Laboratory of Respiratory Diseases and Thoracic Surgery, Department of Chronic Diseases and Metabolism, KU Leuven, Leuven, Belgium.
Research Group for Rehabilitation in Internal Disorders, Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium.
J Appl Physiol (1985). 2021 Jul 1;131(1):339-351. doi: 10.1152/japplphysiol.00733.2020. Epub 2021 Jun 3.
Vitamin D deficiency, which is highly prevalent in the general population, exerts similar deleterious effects on skeletal muscles to those induced by cigarette smoking. We examined whether cigarette smoke (CS) exposure and/or vitamin D deficiency impairs the skeletal muscle hypertrophic response to overload. Male C57Bl/6JolaH mice on a normal or vitamin D-deficient diet were exposed to CS or room air for 18 wk. Six weeks after initiation of smoke or air exposure, sham surgery or denervation of the agonists of the left plantaris muscle was performed. The right leg served as internal control. Twelve weeks later, the hypertrophic response was assessed. CS exposure instigated loss of body and muscle mass, and increased lung inflammatory cell infiltration ( < 0.05), independently of diet. Maximal exercise capacity, whole body strength, in situ plantaris muscle force, and key markers of hypertrophic signaling (Akt, 4EBP1, and FoxO1) were not significantly affected by smoking or diet. The increase in plantaris muscle fiber cross-sectional area in response to overload was attenuated in vitamin D-deficient CS-exposed mice (smoking × diet interaction for hypertrophy, = 0.03). In situ fatigue resistance was elevated in hypertrophied plantaris, irrespective of vitamin D deficiency and/or CS exposure. In conclusion, our data show that CS exposure or vitamin D deficiency alone did not attenuate the hypertrophic response of overloaded plantaris muscles, but this hypertrophic response was weakened when both conditions were combined. These data suggest that current smokers who also present with vitamin D deficiency may be less likely to respond to a training program. Plantaris hypertrophy caused by compensatory overload after denervation of the soleus and gastrocnemius muscles showed increased mass and fiber dimensions, but to a lesser extent when vitamin D deficiency was combined with cigarette smoking. Fatigue resistance was elevated in hypertrophied plantaris, irrespective of diet or smoking, whereas physical fitness, hypertrophic markers, and in situ plantaris force were similar. These data showed that the hypertrophic response to overload is attenuated when both conditions are combined.
维生素 D 缺乏在普通人群中非常普遍，它对骨骼肌肉的有害影响与吸烟相似。我们研究了香烟烟雾（CS）暴露和/或维生素 D 缺乏是否会损害骨骼肌肉对超负荷的肥大反应。雄性 C57Bl/6JolaH 小鼠在正常或维生素 D 缺乏饮食下暴露于 CS 或室内空气 18 周。烟雾或空气暴露开始后 6 周，进行假手术或拮抗剂左比目鱼肌的去神经支配。右腿作为内部对照。12 周后，评估肥大反应。CS 暴露引发体重和肌肉质量下降，并增加肺炎症细胞浸润（<0.05），与饮食无关。最大运动能力、全身力量、原位比目鱼肌力量以及肥大信号的关键标志物（Akt、4EBP1 和 FoxO1）不受吸烟或饮食的影响。对超负荷的比目鱼肌纤维横截面积的增加在维生素 D 缺乏的 CS 暴露小鼠中受到抑制（肥大的吸烟×饮食相互作用，=0.03）。无论是否存在维生素 D 缺乏和/或 CS 暴露，原位疲劳抗性在肥大的比目鱼肌中升高。总之，我们的数据表明，CS 暴露或单独的维生素 D 缺乏本身并没有减弱超负荷比目鱼肌的肥大反应，但当两种情况结合时，这种肥大反应会减弱。这些数据表明，目前吸烟且同时存在维生素 D 缺乏的人可能不太可能对训练计划做出反应。在比目鱼肌和腓肠肌去神经支配后，代偿性超负荷引起的比目鱼肌肥大显示出增加的质量和纤维尺寸，但当与吸烟相结合时，程度较小。无论饮食或吸烟如何，肥大的比目鱼肌的疲劳抗性都升高，而身体适应性、肥大标志物和原位比目鱼肌力量相似。这些数据表明，当两种情况结合时，对超负荷的肥大反应会减弱。
