Rogers Laura Q, Vicari Sandra, Trammell Rita, Hopkins-Price Patricia, Fogleman Amanda, Spenner Allison, Rao Krishna, Courneya Kerry S, Hoelzer Karen S, Robbs Randall, Verhulst Steven
1Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL; 2Department of Psychiatry, SIU School of Medicine, Springfield, IL; 3Department of Internal Medicine, SIU School of Medicine, Springfield, IL; 4Center for Clinical Research, SIU School of Medicine, Springfield, IL; 5Department of Medicine, SIU School of Medicine, Springfield, IL; 6Department of Physical Education and Recreation, University of Alberta, Edmonton, Alberta, CANADA; and 7Department of Hematology Oncology, Springfield Clinic, Sprinfield, IL.
Med Sci Sports Exerc. 2014 Jun;46(6):1077-88. doi: 10.1249/MSS.0000000000000210.
This study aimed to examine mediators of fatigue response to an exercise intervention for breast cancer survivors in a pilot randomized controlled trial.
Postmenopausal breast cancer survivors (n = 46; ≤stage 2), off primary treatment, and reporting fatigue and/or sleep dysfunction were randomized to a 3-month exercise intervention (160 min·wk of moderate-intensity aerobic walking, twice weekly resistance training with resistance bands) or control group. Six discussion group sessions provided behavioral support to improve adherence. Fatigue, serum cytokines, accelerometer physical activity, cardiorespiratory fitness, sleep dysfunction, and psychosocial factors were assessed at baseline and 3 months.
The exercise intervention effect sizes for fatigue were as follows: fatigue intensity d = 0.30 (P = 0.34), interference d = -0.38 (P = 0.22), and general fatigue d = -0.49 (P = 0.13). Using the Freedman-Schatzkin difference-in-coefficients tests, increase in fatigue intensity was significantly mediated by interleukin 6 (IL-6) (82%), IL-10 (94%), IL-6/IL-10 (49%), and tumor necrosis factor-α (TNF-α):IL-10 (78%) with reduced sleep dysfunction increasing the relationship between intervention and fatigue intensity rather than mediating intervention effects (-88%). Decrease in fatigue interference was mediated by sleep dysfunction (35%), whereas IL-10 and pro-anti-inflammatory cytokine ratios increased the relationship between intervention and interference (-25% to -40%). The reduction in general fatigue was significantly mediated by minutes of physical activity (76%), sleep dysfunction (45%), and physical activity enjoyment (40%), with IL-10 (-40%) and IL-6/IL-10 (-11%) increasing the intervention-fatigue relationship. In the intervention group, higher baseline fatigue, anxiety, depression, and perceived exercise barrier interference predicted a greater decline in fatigue interference and/or general fatigue during the intervention.
Biobehavioral factors mediated and enhanced intervention effects on fatigue, whereas psychosocial factors predicted fatigue response. Further study is warranted to confirm our results and to improve understanding of relationships that mediate and strengthen the intervention-fatigue association.
在一项初步随机对照试验中，本研究旨在探讨乳腺癌幸存者运动干预疲劳反应的介导因素。
绝经后乳腺癌幸存者（n = 46；≤2期），已结束主要治疗，且报告有疲劳和/或睡眠功能障碍，被随机分为3个月的运动干预组（每周160分钟中等强度有氧步行，每周两次弹力带抗阻训练）或对照组。六次讨论小组会议提供行为支持以提高依从性。在基线和3个月时评估疲劳、血清细胞因子、加速度计测量的身体活动、心肺适能、睡眠功能障碍和心理社会因素。
运动干预对疲劳的效应量如下：疲劳强度d = 0.30（P = 0.34），干扰d = -0.38（P = 0.22），以及总体疲劳d = -0.49（P = 0.13）。使用弗里德曼-沙茨金系数差异检验，疲劳强度的增加显著由白细胞介素6（IL-6）（82%）、IL-10（94%）、IL-6/IL-10（49%）和肿瘤坏死因子-α（TNF-α）：IL-10（78%）介导，睡眠功能障碍的减轻增加了干预与疲劳强度之间的关系，而非介导干预效果（-88%）。疲劳干扰的减少由睡眠功能障碍介导（35%），而IL-10和促炎/抗炎细胞因子比率增加了干预与干扰之间的关系（-25%至-40%）。总体疲劳的减轻显著由身体活动分钟数（76%）、睡眠功能障碍（45%）和身体活动愉悦感（40%）介导，IL-10（-40%）和IL-6/IL-10（-11%）增加了干预与疲劳之间的关系。在干预组中，更高的基线疲劳、焦虑、抑郁和感知运动障碍干扰预测干预期间疲劳干扰和/或总体疲劳有更大程度的下降。
生物行为因素介导并增强了对疲劳的干预效果，而心理社会因素预测了疲劳反应。有必要进一步研究以证实我们的结果，并增进对介导和加强干预与疲劳关联的关系的理解。
