# Yo, Cardiologists: Help a Nurse Understand Left Ventricle Enlargement
**URL:** https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312
**Category:** Factual Questions
**Created:** [February 8, 2024, 5:18pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312 "2024-02-08T17:18:59Z")
**Posts on this page:** 20
**Page:** 1
### Author:  [@Malienation](https://boards.straightdope.com/u/Malienation)
#### Post date: [February 8, 2024, 5:18pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/1 "2024-02-08T17:18:59Z")
Left ventricle enlargement subsequent to two distinct cases has always puzzled me. Case 1: enthusiastic exerciser has enlargement of the left ventricle due to significant cardio. This is good. Case 2: patient has enlargement of the left ventricle due to significant and long term untreated hypertension. This is bad.
Why are these two cases fundamentally different? I have found elsewhere statements to the effect that the LV enlargement in the case of the hypertensive patients is bad because the walls of the LV become stiff and inflexible, effecting poor pumping efficiency. Okay, but why don’t the walls of the exerciser become stiff and inflexible? Their hearts are both working harder. In the case of the HTN patient I figure this is because of increased afterload making the heart struggle to pump and increased preload filling the heart more, amirite?
You wouldn’t believe how much aggravation I’ve gone through to find the answer to this question. Yeah, I’m looking at you, Reddit. So, please. Bless me with your wisdom.
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### Author:  [@Riemann](https://boards.straightdope.com/u/Riemann)
#### Post date: [February 8, 2024, 5:26pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/2 "2024-02-08T17:26:37Z")
The background discussion in this paper speaks directly to your question.
> **[Aerobic exercise training promotes physiological cardiac remodeling involving...](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/)**
>
> Left ventricular (LV) hypertrophy is an important physiological compensatory mechanism in response to chronic increase in hemodynamic overload. There are two different forms of LV hypertrophy, one physiological and another pathological. Aerobic...
> Physiological cardiac hypertrophy may be exemplified by the LV remodeling induced by exercise training… The LV remodeling induced by physiological stimuli leads to preserved or even enhanced LV function, decreased collagen content, lack of fibrosis, increased angiogenesis, improved myocardial antioxidant capacity ([78](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B78)), and decreased mitochondrial dysfunction ([7](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B7)) and has been shown to prevent cardiomyocyte apoptosis ([44](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B44)).
>
> … [Whereas] LV remodeling induced by pathological stress leads to progressive declines in cardiac output, myocardial rarefaction, increased apoptosis, cardiomyocyte metabolism switch from fatty acid to glucose use, and increased fibrosis ([35](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B35), [49](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B49)).
>
> At the molecular level, reexpression of fetal genes is used as a biomarker of pathological cardiac hypertrophy. Among them, atrial and brain natriuretic peptide, α-skeletal myosin, and α- to β-myosin heavy chain (MHC) expression ratio have been the most frequently reported ([45](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B45), [51](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B51), [102](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B102)). Although the best known effects of atrial and brain natriuretic peptide are natriuresis and blood pressure regulation, these small peptides also contribute to preventing cardiac hypertrophy and fibrosis in the adult heart ([66](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B66)). The main release factor of the atrial peptides factor is the wall strain induced by the increased workload, but other mechanisms are still being uncovered ([96](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B96)).
> … distinct morphological adaptations to the heart; in particular, to the LV. The LV remodeling by pressure overload is characterized by concentric hypertrophy, whereas LV remodeling by volume overload induces eccentric hypertrophy ([70](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B70)). At the cellular level, concentric hypertrophy is characterized by parallel addition of new sarcomeres and lateral growth of individual cardiomyocytes. This hypertrophy generally leads to increased LV wall thickness with either decreased LV chamber diameter (pathological) or no change on LV chamber diameter (physiological exercise training induced) ([34](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4537939/#B34)). The eccentric hypertrophy due to volume overload is characterized by addition of sarcomeres in series and longitudinal cardiomyocyte growth…
And see the diagram of the differences in remodeling.
That seems like a pretty comprehensive summary of what was known at least in 2015.
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### Author:  [@DSeid](https://boards.straightdope.com/u/DSeid)
#### Post date: [February 8, 2024, 6:37pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/3 "2024-02-08T18:37:53Z")
It must be noted though that there are limits to the healthy remodeling associated with recurrent extreme endurance activity. There is damage during those events and it requires recovery.
[Cardiovascular Damage Resulting from Chronic Excessive Endurance Exercise - PMC](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6179786/#:~:text=Abnormally%20increased%20levels%20of%20cardiac,of%20integrity%20of%20desmosomal%20connections).
Lots of good stuff in that article. This just one of the bits.
> [@](#):
>
> In a study of 102 ostensibly healthy male runners ranging from 50 to 72 years old, who had completed at least five marathons during the past three years compared to 102 age-matched control subjects, CMR was used to assess the effects of chronic long distance running on myocardial structure.[45](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6179786/#b45-ms109_p0312)Approximately 12% of these apparently healthy marathon runners showed evidence for patchy myocardial scarring, a rate three-fold higher than that in age-matched control subjects. This study indicates that in endurance athletes, CMR with late gadolinium enhancement can reliably detect areas of patchy fibrosis.[45](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6179786/#b45-ms109_p0312) Of additional concern, the CAD event rate during two-year follow up was significantly higher in the marathon runners than in controls (P \< .0001).
“Athletic heart” is almost always a good thing but there is the almost in there.
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### Author:  [@Malienation](https://boards.straightdope.com/u/Malienation)
#### Post date: [February 8, 2024, 6:39pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/4 "2024-02-08T18:39:49Z")
Holy crap, that was fast. Holy crap #2, you’re right, this appears to be exactly what I’m looking for. Gonna ponder this tonight, there’s a lot to chew on here.
I’ll post here again after reading this in full and will sum up the article for interested Dopers that aren’t up to grinding through a stiff journal article.
And thanks
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### Author:  [@DSeid](https://boards.straightdope.com/u/DSeid)
#### Post date: [February 8, 2024, 6:41pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/5 "2024-02-08T18:41:16Z")
Suck on it Reddit! 😅
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### Author:  [@Malienation](https://boards.straightdope.com/u/Malienation)
#### Post date: [February 8, 2024, 6:46pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/6 "2024-02-08T18:46:49Z")
Yet another interesting article to look at. Thanks.
This certainly would help explain a phenomenon that periodically shows up in popular media, the fact that people who are extremely active throughout their lives don’t live as long as people that are only moderately active. Explanations tend to be sparse, but usually researchers are quoted that they suspect either 1) very active people tend to be risk-takers until their luck runs out, or 2) cumulative effects of chronic inflammation.
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### Author:  [@Riemann](https://boards.straightdope.com/u/Riemann)
#### Post date: [February 8, 2024, 7:02pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/7 "2024-02-08T19:02:31Z")
I should have noted that only the first part that I quoted talks unambiguously about differences such as fibrosis between physiological and pathological hypertrophy. The second part on morphology is describing pressure overload vs volume overload as observed in two types of training, resistance and cardio. And it says
> Both pathological and physiological cardiac hypertrophy may be triggered by pressure or volume cardiac overload.
So I’m not really sure if the second part I quoted on morphology is relevant to your question, at least that paper doesn’t explain if/how it’s relevant.
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### Author:  [@DSeid](https://boards.straightdope.com/u/DSeid)
#### Post date: [February 8, 2024, 9:42pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/8 "2024-02-08T21:42:51Z")
Relevant to the OP question most is their explanation regarding how the physiologic adaptations have matched new blood vessel growth and cardiac muscle mass increase, along with decreased collagen, while in pathological adaptations the new blood vessel growth does not keep up and collagen increases leading to stiffness and poorer function.
The detail though on the miRNA mechanisms of those changes? Glad someone understands it! It’s enough for me to get that there are specific patterns that are part of those responses, which may lead to drug targets for pathological conditions.
The bit about the difference between eccentric and concentric muscle growth as adaptations to aerobic exercise and strength training respectively? Makes me wonder what sort of adaptations happen in those who have a balanced approach?
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### Author:  [@Riemann](https://boards.straightdope.com/u/Riemann)
#### Post date: [February 8, 2024, 9:50pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/9 "2024-02-08T21:50:35Z")
> [@DSeid](#):
>
> The detail though on the miRNA mechanisms of those changes?
I didn’t link the paper for the small RNA research itself that is reported, that doesn’t seem especially interesting, just for the introductory background.
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### Author:  [@DSeid](https://boards.straightdope.com/u/DSeid)
#### Post date: [February 8, 2024, 9:54pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/10 "2024-02-08T21:54:51Z")
But it really is interesting!
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### Author:  [@Riemann](https://boards.straightdope.com/u/Riemann)
#### Post date: [February 8, 2024, 10:00pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/11 "2024-02-08T22:00:13Z")
I mean, all it’s really doing is identifying the species that mediate the regulatory pathways here. It’s not remarkable that small RNAs are involved, they are involved in gene regulation everywhere, I’m not seeing any unusual mechanisms. So I don’t think the highly technical small RNA stuff is as interesting (to anyone other than a specialist researcher) as just what is being regulated and in response to what.
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### Author:  [@DSeid](https://boards.straightdope.com/u/DSeid)
#### Post date: [February 8, 2024, 10:06pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/12 "2024-02-08T22:06:28Z")
The whole field of miRNA developed after my education. 30% of proteins regulated by them. Yeah much more in the weeds than I can absorb but the fact they may be reaching enough understanding and identification to develop as drug targets is interesting to me, anyway.
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### Author:  [@Malienation](https://boards.straightdope.com/u/Malienation)
#### Post date: [February 8, 2024, 10:42pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/13 "2024-02-08T22:42:41Z")
Ah, so collateral circulation develops in the exercisers but not in the hypertensives? Interesting…
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### Author:  [@DavidNRockies](https://boards.straightdope.com/u/DavidNRockies)
#### Post date: [February 8, 2024, 10:50pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/14 "2024-02-08T22:50:41Z")
I was looking into this a couple of years ago. I found this article helpful:
> **[The Athlete Grey Zone: Distinguishing Pathologic From Physiologic Left...](https://www.acc.org/latest-in-cardiology/articles/2014/10/14/11/02/the-athlete-grey-zone-distinguishing-pathologic-from-physiologic-left-ventricular-hypertrophy)**
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### Author:  [@DSeid](https://boards.straightdope.com/u/DSeid)
#### Post date: [February 8, 2024, 10:58pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/15 "2024-02-08T22:58:20Z")
I was envisioning more capillary density?
ETA apparently confirmed on quick search.
> **[Exercise training increases myocardial capillary density rather than coronary...](https://www.physoc.org/abstracts/exercise-training-increases-myocardial-capillary-density-rather-than-coronary-artery-size-or-function-in-the-healthy-and-diabetic-heart/)**
>
> Introduction: Exercise training (EX) is postulated to improve myocardial vascular structure and function, but this idea has not been consistently
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### Author:  [@LSLGuy](https://boards.straightdope.com/u/LSLGuy)
#### Post date: [February 8, 2024, 11:24pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/16 "2024-02-08T23:24:40Z")
Looking at it from a very very rough mechanical analog POV (always dangerous), there’s a big difference between a pump running at sustained high RPM and one lugging at low RPM pushing against heavy resistance.
It’s not surprising to me that when the pump is alive and able to self-redesign in response to its loads, the one stuck lugging at low RPM into high resistance picks a different response than the pump forced to produce high output into low resistance, but for sustained intervals.
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### Author:  [@DSeid](https://boards.straightdope.com/u/DSeid)
#### Post date: [February 8, 2024, 11:49pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/17 "2024-02-08T23:49:18Z")
Very much accurate. The question though was why pumps that grossly look the same function differently.
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### Author:  [@Vlad\_Igor](https://boards.straightdope.com/u/Vlad_Igor)
#### Post date: [February 9, 2024, 3:50pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/18 "2024-02-09T15:50:11Z")
So, in terms of LVEF, exercise produces LVH with a good ejection fraction, and heart failure produces LVH with a poor ejection fraction. Did I get that right?
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### Author:  [@DSeid](https://boards.straightdope.com/u/DSeid)
#### Post date: [February 10, 2024, 11:05pm UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/19 "2024-02-10T23:05:50Z")
Yes. Albeit the question is more the why when both have similar muscle thickness.
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### Author:  [@Vlad\_Igor](https://boards.straightdope.com/u/Vlad_Igor)
#### Post date: [February 12, 2024, 12:44am UTC](https://boards.straightdope.com/t/yo-cardiologists-help-a-nurse-understand-left-ventricle-enlargement/997312/20 "2024-02-12T00:44:31Z")
20 years ago (yeeesh!) I was the coordinator and blood sample procurer for a marker for CHF. I seem to recall pericardial effusion was a feature that created the spiral of more effusion, less LVEF, less pressure to move the fluid out. With exercise-induced LV hypertrophy, I wouldn’t expect effusion. So, my assumption is effusion is the why.