A heart question...

[icomefrombirmingham]

The left ventricle is the one that pumps oxygen rich blood "out" of the heart to the body.
The size of the ventricle walls, which provide the pump with its strength is therefore rather important, but bigger is not necessarily better.
Generally, I understand, a wall thickness of <59 is considered good but greater then 75 is considered a problem as it is an indication that the heart has been working too hard for too long (and is an indication that the heart is having to overcome an underlying problem such as HBP, valve insufficiencies etc. etc.).
However, in my ignorance it seems to me that someone who has been athletic for much of their lives, particularly in their formative years, could well have thicker than "average" ventricle walls, so that the <59->75 range might not be applicable.

Is there any evidence for this?

Thanks,
Brent

[BobD]

Yes this is true according to my cariologist and as you get older the septum (separates the chambers) gets thicker too.

[icomefrombirmingham]

Bob,
Thanks for the info.
As you may have guessed, I have a personal interest in what is considered the average thickness of the left ventricle relative to the thickness of my very own ventricle !
Also, the measurement of the thickness is pretty tricky, at least using ultre-sound machines, as the angle through the heart at which the beam is aimed has to be the same each time to get an accurate read. If the angle is off by a few degrees it can give the appearance of significant thickening (or I suppose thinning) of the wall.
Still, better the inaccuracies of an ultra-sound than the accuracy of an autopsy!
Brent

[canoeguy]

I had an atrial fib in August of 1994 determined to be caused by an enlarged heart. I was 45 years old.

4 months earlier I paddled solo and came in first in a 16.5 mile canoe race which lasted about 3 hours and included 3 steep portages. I was at the peak of training and feeling like the bull of the woods.

One month after my diagnosis I ended up at the National Institute of Health in Bethesda MD to participate in a clinical study protocol. I spent the day being evaluated against the study's entry criteria. Finally at the end of the day I had another echo. As I lay there quietly, the room seemed to fill with white coats as I imagined everyone wanted to see such a rare cardiovascular anomaly.

At the final interview the doc said there was nothing wrong with me and I was to stop all meds. When no pathology is found following an atrial fib the default dx is usually stress. I just hit the mega millions medical lottery!!!!

Based on "interpretation" of my echo, the original cardiologist along with an "objective" review by his partners, determined my atrial fib was caused by an enlarged heart. On a scale of 1 - 10 my heart wall was a 6. He put me on meds that knocked me on my butt despite that all other tests showed high normal heart function.

The cardiologist told my dentist it didn't matter which local anesthesia I got because I could die at any moment. The dentist almost divorced me.

Problem was the angle at which the echo was viewed by the cardiologist. The cordae tendonae lined up to cause the heart wall to appear to be pathologically thickened.

[Snail Space]

I had an atrial fib in August of 1994 determined to be caused by an enlarged heart. I was 45 years old.

4 months earlier I paddled solo and came in first in a 16.5 mile canoe race

If I remember rightly Xeno had atrial fibrillation before winning an Olympic Gold, so you're in good company. He must have been doing huge training volumes over the preceding years, so I presume that his AF might have been related to left ventricular hypertrophy too.

Episodic AF can also be caused by (amongst other things) alcohol bingeing, but I doubt that an Olympic athlete would succumb to that. In Scandinavia, though, alcohol is so expensive that they save up beer money, and then go on kamikaze drinking sprees. It is thereafter quite common to have a few young men, without heart disease, spend a few days in AF. This may be caused by alcohol leaching out magnesium (an element that can help stabilise heart rhythm).

That was nothing to do with erging, but nevertheless interesting I hope.

Cheers
Dave

[Alissa]

Here's a link to a blog entry of Xeno's discussing atrial fibrillation.

Alissa

[icomefrombirmingham]

Jeepers! This is all very interesting to me. I am in Niagara Falls and locally have to rely on an internist not a specialist cardiologist.
He is looking at the thickness of the ventricle....and the measurements have gone 64-70-66 the last three times. That's why I asked the question about thickness in "athletic" types. If 59 or less is considered normal, then it would only take a slight thickening of the heart due to athletic endeavors to make my 66 (average) reading look pretty good.
The other key measurement is the ejection fraction, mine is on the low side of normal according to my guy locally, but in two referrals over the years, the consultants have seen no problem with the EF.
I am being followed regularly because of a bicuspid aortic valve....which the local guy told me once in these words...."you'll have to have a replacement....if you live long enough"!!!!!!......you'd think in 7 or 10 years of training they could spend 20 minutes or so on normal human interaction with patients!!
Thanks for all the info.....I look forward to reading Xeno's log.
Regards,
Brent

[John Rudoff, M. D.]

It is correct that chronic athletic training will 'enlarge' the heart. However:
First, enlargement ('hypertrophy') refers either to the cavity or chamber-dimension of the ventricle; or, to the thickness of the walls. (These 2 processes have unfortunately been named 'eccentric' or 'concentric' hypertrophy in the cardiac literature, which is a bit confusing.)
Second, it is generally (though NOT completely) considered that resistance training causes muscle thickening and that distance or aerobic training causes chamber enlargement. This used to be considered an article of certainty amongst cardiologists, but this is no longer considered to be completely accurate.
Third, the original reason that this has been considered interesting is that there is a quite uncommon congenital abnormality called 'HCM', 'hypertrophic cardiomyopathy' (formerly called 'IHSS'), which causes thickening of some or all of the heart muscle. The distinctive feature of this abnormality, though, is actual disarray of the cardiac fibers, usually only discernible on autopsy or biopsy, and this condition is the leading cause of sudden cardiac death (SCD) among young (under 35) athletes. The reason that this has been interesting is that there are some general similarities in the size and shape of the heart muscle (the 'gross morphology') in the athletics-related hypertrophy and the congenital abnormality. However, only the latter, the congenital form, carries the marker of risk for SCD. Athletic hypertrophy tends to regress pretty rapidly--under 6--10 weeks--after stopping hard training.
Fourth, the work of a cardiologist named P. Spirito in Italy (who by the way trained at NIH) very interestingly demonstrated that of the entire Italian Olympic team, very, very few had significant thickening of the wall between the 2 sides of the heart; but of those, most were rowers or paddlers. The exact mechanism of this is as yet uncertain. This is probably a function of the unusual combination of both resistance and aerobic training to which we subject ourselves.
This is not, repeat and underscore is not, associated with an increased risk of SCD.
Last, echocardiography is the best way non-invasively to measure the size and thickness of the cardiac chambers; but it is technician-dependent; there can frequently be minor variations of measurement according to the exact angle of the ultrasound beam...

[icomefrombirmingham]

It is correct that chronic athletic training will 'enlarge' the heart. However:
First, enlargement ('hypertrophy') refers either to the cavity or chamber-dimension of the ventricle; or, to the thickness of the walls. (These 2 processes have unfortunately been named 'eccentric' or 'concentric' hypertrophy in the cardiac literature, which is a bit confusing.)
Second, it is generally (though NOT completely) considered that resistance training causes muscle thickening and that distance or aerobic training causes chamber enlargement. This used to be considered an article of certainty amongst cardiologists, but this is no longer considered to be completely accurate.
Third, the original reason that this has been considered interesting is that there is a quite uncommon congenital abnormality called 'HCM', 'hypertrophic cardiomyopathy' (formerly called 'IHSS'), which causes thickening of some or all of the heart muscle. The distinctive feature of this abnormality, though, is actual disarray of the cardiac fibers, usually only discernible on autopsy or biopsy, and this condition is the leading cause of sudden cardiac death (SCD) among young (under 35) athletes. The reason that this has been interesting is that there are some general similarities in the size and shape of the heart muscle (the 'gross morphology') in the athletics-related hypertrophy and the congenital abnormality. However, only the latter, the congenital form, carries the marker of risk for SCD. Athletic hypertrophy tends to regress pretty rapidly--under 6--10 weeks--after stopping hard training.
Fourth, the work of a cardiologist named P. Spirito in Italy (who by the way trained at NIH) very interestingly demonstrated that of the entire Italian Olympic team, very, very few had significant thickening of the wall between the 2 sides of the heart; but of those, most were rowers or paddlers. The exact mechanism of this is as yet uncertain. This is probably a function of the unusual combination of both resistance and aerobic training to which we subject ourselves.
This is not, repeat and underscore is not, associated with an increased risk of SCD.
Last, echocardiography is the best way non-invasively to measure the size and thickness of the cardiac chambers; but it is technician-dependent; there can frequently be minor variations of measurement according to the exact angle of the ultrasound beam...

John,
Thank you for this response. I have now run across two rowers who have gone through aortic valve replacement...one on here.....the other yesterday afternoon at the wind-up pig roast for our rec. rowing league. Both of them seem to be doing splendidly with their respective rowing endeavours.
Thanks for clearing up the "athletic thickening" question. If any thickening effect of hard training dissipates in 10 weeks or less, then mine would have returned to normal approximately 25 years ago...I think I can take it from that that any thickening now is due to the regurgitation of blood from the valve!
Next time I see my doctor, in January, I will ask for a full assesment and stress test. This should be in lots of time for next season.
Thanks again,
Brent

[BobD]

Well folks, after having recurring attacks of elevated irregular heartbeats, lasting over a couple of hours, my girlfriend convinced me to see another cardiologist who is her personal friend.

I have a leaking mitral valve, very evident on ultrasound

Every heartbeat is pumping blood back into my lungs and the harder I exercise the worse it is. The chamber has enlarged to compensate for the lost blood volume and that is where the irregular heartbeat is generated. He has limited me to an HRmax of 130-140 and the good news is that they endoscopically repair such. The "Gotcha" is they have to stop and restart ME He says the sooner the better or I will end up with heart insufficiency and water in my lungs which is...not..good.

[douglashaller]

I've seen this mentioned in literature a couple of times, sounds like an enlarged heart could be a sign of a strong heart, anyone have other info about it?

google "Rowers heart", and you will find a number of links.

4. THE ROWER'S HEART- Research from Italy
See #4 on the reference list

The most extensive study I know of regarding the impact of training on heart dimensions was completed by Pelicia et al. in 1991. This group performed echocardiographic analysis on 947 athletes competing in 25 different sports to determine the impact of specific sports training on the heart. 92 of these athletes were rowers. Soccer players, cyclists, runners, weightlifters, volleyball players, yacht racers, etc. were all examined.

Now, I have already told you that the endurance athlete generally has a bigger heart than untrained people due primarily to a greater heart ventricle diameter. Of all the different athletic populations tested in this study, the rowers had the biggest hearts on average, whether measured as LV end diastolic diameter, or mass index. Cyclists, cross country skiers and water polo players weren't far behind though, supporting the general big heart/endurance athlete theme. However, the more interesting finding was this: Rowers also tended to have thicker heart walls, a charecteristic we often ascibe to hypertension or cardiomyopathy. In fact, 12 of the rowers had heart walls that were thick enough to be diagnosed as cardiomyopathic in the untrained population, (along with 3 canoists and one cyclist). This abnormal wall thickness was completely absent among the other athletic groups. Why rowers? Is rowing bad for the heart? Well, it appears that the mechanics of rowing create both a volume overlaod and a pressure overload stress on the heart. This pressure overload is experienced at the catch when a large percentage of muscle mass is statically contracting (and the breath is briefly held). An increase heart wall thickness in response to pressure overload is analogous to an increase in biceps thickness after a weight training program. The heart responds in a functional way to the unique combined volume/force demands created by rowing, by increasing both volume and wall thickness. Is this pathological? Among those athletes with the thickest hearts, 8 were in the top 3 in the world in their sport and 3 were Olympic gold medalists. Six of the athletes with thick heart walls were retested after a 90 day period without heavy training following the 1988 Olympics . The thickness of the heart had decreased dramatically. This demonstrated the adaptive nature of the large wall thickness. So, it seems that "The Rowers Heart" may be a unique hybrid of the "Endurance athlete's heart" in hard training competitive rowers. But, in this group, this difference was functional and adaptive, not pathological.