title: Atrial receptors and heart volumes.
abstract: So now we have a view of the circulation in exercise in the upright posture. The output of the heart depends on the input which is driven by the muscle pumps mainly from the lower limbs but augmented by the upper limbs, and the thoracic and abdominal muscles. The heart thus receives an increasing inflow of blood but the heart volumes change comparatively little-only over a very small range of values. Physiologists, in animals and man, have measured changes in cardiac output and heart volumes-it is difficult to be precise about the results but we can agree on order of magnitude. Cardiac output can increase 5, 6 or 7 times in trained athletes but the stroke volume never more than doubles, the end-diastolic volume increases only 50% and the end-systolic volume decreases by about the same amount (16,43). The heart rate increases about 2 1/2 times in the untrained to 5 times in the trained physically fit athlete. It would also seem that the main influence causing an increase in heart size is an increase in venous return mainly caused by the muscle pumps. An increase in activity in sympathetic nerves to the heart muscle forms a mechanism which assists in the control of heart volumes, decreasing end-systolic volume and increasing stroke volume. It is not known what causes this increase in sympathetic activity during exercise but it may just be concomitant with the increase in activity in nerves to the skeletal muscles and originate in a similar area of the brain. There also seems no doubt that as the heart rate increases, with no other concomitant changes, the heart volumes decrease. Thus is may concluded that any increase in heart rate during exercise would limit the increase in the size of the heart which results from the increase in venous return. Next we must consider mechanisms which might affect the two efferent nerves to the heart, the sympathetic and the vagal nerves, these being the final common path of changes in heart rate.
authors.affiliation: Biomedical Sciences Division, University of London, United Kingdom.
authors.forename: R J
authors.initials: RJ
authors.lastname: Linden
mesh_terms: D000818:Animals; D016275:Atrial Function; D002306:Cardiac Volume / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006325:Heart Atria / Q000294:innervation; D006801:Humans; D009411:Nerve Endings / Q000502:physiology*; D012018:Reflex