INCREASING PHYSICAL ACTIVITY TO AID SMOKING CESSATION

描述(申请人提供)：建议补充的目的是调查戒烟单独和与有组织的体力活动计划一起对由产生活性氧物种(ROS)引起的大分子氧化的影响。ROS的产生超过了内源性抗氧化防御系统的数量，被称为氧化应激。越来越多的证据表明，氧化应激与许多疾病的发病有关，包括糖尿病、癌症和心血管疾病(CVD)。吸烟会加剧体内ROS的形成，并在体内造成显著的氧化应激。戒烟和有组织的体力活动计划都被独立地报道为抑制ROS的形成，并被建议帮助控制疾病的发生和发展。到目前为止，还没有研究确定这些方法对ROS产生和大分子氧化的联合影响。一项正在进行的临床试验(R01 HL68569)提供了一个独特的机会，可以有效和经济地评估戒烟和体力活动对氧化应激生物标记物的综合影响。具体地说，我们假设戒烟干预结合运动干预将导致氧化应激生物标记物比没有运动辅助的相同戒烟干预更大程度的减弱。因此，我们提出以下具体目标：1.在这项正在进行的临床试验中，对120名参与者进行抽样，在这项试验中，久坐或活动最少的吸烟者被随机分为两个治疗组：要么是经过验证的、成本效益高的戒烟计划+基于社区的运动干预，要么是相同的戒烟计划+接触时间控制健康干预)；以及，2.与基线措施相比，在6个月的随访中确定这两种干预措施抑制氧化应激的有效性。试验的主要依赖变量是血清DNA氧化、血浆脂质过氧化、血浆蛋白质氧化和血浆抗氧化还原能力。这项拟议的研究将首次研究戒烟和定期锻炼对抑制氧化应激的作用。随着大约23%的美国成年人仍然吸烟，以及氧化应激在疾病中的作用越来越被认识到，需要尝试确定旨在抑制吸烟者氧化应激的干预措施。因此，这项研究具有重大的公共卫生效用。

DESCRIPTION (provided by applicant): The purpose of the proposed supplement is to investigate the effects of smoking cessation alone and in conjunction with a program of structured physical activity on macromolecule oxidation caused by the generation of reactive oxygen species (ROS). Production of ROS in quantities that overwhelm the endogenous antioxidant defense system has been referred to as oxidative stress. An increasing body of evidence implicates oxidative stress in the pathogenesis of numerous diseases, including diabetes, cancer, and cardiovascular disease (CVD). Cigarette smoking exacerbates ROS formation and poses a significant oxidant stress in vivo. Both smoking cessation and structured physical activity programs have been independently reported to suppress ROS formation and have been suggested to help control disease onset and progression. To date, no study has determined the combined effect of these methods on ROS production and macromolecule oxidation. An ongoing clinical trial (R01 HL68569) presents a unique opportunity to efficiently and cost-effectively assess the combined effects of smoking cessation and physical activity on oxidative stress biomarkers. Specifically, we hypothesize that a smoking cessation intervention with an adjunctive exercise intervention will result in a greater attenuation in oxidative stress biomarkers than the same smoking cessation intervention without the exercise adjunct. Therefore, we propose the following specific aims: 1. To sample 120 participants in this on-going clinical trial, in which sedentary or minimally active cigarette smokers are randomized to one of two treatment arms: either a validated, cost-effective smoking cessation program plus a community-based exercise intervention, or the same smoking cessation program plus a contact time control wellness intervention); and, 2. To determine the efficacy of these two interventions to suppress oxidative stress at a 6-month follow-up compared to baseline measures. The primary dependent variables of the trial are serum DNA oxidation, plasma lipid peroxidation, plasma protein oxidation, and plasma antioxidant reducing capacity. The proposed investigation will be the first to study the role of smoking cessation and regular exercise to suppress oxidative stress. With approximately 23% of U.S. adults still smoking, and the role of oxidative stress in disease becoming increasingly more recognized, attempts to identify interventions aimed at suppressing oxidative stress in smokers are needed. As such, this study has substantial public health utility.