Bloomer Richard J, Fisher-Wellman Kelsey
Cardiorespiratory/Metabolic Laboratory, 161F Elma Neal Roane Field House, The University of Memphis, Memphis, TN 38152, USA.
Nicotine Tob Res. 2009 Jan;11(1):3-11. doi: 10.1093/ntr/ntn005.
Cigarette smoking continues to pose a significant health burden on society. Two well-described mechanistic links associating smoking with morbidity and mortality include elevated blood lipids and increased oxidative stress. These variables have traditionally been measured while an individual is fasting, but evidence suggests that postprandial lipemia and oxidative stress provide more important information concerning susceptibility to disease, in particular cardiovascular disease. Cigarette smokers have elevated levels of biomarkers of oxidative stress at rest and experience impaired postprandial lipid and glucose metabolism. We have confirmed these findings while noting an exaggerated oxidative stress response to high-fat feeding. Smoking cessation is without question the best approach to minimizing smoking-induced ill health and disease, but success rates among those who attempt to quit are dismal. Other means to decrease a smoker's susceptibility to oxidative stress-related disease are needed. We propose that exercise may aid in attenuating postprandial oxidative stress, and we do so in 3 distinct ways. First, exercise stimulates an increase in endogenous antioxidant enzyme activity. Second, exercise improves blood triglyceride clearance via a reduced chylomicron-triglyceride half-life and an enhanced lipoprotein lipase activity. Third, exercise improves blood glucose clearance via an enhanced glucose 4 transport protein translocation and protein content, as well as insulin-insulin receptor binding and postreceptor signaling. Improvements in antioxidant status, as well as lipid and glucose processing, may aid greatly in minimizing feeding-induced oxidative stress in smokers. If so, and in accordance with the recent joint initiative of the American College of Sports Medicine and the American Medical Association, exercise may be viewed as a "medicine" for cigarette smokers at increased risk for postprandial oxidative stress. Research into this area may provide insight into the potential benefits of exercise for this purpose.
吸烟继续给社会带来重大的健康负担。两个已被充分描述的将吸烟与发病率和死亡率联系起来的机制性关联包括血脂升高和氧化应激增加。这些变量传统上是在个体禁食时测量的,但有证据表明,餐后血脂异常和氧化应激能提供更多关于疾病易感性的重要信息,尤其是心血管疾病。吸烟者在静息时氧化应激生物标志物水平升高,并且餐后脂质和葡萄糖代谢受损。我们已经证实了这些发现,同时注意到对高脂饮食的氧化应激反应会加剧。毫无疑问,戒烟是将吸烟所致健康不良和疾病降至最低的最佳方法,但尝试戒烟者的成功率却很低。需要其他方法来降低吸烟者对氧化应激相关疾病的易感性。我们提出运动可能有助于减轻餐后氧化应激,我们将通过三种不同的方式来实现这一点。首先,运动刺激内源性抗氧化酶活性增加。其次,运动通过缩短乳糜微粒 - 甘油三酯半衰期和增强脂蛋白脂肪酶活性来改善血液甘油三酯清除。第三,运动通过增强葡萄糖4转运蛋白的易位和蛋白含量,以及胰岛素 - 胰岛素受体结合和受体后信号传导来改善血糖清除。抗氧化状态以及脂质和葡萄糖处理的改善,可能极大地有助于将吸烟者进食引起的氧化应激降至最低。如果是这样,并且根据美国运动医学学院和美国医学协会最近的联合倡议,运动可被视为对餐后氧化应激风险增加的吸烟者的一种“药物”。对这一领域的研究可能会深入了解运动在此方面的潜在益处。