Leon A S
Med Clin North Am. 1985 Jan;69(1):3-20. doi: 10.1016/s0025-7125(16)31055-0.
Coronary heart disease, the primary health problem in western life, is caused by the interaction of multiple factors. Absolute proof of the contributing role of physical inactivity is not possible owing to the complexity of the CHD problem and the infeasibility of a definitive clinical trial because of logistical and economic constraints. Despite limitations, existing epidemiologic studies strongly suggest, but fall short of proving, the concept that habitual physical exercise offers partial protection against primary or secondary events of CHD and associated mortality. However, experimental data support this hypothesis and provide evidence of possible mechanisms responsible for the protection. The available epidemiologic data also suggest that physical inactivity is probably not as potent an individual risk factor as elevated serum cholesterol levels, hypertension, and cigarette smoking, and that the protective effects of exercise may be overwhelmed by high levels of these major risk factors. On the other hand, there is some evidence that exercise may attenuate other risk factors both directly and through associated weight reduction. Epidemiologic studies also suggest a dose response relationship between physical activity and rates of CHD. About 2000 kcal per week of moderate intensity, dynamic, endurance-type of exercise (such as walking or jogging about 20 miles per week) or at least one hour of intermittent hard physical labor are required to obtain the optimal effect of exercise on coronary heart disease rates. Experimental studies suggest that this amount of exercise should provide sufficient stimulus to favorably alter blood HDL cholesterol levels and perhaps other CHD risk factors, especially if there is an accompanying reduction in weight. Possible mechanisms for the protective effects of exercise against CHD are illustrated in Figure 1. Insistence on final experimental proof prior to prudent medical practice or public health policy on physical inactivity or other coronary risk factors indicates a lack of understanding of the nature of scientific proof and evidence required for health actions.(ABSTRACT TRUNCATED AT 400 WORDS)
冠心病是西方社会的主要健康问题，它由多种因素相互作用引起。由于冠心病问题的复杂性以及由于后勤和经济限制而无法进行确定性临床试验，因此不可能绝对证明缺乏体育活动的促成作用。尽管存在局限性，但现有的流行病学研究强烈表明（但未证明）这样一个概念，即习惯性体育锻炼对冠心病的原发性或继发性事件及相关死亡率提供部分保护。然而，实验数据支持这一假设，并提供了可能的保护机制的证据。现有的流行病学数据还表明，缺乏体育活动可能不像血清胆固醇水平升高、高血压和吸烟那样是一个强大的个体危险因素，而且运动的保护作用可能会被这些主要危险因素的高水平所抵消。另一方面，有证据表明运动可能直接或通过相关的体重减轻来减轻其他危险因素。流行病学研究还表明体育活动与冠心病发病率之间存在剂量反应关系。为了获得运动对冠心病发病率的最佳效果，每周需要约2000千卡的中等强度、动态、耐力型运动（如每周步行或慢跑约20英里）或至少一小时的间歇性高强度体力劳动。实验研究表明，这个运动量应能提供足够的刺激，以有利地改变血液中高密度脂蛋白胆固醇水平以及可能的其他冠心病危险因素，特别是如果同时体重有所减轻。运动对冠心病保护作用的可能机制如图1所示。在针对缺乏体育活动或其他冠心病危险因素制定谨慎的医疗实践或公共卫生政策之前，坚持要求最终的实验证据，表明对健康行动所需的科学证据的性质缺乏理解。（摘要截短为400字）
