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Updated: Aug 4, 2026

An Isolated Working Heart System for Large Animal Models
Published on: June 11, 2014
The size of the heart
1Biomedical Sciences Division, King's College London, University of London, UK.
Insights
Heart size remains remarkably stable during physiological activities. Changes in heart rate, influenced by atrial receptors and blood volume, are proposed as the primary mechanism controlling heart size, not just the Frank-Starling mechanism.
Area of Science:
- Cardiology
- Physiology
Background:
- Heart size shows minimal variation across normal physiological activities.
- Cardiac output increases significantly during exercise, but stroke volume and chamber volumes change less dramatically.
Purpose of the Study:
- To investigate the controlling mechanisms behind heart volume regulation during physiological activities.
- To propose a novel hypothesis for heart size control beyond the Frank-Starling mechanism.
Main Methods:
- Analysis of physiological data on cardiac output, heart rate, stroke volume, and end-diastolic/end-systolic volumes during exercise.
- Consideration of the role of muscle pumps and venous return in cardiac filling.
- Evaluation of the Frank-Starling mechanism and atrial receptor influence.
Main Results:
- Cardiac output can increase severalfold during exercise, while stroke volume and end-diastolic volume increase by approximately 50% and end-systolic volume decreases similarly.
- Heart rate increases significantly, especially in trained athletes.
- The Frank-Starling mechanism alone does not fully explain the observed changes in heart volume.
Conclusions:
- Heart rate changes, modulated by atrial receptors and blood volume, are postulated as the key mechanism controlling heart size.
- This regulatory system ensures the heart maintains a small, efficient size despite varying physiological demands.
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.
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