Sleep medicine · 2025
The impact of exercise training on the obstructive sleep apnea endotypes.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Beatty Caroline J, Landry Shane A, Mann Dwayne L, Joosten Simon A, Collet Jinny, Ferreira-Silva Rosyvaldo, Ueno-Pardi Linda M, Genta Pedro R, Hamilton Garun S, Edwards Bradley A
Аннотация
RATIONALE: Weight-loss interventions such as exercise are often recommended to manage obstructive sleep apnea (OSA). Interestingly, exercise can modestly improve OSA severity even without significant changes in body weight. However, the mechanisms underlying the improvements in OSA severity, separate from those observed with weight loss, are currently unknown. We aimed to assess how exercise affects the OSA endotypes (upper-airway collapsibility, loop gain, arousal threshold and upper-airway muscle compensation) and identify individuals most likely to benefit.
METHODS: We retrospectively analyzed data from participants with OSA (mean age = 52.8 ± 7.0 years) who underwent a 6-month exercise intervention (n = 22). OSA endotypes were calculated from routine polysomnographic recordings before and following the intervention. Paired t-tests were used to compare the OSA endotypes before and after the exercise intervention. Regression analysis was used to assess whether the baseline OSA endotype(s) predict change in OSA severity.
RESULTS: Following exercise training, there was an improvement in the apnea-hypopnea index (AHI; 37.2[17.1, 57.4] to 27.9[15.9, 48.8] events/hr, p = 0.046) but no significant change in body weight. Overall, there was no change in OSA endotypes; however, improvements in AHI were associated with improvements in muscle compensation (r2 = 0.332, p = 0.006) and reductions in the arousal threshold (r2 = 0.256, p = 0.023). Furthermore, poor muscle compensation (r2 = 0.462, p = 0.001) and a high arousal threshold (r2 = 0.397, p = 0.004) at baseline predicted greater reductions in OSA severity.
CONCLUSION: Exercise may improve OSA by strengthening the upper airway muscles. As such, regular exercise may be helpful to improve OSA in those with poor upper airway muscle function (and a high arousal threshold).
METHODS: We retrospectively analyzed data from participants with OSA (mean age = 52.8 ± 7.0 years) who underwent a 6-month exercise intervention (n = 22). OSA endotypes were calculated from routine polysomnographic recordings before and following the intervention. Paired t-tests were used to compare the OSA endotypes before and after the exercise intervention. Regression analysis was used to assess whether the baseline OSA endotype(s) predict change in OSA severity.
RESULTS: Following exercise training, there was an improvement in the apnea-hypopnea index (AHI; 37.2[17.1, 57.4] to 27.9[15.9, 48.8] events/hr, p = 0.046) but no significant change in body weight. Overall, there was no change in OSA endotypes; however, improvements in AHI were associated with improvements in muscle compensation (r2 = 0.332, p = 0.006) and reductions in the arousal threshold (r2 = 0.256, p = 0.023). Furthermore, poor muscle compensation (r2 = 0.462, p = 0.001) and a high arousal threshold (r2 = 0.397, p = 0.004) at baseline predicted greater reductions in OSA severity.
CONCLUSION: Exercise may improve OSA by strengthening the upper airway muscles. As such, regular exercise may be helpful to improve OSA in those with poor upper airway muscle function (and a high arousal threshold).