cardiac remodelling(netherlands heart journal)

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Cardiac remodelling: concentric versus

eccentric hypertrophy in strength and

endurance athletes

Cardiac remodelling is commonly defined as aphysiological or pathological state that may occurafter conditions such as myocardial infarction, pres-sure overload, idiopathic dilated cardiomyopathy

or volume overload. When training excessively, theheart develops several myocardial adaptationscausing a physiological state of cardiac remodelling.These morphological changes depend on the kindof training and are clinically characterised bymodifications in cardiac size and shape due to in-creased load. Several studies have investigatedmorphological differences in the athletes heartbetween athletes performing strength training andathletes performing endurance training. Endurancetraining is associated with an increased cardiacoutput and volume load on the left and right

ventricles, causing the endurance-trained heart togenerate a mild to moderate dilatation of the left

ventricle combined with a mild to moderate in-crease in left ventricular wall thickness. Strengthtraining is characterised by an elevation of bothsystolic and diastolic blood pressure. This pressureoverload causes an increase in left ventricular wallthickness. This may or may not be accompaniedby a slight raise in the left ventricular volume.However, the development of an endurance-trained heart and a strength-trained heart shouldnot be considered an absolute concept. Both formsof training cause specific morphological changesin the heart, dependent on the type of sport. (NethHeart J2008;16:129-33.)

Keywords: ventricular remodelling, heart, sports,hypertrophy

Cardiac remodelling is commonly defined as aphysiological or pathological state that may occurafter conditions such as myocardial infarction, pressureoverload, idiopathic dilated cardiomyopathy or volume

overload.

1

The athletes heart is a physiological condition thatcan be defined as a morphological consequence ofsystematic training in athletes with the followingfeatures: increase in maximal cardiac output, increasein stroke volume, decrease in resting heart rate andelectrocardiographic changes in conduction andrepolarisation. A broad variety of cardiovascularadaptations can be achieved after either dynamic orisometric exercise, or a combination of both.2

First, we address the question how exercise-inducedhypertrophy of the heart differs from cardiac hyper-trophy of pathological origin. Second, we review themorphological changes in the heart that are typical for

both endurance training and strength training.

Remodelling: physiological vs. pathological

Cardiac remodelling is clinically manifested by changesin cardiac size, shape and function in response tocardiac injury or increased load.1Various causes ofcardiac remodelling share several molecular, bio-chemical, and mechanical pathways. The process ofcardiac remodelling is largely influenced by haemo-dynamic load, neurohumoral activation and additionalfactors such as endothelin, cytokines, nitric oxideproduction and oxidative stress.1

The heart is considered a supplier of a stable flowof blood, which responds to an increase in demand byraising stroke volume and heart rate.3Volume overloadand increased filling pressures lead to increasedstretching force on the myocardium.4 Due to theFrank-Starling mechanism the heart muscle is able toincrease contractile force when the ventricular wall isstretched. Cardiac remodelling can be a physiologicalor pathological condition:1

physiological remodelling is a compensatory changein the proportions and function of the heart; thistype of remodelling can be seen in athletes;

pathological remodelling may occur after conditionssuch as myocardial infarction (pressure overload),

C. Mihl, W.R.M. Dassen, H. Kuipers

C. Mihl

W.R.M. Dassen

H. Kuipers

Department of Cardiology, Maastricht University Hospital,

Maastricht, the Netherlands

Correspondence to: W.R.M. Dassen

Department of Cardiology, Maastricht University Hospital,

PO Box 5800, 6202 AZ Maastricht, the Netherlands

E-mail: [email protected]

REVIEW ARTICLE

Netherlands Heart Journal, Volume 16, Number 4, April 2008 129


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inflammatory myocardial disease, with idiopathicdilated cardiomyopathy, or with volume overload.

The cardiac cell that is particularly involved in theremodelling process is the cardiomyocyte.

Stretching caused by the increase of haemodynamic

load causes the heart to undergo a hypertrophicresponse. Cardiomyocytes expand by synthesis of newcontractile proteins and the assembly of new sarcomeresin-parallel.3 This will increase the contractile force percell. This form of remodelling is homogeneous andleads to an increase in the myocyte of the myocardium.5

This hypertrophic response induced by exercise isreferred to as physiological remodelling.

When the heart is subject to chronic increases indemand (such as myocardial infarction) a different formof remodelling takes place. The majority of this categoryof remodelling is irreversible. The type of cardiac re-modelling, due to conditions such as chronic overload,is associated with an inhomogeneous, disproportionatecontribution of cardiac fibroblasts that produce inter-stitial fibrillar collagen. Collagen is principallysynthesised by fibroblasts but also by vascular smoothmuscle cells in response to a variety of pathologicalstimuli, including increased oxidative and mechanicalstress, ischaemia and inflammation.6 Fibroblaststimulation increases collagen synthesis and causesfibrosis of both the infarcted and noninfarcted regionsof the ventricle.7 This can lead to a loss of cardiomyo-cytes by apoptosis or necrosis and eventually thesecardiomyocytes are replaced by fibroblasts and extra-cellular collagen.3 Fibrosis increases the stiffness of themyocardium, which interferes with filling of the heart.8

Loss of myocytes is an important mechanism in thedevelopment of cardiac failure.9 The apoptosis of car-diomyocytes will reduce the contractile force anddiminish myocardial wall thickness. This is termeddilated cardiomyopathy. When the heart is exposed toa pressure overload and fails to undergo hypertrophy,this can also lead to ventricular dilatation.3,10 The in-creased stiffness of the myocardium and the diminishedcontractility are consequences of pathological remodel-ling and a strong predictor of heart failure.10

Remodelling: endurance vs. strength training

Morganroth et al. were the first to uncover two differentmorphological forms of athletes hearts: a strength-trained heart and an endurance-trained heart.11

Endurance sports such as cycling, running andtriathlon induce physical loads with high dynamic andhigh static components. In training and competition,endurance-trained athletes sustain long intervals withhigh cardiac output, high heart rate, high strokevolume and a moderate increase in mean arterial bloodpressure.2,12 Dynamic exercise imposes a volume loadon the left ventricle. The cardiac output of trained en-durance athletes may increase from 5 to 6 l/min atrest to up to 40 l/min during maximal exercise.13

Besides an increase in cardiac output, the blood

pressure increases as well, although not to the sameextent as during strength training. Consequently, theendurance-trained heart needs to adapt to both volumeand pressure load. The heart responds by increasingleft ventricular internal diameter and left ventricularwall thickness.14

Ventricular dilation is caused by volume overload.Hereby, new sarcomeres are added in-seriesto existingsarcomeres. Volume overload-induced cardiac hyper-trophy is known as eccentric hypertrophy (figure 1). Inendurance training, the volume load is a predominantfactor; therefore, the endurance-trained heart developseccentric hypertrophy.15

Cardiovascular adaptations in power athletes vary fromthose in endurance-trained athletes. Strength training

is considered a static exercise. In static exercises thestroke volume of the heart is not affected but the over-load is characterised by marked elevations in systolic anddiastolic blood pressure and a modest increase incardiac output, heart rate and oxygen consumption.16,17

High level resistance training is associated with suddenand large pressor responses. The blood pressureresponse during weightlifting can increase to levels ashigh as 320/250 mmHg.18

Due to an increased afterload, high intraventricularpressure is needed to open the aortic valve. During theejection phase, the high levels of afterload and intra-ventricular pressure lead to an increase in myocardialwall stress, which is the major stimulus for cardiachypertrophy in the pressure-overloaded heart.19

There is a substantial increase in systolic bloodpressure with high-intensity isometric activity.18 Theheart responds to a pressure overload in strengthtraining by adding new sarcomeres in-parallelto exist-ing sarcomeres. As a consequence, the wall thicknessincreases. This pathological condition is called con-centric hypertrophy (figure 1).

Combined with a reduced compliance due toincreased stiffness of the ventricle, this leads to diastolicdysfunction. Maron et al. found that the early fillingphase of diastole is significantly prolonged and associ-

Cardiac remodelling: concentric versus eccentric hypertrophy in strength and endurance athletes

130 Netherlands Heart Journal, Volume 16, Number 4, April 2008

Normalheart condition

Eccentrichypertrophy

Concentrichypertrophy

Pathological heart remodelling

Figure 1. Pathological heart remodelling.


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ated with a decreased rate and volume of rapid filling.20

Figures 2 and 3 depict ultrasound images of heartswith concentric and eccentric hypertrophy.

ResultsPellicia et al. described a variety of morphologicalchanges in the left ventricular chambers of athletes per-forming endurance sports.21,22 These findings seemedto be associated with the haemodynamic overload.They concluded that endurance sports had a strongimpact on left ventricular wall thickness and leftventricular cavity size. The authors measured leftventricular dimensions above the upper limit of normal(>55 mm).21,22Hoogsteen et al. reported that in cycliststhe onset of the process of dilatation of the left ventricleand left atrium takes place at a relatively early stage.The process of dilatation seems to continue during theathletes career. There is also evidence that in cycliststhe left ventricular mass is increased at an early age.Over time, the athletes show no significant changes indiastolic function of the left ventricle.23

Several studies have described morphologicalcharacteristics that differed between various endurancesports. Hoogsteen et al. found myocardial adaptationsthat differed between endurance sports, includingcycling, marathon and triathlon. These differences incardiac adaptation are induced by various pressure loads

and exercise-related volumes.16 Pluim et al. found that

runners show predominantly increased left ventricularwall thickness, whereas cyclists particularly demonstratedilatation of the left ventricle.14

Hoogsteen et al. investigated the effects of cardiacremodelling on different groups of these highly trainedendurance athletes; a prevalence of eccentric remodel-ling was found, being most apparent in cyclists.16,23 Thecombination of volume loading and pressure loadingcreates a physiological trigger that induces differenti-ation in left ventricular systolic and diastolic parameterssuch as dilatation, increased left ventricular mass anddiastolic profile.3,16

These findings differ from the remodelling of thestrength-trained heart. Martin et al. found that theeffects of isometric exercise on left ventricular per-formance depend on two factors: the intensity ofisometric exercise and the muscular mass involved inthe contraction.24 Spirito et al. investigated the haemo-dynamic responses to isometric exercise in 947 eliteathletes and concluded that athletes performing iso-metric exercise show increased myocardial mass withor without a slight increase in left ventricular volume.25

Kasikcioglu et al. presented comparable results.19

However, left ventricular end-systolic wall stress provedto be lower in the athletes than in the control group.This is believed to be due to the cardiovascular



Figure 2. Ultrasound showing concentric hypertrophy of the heart. Figure 3. Ultrasound showing eccentric hypertrophy of the heart.


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adaptation factors that affect left ventricular hyper-trophy.19 No further research on this matter has beenconducted. Fisman et al. reported similar results andalso make mention of a thicker interventricular septumin hearts of weightlifters than in hearts of sedentaryindividuals.17

Spirito et al. found that power disciplines do havea disproportionately larger impact on left ventricular wallthickness than on cavity size.25 Pelicia et al. reportedan increase in absolute wall thicknesses; however, theyrarely exceeded the upper normal limits (


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18 MacDougall JD, Tuxen D, Sale DG, Moroz JR. Arterial bloodpressure response to heavy resistance exercise.J Appl Physiol1985;58:785-90.

19 Kasikcioglu E, Oflaz H, Akhan H, Kayserilioglu A, MercanogluF, Umman B, et al. Left ventricular remodelling and aortic dis-tensibility in elite power athletes. Heart Vessels2004;19:183-8.

20 Maron BJ. Hypertrophic cardiomyopathy. Lancet1997;350:127-33.

21 Pellicia A, Di Paolo FM, Maron BJ. The athletes heart: remodel-ling, electrocardiogram and preparticipation screening. CardiolRev2002;10:85-90.

22 Pellicia A, Maron BJ, Sparato A, Proschan MA, Spirito P. Theupper limit of physiologic cardiac hypertrophy in highly trainedelite athletes. N Engl J Med1991;324:295-301.

23 Hoogsteen J, Hoogeveen A, Schaffers H, Wijn PFF, van der WallEE. Left atrial and ventricular dimensions in highly trained cyclists.Int J Cardiol Imaging2003;19:211-7.

24 Martin CE, Shaver JA, Leon DF, Thompsom ME, Reddy PF,Leonard JJ. Autonomic mechanisms in hemodynamic responses toisometric exercise.J Clin Invest1974;54:104-15.

25 Spirito P, Pelliccia A, Proschan M, Granata M, Spataro A, BelloneP, et al. Morphology of the athletes heart assessed by echo-cardiography in 947 elite athletes representing 27 sports.Am JCardiol1994;74:802-6.

26 Pelliccia A, Spataro A, Caselli G, Maron BJ. Absence of leftventricular wall thickening in athletes engaged in intense powertraining.Am J Cardiol1993;72:1048-54.



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