EXSS2028 Lecture Notes - Lecture 11: Stroke Volume, Pulmonary Circulation, Sympathetic Nervous System
4 Sep 2018
School
Department
Course
Professor
Document Summary
Plateaus at vo2 max (not always observable in all individuals) Heart also works strenuously during exercise = higher blood flow to heart. With increasing power output/vo2 > heart rate increases linearly until it reaches a max. After training, heart rate will decrease > training bradycardia. Sinoatrial node/pacemaker (actual heart rate is lower than sa node discharge) Parasympathetic = decreases heart rate: hormonal control. Noradrenaline secreted at sympathetic nerve ending and adrenal gland. During exercise > not a linear increase. Heart rate not allowing ventricles to fill - slower increase. More volume returning to ventricle = higher stretch = higher contractility = more blood ejected (left ventricle > aorta) (right ventricle > pulmonary circulation) Determinants of sv: increased diastolic filling (increased venous return - muscle pump, valves, greater systolic emptying - due to greater stroke output via catecholamine release (dopamine) Towards higher intensity, lower end systolic volume - ventricles contracting more forcefully and releasing more volume.
