The size of the heart varies very little over a whole range of normal
physiological activities. Physiologists, in animals and man, measure c
hanges in cardiac output and heart volumes during exercise. Cardiac ou
tput can increase 5, 6, or 7 times in athletes but the stroke volume n
ever more than doubles, the end-diastolic volume increases only by abo
ut 50% and the end-systolic (residual) volume decreases by the same am
ount; the heart rate increases about two and a half times in the untra
ined to 5 times in the physically fit athlete. It certainly appears as
though there are some controlling mechanisms. The best way to conside
r these potential controlling mechanisms is not to accept the proposit
ion 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 me
chanisms 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 F
rank-Starling mechanism allows an increased force of contraction to fo
llow an increase in volume of each chamber, but from the evidence prov
ided above this is by no means the whole story. It is proposed that ch
anges in heart rate form the basis of the mechanism controlling the he
art volumes and its size. Evidence is provided to allow me to postulat
e that the atrial receptors and the effect on blood volume and the eff
ect on heart rate together form a remarkable control system which cont
rols the size of the heart-and keeps it small.