INCREASING PHYSICAL ACTIVITY TO AID SMOKING CESSATION

描述（由申请人提供）：拟议补充的目的是研究戒烟单独和结合结构化身体活动计划对活性氧（ROS）产生引起的大分子氧化的影响。ROS的大量产生压倒内源性抗氧化防御系统被称为氧化应激。越来越多的证据表明氧化应激与许多疾病的发病机制有关，包括糖尿病、癌症和心血管疾病（CVD）。吸烟加剧ROS的形成，并在体内造成显著的氧化应激。戒烟和有组织的体育锻炼计划都有独立的报道可以抑制ROS的形成，并被认为有助于控制疾病的发生和进展。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综合影响。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育活动对氧化应激生物标志物的综合影响。具体来说，我们假设戒烟干预与辅助运动干预相比，没有运动辅助的戒烟干预会导致氧化应激生物标志物的更大衰减。因此，我们提出以下具体目标：在这项正在进行的临床试验中，对120名参与者进行抽样，其中久坐或最低限度活动的吸烟者随机分为两组：一组是经过验证的、具有成本效益的戒烟计划加社区运动干预，一组是相同的戒烟计划加接触时间控制健康干预)；, 2。在6个月的随访中，与基线测量相比，确定这两种干预措施抑制氧化应激的有效性。试验的主要因变量是血清DNA氧化、血浆脂质过氧化、血浆蛋白氧化和血浆抗氧化还原能力。这项拟议中的调查将首次研究戒烟和定期锻炼对抑制氧化应激的作用。由于大约23%的美国成年人仍在吸烟，并且氧化应激在疾病中的作用越来越被认识到，因此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.