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K SRINIVAS

ATHLETE’S HEART

HISTORY

Heneschen(1890) used physical

examination to determine increased

cardiac dimensions in elite nordic skiers.

Eugene darling in the same year in

rowers of harvard university.

2/1/2015 2ATHLETE'S HEART

Paul dudely white(1900)

studied radial pulse rate

among boston marathon

competitors and was the

first to report marked

resting sinus bradycardia in

long distance runners.2/1/2015 3ATHLETE'S HEART

Earlier it was thought to be beneficial

adaptations to exercise.

But later it was postulated as a form of

overuse pathology and prolonged

participation in sport can lead to

premature cardiovascular system

collapse.


Athlete’sheart syndrome , a term often

applied to athletic patient who present

with subjective symptoms or abnormal

CVS findings.


Aerobic /endurance exercises

execises requiring primarily an increase in o2 transpot.


Resting /strength exercises

exercises primarily stressing the skeletal muscle.


PHYSIOLOGY

Physical activity acutely increases o2

demand which increases cardiac output

(Q) and arteriovenous difference (A-

V)O2.

1 lit of oxygen consumption (VO2)

produces 5-6 lit increase in Q.


The CV response to exercise has both

external and internal work rate,

External work rate is VO2 required for

exercise task and is direct determination

of Q.

Internal work rate is MO2 required for

exercise task and is direct determinant

of HR


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Repetitive excercises to increase exercise capacity

Increases VO2

Increased Q(HR and SV)

Increased stroke volume

The increase in SV means that

performing the same exercise task which

requires the same VO2 can be performed

at a slower HR and a lower MO2 or

internal work rate.


The physiologic mediators of these CV

adaptations may be produced by

increased resting vagal tone and reduced

resting sympathetic tone resulting in

resting sinus bradycardia


LEFT VENTRICLE

Studies revealed LV hypertrophy and

dilation.

Pellica.et.al showed increased LV end

diastolic diameter and small percentage

had LV wall thickness more than 13mm.


MORGANROTH HYPOTHESIS

Morganroth.et.el studies demonstrated

concentric LV hypertrophy in strength

training and eccentic LV hypertrophy in

aerobic training.


Figure 3. Impact of different clinical variables on LV end-diastolic cavity dimensions in a large

population of male and female elite athletes.

Maron B J , and Pelliccia A Circulation. 2006;114:1633-

1644

Copyright © American Heart Association, Inc. All rights reserved.2/1/2015 18ATHLETE'S HEART

On LV systolic function

demonstrated preserved LV ejection

fraction except for one study

On LV diastolic function

improved LV diastolic function is essential

mechanism in preserving stroke volume


RIGHT VENTRICLE

Cardiac remodelling is not confined to LV

Scharhag et al study demonstrated RV

enlargement parallels LV enlargement

supporting the concept of biventricular

enlargement.


AORTA

Experiences a significant hemodynamic

load during exercise.

Aerobic exercise- high volume aortic

flow with modest systemic hypertension

Strength exercises-normal volume with

profound systemic hypertension.


Babee et al studies revealed increased

aortic dimensions in strength exercise

training.

Pellica et al studies revealed incresed

aortic dimensions in aerobic training

exercises.


LEFT ATRIUM

Studies confirmed high prevalnce of left

atrial enlargement in athletes

SEX AND RACE


PATHOLOGY VS PHYSIOLOGICAL ADAPTATION


A, An electrocardiogram of a 46-year-old male triathlete who presented after long-standing

palpitations and a recent episode of syncope.

Baggish A L , and Wood M J Circulation. 2011;123:2723-

2735

Copyright © American Heart Association, Inc. All rights reserved.2/1/2015 25ATHLETE'S HEART

ARRHYTHMIAS

Brady arrhythmias such as

Sinus bradycardia

Junctional bradycardia

AV block

The reduced AV conduction velocity may take

accessory pathway such as WPW syndrome.


Increased vagal tone may be responsible

for early repolarisation and ST

abnormalities.


VALVE DISEASE IN ATHLETS

AORTIC STENOSIS

Careful evaluation of symptoms and

maximal exercise testing

Warm up dyspnea indicates clinically

important AS


AORTIC REGURGITATION

Generally tolerate AR,because of

increased HR during exercise, decreases

diastole and regurgitant.

Rarely restrict the patients with AR

unless there is ventricular deterioration.


AORTIC DISSECTION IN BAV

We do not restrict the patient unless the

patient aortic root dimensions are more

than 45 mm

Annual screening.


SYNCOPE

Majority of syncope in athlete’s is

attributed to neurocardiogenic syncope.

Manifests in the immediate post exercise

testing owing to sudden reduction in

venous return, which facilitates transient

cerebral hypoperfusion.


Syncope during exercise, there is a

possibility of malignant arrhythmias,

valvular heart disease and myocardial

ischemia.


DECREASED EXERCISE CAPACITY

Hyperthyroididm

Exercise induced asthma

Disease of the skeletal muscles

Anemia

AF

Viral illness


ELEVATED CARDIAC ENZYMES

Increase in cTnT occurs in athletes

following prolonged exertion.

Endurance athletes were documented to

have increased concentrations of CK-MB

and satellite cells in their leg muscles.


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