Cardiovascular System

Amount of blood pumped by the left ventricle in 1 minute, measured in l/min Product of stroke volume and heart rate = stroke volume (SE) × beats per minute (HR)

Averages at 90–110 ml/beat

Increase in stroke volume prior to start of exercise period, due to release of hormones (adrenaline & noradrenaline) More blood is pumped out of ventricles Increased venous return, increased myocardial contraction during ventricular systole Increases to maximal values during submaximal work. Doesn’t increase further as work increases towards maximal effort - heart already expanding & contracting to fullest size

2 phases in cycle: relaxation – diastolic 0.5 and contraction – systolic 0.3 secs Diastolic: Right & left atria fill with blood & atrioventricular valves closed (mitral & tricuspid) Rising atrial pressure forces open atrioventricular valves & ventricles begin to fill Semi-lunar valves to aorta & pulmonary arteries closed Systolic SA node initiates impulse causing wave of contraction across atrial myocardium, forcing remaining blood out of atria into ventricles Semi-lunar valves remain closed, atrioventricular valves close after passage of blood Impulse reaches AV node - spreads 2nd contraction through ventricle walls Rising ventricular pressure forces open semi-lunar valves to lungs & systemic arteries (pulmonary artery & aorta) Once blood has left heart &contraction ceases, semi-lunar valves shut

Structural: With exercise heart becomes stronger and bigger, cardiac hypertrophy Increase in RBCs – RBC volume & haemoglobin content is higher in trained athlete, which facilitates the transport of O2 around body Body parts where O2 required may experience growth of new capillaries. Increased vascularisation Functional: Increase in rates of diffusion, moving from area of high pressure to low. Vascular shunting occurs where blood is diverted to skeletal muscle tissue where it’s needed Increase in RBC & haemoglobin levels - higher in trained athletes, which facilitates transport of O2 around body Increased lactate threshold BC LIVID

Muscle cell respiration increases – increased use of glycogen & O2 & increased production of CO2 Fatigue – muscle fatigue = short-term decline in ability of muscle to generate force - result of training or overexertion during exercise HR - increases, to transport oxygenated blood to muscles quicker & return deoxygenated blood to heart & lungs Muscles involved in breathing can themselves utilise up to 10% of total O2 uptake Gaseous exchange rate increases to deliver increased O2 to working muscles & remove CO2 & lactic acid MFHUG

Cardiac hypertrophy = heart muscle becomes larger & stronger - heart pumps a larger volume of blood out per beat, hence stroke volume is greater Enlargement caused by increase in thickness of cardiac muscle in ventricular wall & increase in size of ventricular chamber Can lead to a greater stroke volume, reduced resting heart rate & increased maximum cardiac output Increases RBCs

Increase in stroke volume Increased heart rate Increased cardiac output Redistribution of blood flow to the working muscles

Automatic opening up of blood vessels (arterioles) to active muscle tissue & constriction of blood vessels to non-active tissue as response to increase in exercise Vascular shunting refers to distribution of blood around body During exercise blood is redistributed to muscles – away from organs (stomach, kidneys, liver) where majority of blood is at rest

Vasomotor control diverts blood to skeletal muscle tissue where it’s needed Vasodilation = increase//Vasoconstriction = reduces Vascular shunting aids performance by increasing blood flow to working muscles. O2 facilitates energy production & performer can work for longer

Diastolic blood pressure decreases in trained performers Diastolic blood pressure increases during maximal intensity exercise/in activities involving isometric muscular contractions Age, anxiety/stress, caffeine consumption, medical conditions (obesity, CHD) & environmental factors (heat, humidity) may affect systolic blood pressure