Their baseline characteristics are presented in Table 1. The thirteen participants had moderate to moderately severe airflow obstruction (Knudson et al 1983) and only two patients were slightly breathless at rest (ie, breathlessness = 1 and 0.5 out of 10). One physiotherapist delivered the interventions Buparlisib chemical structure at the Pulmonary Research Room of the Physical Therapy Department

at Khon Kaen University in Thailand. The therapist had a degree in physiotherapy and three years experience working in the Easy Asthma and COPD Clinic of Srinakharind Hospital. The participants found breathing through conical-PEP during exercise to be acceptable and there were no complications or adverse events. The exercise resulted in heart rates that were approximately GW3965 in vivo 70% of the age-predicted maximum. The following criteria would have been considered unsafe: SpO2 < 88%, PETCO2 > 50 mmHg, or changes > 20% from control values while using conical-PEP. Oxygen saturation (SpO2) was ≥ 92% during exercise, and there was no evidence of hypercapnia or abnormal electrocardiogram. Group data for lung capacity are presented in Table 2 and for cardiorespiratory function in Table 3. Individual data is presented in Table 4 (see eAddenda for Table 4). Inspiratory capacity increased 200 ml (95% CI 0 to 400) more

after the experimental intervention and slow vital capacity increased 200 ml (95% CI 0 to 400) more after the experimental intervention than the control intervention. Participants exercised for 687 s (SD 287) during the experimental intervention compared with 580 s (SD 248) during the control intervention (mean difference 107 s, 95% CI −23 to 238). Participants stopped exercising either because of breathlessness (n Levetiracetam = 6) or

because of leg discomfort (n = 7). The median breathlessness score for all patients was 4 out of 10 (IQR 2.0–5.0) immediately after the experimental intervention, and 4 (IQR 3.0–5.0) after the control intervention. The median leg discomfort was 10 out of 10 (IQR 0–10) immediately after the experimental intervention, and 10 (IQR 0–10) after the control intervention. Change in cardiorespiratory function (heart rate, tidal volume, minute ventilation, PETCO2 or SpO2) from rest to the last 30 s of exercise was not different between the interventions. A longer inspiratory time during the experimental intervention compared with the control intervention (mean difference 0.3 s, 95% CI 0.0 to 0.7) and longer expiratory time (mean difference 0.9 s, 95% CI 0.3 to 1.5) resulted in a slower respiratory rate (mean difference −6.1 breaths/min, 95% CI −10.8 to −1.4). However, this slower respiratory rate did not have any adverse effects on CO2 retention or oxygen saturation. In addition, mouth pressure was 8.5 cmH2O (95% CI 5.9 to 11.2) higher and respiratory flow rate 0.21 L/s (95% CI 0.12 to 0.31) slower during the experimental intervention compared to the control intervention. The I:E ratio went from 1:1.5 to 1:1.