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Konstantinos Bitos,1 Tobias Kuehne,1 Tsogyal D Latshang,1 Sayaka S Aeschbacher,1 Fabienne Huber,1 Deborah Flueck,1 Elisabeth D Hasler,1 Philipp M Scheiwiller,1 Mona Lichtblau,1 Silvia Ulrich,1 Konrad E Bloch,1 Michael Furian1,2 1University Hospital Zurich, Department of Respiratory Medicine, Zurich, Switzerland; 2Swiss University of Traditional Chinese Medicine, Research Department, Bad Zurzach, SwitzerlandCorrespondence: Michael Furian, University Hospital Zurich, Department of Pulmonology, Raemistrasse 100, Zurich, 8092, Switzerland, Email michael.furian@usz.chBackground: Amongst the millions of travelers to high altitude worldwide are many with chronic obstructive pulmonary disease (COPD), but data regarding the effects of acute exposure to altitude on exercise performance are limited. The current study investigated how acute exposure to moderate altitude influences exercise performance in COPD patients, providing novel insights to the underlying physiological mechanisms.Methods: Twenty-nine COPD patients, GOLD grade 2– 3, median (quartile) forced expiratory volume in 1 second (FEV1) of 60% predicted (46; 69) performed cycling incremental ramp exercise test (IET) at 490 m and after acute exposure of 2– 6 hours to 2048 m or vice versa, according to a randomized cross-over design. Exercise performance and breath-by-breath analyses of the last 30 seconds of each IET were compared between locations.Results: At 2048 m compared to 490 m, the maximum power output (Wmax) was 77 watts (62;104) vs 88 watts (75;112), median reduction 5 watts (95% CI, 2 to 8, P< 0.05), corresponding to a median reduction of 6% (95% CI, 2 to 11, P< 0.05) compared to 490 m. The peak oxygen uptake (V’O2peak) was 70% predicted (56;86) at 2048 m vs 79% predicted (63;90) at 490 m, median reduction of 6% (95% CI, 3 to 9, P< 0.05). The oxygen saturation by pulse oximetry (SpO2) at 2048 m was reduced by 8% (95% CI, 4 to 9, P< 0.05) compared to 490 m. The minute ventilation (V’E) increased by 2.8L/min (95% CI, 0.9 to 4.2, P< 0.05) at 2048 m. The maximum heart rate and the subjective sense of dyspnea and leg fatigue did not change.Conclusion: Lowlanders with moderate-to-severe COPD acutely exposed to 2048 m reveal small but significant reduction in cycling IET along with a reduced V’O2peak. As dyspnea perception and maximal heart rate were unchanged, the lower blood oxygenation and exaggerated ventilatory response were culprit factors for the reduced performance.Keywords: COPD, exercise, high altitude, hypoxia, hypoxemia, cardiopulmonary exercise testing

Martina Meszaros,1 Tsogyal D Latshang,1 Sayaka S Aeschbacher,1 Fabienne Huber,1 Deborah Flueck,1 Mona Lichtblau,1 Stefanie Ulrich,1 Elisabeth D Hasler,1 Philipp M Scheiwiller,1 Lukas Reinhard,1 Silvia Ulrich,1,2 Konrad E Bloch,1– 3 Michael Furian,1 Esther I Schwarz1,3 1Department of Pulmonology and Sleep Disorders Centre, University Hospital Zurich, Zurich, Switzerland; 2Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland; 3Centre of Competence Sleep & Health, University of Zurich, Zurich, SwitzerlandCorrespondence: Esther I SchwarzDepartment of Pulmonology and Sleep Disorders Centre, University Hospital Zurich, Zurich, SwitzerlandTel +41 44 255 11 11Fax +41 44 255 44 51Email estherirene.schwarz@usz.chPurpose: Patients with chronic obstructive pulmonary disease (COPD) are particularly vulnerable to hypoxia-induced autonomic dysregulation. Hypoxemia is marked during sleep. In COPD, altitude exposure is associated with an increase in blood pressure (BP) and a decrease in baroreflex-sensitivity (BRS). Whether nocturnal oxygen therapy (NOT) may mitigate these cardiovascular autonomic changes in COPD at altitude is unknown.Materials and Methods: In a randomized placebo-controlled cross-over trial, 32 patients with moderate-to-severe COPD living < 800 m were subsequently allocated to NOT and placebo during acute exposure to altitude. Measurements were done at low altitude at 490 m and during two stays at 2048 m on NOT (3 L/min) and placebo (3 L/min, ambient air) via nasal cannula. Allocation and intervention sequences were randomized. Outcomes of interest were BP, BRS (from beat-to-beat BP measurement), BP variability (BPV), and heart rate.Results: About 23/32 patients finished the trial per protocol (mean (SD) age 66 (5) y, FEV1 62 (14) % predicted) and 9/32 experienced altitude-related illnesses (8 vs 1, p < 0.05 placebo vs NOT). NOT significantly mitigated the altitude-induced increase in systolic BP compared to placebo (Δ median − 5.8 [95% CI − 22.2 to − 1.4] mmHg, p = 0.05) but not diastolic BP (− 3.5 [95% CI − 12.6 to 3.0] mmHg; p = 0.21) or BPV. BRS at altitude was significantly higher in NOT than in placebo (1.7 [95% CI 0.3 to 3.4] ms/mmHg, p = 0.02).Conclusion: NOT may protect from hypoxia-induced autonomic dysregulation upon altitude exposure in COPD and thus protect from a relevant increase in BP and decrease in BRS. NOT may provide cardiovascular benefits in COPD during conditions of increased hypoxemia and may be considered in COPD travelling to altitude.Keywords: COPD, altitude, oxygen, hypoxia, blood pressure, blood pressure variability, baroreflex sensitivity

Background: Asthma rehabilitation at high altitude is common. Little is known about the acute and subacute cardiopulmonary acclimatization to high altitude in middle-aged asthmatics without other comorbidities. Methods: In this prospective study in lowlander subjects with mostly mild asthma who revealed an asthma control questionnaire score >0.75 and participated in a three-week rehabilitation program, we assessed systolic pulmonary artery pressure (sPAP), cardiac function, and extravascular lung water (EVLW) at 760 m (baseline) by Doppler-echocardiography and on the second (acute) and last day (subacute) at a high altitude clinic in Kyrgyzstan (3100 m). Results: The study included 22 patients (eight male) with a mean age of 44.3 ± 12.4 years, body mass index of 25.8 ± 4.7 kg/m², a forced expiratory volume in 1 s of 92% ± 19% predicted (post-bronchodilator), and partially uncontrolled asthma. sPAP increased from 21.8 mmHg by mean difference by 7.5 [95% confidence interval 3.9 to 10.5] mmHg (p < 0.001) during acute exposure and by 4.8 [1.0 to 8.6] mmHg (p = 0.014) during subacute exposure. The right-ventricular-to-pulmonary-artery coupling expressed by TAPSE/sPAP decreased from 1.1 by -0.2 [-0.3 to -0.1] mm/mmHg (p < 0.001) during acute exposure and by -0.2 [-0.3 to -0.1] mm/mmHg (p = 0.002) during subacute exposure, accordingly. EVLW significantly increased from baseline (1.3 ± 1.8) to acute hypoxia (5.5 ± 3.5, p < 0.001) but showed no difference after 3 weeks (2.0 ± 1.8). Conclusion: In otherwise healthy asthmatics, acute exposure to hypoxia at high altitude increases pulmonary artery pressure (PAP) and EVLW. During subacute exposure, PAP remains increased, but EVLW returns to baseline values, suggesting compensatory mechanisms that contribute to EVLW homeostasis during acclimatization. [ABSTRACT FROM AUTHOR]

Background: Asthma rehabilitation at high altitude is common. Little is known about the acute and subacute cardiopulmonary acclimatization to high altitude in middle-aged asthmatics without other comorbidities. Methods: In this prospective study in lowlander subjects with mostly mild asthma who revealed an asthma control questionnaire score >0.75 and participated in a three-week rehabilitation program, we assessed systolic pulmonary artery pressure (sPAP), cardiac function, and extravascular lung water (EVLW) at 760 m (baseline) by Doppler-echocardiography and on the second (acute) and last day (subacute) at a high altitude clinic in Kyrgyzstan (3100 m). Results: The study included 22 patients (eight male) with a mean age of 44.3 ± 12.4 years, body mass index of 25.8 ± 4.7 kg/m2, a forced expiratory volume in 1 s of 92% ± 19% predicted (post-bronchodilator), and partially uncontrolled asthma. sPAP increased from 21.8 mmHg by mean difference by 7.5 [95% confidence interval 3.9 to 10.5] mmHg (p < 0.001) during acute exposure and by 4.8 [1.0 to 8.6] mmHg (p = 0.014) during subacute exposure. The right-ventricular-topulmonary-artery coupling expressed by TAPSE/sPAP decreased from 1.1 by −0.2 [−0.3 to −0.1] mm/mmHg (p < 0.001) during acute exposure and by −0.2 [−0.3 to −0.1] mm/mmHg (p = 0.002) during subacute exposure, accordingly. EVLW significantly increased from baseline (1.3 ± 1.8) to acute hypoxia (5.5 ± 3.5, p < 0.001) but showed no difference after 3 weeks (2.0 ± 1.8). Conclusion: In otherwise healthy asthmatics, acute exposure to hypoxia at high altitude increases pulmonary artery pressure (PAP) and EVLW. During subacute exposure, PAP remains increased, but EVLW returns to baseline values, suggesting compensatory mechanisms that contribute to EVLW homeostasis during acclimatization. [ABSTRACT FROM AUTHOR]