European Journal of Cardiovascular Medicine

Bronchial asthma is a chronic inflammatory disease of the airways characterised by reversible airflow obstruction, airway hyperresponsiveness, and recurrent episodes of wheezing, dyspnoea, chest tightness, and cough. It affects more than 300 million individuals globally and represents one of the most common chronic respiratory disorders across all age groups.¹ In India, prevalence ranges from 2–5% in adults and 5–10% in children, with rising incidence attributable to urbanisation, environmental pollution, and lifestyle transitions.²

Pharmacological therapy — including inhaled corticosteroids (ICS), long-acting beta-2 agonists (LABA), and leukotriene receptor antagonists — remains the cornerstone of asthma management.³ However, a substantial proportion of patients continue to experience suboptimal symptom control, frequent exacerbations, and reduced quality of life despite adequate pharmacotherapy. Long-term medication use is also associated with adverse effects including oral candidiasis and osteoporosis.⁴

These limitations have generated considerable interest in non-pharmacological adjunct therapies, particularly structured breathing exercises. Breathing exercise modalities studied in asthma include diaphragmatic breathing, pursed-lip breathing (PLB), the Buteyko technique, and yoga-based Pranayama techniques.⁵ These exercises aim to improve respiratory muscle strength, optimise breathing patterns, reduce airway resistance, and modulate autonomic nervous system activity.⁶

Existing systematic reviews report improvements in asthma-related quality of life and symptom control following breathing exercise interventions; however, evidence regarding objective pulmonary function improvement remains inconsistent, largely attributable to heterogeneous protocols, small sample sizes, and variable outcome measures.⁷ There is a need for well-designed, adequately powered randomised controlled trials using standardised spirometry and validated patient-reported outcomes.

The present study was therefore designed to evaluate the effect of a structured, multimodal eight-week breathing exercise programme on objective pulmonary function parameters and patient-reported asthma outcomes in a randomised controlled trial setting.

2.1 Study Design and Setting A prospective, open-label, parallel-group, randomised controlled interventional study was conducted at the Department of Pulmonary Medicine and Physiology, Outpatient Department (OPD) of a tertiary care teaching hospital. The study was approved by the Institutional Ethics Committee (IEC) and conducted in accordance with the Declaration of Helsinki (2013 revision) and ICMR National Ethical Guidelines for Biomedical and Health Research. Written informed consent was obtained from all participants prior to enrolment. 2.2 Participants Adults aged 18–60 years with a confirmed diagnosis of bronchial asthma as per Global Initiative for Asthma (GINA) criteria, with clinically stable disease (no acute exacerbation or change in maintenance medication in the preceding four weeks), and the ability to perform reproducible spirometric manoeuvres were eligible. Key exclusion criteria included: severe/uncontrolled asthma (FEV1 < 40% predicted), concurrent COPD, significant cardiovascular disease, neuromuscular disorders, active respiratory tract infection, pregnancy, thoracic cage deformities, and concurrent participation in another clinical trial. 2.3 Sample Size Sample size was calculated using the two-sample t-test formula for comparison of means. Assuming a standard deviation of 0.35 L for FEV1 change (based on published literature), a minimum clinically important difference of 0.10 L, two-tailed α = 0.05 (Zα/2 = 1.96), and 80% power (Zβ = 0.842), the minimum required sample was 97 per group. Accounting for 15% attrition, the final adopted sample size was 120 per group (total n = 240). 2.4 Randomisation and Allocation Concealment Computer-generated block randomisation (alternating block sizes of 4 and 6) was used. The allocation sequence was concealed in sequentially numbered, opaque, sealed envelopes maintained by a research co-ordinator not involved in participant assessment. 2.5 Interventions Group A (Control, n = 120) received standard maintenance pharmacological therapy as prescribed by the treating pulmonologist (ICS ± LABA ± LTRA, with SABA as rescue), with standard OPD follow-up at weeks 4 and 8. Group B (Intervention, n = 120) received identical standard pharmacological therapy plus a structured, physiotherapist-supervised breathing exercise programme comprising three core components: (i) Diaphragmatic breathing: Supine/semi-recumbent position; slow nasal inhalation with abdominal expansion; slow oral exhalation with abdominal contraction; rate ~8–10 breaths/min. (ii) Pursed-lip breathing (PLB): Slow nasal inhalation (count of 2) followed by slow exhalation through pursed lips (count of 4); inhalation:exhalation ratio 1:2. (iii) Pranayama techniques: Anulom-Vilom (alternate nostril breathing), Bhramari (humming bee breathing), and Kapalbhati (forceful exhalation technique). Sessions lasted 30 minutes daily (10 min per technique), six days per week, for eight weeks. The first two weeks included three supervised physiotherapy sessions per week; remaining sessions were conducted independently at home following instruction. Compliance was monitored using self-maintained exercise diaries and weekly telephonic follow-up. 2.6 Outcome Measures The primary outcome was change in FEV1 (litres and % predicted) from baseline to week 8. Secondary outcomes included changes in FVC, FEV1/FVC ratio, PEFR, Asthma Control Test (ACT) score, and modified Medical Research Council (mMRC) Dyspnoea Scale score. Spirometry was performed using a calibrated electronic spirometer in accordance with ATS/ERS Technical Standards (2019 update).⁸ A minimum of three acceptable reproducible manoeuvres were obtained; the best effort was recorded. Bronchodilators were withheld prior to testing (SABA ≥4 h; LABA ≥12 h). Post-intervention spirometry was conducted at the same time of day as baseline assessment. 2.7 Statistical Analysis All analyses were performed using IBM SPSS Statistics v26. Continuous variables are presented as mean ± standard deviation (SD); categorical variables as frequencies and percentages. Normality was assessed using the Shapiro-Wilk test. Pre- vs post-intervention comparisons within groups were performed using the paired t-test (or Wilcoxon signed-rank test where non-normal). Between-group comparisons used the independent samples t-test (or Mann-Whitney U test). Categorical variables were compared using chi-square or Fisher's exact test. Effect sizes were calculated as Cohen's d. Pearson's correlation coefficient was used to assess the compliance–FEV1 improvement relationship. ANCOVA was applied to control for baseline covariates. A two-tailed p < 0.05 was considered statistically significant.

3.1 Baseline Characteristics

A total of 240 participants were enrolled and randomised; all completed the eight-week study period (100% retention). Baseline demographic and clinical characteristics were comparable between the two groups (Table 1), confirming adequacy of randomisation (p > 0.05 for all parameters).

3.2 Baseline Pulmonary Function Parameters

No statistically significant inter-group differences were found in any spirometric parameter at baseline (Table 2), further confirming group homogeneity.

Table 1. Baseline Demographic and Clinical Characteristics

BMI = Body Mass Index; ACT = Asthma Control Test. Values are Mean ± SD or n (%). p-values from independent t-test or chi-square test.

Table 2. Baseline Pulmonary Function Parameters

FVC = Forced Vital Capacity; FEV1 = Forced Expiratory Volume in 1 second; PEFR = Peak Expiratory Flow Rate. p > 0.05 for all = not significant.

3.3 Within-Group Comparison: Pre- vs Post-Intervention

3.3.1 Group A (Control)

The control group demonstrated modest but statistically significant improvements in FVC, FEV1, and PEFR (p < 0.05), likely attributable to improved pharmacotherapy adherence during the study period. The FEV1/FVC ratio showed a marginal non-significant improvement (p = 0.061) (Table 3).

Table 3. Pre- vs Post-Intervention PFT Values — Control Group (Group A)

* p < 0.05 (statistically significant); NS = Not Significant. Paired t-test.

3.3.2 Group B (Intervention)

The intervention group demonstrated highly significant improvements across all spirometric parameters (p < 0.001 for all). FEV1 improved from 1.76 ± 0.29 L to 2.24 ± 0.24 L (absolute gain +0.48 L; +27.3%). PEFR increased from 298.7 ± 33.8 to 368.2 ± 28.9 L/min (+23.3%) (Table 4).

Table 4. Pre- vs Post-Intervention PFT Values — Intervention Group (Group B)

*** p < 0.001 (highly statistically significant). Paired t-test.

3.4 Between-Group Comparison: Post-Intervention

Statistically highly significant differences were observed in all spirometric parameters in favour of the intervention group (Table 5). Cohen's d for FEV1 was 1.84, indicating a very large effect.

Table 5. Post-Intervention Between-Group Comparison

** p < 0.01; *** p < 0.001. Independent samples t-test. Cohen's d > 0.8 = large effect; > 1.2 = very large effect.

3.5 Patient-Reported Outcome Measures

The proportion of patients achieving well-controlled asthma (ACT ≥ 20) increased from 9.2% to 61.7% in Group B, compared with 10% to 15% in Group A (p < 0.001). The mMRC dyspnoea score decreased by 1.0 point in Group B versus 0.3 points in Group A (p = 0.002) (Table 6).

Table 6. Patient-Reported Outcome Measures

ACT range: 5–25 (≥ 20 = well-controlled); mMRC range: 0–4 (lower = less dyspnoea). ** p < 0.01; *** p < 0.001.

3.6 Exercise Compliance and Dose-Response Relationship

Overall exercise compliance in Group B was 77.4 ± 11.8% (range 41–100%). High compliance (≥ 80%, n = 52) was associated with a mean FEV1 improvement of +0.61 ± 0.11 L, compared with +0.18 ± 0.12 L in low-compliance participants (< 60%, n = 20). A strong positive correlation was demonstrated between compliance and FEV1 improvement (Pearson r = 0.71, p < 0.001), establishing a clear dose-response relationship.

The principal finding of this randomised controlled trial is that an eight-week structured multimodal breathing exercise programme — comprising diaphragmatic breathing, pursed-lip breathing, and Pranayama techniques — produced clinically meaningful and statistically highly significant improvements in all measured pulmonary function parameters and patient-reported outcomes when added to standard pharmacological therapy in stable adult asthma patients.

The mean FEV1 improvement of +0.48 L (+27.3%) in the intervention group substantially exceeds the established minimal clinically important difference (MCID) for FEV1 in asthma (0.10–0.20 L) and is approximately four times the improvement observed in the control group (+0.12 L).⁹ This magnitude surpasses single-modality studies by Singh et al. (Pranayama, +0.21 L over 6 weeks)¹⁰ and Saxena & Saxena (Buteyko, ~18% FEV1 gain).¹¹ The superior outcomes observed in the present study are plausibly attributable to the multimodal design integrating three complementary techniques, each targeting distinct physiological pathways.

Diaphragmatic breathing conditioning strengthens the primary inspiratory muscle, increases diaphragmatic excursion and tidal volume, reduces accessory muscle recruitment, and slows the respiratory rate — collectively improving ventilation-perfusion matching and contributing to FVC and FEV1 gains.¹² PLB generates a positive end-expiratory pressure effect within the airways, preventing premature expiratory airway collapse and reducing air trapping, thereby improving FEV1/FVC ratios and PEFR.¹³ Pranayama components offer complementary mechanistic contributions: Anulom-Vilom enhances parasympathetic tone, reducing bronchomotor activity; Bhramari increases nitric oxide production via nasal sinus resonance, contributing to bronchodilation; and Kapalbhati strengthens expiratory muscles and facilitates mucus clearance.¹⁴

The PEFR improvement of +69.5 L/min (+23.3%) is clinically relevant as it directly reflects large central airway patency, correlates with daily symptom burden, and is self-monitorable by patients. Similar findings were reported by Nagarathna and Nagendra in their landmark yoga-asthma trial¹⁵ and by Sabina et al.¹⁶ The normalisation of FEV1/FVC ratio from 72.4% to 80.3% (+7.9 percentage points) represents a clinically significant shift away from the obstructive pattern, reflecting reduced airway resistance and bronchospasm.

The patient-reported outcomes reinforce the spirometric findings. The sixfold increase in well-controlled asthma status (ACT ≥ 20: 9.2% to 61.7%) — compared with a negligible increase in controls (10% to 15%) — is among the largest ACT improvements reported in breathing exercise trials and aligns with systematic review evidence.¹⁷ The 1.0-point reduction in mMRC dyspnoea score translates to a meaningful decrease in perceived breathlessness severity, with direct implications for exercise tolerance and functional capacity.

The strong dose-response relationship (r = 0.71, p < 0.001) between exercise compliance and FEV1 improvement provides compelling evidence of causal attribution. Patients with high compliance (≥ 80%) achieved 3.4-fold greater FEV1 improvement than low-compliance participants, underscoring that adherence support is a critical determinant of therapeutic efficacy.

The modest control-group improvements are most plausibly attributable to improved medication adherence facilitated by study participation (Hawthorne effect) and regression to the mean, rather than natural disease progression.

The findings are consistent with and extend the existing Cochrane review evidence,¹⁸ which reported improvements in quality of life but inconsistent lung function gains. The present study, with its larger sample (n = 240), multimodal design, validated outcome measures, and robust randomisation, addresses key methodological limitations of prior studies.

This study has several limitations. Blinding of participants was not feasible given the nature of the intervention, introducing potential performance bias. The single-centre design may limit generalisability to primary care or rural settings. The eight-week follow-up does not address long-term sustainability of benefits. Compliance relied partly on self-report, susceptible to recall bias. Inflammatory biomarkers were not assessed, precluding mechanistic insights at the molecular level.

A structured multimodal breathing exercise programme comprising diaphragmatic breathing, pursed-lip breathing, and Pranayama techniques produces clinically meaningful and statistically highly significant improvements in pulmonary function (FEV1, FVC, FEV1/FVC, PEFR), asthma control (ACT), and dyspnoea (mMRC) when added to standard pharmacological therapy in stable adult asthma patients. A clear compliance–benefit dose-response relationship was demonstrated. Structured breathing exercise therapy should be considered a cost-effective, safe, and evidence-based adjunct to pharmacological management in asthma, particularly for patients with suboptimal symptom control.

1. Masoli M, Fabian D, Holt S, Beasley R. The global burden of asthma: executive summary of the GINA Dissemination Committee report. Allergy. 2004;59(5):469–78.

2. Ghoshal AG, Ghosh A, Chatterjee S, et al. Asthma in India: results from a nationwide cross-sectional study (ICSA). Lung India. 2022;39(1):8–17.

3. Bateman ED, Hurd SS, Barnes PJ, et al. Global strategy for asthma management and prevention: GINA executive summary. Eur Respir J. 2008;31(1):143–78.

4. Barnes PJ. Inhaled corticosteroids. Pharmaceuticals (Basel). 2010;3(3):514–40.

5. Freitas DA, Holloway EA, Bruno SS, et al. Breathing exercises for adults with asthma. Cochrane Database Syst Rev. 2013;(10):CD001277.

6. Courtney R. The functions of breathing and its dysfunctions and their relationship to breathing therapy. Int J Osteopath Med. 2009;12(3):78–85.

7. Thomas M, McKinley RK, Mellor S, et al. Breathing exercises for asthma: a randomised controlled trial. Thorax. 2009;64(1):55–61.

8. Graham BL, Steenbruggen I, Miller MR, et al. Standardization of spirometry 2019 update. Am J Respir Crit Care Med. 2019;200(8):e70–e88.

9. Reddel HK, Taylor DR, Bateman ED, et al. An official ATS/ERS statement: asthma control and exacerbations. Am J Respir Crit Care Med. 2009;180(1):59–99.

10. Singh V, Wisniewski A, Britton J, Tattersfield A. Effect of yoga breathing exercises (pranayama) on airway reactivity in subjects with asthma. Lancet. 1990;335(8702):1381–3.

11. Saxena T, Saxena M. The effect of various breathing exercises (pranayama) in patients with bronchial asthma of mild to moderate severity. Int J Yoga. 2009;2(1):22–5.

12. Cahalin LP, Braga M, Matsuo Y, Hernandez ED. Efficacy of diaphragmatic breathing in persons with chronic obstructive pulmonary disease: a review. J Cardiopulm Rehabil. 2002;22(1):7–21.

13. Mueller RE, Petty TL, Filley GF. Ventilation and arterial blood gas changes induced by pursed lips breathing. J Appl Physiol. 1970;28(6):784–9.

14. Weitzberg E, Lundberg JO. Humming greatly increases nasal nitric oxide. Am J Respir Crit Care Med. 2002;166(2):144–5.

15. Nagarathna R, Nagendra HR. Yoga for bronchial asthma: a controlled study. Br Med J (Clin Res Ed). 1985;291(6502):1077–9.

16. Sabina AB, Williams AL, Wall HK, et al. Yoga intervention for adults with mild-to-moderate asthma: a pilot study. Ann Allergy Asthma Immunol. 2005;94(5):543–8.

17. Cramer H, Posadzki P, Dobos G, Langhorst J. Yoga for asthma: a systematic review and meta-analysis. Ann Allergy Asthma Immunol. 2014;113(4):383–90.

18. Holloway EA, West RJ. Integrated breathing and relaxation training (the Papworth method) for adults with asthma: a randomised controlled trial. Thorax. 2007;62(12):1039–42.