Respiratory muscle strength effect onheart rate variability in COPD patients

What is it about?

Introduction: Chronic obstructive pulmonary disease (COPD) is recognized as a multisystemic inflammatory disease associated with extrapulmonary comorbidities, including respiratory muscle weakness and cardiovascular and cardiac autonomic regulation disorders. We investigated whether alterations in respiratory muscle strength (RMS) would affect cardiac autonomic modulation in COPD patients. Methods: This study was a cross-sectional study done in ten COPD patients affected by moderate to very severe disease. The heart rate variability (HRV) signal was recorded using a Polar cardiofrequencimeter at rest in the sitting position (10 minutes) and during a respiratory sinus arrhythmia maneuver (RSA-M; 4 minutes). Linear analysis in the time and frequency domains and nonlinear analysis were performed on the recorded signals. RMS was assessed using a digital manometer, which provided the maximum inspiratory pressure (Pimax) and the maximum expiratory pressure (Pemax). Results: During the RSA-M, patients presented an HRV power increase in the low-frequency band (LFnu) (46.9±23.7 vs 75.8±27.2; P=0.01) and a decrease in the high-frequency band (HFnu) (52.8±23.5 vs 24.0±27.0; P=0.01) when compared to the resting condition. Significant associations were found between RMS and HRV spectral indices: Pimax and LFnu (r=-0.74; P=0.01); Pimax and HFnu (r=0.74; P=0.01); Pemax and LFnu (r=-0.66; P=0.01); Pemax and HFnu (r=0.66; P=0.03); between Pemax and sample entropy (r=0.83; P,0.01) and between Pemax and approximate entropy (r=0.74; P=0.01). Using a linear regression model, we found that Pimax explained 44% of LFnu behavior during the RSA-M. Conclusion: COPD patients with impaired RMS presented altered cardiac autonomic control, characterized by marked sympathetic modulation and a reduced parasympathetic response; reduced HRV complexity was observed during the RSA-M.

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Why is it important?

In conclusion, patients affected by COPD presented increased parasympathetic activity and ANS complexity at rest in the sitting position when compared to the RSA-M. This suggests an autonomic modulation alteration in basal conditions. During the RSA-M, a marked sympathetic modulation and a reduced parasympathetic response, with an HRV complexity reduction, were induced. Finally, RMS was found to be strongly associated with the sympathovagal response in COPD patients. These findings are relevant to understanding of COPD effects on HR autonomic modulation, and this is important to elucidate pathobiological mechanisms linking COPD to its comorbidities.