cardiovascular response to training Flashcards
CV system adaptation
acute and chronic
acutely- to increase o2 delivery to working muscles by increasing blood flow to muscles and reducing delivery to low activity tissues
chronically- to deliver more o2 to active muscle mass- more effective o2 delivery during submaximal exercise and increased maximum o2 consumption (vo2 max)
CV factors affecting o2 uptake and vo2 max
- cardiac structure and function
- blood (plasma) volume
- blood flow and distribution
- oxygen extraction (AV difference)
fick equation
VO2= HR xSV x (a-v) diff
a-v= arterio mixed venous
Q= SV xHR
oxygen extraction- avo2 diff
training increases sub maximal and maximal o2 values in muscle
active muscles can utlise o2 more efficiently by increasing oxidative capacity eg higher oxidative enzyme content
can be measured by extracting blood from an artery and a vein while subject is excercising
mass of heart
greater in trained athletes and on average is greater in males
highest seen in college wrestlers and shot putters
cardiac adaptations- power vs endurance
trends show that power athletes (wrestlers and shot putters) have greater mass and size of left ventricle and septum but lower volume of blood in the LV
endurance athletes are the opposite- higher volume of blood in LV but less mass
preload + afterload
pre
amount of blood in ventricle before contraction (EDV), this determines cardiac muscle length before contraction- most important determining factor for preload is venous return
afterload
pressure against which the ventricle must contract (vascular resistance, proportional to arterial mean pressure)
the higher the afterload, less blood will be ejected per heartbeat
frank starling mechanism
based on the length tension relationship within the ventricle- greater stretch= greater contraction (increased SV)
Increased Venous Return → Increased End-Diastolic Volume (EDV) → Increased Preload → Enhanced Stretching of Cardiac Muscle Fibers → Increased Force of Contraction → Increased Stroke Volume
potential mechanisms for heart changes
left ventricular mass= heavier in athletes
LV volume= higher in endurance athletes–> increased preload= increased stroke volume- eccentric hypertrophy
posterior wall thickness and septal thickness- larger in reisstance athletes–> increased afterload- decreased SV= concentric hypertrophy
SV + Q determined
SV- determines by 3 factors= afterload, preload and contractiltity
Q- directly related to venous return and vascular resistance
endurance adaptations- SV
increased preload (ventricular filling)–> increased ventricular dimensions
increased diastolic filling time due to bradycardia (slow HR)
increased contractiltity
increased maximal SV
adaptations- HR
increased SV = decreased HR for the same Q - at submaximal exercise
different HRs for same intensity
maximal HR is unchanged
cardiac output
most significant adaptation is vo2 max
training adaptation at submaximal exercise- Q decreases as increased o2 extraction - due to better muscle oxidative capacity - higher avo2 difference
acute blood flow redistrbution
during heavy exercise Q will increase (~25l/min) and the majority ~70-85% of blood will go to muscle (~20l/min)
at rest Q is ~ 5l/min with blood flow to all major sustems and 15-20% to muscle (~0.75l/min)
acute blood flow regulation
controlled by:
muscle metabolites and temp
dilator substances produced by endothelium (nitric oxide)
pressure changes within the blood vessel
sympathetic activity- reduced blood flow to low activity tissues- related to stress hormone response- adrenaline produced during exercise and receptors can open or close vessels to certain tissues