Validation of the Slovene Version of the Stop-Bang Questionnaire in a Primary Practice Setting.

Aim: The aim of our study was to validate the Slovene translation of the STOP-BANG (SBQ) questionnaire for use in the primary practice setting. Methods: We recruited 158 randomly selected visitors at four primary practice clinics who came to the practice for any reason. Participants completed the Slovene SBQ and underwent type 3 respiratory polygraphy, which was analysed by an experienced somnologist. The SBQ was previously translated in to Slovene and validated for the sleep clinic. Results: Of 158 participants, 153 had valid recordings. The mean age of the participants was 49.5 years (±13.0 years), and 47.7% were male. OSA was identified in 49.0% of the participants. The questionnaire, with a cutoff of ≥3, demonstrated an area under the curve of 0.823 for any OSA (REI≥5), 0.819 for moderate and severe OSA (REI≥15) and 0.847 for severe OSA (REI≥30). Sensitivity was 65.3%, 81.8%, and 90.0%, and specificity was 87.2%, 73.3% and 65.0% for any, moderate to severe and severe OSA, respectively. Conclusions: The Slovene translation of the SBQ is a reliable instrument for OSA risk stratification in the primary practice setting.

Translation and validation of the STOP-Bang questionnaire into Slovene.

PURPOSE: To translate, culturally adapt and evaluate the Slovene version of the STOP-Bang questionnaire (SBQ) for use in the sleep clinic. METHODS: Standard forward-backward translation and harmonisation of the Slovene translation of the SBQ were performed. Test-retest reliability was performed on a sample of healthy subjects. A cross-sectional study was performed with patients referred for a sleep study. Patients filled out the Slovene translation of the SBQ before undergoing sleep study. RESULTS: The validation group consisted of 256 patients, of which 237 (92.6%) were included. Mean age was 52.5 ± 14.6, 63.3% of patients were male. Obstructive sleep apnoea (OSA) (apnoea-hypopnea index (AHI) ≥ 5) was present in 69.6% of patients, of whom 22.4% had mild (AHI ≥ 5 and < 15), 21.9% moderate (AHI ≥ 15 and < 30), and 25.3% severe (AHI ≥ 30) OSA. A SBQ score of 3 had a sensitivity of 92.1 (86.9-95.7), specificity of 44.4 (32.7-56.6), PPV of 79.2 (75.5-82.4) and AUC of 0.757 (95% CI 0.692-0.823; p < 0.001) for all OSA (AHI ≥ 5). Each increase in the SBQ score was associated with an increase in the probability of OSA. CONCLUSION: This study shows that the Slovene version of the SBQ is a valid tool for evaluating the risk of OSA in a sleep clinic.

Exercise during Short-Term and Long-Term Continuous Exposure to Hypoxia Exacerbates Sleep-Related Periodic Breathing.

STUDY OBJECTIVES: Exposure to hypoxia elevates chemosensitivity, which can lead to periodic breathing. Exercise impacts gas exchange, altering chemosensitivity; however, interactions between sleep, exercise and chronic hypoxic exposure have not been examined. This study investigated whether exercise exacerbates sleep-related periodic breathing in hypoxia. METHODS: Two experimental phases. Short-Term Phase: a laboratory controlled, group-design study in which 16 active, healthy men (age: 25 ± 3 y, height: 1.79 ± 0.06 m, mass: 74 ± 8 kg) were confined to a normobaric hypoxic environment (FIO2 = 0.139 ± 0.003, 4,000 m) for 10 days, after random assignment to a sedentary (control, CON) or cycle-exercise group (EX). Long-Term Phase: conducted at the Concordia Antarctic Research Station (3,800 m equivalent at the Equator) where 14 men (age: 36 ± 9 y, height: 1.77 ± 0.09 m, mass: 75 ± 10 kg) lived for 12-14 months, continuously confined. Participants were stratified post hoc based on self-reported physical activity levels. We quantified apnea-hypopnea index (AHI) and physical activity variables. RESULTS: Short-Term Phase: mean AHI scores were significantly elevated in the EX group compared to CON (Night1 = CON: 39 ± 51, EX: 91 ± 59; Night10 = CON: 32 ± 32, EX: 92 ± 48; P = 0.046). Long-Term Phase: AHI was correlated to mean exercise time (R(2) = 0.4857; P = 0.008) and the coefficient of variation in night oxyhemoglobin saturation (SpO2; R(2) = 0.3062; P = 0.049). CONCLUSIONS: Data indicate that exercise (physical activity) per se affects night SpO2 concentrations and AHI after a minimum of two bouts of moderate-intensity hypoxic exercise, while habitual physical activity in hypobaric hypoxic confinement affects breathing during sleep, up to 13+ months' duration.

Effect of exercise on night periodic breathing and loop gain during hypoxic confinement.

BACKGROUND AND OBJECTIVE: Hypoxic exercise exacerbates periodic breathing in otherwise healthy, awake humans. Interactions between sleep, exercise and hypoxic exposure have not been fully elucidated. METHODS: Fourteen men were confined 10 days to a simulated altitude of 4175 m (FIO2 = 0.139; PIO2 = 88 mm Hg). They were randomly assigned to an exercise intervention of 2 × 60-min cycle exercise/day at 50% of their hypoxia-specific peak power output (exercise, n = 8), or they completed no exercise (control, n = 6, random order). Sleep and breathing were objectively assessed via full polysomnography on night 1, after 14-h acute exposure (N1), and again on night 10 (N10). RESULTS: The exercise group spent more time in light sleep than control on N10 (95% confidence interval (CI): 8.5-15.0%; P = 0.013) and experienced more stage shifts (CI: 13-44; P = 0.023) on both nights compared with control. The exercise group experienced more apnoea-hypopnoea (AH) events per hour compared with control (CI: 1-110; P = 0.046); AH events that were associated with night desaturations were also higher on N1 (exercise: 397 ± 320, control: 124 ± 205, P = 0.047) and N10 (exercise: 375 ± 229, control: 110 ± 138, P = 0.028, CI: 49-489 total events; P = 0.020). The length of hyperpnoea was increased from 12.8 ± 2.2 s on N1 to 14.6 ± 2.7 s on N10 (P = 0.008), and thus, total cycle length also increased (P = 0.002) in both cohorts. Mean pooled duty ratios were 0.68 ± 0.02 on N1 and 0.69 ± 0.02 on N10 (group effect P = 0.617). CONCLUSION: Daily, moderate-intensity exercise in normobaric hypoxia equivalent to 4175 m exacerbated AH events, and negatively affected sleep architecture in exercisers compared with matched controls.