Figure 3. Impact of different clinical variables on LV end-diastolic cavity dimensions in a large population of male and female elite athletes. The relative impact of the examined variables (body size, gender, age, and type of sport) are shown here as a proportion of overall variability in LV cavity size.
A, An electrocardiogram of a 46-year-old male triathlete who presented after long-standing palpitations and a recent episode of syncope. The findings of diffuse T-wave inversions prompted an echocardiogram (B), which revealed normal left ventricular (LV) dimensions and function. C, A subsequent magnetic resonance imaging study confirmed the presence of focal asymmetric LV hypertrophy (yellow arrow) consistent with the apical variant form of hypertrophic cardiomyopathy.
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.
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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.
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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
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Athlete’sheart syndrome , a term often
applied to athletic patient who present
with subjective symptoms or abnormal
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Aerobic /endurance exercises
execises requiring primarily an
increase in o2 transpot.
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Physical activity acutely increases o2
demand which increases cardiac output
(Q) and arteriovenous difference (A-
1 lit of oxygen consumption (VO2)
produces 5-6 lit increase in Q.
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The CV response to exercise has both
external and internal work rate,
External work rate isVO2 required for
exercise task and is direct determination
Internal work rate is MO2 required for
exercise task and is direct determinant
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Repetitive excercises to increase
Increased Q(HR and SV)
Increased stroke volume
The increase in SV means that
performing the same exercise task which
requires the sameVO2 can be performed
at a slower HR and a lower MO2 or
internal work rate.
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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
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Studies revealed LV hypertrophy and
Pellica.et.al showed increased LV end
diastolic diameter and small percentage
had LV wall thickness more than 13mm.
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Morganroth.et.el studies demonstrated
concentric LV hypertrophy in strength
training and eccentic LV hypertrophy in
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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
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Cardiac remodelling is not confined to LV
Scharhag et al study demonstrated RV
enlargement parallels LV enlargement
supporting the concept of biventricular
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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.
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Babee et al studies revealed increased
aortic dimensions in strength exercise
Pellica et al studies revealed incresed
aortic dimensions in aerobic training
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Studies confirmed high prevalnce of left
atrial enlargement in athletes
SEX AND RACE
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PATHOLOGY VS PHYSIOLOGICAL
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Brady arrhythmias such as
The reduced AV conduction velocity may take
accessory pathway such as WPW syndrome.
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Increased vagal tone may be responsible
for early repolarisation and ST
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VALVE DISEASE IN ATHLETS
Careful evaluation of symptoms and
maximal exercise testing
Warm up dyspnea indicates clinically
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Generally tolerate AR,because of
increased HR during exercise, decreases
diastole and regurgitant.
Rarely restrict the patients with AR
unless there is ventricular deterioration.
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AORTIC DISSECTION IN BAV
We do not restrict the patient unless the
patient aortic root dimensions are more
than 45 mm
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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
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Syncope during exercise, there is a
possibility of malignant arrhythmias,
valvular heart disease and myocardial
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DECREASED EXERCISE CAPACITY
Exercise induced asthma
Disease of the skeletal muscles
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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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