Differences in Respiratory Muscle Responses to Hyperpnea or Loaded Breathing in COPD.

INTRODUCTION: We aimed to compare acute mechanical and metabolic responses of the diaphragm and rib cage inspiratory muscles during two different types of respiratory loading in patients with chronic obstructive pulmonary disease. METHODS: In 16 patients (age, 65 ± 13 yr; 56% male; forced expiratory volume in the first second, 60 ± 6%pred; maximum inspiratory pressure, 82 ± 5%pred), assessments of respiratory muscle EMG, esophageal pressure (Pes) and gastric pressures, breathing pattern, and noninvasive assessments of systemic (V˙O2, cardiac output, oxygen delivery and extraction) and respiratory muscle hemodynamic and oxygenation responses (blood flow index, oxygen delivery index, deoxyhemoglobin concentration, and tissues oxygen saturation [StiO2]), were performed during hyperpnea and loaded breathing. RESULTS: During hyperpnea, breathing frequency, minute ventilation, esophageal and diaphragm pressure-time product per minute, cardiac output, and V˙O2 were higher than during loaded breathing (P < 0.05). Average inspiratory Pes and transdiaphragmatic pressure per breath, scalene (SCA), sternocleidomastoid, and intercostal muscle activation were higher during loading breathing compared with hyperpnea (P < 0.05). Higher transdiaphragmatic pressure during loaded breathing compared with hyperpnea was mostly due to higher inspiratory Pes (P < 0.05). Diaphragm activation, inspiratory and expiratory gastric pressures, and rectus abdominis muscle activation did not differ between the two conditions (P > 0.05). SCA-blood flow index and oxygen delivery index were lower, and SCA-deoxyhemoglobin concentration was higher during loaded breathing compared with hyperpnea. Furthermore, SCA and intercostal muscle StiO2 were lower during loaded breathing compared with hyperpnea (P < 0.05). CONCLUSION: Greater inspiratory muscle effort during loaded breathing evoked larger rib cage and neck muscle activation compared with hyperpnea. In addition, lower SCA and intercostal muscle StiO2 during loaded breathing compared with hyperpnea indicates a mismatch between inspiratory muscle oxygen delivery and utilization induced by the former condition.

Inspiratory muscle training reduces diaphragm activation and dyspnea during exercise in COPD.

Among patients with chronic obstructive pulmonary disease (COPD), those with the lowest maximal inspiratory pressures experience greater breathing discomfort (dyspnea) during exercise. In such individuals, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. Therefore, we aimed to identify physiological mechanisms of improvement in dyspnea and exercise endurance following inspiratory muscle training (IMT) in patients with COPD and low maximal inspiratory pressure (Pimax). The effects of 8 wk of controlled IMT on respiratory muscle function, dyspnea, respiratory mechanics, and diaphragm electromyography (EMGdi) during constant work rate cycle exercise were evaluated in patients with activity-related dyspnea (baseline dyspnea index <9). Subjects were randomized to either IMT or a sham training control group ( n = 10 each). Twenty subjects (FEV1 = 47 ± 19% predicted; Pimax = -59 ± 14 cmH2O; cycle ergometer peak work rate = 47 ± 21% predicted) completed the study; groups had comparable baseline lung function, respiratory muscle strength, activity-related dyspnea, and exercise capacity. IMT, compared with control, was associated with greater increases in inspiratory muscle strength and endurance, with attendant improvements in exertional dyspnea and exercise endurance time (all P < 0.05). After IMT, EMGdi expressed relative to its maximum (EMGdi/EMGdimax) decreased ( P < 0.05) with no significant change in ventilation, tidal inspiratory pressures, breathing pattern, or operating lung volumes during exercise. In conclusion, IMT improved inspiratory muscle strength and endurance in mechanically compromised patients with COPD and low Pimax. The attendant reduction in EMGdi/EMGdimax helped explain the decrease in perceived respiratory discomfort despite sustained high ventilation and intrinsic mechanical loading over a longer exercise duration. NEW & NOTEWORTHY In patients with COPD and low maximal inspiratory pressures, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. This study showed that 8 wk of home-based, partially supervised IMT improved respiratory muscle strength and endurance, dyspnea, and exercise endurance. Dyspnea relief occurred in conjunction with a reduced activation of the diaphragm relative to maximum in the absence of significant changes in ventilation, breathing pattern, and operating lung volumes.