Rogers Laura Q, Fogleman Amanda, Trammell Rita, Hopkins-Price Patricia, Spenner Allison, Vicari Sandra, Rao Krishna, Courneya Kerry S, Hoelzer Karen, Robbs Randall, Verhulst Steven
University of Alabama at Birmingham, Birmingham, AL, USA.
Psychooncology. 2015 Mar;24(3):302-10. doi: 10.1002/pon.3594. Epub 2014 Jun 11.
To improve mechanistic understanding, this pilot randomized controlled trial examined mediators of an exercise intervention effects on sleep in breast cancer survivors (BCS).
Forty-six postmenopausal BCS (≤Stage II, off primary treatment) were randomized to a 3-month exercise intervention or control group. Intervention included 160 min/week of moderate intensity aerobic walking, twice weekly resistance training (resistance bands), and six discussion groups (to improve adherence). Blinded assessments at baseline and post-intervention included sleep disturbance (PSQI and PROMIS®), objective sleep quality (accelerometer), serum cytokines, accelerometer physical activity, cardiorespiratory fitness, body composition, fatigue, and psychosocial factors. Mediation was tested using Freedman-Schatzkin difference-in-coefficients tests.
When compared with control, the intervention group demonstrated a significant increase in PSQI sleep duration (i.e., fewer hours of sleep/night) (d = 0.73, p = .03). Medium to large but non-significant standardized effect sizes were noted for PSQI daytime somnolence (d = -0.63, p = .05) and accelerometer latency (d = -0.49, p = .14). No statistically significant mediators were detected for PSQI sleep duration score or accelerometer latency. Daytime somnolence was mediated by tumor necrosis factor-alpha (mediated 23% of intervention effect, p < .05), interleukin (IL)-6:IL-10 (16%, p < .01), IL-8:IL-10 (26%, p < .01), and fatigue (38%, p < .05). Mediating or enhancing relationships for several of the sleep outcomes were noted for accelerometer physical activity, PROMIS® fatigue, exercise social support, and/or physical activity enjoyment.
Inflammation and psychosocial factors may mediate or enhance sleep response to our exercise intervention. Further study is warranted to confirm our results and translate our findings into more effective interventions aimed at improving sleep quality in BCS.
为了加深对作用机制的理解，这项初步随机对照试验研究了运动干预对乳腺癌幸存者（BCS）睡眠影响的中介因素。
46名绝经后BCS（≤II期，未接受主要治疗）被随机分为3个月运动干预组或对照组。干预措施包括每周160分钟的中等强度有氧步行、每周两次的阻力训练（弹力带）以及六个讨论组（以提高依从性）。在基线和干预后进行的盲法评估包括睡眠障碍（匹兹堡睡眠质量指数[PSQI]和患者报告结果测量信息系统[PROMIS®]）、客观睡眠质量（加速度计）、血清细胞因子、加速度计身体活动、心肺适能、身体成分、疲劳和心理社会因素。使用弗里德曼 - 沙茨金系数差异检验来检验中介作用。
与对照组相比，干预组的PSQI睡眠时间显著增加（即每晚睡眠时间减少）（d = 0.73，p = 0.03）。PSQI日间嗜睡（d = -0.63，p = 0.05）和加速度计入睡潜伏期（d = -0.49）的标准化效应量为中等至大，但无统计学意义（p = 0.14）。未检测到PSQI睡眠时间得分或加速度计入睡潜伏期的统计学显著中介因素。日间嗜睡由肿瘤坏死因子 - α介导（介导干预效应的23%，p < 0.05）、白细胞介素（IL）-6:IL-10（16%，p < 0.01）、IL-8:IL-10（26%，p < 0.01）和疲劳（38%，p < 0.05）。对于加速度计身体活动、PROMIS®疲劳、运动社会支持和/或身体活动乐趣，发现了与几种睡眠结果的中介或增强关系。
炎症和心理社会因素可能介导或增强对我们运动干预的睡眠反应。有必要进行进一步研究以证实我们的结果，并将我们的发现转化为更有效的干预措施，旨在改善BCS的睡眠质量。
