SBE in the integrated management of CHF.

In light of the aforementioned limitations, future research should advance the study of SBE. First, it is essential to establish a unified standard framework for Baduanjin-based cardiac rehabilitation. This includes defining the training frequency, session duration, postural specifications, and exercise intensity monitoring indicators (e.g., heart rate zones, Borg Rating of Perceived Exertion), thereby creating a quantifiable and reproducible exercise prescription model. Second, future studies should adopt a stratified design based on heart failure subtypes—HFrEF, HFmrEF, and HFpEF—to explore the differential efficacy, safety boundaries, and adaptability of SBE across distinct pathophysiological categories, ultimately facilitating precision rehabilitation. Third, there is a pressing need for multicenter, large-sample, and long-term RCTs conducted in diverse populations and geographic regions. Such studies should verify the sustained effects of SBE on cardiac function, rehospitalization rate, and mortality, while systematically documenting adverse events to evaluate long-term safety and clinical sustainability. Fourth, mechanistic investigations should be strengthened by integrating heart rate variability (HRV) analysis, inflammatory cytokine profiling, vascular endothelial function assessment, and multi-omics approaches. These studies can help clarify the biological underpinnings of SBE in regulating autonomic balance, anti-inflammatory and antioxidative pathways, and myocardial remodeling. Moreover, objective multimodal assessments using cardiac magnetic resonance imaging (MRI), cardiopulmonary exercise testing (CPET), and wearable monitoring devices should be incorporated to bridge the gap between clinical efficacy observation and mechanistic validation. In the future, efforts should focus on integrating SBE into modern cardiac rehabilitation systems, promoting it as a scalable, quantifiable, and sustainable model for global heart failure rehabilitation.