L
eft
V
entric
u
lar
Hypertrophy
of
Athletes
.
Adaptati
v
e
P
hysiolo
g
ic
Response
of
the
Heart
Nabil Ghorayeb, Michel Batlouni, Ibraim M. F. Pinto, Giuseppe S. Dioguardi
Instituto Dante Pazzanese de Cardiologia - São Paulo, SP - BrazilO
BJECTIVE
To verif y whether left ventricular hypertrophy (LVH) of elite c om p et i t i on at h l et es (m arat h on ers) r ep r esen t s a p u r el y physiological, adaptative process, or it may involve pathological aspects in its anatomical and functional characteristics.
M
ETHODS
From November 1999 to December 2000, consecutive samples from 30 under 50-year-old marathoners in full sportive activity, with previously documented LVH and absence of cardiopathy were selected. They were submitted to clinical exams, electrocardiogram, color Doppler echocardiogram and exercise treadmill test (ETT). Fifteen were assorted to be also submitted to ergoespirometric test and heart magnetic resonance imaging (MRI).
R
ESULTS
In ETT, all of them showed good physical pulmonary capacity, with no evidences of ischemic response to exercise, symptoms or arrhythmias. In Doppler echocardiogram, values of diameter and diastolic thickness of LV posterior wall, interventricular septum, LV mass and left atrium diameter, were significantly higher when compared to non-athlete control group, with similar ages and anthropometric measurements. The mean of LV mass of at hl et es i ndexed t o body sur f ace (1 2 6 g/m2 ) was significantly greater than the one in control group (70 g/m2) (p< 0.001). Magnetic resonance imaging (MRI) showed there was not impairment of contractile strength or LV performance, and values of end diastolic volume, end systolic volume and EF within limits of normality. On the other hand, average ventricular parietal mass, 162.93± 17.90 g, and LV parietal thickness, 13.67± 2.13 mm, at the end of diastole in athlete group, differed significantly from control group: 110± 14.2 g (p= 0.0001) and 8± 0.9 mm, respectively (p= 0.0001). The same happened to the thickness at the end of systole, which was 18.87± 3.40 mm (control group: 10± 1.80 mm, p= 0.0001).
M a i l i n g a d d r e s s : N a b i l G h o r a y e b • R u a B o m P a s t o r , 1 1 6 3 • 0 4 2 0 3 - 0 5 1 • S ã o P a u l o , S P - B r a z i l E-mail: [email protected] Received on 09/12/04 • Accepted on 03/04/05
C
ONCLUSION
Results allowed for concluding that LVH in marathoners in full spor t i ve act i vi t y peri od, assessed by non- i nvasi ve met hods, represents an adaptative response to intensive and prolonged physical training, with purely physiological characteristics.
K
EY
WORDS
Cardiac hypertrophy of highly trained athletes has b e e n a c kn ow le d ge d for m ore t h a n a c e n t u r y b y Bergm a nn (1 8 8 4 ) a nd Pa rrot (1 8 9 3 ), m entioned by Rost1, and consists of one of the m ost frequent findings in athletic hearts.
How e ve r, c on t rove rs ie s s t ill p e rs is t on it s re a l m ea ning. Would it be a bout a p urely p h ys iologica l p roce s s , com p e n s a tor y or a d a p ta tive h yp e rtrop h y, necessary to keep excellent cardiac perform ance under increa s ed circula tory overloa d conditions , or would in vo lve t h e p o t e n t ia l o f in d u c in g, in lo n g t e rm , pa thologica l cha nges, rela ted to m yoca rdia l structure and compromising of cardiac performance? Most authors support the first hypothesis1 -5. Elsewhere, som e authors have questioned that point of view, by acknowledging that left ventricular hypertrophy in athletes m ay have pathological consequences, considering that, very often, em phatically increased values of parietal thickness and ventricular dilatation superim pose those of hypertrophic or dilated cardiom yopathy6.
Intensive and prolonged physical training induces to cardiovascular adjustments that allow for an exceptional physical performance of athletic heart7 -9. However, those adjustments include functional and anatomical changes that may be placed out of normality limits and whose clinical and prognostic meanings have been a matter of intense discussion and controversies1 ,6 .
There are manywell-known cardiovascular effects of energetic physical training, which is done throughout long periods of time, experimentally observed and in highly-trained competitive athletes2 ,1 0 ,1 1. It is also verified a higher mechanical efficiency of skeleton musculature, increase in capillarization, enzyme activities, increase of pulmonary function capacity and a better ventilation/perfusion rate. Those ca rdiova scula r cha nges result from a com plex in te ra ction of ce n tra l a n d p e rip h e ra l m e ch a n is m s , operating in structural, electrophysiological, biochemical, metabolic and neurogenic levels1 2. They depend on the intensity and length of training, type of athletic activity and genetic factors.
M
E
T
H
O
D
S
In the period from November 1 9 9 9 to December 2 0 0 0 , 3 0 6 athletes were seen, routinely sent by their respective sports entities, for pre-participation cardiologic assessment. From those, we consecutively selected 3 0 athletes, being eighteen whites, eleven blacks and one Far Eastern athlete, who fulfilled all inclusion criteria: male sex, age under 5 0 years old (ages varied from 2 4 to 4 8 years old, mean of 3 7 .5 ± 6 .2 1 ); high endurance aerobic sports performers (marathoners) for more than three years and in a full athletic activity period; left ventricular hypertrophy at color two-dim ensiona l Doppler echoca rdiogra m (left ventricula r thickness and mass over normality limits); absence of subjacent cardiovascular disease. From those 3 0 athletes,
1 5 were randomly selected to submit to heart magnetic resonance imaging (MRI).
The protocol of Seção Médica de Cardiologia do Esporte (Sports Cardiology Medical Section) do Instituto Dante Pazzanese de Cardiologia, do Estado de São Paulo was followed: clinica l interview, with specia l a ttention to cardiovascular symptoms and signs, at rest or exercise-induced, tra ining dura tion, intens ity a nd frequency, electrocardiogram at rest1 3, exercise treadm ill test on trea dm ill, by using Bruce’s protocol1 4, even lim iting s ym p t o m o r s ign , a n d c a rd io p u lm o n a r y o r ergoespirometric test, with incline protocol standardized for athletes, in the 1 5 selected athletes submitted to heart magnetic resonance imaging. Records from color Doppler echocardiogram from 3 0 athletes were carried out under rest conditions and without medication administration. Each exam consisted of M-mode, two-dimensional, pulse and continuous Doppler mode assessments and through color flow mapping modalities1 5 ,1 6.
Th ro u gh m a gn e t ic re s o n a n c e im a gin g (MRI), m yo c a rd ia l m a s s w a s q u a n t ifie d , c a rd ia c fib e r contraction was analyzed, and global ventricular function and left ventricular regional contractility was assessed, th rou gh ta ggin g1 7. Su ch a n a lys is is s u b je ctive a n d d eterm in es wh eth er th ere a re region a l con tra ctility defects, by com pa ring a thletes’ hea rts with those of n orm a l p op u la t ion . Th e s e q u e n c e u s e d w a s c in e m a gn etic res on a n ce im a gin g “FIESTA” with a p n ea . De fin ition of ve n tricu la r rim s a n d d e te rm in a tion of ventricular volum es were carried out at com puter-aided workstation itself, dedicated to that purpose, with the manufacturer’s program.
Results obtained in the group of athletes were compared with those observed in control group of 3 0 normal sedentary individuals, with similar anthropometric characteristics.
R
E
SULTS
None of the 3 0 athletes showed clinical history of family diseases or sudden death, or personal history of clinical importance. The physical exams did not show significant abnormalities.
Results obta ined in 3 0 exercise trea dm ill test a re shown in table I and the results from 1 5 cardiopulmonary tests are displayed in table II.
In exercise treadmill and cardiopulmonary tests, clinical a nd electroca rdiogra p h ic p a ra m eters , obs erved a nd recorded during a nd a fter them , were considered a s compatible with normality. In no case there was ischemic re s p on s e t o e xe rc is e , a n d n o c lin ic a l s ym p t om s , arrhythmias, abnormal behavior of heart rate or ventricular function were observed. The reasons for interruption of e xe rcis e in a ll ca s e s wa s p h ys ica l e xh a u s tion th a t u s u a lly h a p p e n e d clos e to m a xim u m fore ca s t HR. Ca rd iore s p ira tor y ca p a city of th e 3 0 a th le te s wa s considered as “well-conditioned” functional level, higher than those found in normal sedentary individuals1 9.
Doppler echocardiogram – Absolute values and values indexed to body mass and compared to control group of 3 0 non-athletes, with similar ages and anthropometric measurements were obtained (tables III and IV).
The means of left atrium diameter, LV systolic diameter, in t e r ve n t ric u la r s e p t u m a n d LV p o s t e rio r w a ll dia stolic thicknesses, ventricula r m a ss, ejection fra c-tion a n d s h orte n in g p e rc e n ta ge we re s ign ific a n tly higher (p< 0 .0 0 1 ) in athlete group, in comparison with control group (tab. III).
Those same body surface-indexed variables were also significantly higher in athlete group (tab. IV).
Specifically, the mean of left ventricular mass (LVM) of a th letes, indexed to body m a ss (1 2 6 g/m2), wa s significantly greater than the one of control group (7 0 g/ m2) (p< 0 .0 0 1 ). The mean of left ventricular function, assessed through ejection fraction, was also significantly greater in athlete group (0 .7 0 ) when compared to the one of control group (0 .6 0 ) (p< 0 .0 0 1 ). LV dia stolic function variables were normal among all athletes.
Magnetic resonance imaging (MRI) – Results from 1 5 a t h le t e s s h ow e d va lu e s of e n d d ia s t olic volu m e , end systolic volum e a nd ejection fra ction within the limits of normality.
The comparison of results found in athletes with values from 3 0 normal controls (tables V and VI) did not reveal any significant difference concerning end diastolic volume (p= 0 .7 ), end systolic volum e (p= 0 .1 4 ) and ejection fra ction (p= 0 .2 0 ). On th e oth er h a nd, th ere wa s a s ign ifica n t d iffe re n ce in le ft ve n tricu la r m a s s a n d ventricular thicknesses, at the end of diastole and systole. So, the average mass defined by magnetic resonance imaging was 1 6 2 .9 3 ± 1 7 .9 0 g in athlete group against 1 1 0 ± 1 4 .2 g, in control group (p= 0 .0 0 0 1 ); the mean of thickness at the end of diastole was 1 3 .6 7 ± 2 .1 3 mm in a t h le t e grou p a n d 8 ± 0 . 9 m m , in c on t rol grou p (p= 0 .0 0 0 1 ); and the mean of thickness at the end of systole was 1 8 .8 7 ± 3 .4 0 mm among athletes versus 1 0 ± 1 .8 0 mm, in control individuals (p= 0 .0 0 0 1 ).
Despite the magnitude of changes found, there was not dyssynergy in any case, nor impairment of ventricular
perform a nce, which wa s confirm ed not only through global ejection fraction quantification, but also due to the fact that left ventricular regional movement, assessed through tagging, did not show significant changes in any of the cases. Regional thickening measurement of all assessed athletes was found within normality limits and diastolic function of athletes was shown, similarly, normal with discreet changes, without clinical meaning (tab. VII).
D
IS
C
USSION
Athletic heart shows a variety of morphological and fu n ction a l ch a n ge s , re s u ltin g from d e m a n d in g a n d systematic physical training, to improve heart function as a pump and the ability of cardiovascular system to supply oxygen to m uscles under exercise. Preva iling adjustments include: increase of end diastolic dimension of left ventricula r ca vity, of pa rieta l thickness a nd of left ventricula r m a ss, im provem ent of dia stolic filling and heart rate reduction.
Le ft ve n t ric u la r h yp e r t ro p h y d e ve lo p s w a s a compensatory or adaptative process to a hemodynamic stimulus, representing pressure and/or volume overload. The theory, which best describes hypertrophy patterns, ta kes into considera tion th a t ventricula r response is processed in a way to maintain ventricular parietal stress relatively constant and the suitable systolic volume.
Physical exercise is a well-identified stimulus for left ventricular hypertrophy development. Structural changes, res ulting from p h ys ica l tra ining, dep end on na ture, duration and intensity of the exercise. Many sports have b e e n fu n d a m e n t a lly c la s s ifie d in t wo b ig grou p s : endurance sports, in which isotonic or dynamic forms of exercise prevail, and strength sports, in which isometric or sta tic form s of exercise preva il. However, a thletic conditioning is rarely purely isotonic or isometric. Most p h ys ic a l a c t ivit ie s in volve a d yn a m ic a n d s t a t ic com ponent, a lth ough with prepondera nce of one of them8 ,2 0 -2 2.
Another relevant aspect is that exercise-associated overload probably represents the prim ary m echanism responsible for ca rdia c structure cha nges. In a nim a l m od e ls2 3, it h a s b e e n ob s e r ve d t h a t m yoc a rd ia l hypertrophy had a very close relation with hemodynamic ove rloa d in t e n s it y, w h e re a s p la s m a a n d c a rd ia c catecholamines and alpha- and beta-adrenergic activities exerted minimum effect.
Table III - M ain echocardiographic variables in athlete and control groups
Echocardiographic variables Athletes (n= 3 0 ) Control (n= 3 0 ) p
Mean (sd) Va ria tion Mean (sd) Va ria tion
Diam eter of the aorta (m m ) 3 3 ± 3 2 6 a 3 8 3 2 ± 4 2 4 a 3 8 NS
Left atrium diam eter 3 9 ± 4 2 5 a 4 2 3 4 ± 4 2 4 a 4 0 < 0 .0 0 1
LV diastolic diam eter 5 4 ± 5 4 4 a 6 6 5 0 ± 4 4 0 a 5 6 < 0 .0 0 1
LV systolic diam eter 3 2 ± 4 2 4 a 3 9 3 2 ± 4 2 6 a 3 7 < 0 .0 0 1
Ventricular septum diastolic thickness 1 1 .0 ± 0 .5 1 0 a 1 2 7 .6 ± 0 .7 6 a 9 < 0 .0 0 1
Posterior wall diastolic thickness 1 1 .0 ± 0 .6 1 0 a 1 2 7 .6 ± 0 .7 6 a 9 < 0 .0 0 1
Left ventricular m ass (g) 2 3 4 ± 4 1 1 5 6 a 2 9 4 1 3 4 ± 2 7 8 1 a 1 7 1 < 0 .0 0 1
Ejection fra ction 0 .7 0 ± 0 .0 5 0 .6 1 a 0 .7 9 0 .6 0 ± 0 .0 5 0 .5 3 a 0 .7 3 < 0 0 0 1
% D (Shortening fraction) 4 0 ± 4 3 3 a 4 9 3 6 ± 4 3 1 a 4 7 < 0 .0 0 1
Table IV - M eans of main echocardiographic variables obtained in athlete and control groups, indexed to body surface
Echocardiographic variables Athletes (n= 3 0 ) Control (n= 3 0 ) p
Diam eter of the aorta (m m /m 2 ) 1 8 ± 2 1 7 ± 2 0 .0 4
Left atrium diam eter (m m /m 2 ) 2 1 ± 2 1 7 ± 2 < 0 .0 0 1
LV diastolic diam eter (m m /m 2 ) 2 9 ± 4 2 6 ± 4 < 0 .0 0 1
LV systolic diam eter (m m /m 2 ) 1 7 ± 3 1 7 ± 3 NS
Ventricular septum diastolic thickness (m m /m 2 ) 5 .9 ± 0 .5 3 .9 ± 0 .4 < 0 .0 0 1
Posterior wall diastolic thickness (m m /m 2 ) 5 .7 ± 0 .5 3 .9 ± 0 .4 < 0 .0 0 1
Left ventricula r m a ss (g/m 2 ) 1 2 6 ± 2 4 7 0 ± 1 5 < 0 .0 0 1
Table V - Maximum and minimum values, mean and standard deviation of end diastolic volume (EdV), end systolic volume (EsV), ejection fraction (EF), ventricular wall diastolic and systolic thickness, in the athlete group
EdV (m l) EsV (m l) EF (%) Mass (g) Diastolic thickness (m m ) Systolic thickness (m m )
Min. 7 0 2 0 5 7 1 3 0 1 1 1 5
Ma x. 1 4 0 5 3 7 2 2 4 0 1 9 2 6
Mea n 9 9 .0 7 3 6 .8 6 3 .6 7 1 6 2 .9 3 1 3 .6 7 1 8 .8 7
SD 2 0 .0 9 7 .9 7 4 .5 3 1 7 .9 0 2 .1 3 3 .4 0
Table VI - Maximum and minimum values, mean and standard deviation of end diastolic volume (EdV), end systolic volume (EsV), ejection fraction (EF), ventricular wall diastolic and systolic thickness, in the control group
EdV (m l) EsV (m l) EF (%) Mass (g) Diastolic thickness (m m ) Systolic thickness (m m )
Min. 8 5 1 8 5 6 9 0 7 9
Ma x. 1 3 5 4 2 7 5 1 3 5 1 1 1 1
Mea n 1 3 0 .0 0 3 0 .0 0 6 0 .0 0 1 1 0 .0 0 8 .0 0 1 0 .0 0
SD 1 5 .0 0 5 .4 5 8 .2 0 1 4 .2 0 0 .9 0 1 .8 0
Table I - M inimum and maximum values, means and standard deviations of data obtained from simple exercise treadmill test
HR BP T VO2 m a x MET
In itia l Fin a l In itia l Fin a l m in m l/kg/m in
Min. 3 6 1 6 3 1 1 0 x 6 0 1 7 0 x 7 0 1 0 4 6 1 4 .6
Ma x. 6 7 1 9 7 1 4 0 x 9 0 2 2 0 x 9 0 2 1 7 7 .3 2 2 .4
Mean 5 5 .7 1 7 9 .9 1 2 7 .7 x 8 0 .5 1 9 1 .5 x 8 0 .2 1 2 .6 6 3 .6 4 1 9 .1
SD 7 .3 1 0 .3 1 0 x 8 .1 1 4 .2 x 9 .5 2 .6 1 0 .3 8 2 .8 3
Table II - Minimum and maximum values, means and standard deviations of data obtained from cardiopulmonary tests
HR BP T VO2 M E T LA2 VO % HR m a x % LA HR
I n i ti a l F i n a l I n i ti a l F i n a l m i n m l / k g / m i n m l / k g / m i n max
Min 5 5 1 6 5 1 1 0 x 8 0 1 7 0 x 7 0 1 0 :4 4 4 8 .6 1 4 2 8 .1 9 2 .4 7 0 .2
Ma x 6 7 1 9 7 1 4 0 x 9 0 2 1 0 x 8 5 1 2 :1 8 5 2 .1 1 5 3 8 .6 1 0 7 .7 8 9 .8
Mea n 6 1 1 7 8 1 2 8 x 8 1 1 9 0 x 7 7 1 1 :3 5 5 1 .3 1 4 .6 3 2 .4 9 9 .2 7 9 .4
level of training1 ,2 4 ,2 6. For Pelliccia2 7, hereditary factors influence ca rdia c dim ensions, either through genetic control of hypertrophic response to athletic conditioning, or through genetic predisposition to support a m ore intensive physical training and reach higher performance levels during competition. Recently, Montgomery et al.2 8 studied 4 0 0 army rookies before and after a 1 0 -week period of strength and endurance training. At the end of the study, they observed an increase of the average left ventricular mass from 1 6 7 g to 1 9 7 g (an increase of 1 8 %). Individuals were divided in three groups, according to a n giote n s in con ve rtin g e n zym e (ACE) ge n otyp e polymorphism: homozygotic insertion (I/I), heterozygotic insertion/deletion (I/D) and homozygotic deletion (D/D). The three groups, with deletion allele, had the greatest increase of left ventricular mass, which suggested that increased ACE levels play an important role in training-induced myocardial hypertrophy development.
In this study, echocardiographic assessment of left ventricula r systolic function, represented by ejection fraction (0 .6 1 to 0 .7 9 , mean of 0 .7 0 ± 0 .0 5 ) and by the fiber systolic shortening percentage (3 3 to 4 9 %, mean of 4 0 %± 4 ), evidenced normal values in all cases, inclusively significantly higher than those from control group (0 .5 3 to 0 .7 3 , mean of 0 .6 0 ± 0 .0 0 5 , and 3 1 to 4 7 %, mean of 3 6 . 0 % ± 4 , re s p e c t ive ly). Th os e fin d in gs a re in accordance to results from many cross-section studies, which compared groups of athletes from most different sports with sedentary control individuals3 ,2 9 -3 1.
Tw o s t u d ie s d e s e r ve s p e c ia l a t t e n t ion . Am on g endurance and strength sports athletes, it was observed that several non-invasive contractility indexes used to assess left ventricular function were normal, despite the pronounced increase of ventricular cavity and thickness3 0. Another study5 assessed the echocardiographic dimension of left ventricular cavity in 1 ,3 0 9 elite athletes, from 3 8 different sports modalities. According to a cut-off arbitrary level of 6 0 mm, they considered that left ventricular cavity was substantially increased in 1 8 5 athletes (1 4 %). All of them had global systolic left ventricular function within norm ality lim its and did not show segm ental parietal m otility abnorm alities. After a 1 -to-1 2 -year follow-up (a vera ge of 4 . 7 yea rs ), th e 1 8 5 a th letes rem a ined asymptomatic and did not show cardiac performance anomaly. The main determinants of left ventricular cavity d im e n s ion w e re t h e la rge r b od y s u rfa c e a n d t h e participation in certain endurance sports (cycling, cross-country skiing and canoeing).
Results from assessment through magnetic resonance imaging (MRI) in this study equally show that, despite the increase of left ventricular mass and parietal thickness, athletes had normal ejection fraction (5 7to 7 2 %, average o f 6 3 . 6 7 % ± 4 . 5 3 ). N o rm a l fin d in gs o f re gio n a l movement, assessed by tagging, and measurement of regional thickening reinforce the conclusion that there was no impairment of heart contractile strength or left ventricular performance. Pluim et al.3 2 assessed cardiac a na tom y, function a nd m eta bolism through m a gnetic resonance imaging and spectroscopy among highly trained cyclists and control individuals. Left ventricular mass and end diastolic volumes, indexed by body surface, were s ign ific a n tly h igh e r a m on g c yc lis ts . Howe ve r, le ft ventricular ejection fraction, cardiac index and systolic parietal stress did not differ from those among control individua ls. P h osph ocrea tine/a denosine triph osph a te index was similar in both groups. For the authors, those findings indica te th a t ph ysica l exercise-induced left ventricular hypertrophy is only physiological adjustment.
As s e s s m e n t of s e ve ra l e ch oca rd iogra p h ic of le ft ventricular diastolic function – velocity of E and A waves of mitral flowchart, E/A rate, E wave deceleration time, and isovolumetric relaxation time – in athletes from this study showed values uniformly within normality limits, under basal conditions.
By using angiography with radionuclides, Granger et al.3 3 observed that athletes did not show changes in left ventricular filling, although left ventricular mass was 4 3 % greater than the one in sedentary control group.
As opposed to athlete hypertrophy, diastolic ventricular dysfunction is identified in the vast majority of patients w it h s ys t e m ic h yp e r t e n s io n o r h yp e r t ro p h ic myocardiopathy, regardless of hypertrophy level, presence of symptoms or outlet way blocking3 2.
Myocardial texture nature, like echo intensity, can be examined in many ways. The simple codification through the color or pathological myocardial reflectivity shows an increase of fibrosis-associated echo amplitude. On the other hand, in athlete hypertrophy, echo amplitude or ultrasonic myocardial reflectivity are within normal limits, suggesting that physiological hypertrophy does not come along with fibrosis and other structural changes, observed under pathological conditions3 3.
Response to exercise – It has been acknowledged for a long tim e th a t, under presence of left ventricula r hypertrophy, exercise tests may show changes of ST-T typical of ischemic response due to disproportion between oxygen offer a nd cons um p tion, even in a b s ence of obstructive coronary atherosclerotic disease. In patients with left ventricular hypertrophy and normal coronary arteries at angiographic study, exercise treadmill test with typical ischemic response were reported in 3 8 %3 7 and 5 8 %3 8 of individuals.
In the present study, exercise treadmill test did not evidence, in any case, ischemic response to exercise, nor
Table VII - Analysis of heart segmental contractility (assessed through tagging), of regional thickening
and diastolic function of 1 5 athletes
Regional thickening Ta gging Dia stolic function
Norm a l 1 5 1 3 1 1
Non-significa nt - 0 2 0 4
symptoms, arrhythmias, abnormal behavior of heart rate or ventricular function were observed. Those results indicate th a t left ventricula r h ypertroph y does not induce to disproportion between oxygen offer and consumption, even under maximum exercise conditions. Such findings are in accordance to those reported among long distance runners2, basketball players3 and professional soccer players2 9, many of which had documented left ventricular hypertrophy.
Maximum oxygen consumption (VO2 max) is the main indicator of those adjustments and probably the most objective single indicator of physical training level. While a normal young adult, non-athlete, shows VO2 max of approximately 3 5 ml/kg/min, among endurance athletes, t h a t va ria b le in c re a s e s s ign ific a n t ly (5 0 % , in average)2 2 ,2 4 ,3 0, sometimes exceeding 7 0 ml/kg/min2 0 ,2 1.
Physical capacity of the 3 0 athletes was determined th rough m a xim um oxygen cons um p tion (VO2 m a x), indirectly obtained, and its equivalent in MET. Fifteen athletes were randomly selected to be submitted to MRI, through direct measurement of O2 consumption. Result cla s s ifica tion wa s b a s e d on O2 con s u m p tion ta b le elaborated by Barros et al.1 9, subdivided in four categories: unconditioned, conditioned, well-conditioned and elite athlete. Indexes achieved in this work were from well-conditioned athletes.
Ma ny s tud ies d em ons tra ted th a t ch a nges in left ventricular mass and ventricular cavity size with physical training and conditioning take place simultaneously with cha nges of VO2 m a x3 2 ,3 6 ,3 7 ,3 8,strongly suggesting tha t ven tricu la r h yp ertrop h y is a s s ocia ted with a b etter cardiac function2 0.
Summarizing, results from this study evidenced that left ventricular hypertrophy of marathoners, with excellent level of training, has normal left ventricular function, both systolic and diastolic, high oxygen consumption and does not show anomalous responses at exercise treadmill test.
The reasons why left ventricular hypertrophy (LVH) of a th le te s h a s c le a rly d iffe re n t c h a ra c te ris tic s from hypertrophy a ssocia ted to hypertension, hypertrophic cardiomyopathy and other pathological conditions, are not established, but some suggestions may be given, based on clinical and/or experimental findings.
The first and, probably, the most important is that pressure and volume overload resulting from intensive physical training only represents a hemodynamic stimulus for LVH development, without necessarily being followed by neurohumoral changes, as occurring in pathological hypertrophies. Experiments with animals2 3 showed that exercise-a ssocia ted hem odyna m ic overloa d is closely related with myocardial hypertrophy, whereas cardiac and plasma catecholamines and alpha- and beta-adrenergic activity only exert discreet effect.
More recent studies, using animal models with volume overload without activation of rennin-angiotensin system, in d u ced m yocytes h yp ertrop h y, b u t n ot m yoca rd ia l
fibrosis. So, the m a in initia l stim ulus for m yoca rdia l hypertrophy is mechanical straining, whereas fibrosis-resulting stimuli are humoral2 1 ,2 2 ,2 7. Consequently, athlete’s hypertrophy seems to be restricted to myocytes, without changing extracellular matrix and without causing interstitial fib ros is1 , 2 0 , 2 1. Som e s tu d ie s p rove d , th rou gh c olor codification or through ultrasonic myocardial reflectivity that pathologically hypertrophied myocardium shows and increase of fibrosis-associated echo amplitude, which does not happen in ventricular hypertrophy of athletes3 4.
During physical training, sympathetic nervous system is activated. However, in rest periods, much longer every day, vagal preponderance2 1 ,2 2 takes place that, probably, compensates for deleterial effects of catecholamines in myocardium, as well as activation of other neurohormonal systems by sympathetic nervous system.
The increase in the number of mitochondrias, capillary neoformation, normal activity of myosin ATPase observed in hypertrophied myocardium due to physical training, prevent from the disproportion between oxygen offer and consumption and the occurrence of ischemia, as opposed to what was observed in pathological hypertrophies2 1 ,2 2.
Results from the present study, in a group of marathoners in a full sports activity period, allow for concluding that left ventricular hypertrophy observed in those athletes, assessed through non-invasive methods, represents an adaptative response to intensive and prolonged physical training, with purely physiological characteristics.
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KNOWL
ED
G
E
M
E
NTS
1 . Ros t R. At h le t ic s a n d t h e h e a r t . Ch ic a go, Ye a r Book Me d ic a l Publishers, 1 9 8 6 .
2 . Raskoff WJ, Goldman S, Cohn K. The athletic heart: prevalence and
physiological significance of left ventricular enlargement in distance
runners. JAMA1 9 7 6 ; 2 3 6 : 1 5 8 -6 2 .
3 . Roes ke WR, O’Rou rke RA, Klein A et a l. Non in va s ive eva lu a tion
of ve n tricu la r h yp e rtrop h y in p rofe s s ion a l a th le te s . Circu la tion 1 9 7 6 ; 5 3 : 2 8 6 -9 2 .
4 . Morga nroth J , Ma ron BJ , Henry WL. Com pa ra tive left ventricula r
dim ensions in trained athletes. Ann Intern Med 1 9 7 5 ; 8 2 : 5 2 1 -4 .
5 . Pe lliccia A, Cu la s s o F, Di Pa olo FM, Ma ron BJ . P h ys iologic le ft ve n t ric u la r c a vit y d ila t a t ion in e lit e a t h le t e s . An n In t e rn Me d 1 9 9 9 ; 1 3 0 : 2 3 -3 1 .
6 . Ccann GP, Muir DF, Hills WS. Athletic left ventricular hypertrophy:
long-term studies are required. [Editorial]. Eur Heart J 2 0 0 0 ; 2 1 : 3 5 1 -3 .
7 . Bevega rd S, Holm gren A, J oh ns on B. Circula tory s tudies in
well-trained athletes at rest and during exercise, with special reference to stroke volum e a nd influence of body position. Acta P h ysiol Sca nd 1 9 6 3 ; 5 7 : 2 6 -3 8 .
8 . Frick MH, Konttinen A, Sa ra ja s HSS. Effects of physica l tra ining on
circulation at rest and during exercise. Am J Cardiol 1 9 6 3 ; 1 2 : 1 4 2 -7 .
9 . Saltin B, Astran PO. Maximal oxygen uptake in athletes. J Appl Physiol
1 9 6 7 ; 2 3 : 3 5 3 -8 .
1 0 . Scheur J, Pehpa rgkul S, Bha n A. Experim enta l observa tions on the effects of physical training upon intrinsic physiology and biochemistry. Am J Cardiol 1 9 7 4 ; 3 3 : 7 4 4 -5 1 .
1 1 . Blom q vis t G, Sa ltin B. Ca rd iova s c u la r a d a p ta tion s to p h ys ic a l training. Annu Rev Physical 1 9 8 3 ; 4 5 : 1 6 9 -8 9 .
1 2 . Ma ro n BJ . S u d d e n c a rd ia c d e a t h d u e t o h yp e r t ro p h ic ca rdiom yopa thy in young a thletes. In: Thom pson PD, ed. Exercise and Sports Cardiology. New York: McGraw-Hill 2 0 0 1 : 1 8 9 -2 1 0 .
1 3 . Schwartz HJ, Abraão HD. Eletrocardiografia - vectocardiografia. In: Gh ora ye b N, Me n e gh e lo RS (e d s ). Mé t od os Dia gn ós t ic os e m Cardiologia, Rio de Janeiro: Atheneu 1 9 9 7 : 2 -8 .
1 4 . Bruce RA. Exercise testing of pa tients with corona ry hea rt disea se. Ann Clin Res 1 9 7 1 ; 3 : 3 2 3 .
1 5 . Weim an AE. Appendix A, norm al cross-sectional echocardiographic m easurem ents. In: Principles and Practice of Echocardiogram . 2 nd Ed. Pennsylvania: Lea & Febiger 1 9 9 4 : 1 2 8 8 -9 8 .
1 6 . Martin ET, Fuisz AR, Pohost GM. Imaging cardiac structure and pump function. Cardiol Clin 1 9 9 8 ; 1 6 : 1 3 5 -6 0 .
1 7 . S a ya d D, Wille t DW, Ch w ia lk o w s k i M e t a l. N o n in va s ive qua ntita tion of regiona l left ventricula r function using gra dient-echo MRI with m yoc a rd ia l ta ggin g: in te rs tu d y re p rod u c ib ility. Am J Ca rdiol 1 9 9 5 ; 7 6 : 9 8 5 -8 .
1 8 . S im o n s o n E. Diffe re n t ia t io n Be t w e e n No rm a l a n d Ab n o rm a l Eletrocardiography. St Louis: CV Mosby 1 9 6 1 : 1 5 0 -5 .
1 9 . Barros Neto TL, César MC, Tambeiro VL. Avaliação da aptidão física ca rd iorre s p ira tória . In : Gh ora ye b N, Ba rros T, e d s . O Exe rcício: Prep a ra çã o Fis iológica , Ava lia çã o Mé d ica , As p ectos Es p ecia is e Preventivos. Rio de Janeiro: Atheneu 1 9 9 9 : 1 5 -2 4 .
2 0 . Gh ora ye b N, Ba tlou n i M. Hip e rtrofia ve n tric u la r: m e c a n is m os envolvidos na indução e possibilidades de regressão. Rev Soc Cardiol Est São Paulo: 1 9 9 8 ; 8 : 2 9 8 -3 0 1 .
2 1 . Batlouni M. Coração de atleta. In: Ghorayeb N, Barros Neto TL, eds. O Exercício: Prepa ra çã o Fis iológica , Ava lia çã o Médica , As pectos Especiais e Preventivos. Rio de Janeiro: Atheneu 1 9 9 9 : 1 4 7 -7 2 .
REFERENCES
2 2 . Barros Neto TL. Hipertrofia ventricular secundária ao exercício físico. Rev Soc Cardiol Est São Paulo 1 9 9 4 ; 4 : 3 7 6 -8 1 .
2 3 . Coop e r IV G, Ke n t RL, Ub oh CE, Th om p s on EW, Ma rin o TA. He m od yn a m ic ve rs u s a d re n e rgic con trol of ca t righ t ve n tricu la r hypertrophy. J Clin Invest 1 9 8 5 ; 7 5 : 1 4 0 3 -1 4 .
2 4 . Maron BJ. Structural features of the athletes heart as defined by echo-cardiography. J Am Coll Cardiol 1 9 8 6 ; 7 : 1 9 0 -2 0 3 .
2 5 . Dougla s P S, O’Toole ML, Ka tz SE. Left ventricula r h ypertroph y in athletes. Am J Cardiol 1 9 9 7 ; 8 0 : 1 3 8 4 -9 0 .
2 6 . Os b orne G, Wolfe LA, Burggra f GW et a l. Rela tions h ip s b etween ca rdia c dim ensions, a nth ropom etric ch a ra cteristics a nd m a xim a l aerobic power in young m en. Int J Sports Med 1 9 9 2 ; 1 3 : 2 1 9 -2 4 .
2 7 . Pelliccia A. Determ inants of m orphologic cardiac adaptation in elite athletes: the role of athletic training and constitutional factors. Int J Sports Med 1 9 9 6 ; 1 7 (suppl.): 1 5 7 -6 3 .
2 8 . Mon t gom e r y HE, Cla rks on P, Dolle r y CM e t a l As s oc ia t ion of a n giot e n s in -c on ve rt in g e n zym e s ge n e I/D p olym orp h is m w it h ch a n ge in le ft ve n tricu la r m a s s in re s p on s e to p h ys ica l tra in in g. Circula tion 1 9 9 7 ; 9 6 : 7 4 1 -7 .
2 9 . Ba tlouni M, Abrã o HD, Gh ora yeb N, Gizzi LC, Zorzo D, Sa ua ia N. Alt e ra ç õ e s e le t ro c a rd io grá fic a s e m a t le t a s p ro fis s io n a is : l. Sobreca rga s ventricula res. Arq Bra s Ca rdiol 1 9 8 0 ; 3 5 : 9 5 -1 1 0 .
3 0 . P e llic c ia A, Ma r o n B J , S p a t a r o A e t a l. Th e u p p e r lim it o f p h ys iologic ca rdia c h yp ertrop h y in h igh ly tra ined elite a th letes . N Engl J Med 1 9 9 1 ; 3 2 4 : 2 9 5 -3 0 1 .
3 1 . Cola n SD, Sa n d e rs SP, Borow KM. P h ys iologic a l h yp e rt rop h y: effects on left ventricula r systolic m echa nics in a thletes. J Am Coll Ca rdiol 1 9 8 7 ; 9 : 7 7 6 -9 .
3 2 . P lu im BM, Zwin d e rm a n AH, La a rs e A e t a l. Th e a th le te ’s h e a rt: a m e t a -a n a lys is of c a rd ia c s t ru c t u re a n d fu n c t ion. Circ u la t ion 1 9 9 9 ; 1 0 0 : 3 3 6 -4 4 .
3 3 . Granger CB, Karimeddini MK, Smith VE et al. Rapid ventricular filling in left ventricula r h ypertroph y. Ph ysiologic h ypertroph y. J Am Coll Cardiol 1 9 8 5 ; 5 : 8 6 2 -8 .
3 4 . Lewis J F, Sp irito P, Pelliccia A, Ma ron BJ . Us efulnes s of Dop p ler ech oca rdiogra ph ic a ssessm ent of dia stolic filling in distinguish ing “a th le te ’s h e a rt” from h yp e rtrop h ic ca rd iom yop a th y. Br He a rt J 1 9 9 2 ; 6 8 : 2 9 6 -3 0 0 .
3 5 . La tta nzi F, Di Bello V, Pica no E et a l.Norm a l ultra sonic m yoca rdia l reflectivity in athletes with increased left ventricular mass. Circulation 1 9 9 2 ; 8 5 : 1 8 2 8 -3 4 .
3 6 . Ba t lo u n i M. H ip e r t ro fia c a rd ía c a : fa t o re s d e t e rm in a n t e s e m eca nism os m olecula res. Arq Bra s Ca rdiol 1 9 9 5 ; 6 5 : 5 3 3 -9 .
3 7 . Ehsani AA, Hagberg JM, Hickson RC. Rapid changes in left ventricular di-mension and mass in response to physical conditioning deconditioning. Am J Cardiol 1 9 7 8 ; 4 2 : 5 2 -6 .
3 8 . Ha rris CN, Aronow WS, Pa rker DP et a l. Trea dm ill stress test in left ventricula r hypertrophy. Chest 1 9 7 3 ; 6 3 : 3 5 3 -7 .
3 9 . Roitman D, Jones WB, Sheffield LT. Comparison of submaximal exercise test with coronary cineangiogram. Ann Intern Med 1 9 7 0 ; 7 2 : 6 4 1 -7 .
4 0 . Grossm a n W. Ca rdia c hypertrophy: useful a da pta tion or pa thologic process? Am J Med 1 9 8 0 ; 6 9 : 5 7 6 -8 4 .
4 1 . Wikman-Coffel TJ, Parmley WW, Mason DT. The cardiac hypertrophy process. Circ Res 1 9 8 0 ; 4 5 : 6 9 7 -7 0 7 .
