{"title":"The size of the heart.","authors":"R J Linden","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The size of the heart varies very little over a whole range of normal physiological activities. Physiologists, in animals and man, measure changes in cardiac output and heart volumes during exercise. Cardiac output can increase 5, 6, or 7 times in athletes but the stroke volume never more than doubles, the end-diastolic volume increases only by about 50% and the end-systolic (residual) volume decreases by the same amount; the heart rate increases about two and a half times in the untrained to 5 times in the physically fit athlete. It certainly appears as though there are some controlling mechanisms. The best way to consider these potential controlling mechanisms is not to accept the proposition that the heart provides most of the force necessary to propel the blood round the body during these various activities; this only occurs when you are flat on your back with your chest and abdomen open--not a very common occurrence. It is easier to regard the heart as having mechanisms available to it which allow the heart to accept all the blood which is pumped back to it during activity by the muscle pumps. The Frank-Starling mechanism allows an increased force of contraction to follow an increase in volume of each chamber, but from the evidence provided above this is by no means the whole story. It is proposed that changes in heart rate form the basis of the mechanism controlling the heart volumes and its size. Evidence is provided to allow me to postulate that the atrial receptors and the effect on blood volume and the effect on heart rate together form a remarkable control system which controls the size of the heart--and keeps it small.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"5 4","pages":"225-33"},"PeriodicalIF":0.0000,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardioscience","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The size of the heart varies very little over a whole range of normal physiological activities. Physiologists, in animals and man, measure changes in cardiac output and heart volumes during exercise. Cardiac output can increase 5, 6, or 7 times in athletes but the stroke volume never more than doubles, the end-diastolic volume increases only by about 50% and the end-systolic (residual) volume decreases by the same amount; the heart rate increases about two and a half times in the untrained to 5 times in the physically fit athlete. It certainly appears as though there are some controlling mechanisms. The best way to consider these potential controlling mechanisms is not to accept the proposition that the heart provides most of the force necessary to propel the blood round the body during these various activities; this only occurs when you are flat on your back with your chest and abdomen open--not a very common occurrence. It is easier to regard the heart as having mechanisms available to it which allow the heart to accept all the blood which is pumped back to it during activity by the muscle pumps. The Frank-Starling mechanism allows an increased force of contraction to follow an increase in volume of each chamber, but from the evidence provided above this is by no means the whole story. It is proposed that changes in heart rate form the basis of the mechanism controlling the heart volumes and its size. Evidence is provided to allow me to postulate that the atrial receptors and the effect on blood volume and the effect on heart rate together form a remarkable control system which controls the size of the heart--and keeps it small.