Cardiac changes Flashcards
who should be excluced from the exercise part
Unstable angina Resting SBP>200mmHg or DBP >110mmHg Uncontrolled tachycardia >120b.min-1 Significant resting ST segment depression Uncontrolled atrial or ventricular arrhythmias Aortic stenosis Febrile illness Recent embolism Uncompensated congestive heart failure
why does SV increase in healthy individuals following areobic training
↑ contractile function
↑ LV chamber volume (eccentric)
↑ LV muscle mass (concentric)
↑ in plasma volume
why does contractile function increase
• ↑ calcium handling proteins in cell wall and SR
why does LV chamber volume increase
Myocyte elongation as sarcomeres added in series: occurs after 5 weeks
why does LV muscle mass increase
More myocytes added in parallel (hypertrophy)
why does plasma volume increase
10% PV expansion may occur in just 10 days
la place’s law
T = ( P * R ) / M
• Where T is the tension in the walls • P is the pressure difference across the wall • R is the radius of the cylinder • M is the thickness of the wall
To keep wall tension the same, the radius and the wall thickness must be proportional
what alters myocradial oxygen consumption
tennison development
myocardial contractility
heart rate
- wall tension is an imporatant determinant of MVO2
what causes growth
NE and Epinephrine Renin-angiotensin-aldosterone GH and IGF Thyroid hormones mechanical stress
effect of NE and Epinephrine
Growth
stimulation of alpha and beta receptors in the myocardium cause cardiac growth
effect of Renin-angiotensin-aldosterone
Growth
– ↑ SNS activity reduces renal blood flow during exercise, ↑ renin release, thus ↑ RAA levels
– ↑ RAA levels stimulate cardiac myocytes to hypertrophy
effect of GH and IGF:
Growth
Cardiac myocytes have receptors for both GH and IGF
– Stretching of heart muscle is trigger for these hormones to activate gene expression
– IGF increases myofilament sensitivity to Ca++ thus ↑ contractile forc
what is the effect of thyroid hormones
Growth
Exercise stimulates TSH, thus thyroxin production
Thyroxin causes myocyte hypertrophy
effect of mechanical stress
Pressure overload = ↑ resistance = hypertrophy through ↑ cross sectional area (Concentric)
↑ volume overload = hypertrophy through ↑ myocyte lengthening (Eccentric)
Mechano-sensors in myocyte activated by stress:
– Surface receptors (integrins) and stretch activated ion channels ↑ CA++ influx → activate protein kinase pathways → hypertrophy
Physiological adapltaions to areobic training in healthy individuals
imporved contractility
Angiogensis
effect of imporved contracitility
Improved % shortening, time to peak shortening, relaxation time – ↑ calcium binding sites in myocytes – ↑ Na+ - Ca++ exchanger pumps speed removal of Ca back into SR – ↑ Ca stored in SR = more Ca = more contractile force – ↑ Ca sensitivity of myofilaments • Increased ATPase expression
effect of Angiogensis
Myocyte hypertrophy comes with angiogensis to increase blood flow • Increased arterial size to be equal or greater than increase in cardiac mass (over adaptation!) • Increased capillarisation
adaptaions to areobic training cardiovascular
Stroke volume
↑ Stroke volume 0 - 18% – ↑ blood volume 6-10% – Myocardial hypertrophy – Improved contractile force - ↓ ESV – ↑ ejection fraction
adaptaions to areobic training cardiovascular
parasympathetic tone
increased parasympathetic tone
• ↑ Heart rate variability
• Slower heart rate, thus more filling time
adaptaions to areobic training cardiovascular
↑ SV ↑ parasympathetic tone ↑ coronary collaterals ↑ in cardiac capillary and arteriole blood flow ↓ blood viscosity ↓ endothelial dysfunction
why does endothelial dysfunction reduce
Improved NO production promotes vasodilation
• Improved production of superoxide dismutase which mops up Reactive Oxygen Species (ROS stops NO working)
adaptaions to areobic training cardiovascular during exercise
↑ in max SV
↓ In sub-maximal exercise heart rate - but this may arise without increase in SV
↓ Systolic blood pressure response
↑ Nitric oxide production, ↑ vasodilation thus ↓ TPR
↓ In myocardial oxygen demand (measured by RPP)
Small ↓ in Submax exercise Q
Improvement in max cardiac output
↑ Arteriovenous difference - more O2 extracte
adaptaions to muscle from areobic training cardiovascular
↑ Arteriovenous difference
- V. important as may cause ↑ in peak VO2 without ↑ in Q.
↑ Mitochondrial number and quantity of aerobic enzymes
Shift towards a more aerobic muscle fibre type profile
↓ submaximal exercise muscle blood flow because of ↑ usage of delivered O2
↑ Maximal muscle blood flow
↑ Muscle capillary density
↑ Muscle fibre recruitment
↓ Blood lactate concentration during sub-maximal exercise
effect of 1 MET increase
15% better surival
effect of aerobic training on total exercise capacity
18-35% increase
effect of aerobic training on angina threshold
10-20% increase