10 Reasons Why a Large “Athlete’s Heart” is Usually Not Dangerous

By Armi Legge | January 31, 2013

 

A large heart helps athletes perform better. However, some researchers think having “athlete’s heart” might decrease their long-term health.

If you’re an athlete, you may have an enlarged heart.

If you train more than a few hours a week, especially for endurance sports, your heart is probably much larger. So large in fact, that it could be mistaken for heart disease.

Having a large heart usually a sign of heart disease. However, there are 10 reasons why most researchers don’t think having a large heart is dangerous if you’re an athlete.(1-13)

1. Athlete’s with large hearts tend to have excellent heart function.

If “athlete’s heart” was a sign, or form, of heart disease, you would expect two things to be true:

1. Training that increases heart size should decrease heart function.

2. Athletes with large hearts should have poorer heart function than non-athletes.

Neither of these conclusions are usually true.

First, training that increases heart and coronary artery size generally improves heart function or has no effect.(14-19)

Second, endurance athletes with large hearts tend to have as good or better heart and blood vessel function compared to healthy non-athletes and other athletes.(20-47)

This is also true for football(48-50), handball(51,52), tennis(53), soccer(54), hockey(55), and basketball players.(56-58)

Athletes with enlarged hearts also tend to have better heart function during exercise, when the heart is under the most stress.(59-63) This isn’t surprising, but exercise tolerance is usually considered an excellent measure of heart function.(64-68)

On the other hand, there is some data showing athletes with larger hearts may have worse heart function.

One study found that 11.6% of Tour de France cyclists with enlarged hearts had a reduced “ejection fraction” — the percentage of blood ejected from the heart with each beat.(69) A normal left ventricle ejection fraction (LVEF) is around 55-70%.(70) These cyclist’s LVEF’s were less than 52%.

A previous study found similar results on other pro cyclists.(71)

In both cases, the researchers concluded that extreme athlete’s heart may decrease heart function.

That’s possible, but there are other explanations.

First, athletes tend to have slightly lower heart rates. They also tend to have a higher blood volume, which drops with detraining. Both of these variables could have affected the results.(72)

Second, most of the formulas used to calculate ejection fraction are designed for people with a normal sized heart. It’s possible that having a large athlete’s heart could have caused a “mathematical underestimation” of their actual ejection fractions.(73)

This seems likely, since the cyclists had larger stroke volumes (total heart volume) and a normal cardiac output at rest (the total amount of blood being pumped out of the heart).

This is a little confusing, so here’s an analogy:

You need to fill two glasses with four ounces of orange juice. The glasses represent how much blood your heart needs to pump.

You have two oranges — a large one (an athlete’s heart), and a small one (a normal heart).

The large orange has eight ounces of juice, and the small orange has six. Both of the oranges have enough juice to fill the glasses (supply the needs of the body). However, you’re going to have a lot more juice left over after “pumping” the larger orange.

This means a smaller percentage (50%) of the juice was “ejected” from the large orange, because it had more total juice (it was bigger). The smaller orange ejected 75% of its juice, but the total amount was the same (four ounces).

The same thing is true with your heart. A larger heart doesn’t need to eject as much of a percentage of its blood with each beat, because it has a larger total volume of blood.

As long as the total amount of blood exiting the heart (cardiac output) is sufficient to meet the demands of the body, it’s unlikely a low ejection fraction is a major concern in otherwise healthy athlete’s with enlarged hearts.(74)

That said, however, there isn’t enough data to know for sure. There are other studies that also seem to indicate having a large “athlete’s heart” may be bad. But, they have confounders that need to be considered.

Circling back to the study on the cyclists, it’s important to remember that these measurements were taken at rest, not during exercise. A study on football players with a borderline low ejection fraction of around 58% found that it increased to normal levels during exercise.(75) This doesn’t usually happen in people with heart failure, at least to the same degree.(76,77)

That said, an earlier study found that a few pro soccer player’s ejection fractions did not increase during exercise.(78) The researchers weren’t sure why, and it wasn’t clear if this caused any problems.

Since we’re talking about pro athletes, especially cyclists, we also need to keep in mind that performance enhancing drugs may have affected their hearts.(79-95) For example, in study one on “athlete’s heart,” 71% of former pro cyclists admitted to using performance enhancing drugs during their careers.(96) Steroid abuse may have also affected some of the studies on football players.(97)

In another study, researchers followed 104 old and young professional cyclists for two years.(98) The older cyclists had slower diastolic filling compared to the younger athletes and controls. This means their hearts didn’t fill with blood as efficiently when relaxed, which can be a sign of heart disease.

However, this only occurred in nine cyclists, a small number. This study also doesn’t tell us why they had slower diastolic filling, and it’s possible it was from causes other than their training. Most other studies also indicate that diastolic filling in “athlete’s heart” is either normal or improved at rest, and enhanced during exercise.(99-106)

Another study found similar results in retired pro cyclists with enlarged hearts. They also had slightly higher levels of BNP, which is a chemical marker for heart dysfunction.(107)

In most cases, however, the BNP levels were not significant, and were mostly high in the few athletes who had atrial fibrillation (a form of electrical dysfunction of the heart that we’ll cover in another article) and other symptoms.

The differences in heart function between the athletes and controls were also not significant.

On the other hand, the control group had twice as many previous smokers. The study also didn’t track how many athletes or controls died, or any differences in quality of life, so it’s hard to tell if the athlete’s larger heart size had a negative impact in the long-term.

It’s also questionable if slightly slower diastolic filling is a problem for healthy athletes. Another study found that diastolic filling was only reduced during the off-season in professional cyclists, when their hearts were smaller from not training as hard.(108)

When they returned to regular training, their diastolic filling improved to that of the controls. The researchers “think it unlikely that the impaired Vp, DT, and AR data [measures of heart function] we observed in the inactive athletes are indicative of diastolic dysfunction.”(109)

This was because the athletes were “young, healthy and capable of performing at extremely high levels.”(110) There was no “evidence that the heart fills inadequately, or at higher pressures than normal or that it cannot sustain higher levels of venous return during exercise,” which led them to conclude that it would “‘be inappropriate to infer diastolic ‘dysfunction’” from this study.(111)

In these two studies the cyclists’s heart function was different, but not necessarily worse.

Finally, a recent meta-analysis concluded that systolic function (when the heart contracts) is “similar to that of sedentary control subjects,” and diastolic function (when the heart relaxes) is “normal or slightly enhanced” in athletes with enlarged hearts.(112)

Most of the time, athletes with large hearts have normal heart function when they aren’t exercising, and excellent heart function when they are.

2. Athlete’s heart is not entirely permanent.

In many cases, athlete’s heart reverses completely or largely with de-training.(113-118) Heart disease generally doesn’t regress, at least without surgery, drugs, or other treatments.(119-122)

Many of the changes in “athlete’s heart” start to reverse themselves after just 8-12 weeks.(123-127) Hearts of athletes even shrink during the rest season when they reduce their training levels.(128-130) This would probably not happen if “athlete’s heart” was a form of heart disease.(131,132)

In highly trained athletes with more advanced “athlete’s heart,” however, the changes sometimes don’t completely go away years after they stop training.(133-137) They mostly regress, but not completely.

This is especially true for endurance athletes, who usually have much larger hearts.

But most measures still fall back to the upper end of the normal range.(138-142)

One study found that retired pro cyclists still had significantly enlarged hearts 30 years after retirement. However, the absolute differences in heart size were minor. There was also no evidence this caused any long-term problems.(143)

Another study on elite athletes found that after six years of no intense training, most changes in heart size and function were back to the normal. About 20% of the athletes still had higher than normal heart volumes, but there was “no clinical or echocardiographic evidence of systolic or diastolic LV [left ventricle] dysfunction, cardiac symptoms, or impaired physical performance.”(144)

These athletes also tended to remain more active later in life and/or gain more weight, which explained about 50% of their persistently enlarged hearts.

That said, the authors could not “exclude the possibility that this marked residual chamber enlargement” (that was not explained by continued training and increased body weight), “could ultimately lead to clinical consequences [heart problems] later in life.”(145)

The largest study of this kind, using a cohort of 947 Olympic endurance athletes, found that after an extended break there were significant reductions in heart size and no evidence of heart dysfunction.(146) However, these athletes were much younger on average, so it could be that heart damage only occurs after a longer period of time.

Most other studies, however, have also shown that athlete’s with persistently enlarged hearts tend to have heart function that is about the same as the average population.(147,148)

Other studies indicate that heart function does sometimes change when the heart does not completely go back to normal, but there’s little evidence these changes are bad.(149,150)

We already discussed the studies that seem to disagree with this conclusion in the previous part of this article.(151-153)

In all of these studies, most of the athlete’s hearts substantially shrunk after they stopped exercising. It didn’t always completely return to normal, but it did regress as you would expect any adaptation to do if you stop training. It’s also possible that in some athletes whose hearts don’t atrophy as much, there may be some damage. We don’t know.

3. Athlete’s hearts are symmetrical and uniform.(154-160)

In heart disease, certain patches of heart tissue often become disproportionately thicker or thinner.(161-165) This is a sign the heart is being overwhelmed and may be failing.

Certain chambers of athlete’s hearts can become slightly larger than others. Runners often develop wider ventricles, and cyclists sometimes develop thicker heart walls, mainly due to differences in blood flow during these sports.(166-169) Yet the thickness of the heart walls are still uniform and the other chambers are significantly larger in “athletes heart.”(170-172)

This distinction is not always 100 percent accurate, as some forms of heart disease are symmetrical, and healthy hearts sometimes have small asymmetries.(173)

4. Athlete’s hearts are well vascularized.

Large athlete’s hearts have greater blood vessel density than people with heart disease and healthy non-athletes.

Athlete’s hearts have increased vascularization (more blood vessel density) compared to heart disease patients and sedentary people.(174,175)

When athletes do have heart scarring, there is sometimes a decrease in perfusion — the ability to circulate blood through the heart.(176-177) This kind of heart damage is rare for most athletes, but we’ll take a closer look at it in another article. It’s a valid concern.

5. Coronary arteries are generally larger in athletes.(178-184)

People with heart disease also have enlarged coronary arteries. However, their arteries are disproportionately smaller compared to their hearts.(185-187)

When injected with nitroglycerine (a chemical that makes the arteries relax and expand), the coronary arteries of athletes also expand proportionally to their size, which is what they’re supposed to do. This is generally not the case in heart disease patients.(188-191)

6. Athlete’s heart is not cumulative.

Athlete’s who keep training later in life have no significant further increase in heart size.(192-195) The heart seems to increase in size to meet the demands of exercise, and no more.

It’s possible that “athlete’s heart” is still a form of mild damage, but has a longer progression than other forms of heart disease. If this is the case, it could be that lots of exercise is still bad for the heart, but it takes longer for it to cause problems. However, this seems unlikely after looking at the rest of the evidence.

Heart failure also tends to get worse in a short time.(196-198)

7. Athlete’s with big hearts are usually asymptomatic.

Athletes with enlarged hearts rarely have obvious symptoms of heart disease, like chest pain, nausea, exercise intolerance, and trouble breathing.(199-201)

However, this doesn’t prove athlete’s heart is not a sign of heart disease. Several studies have found that asymptomatic athletes can have extensive heart damage and atherosclerosis.(202-205) There are several problems with these studies that we’ll cover in another article, but they do show that an athlete without symptoms is not 100% safe.

8. Athlete’s hearts usually have healthy mitochondria.

As the heart grows larger in heart failure, there is a decrease in mitochondrial density and function.(206-208)

In “athlete’s heart,” there is an increase in mitochondrial density and function of the heart and other muscles.(209-210) This is one of the reasons moderate endurance training is used to help rehabilitate heart failure patients — it helps increase mitochondrial density and protect heart cells from dying.(211)

That said, mitochondrial function is only one measurement of heart health. It’s possible that extreme training can damage the heart in other ways while improving mitochondrial density and performance.

9. “Athlete’s heart” is largely caused by different genes and signaling pathways than heart disease.

There are major differences in gene expression and molecular signaling between heart disease and “athlete’s heart.”(212,213) In fact, many studies are looking at activating some of the same pathways that cause “athlete’s heart” to prevent or treat heart disease.(214-217)

On the other hand, many of these studies were done on animals, and it’s not clear how relevant they are for humans. There are also several chemical pathways that are activated in heart disease *and* “athlete’s heart.”(218,219) It’s also possible that “athlete’s heart” is a different kind of heart disease and is mediated through different pathways. At this point we don’t know.

10. Elite athletes live a long time.

Elite athletes, of any kind, who often have enlarged hearts, tend to live longer than the average population.(2202-223) Interestingly, endurance athletes generally live the longest, despite usually having the largest hearts.

The studies that found elite athletes live longer didn’t measure heart size, and it’s possible that the athletes with the largest hearts were also the most likely to die. It’s also possible that the reason these athletes lived longer was mainly due to other factors, but a recent review found that “lower cardiovascular disease mortality is likely the primary reason for their better survival rates.”(224)

These are observational studies, and they don’t prove having a large heart improves your quality of life or lifespan. However, they do indicate that “athlete’s heart” probably won’t increase your chances of dying, despite any potential problems it may or may not cause.

The Risks of Having a Large, Athlete’s Heart

Most data suggests that “athlete’s heart” and heart disease are two distinct conditions, and “most authors… believe that athletic left ventricular hypertrophy [heart enlargement] is a purely physiological [safe] condition.”(225-239)

It’s not clear if this means athlete’s hearts are *healthier*, but it does indicate they aren’t *less* healthy.

According to Dr. Aaron L. Baggish, the author of a recent review on this topic, athlete’s heart is most likely a “beneficial physiologic adaptation” to exercise.(240,241)

However, there are researchers who disagree.(242-246) Some data indicates that in certain people, “athlete’s heart” might not be completely benign. It’s not clear if training caused their heart problems, and there’s some question as to whether or not these abnormalities are even problems in the long-run.

There is no direct evidence that the *structural* changes in “athlete’s heart” are dangerous.

Nevertheless, there are studies that seem to provide indirect evidence that too much exercise, especially endurance training, can damage the heart and blood vessels, and may cause dangerous heart rhythm disorders.

 

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200. Baggish AL, Wood MJ. Athlete’s heart and cardiovascular care of the athlete: scientific and clinical update. Circulation. 2011 Jun 14;123(23):2723-35. Abstract: https://pmid.us/21670241 | Full Text: https://goo.gl/fWiEj

201. Pelliccia A, Maron BJ, De Luca R, et al. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation. 2002 Feb 26;105(8):944-9. Abstract: https://pmid.us/11864923 | Full Text: https://goo.gl/AhVWw

202. Wilson M, O’Hanlon R, Prasad S, et al. Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes. J Appl Physiol. 2011 Jun;110(6):1622-6. Abstract: https://pmid.us/21330616 | Full Text: https://goo.gl/IQF8f

203. Breuckmann F, Möhlenkamp S, Nassenstein K, et al. Myocardial late gadolinium enhancement: prevalence, pattern, and prognostic relevance in marathon runners. Radiology. 2009 Apr;251(1):50-7.  Abstract: https://pmid.us/19332846 | Full Text: https://goo.gl/RK4cr

204. La Gerche A, Burns AT, Mooney DJ, et al. Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes. Eur Heart J. 2012 Apr;33(8):998-1006. Abstract: https://pmid.us/22160404 | Full Text: Received from author (with editorial).

205. Nassenstein K, Breuckmann F, Lehmann N, et al. Left ventricular volumes and mass in marathon runners and their association with cardiovascular risk factors. Int J Cardiovasc Imaging. 2009 Jan;25(1):71-9. Abstract: https://pmid.us/18677576 | Full Text: NA

206. Goffart S, von Kleist-Retzow JC, Wiesner RJ. Regulation of mitochondrial proliferation in the heart: power-plant failure contributes to cardiac failure in hypertrophy. Cardiovasc Res. 2004 Nov 1;64(2):198-207. Abstract: https://pmid.us/15485678 | Full Text: https://goo.gl/WZmsf

207. Karamanlidis G, Bautista-Hernandez V, Fynn-Thompson F, et al. Impaired mitochondrial biogenesis precedes heart failure in right ventricular hypertrophy in congenital heart disease. Circ Heart Fail. 2011 Nov;4(6):707-13. Abstract: https://pmid.us/21840936 | Full Text: https://goo.gl/jcpaF

208. Abel ED, Doenst T. Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy. Cardiovasc Res. 2011 May 1;90(2):234-42. Abstract: https://pmid.us/21257612 | Full Text: https://goo.gl/jHPWe

209. Goffart S, von Kleist-Retzow JC, Wiesner RJ. Regulation of mitochondrial proliferation in the heart: power-plant failure contributes to cardiac failure in hypertrophy. Cardiovasc Res. 2004 Nov 1;64(2):198-207. Abstract: https://pmid.us/15485678 | Full Text: https://goo.gl/WZmsf

210. Abel ED, Doenst T. Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy. Cardiovasc Res. 2011 May 1;90(2):234-42. Abstract: https://pmid.us/21257612 | Full Text: https://goo.gl/MvAMo

211. Ventura-Clapier R, Mettauer B, Bigard X. Beneficial effects of endurance training on cardiac and skeletal muscle energy metabolism in heart failure. Cardiovasc Res. 2007 Jan 1;73(1):10-8. Abstract: https://pmid.us/17045979 | Full Text: https://goo.gl/FMBct

212. Weeks KL, McMullen JR. The athlete’s heart vs. the failing heart: can signaling explain the two distinct outcomes? Physiology (Bethesda). 2011 Apr;26(2):97-105. Abstract: https://pmid.us/21487028 | Full Text: https://goo.gl/54BdI

213. Dorn GW 2nd. The fuzzy logic of physiological cardiac hypertrophy. Hypertension. 2007 May;49(5):962-70. Abstract: http:/pmid.us/17389260 | Full Text: https://goo.gl/oTrHf

214. Bernardo BC, Weeks KL, Pretorius L, et al. Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. Pharmacol Ther. 2010 Oct;128(1):191-227. Abstract: https://pmid.us/20438756 | Full Text: NA

215. Fernandes T, Soci UP, Oliveira EM. Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants. Braz J Med Biol Res. 2011 Sep;44(9):836-47. Abstract: https://pmid.us/21881810 | Full Text: https://goo.gl/1zr81

216. McMullen JR, Jennings GL. Differences between pathological and physiological cardiac hypertrophy: novel therapeutic strategies to treat heart failure. Clin Exp Pharmacol Physiol. 2007 Apr;34(4):255-62. Abstract: https://pmid.us/17324134 | Full Text: https://goo.gl/GGr8F

217. Ellison GM, Waring CD, Vicinanza C, et al. Physiological cardiac remodelling in response to endurance exercise training: cellular and molecular mechanisms. Heart. 2012 Jan;98(1):5-10. Abstract: https://pmid/21880653 | Full Text: https://goo.gl/XeKw8

218. O’Neill BT, Abel ED. Akt1 in the cardiovascular system: friend or foe? J Clin Invest. 2005 Aug;115(8):2059-64. Abstract: https://pmid.us/16075047 | Full Text: https://goo.gl/DMhov

219. Shiojima I, Sato K, Izumiya Y, et al. Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. J Clin Invest. 2005 Aug;115(8):2108-18. Abstract: https://pmid.us/16075055 | Full Text: https://goo.gl/jo8z0

220. Teramoto M, Bungum TJ. Mortality and longevity of elite athletes. J Sci Med Sport. 2010 Jul;13(4):410-6.  Abstract: https://pmid.us/19574095 | Full Text: https://goo.gl/Maal6

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222. Reimers CD, Knapp G, Reimers AK. Does physical activity increase life expectancy? A review of the literature. J Aging Res. 2012;2012:243958. Abstract: https://pmid.us/22811911 | Full Text: https://goo.gl/3u0jC

223. Grimsmo J, Maehlum S, Moelstad P, et al. Mortality and cardiovascular morbidity among long-term endurance male cross country skiers followed for 28-30 years. Scand J Med Sci Sports. 2011 Dec;21(6):e351-8. Abstract: https://pmid.us/21477204 | Full Text: NA

224. Teramoto M, Bungum TJ. Mortality and longevity of elite athletes. J Sci Med Sport. 2010 Jul;13(4):410-6. Abstract: https://pmid.us/19574095 | Full Text: https://goo.gl/Maal6

225. Baggish AL, Wood MJ. Athlete’s heart and cardiovascular care of the athlete: scientific and clinical update. Circulation. 2011 Jun 14;123(23):2723-35. Abstract: https://pmid.us/21670241 | Full Text: https://goo.gl/fWiEj

226. Maron BJ, Pelliccia A. The heart of trained athletes: cardiac remodeling and the risks of sports, including sudden death. Circulation. 2006 Oct 10;114(15):1633-44. Abstract: https://pmid.us/17030703 | Full Text: https://goo.gl/qirCb | Author Contact: <hcm.maron@mhif.org>

227. Hildick-Smith DJ, Shapiro LM. Echocardiographic differentiation of pathological and physiological left ventricular hypertrophy. Heart. 2001 Jun;85(6):615-9. Abstract: https://pmid/11359735 | Full Text: https://goo.gl/kr8wy

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Posted in Articles, Endurance, Health

374 Comments

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