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Tuesday, January 15, 2019

Comments on the "Extreme Exercise Hypothesis"

Dr. THM Eijsvogels  from the Netherlands has written extensively about the relationship between endurance exercise levels and various cardiovascular outcomes and findings.

His  recent (1) review with an annotated references list  is available in full text on line.

Maybe the first question should be "what do you  mean "extreme'?

U.S. National and WHO guidelines  recommend 250 minutes of moderate exercise per week or 125 minutes of vigorous ( greater than 7 METS) per week based on in part a well established  reduction in cardiovascular mortality and morbidity as well as numerous other health benefits. However ,US guidelines also state that exercise above that levels is associated with added benefits. But how far "above" should one go. Can you go too far?

Is there a U-shaped curve when you plot health risk of the Y axis and exercise training volume on the x axis? If so, can the inflection point be defined?

Arem (2015) combined data from six prospective population based cohorts ( 661,137 individuals).Maximal all-cause mortality risk reduction was noted at exercise level of 3-5 times current recommendations and even  those exercising at 10 times current recommendation had a lower mortality risk  ( HR 0.69, 95% CI 0.59-0.78). But at the highest level the degree of risk reduction was  less than that achieved by lower exercise levels,

Ten times would be 25 hours ( one full day) of moderate exercise per week,I suggest very few exercise at that level while many preparing for a marathon would likely exercise  as much as 7 or 8 hours a week (3-5 the recommend levels). Olympic rowers might exercise as much as 17-18 hours a week .The relatively few exercisers at the highest volume make the confidence intervals for HR estimation at that exercise level so large as to not be reliable or useful.

Eijsvogels summarizes the quest for "what do mean by extreme" with this understatement:

" Based on limited current evidence and numerous potential confounders, it is difficult to delineate an upper limit for the for the benefits of physical activity at this time."

So there is no epidemiologic support for a U shaped relationship between exercise volume and health risk at least as measuring all-cause mortality. But what about certain medical conditions that have been reported to be increased in long time endurance athletes at levels said to be higher than those who exercise less.

The usual suspects include 1) atrial fibrillation 2)cardiac fibrosis 3)coronary artery calcifications.

I have commented on atrial fibrillation before ( see here) and will likely have more to say later and have blogged about the coronary  calcification paradox before( see here).

Cardiac or myocardial fibrosis (MF) is detected by cardiac MRI imaging with injection of gadolinium  and  is referred to as late gadolinium enhancement (LGE).There is a recognized pattern of LGE designating the  localized fibrosis following a heart attack. The  LGE pattern at issue in endurance athletes is something different-, i.e. a non-ischemic pattern. .

Van de Schoor et al did a systematic Pub Med search (2) and identified 65 athletes with MR imaging. A subgroup (30 subjects) were identified in an MRI study of 509 athletes.

The most frequent pattern was that located near the interventricular septum  and right ventricular insertion points. The significance of this type of myocardial fibrosis is unclear.

Levine (3) et al have suggested that LGE in endurance athletes may not represent irreversible fibrosis and note that a similar pattern of LGE at the insertion points is seen in hypertrophic cardiomyopathy and also pulmonary hypertension.

Chan et al (4) described the histopathology in patients with hypertrophic cardiomyopathy (HCM). In a multi institutional study of 1293 HCM 10% demonstrated small areas of LGE in the area of  ventricular insertion into the ventricular septum. Biopsies showed " greatly expanded extracellular space" with intestinal fibrosis and disorganized myocyte patterns." The authors emphasized the pattern was not that of myocyte death and replacement fibrosis.

Perhaps a similar histologic pattern would be found in the endurance athletes but to my knowledge that information is not available.

LGE has been reported in participants in various sports , the first case was a soccer player. Its significance and underlying mechanism  ( repetitive microtrauma, transient pulmonary artery pressure over load ??) are  not known.

 I have to agree with Eijsvogels' summary statement :  )"There is limited evidence that supports the "extreme exercise hypothesis",the most compelling relating to the increased risk of atrial fibrillation at high volume of exercise. 2) cardiac abnormalities may be present in a small proportion of the most active veteran athletes …"

1)Eijsvogels, TMH, er al The "Extreme Exercise Hypothesis:Recent findings and cardiovascular
health Implications. C"urr Teat Options Cardio Med 2018 20:84

2)Van de Schoor, F ,et all Myocardial Fibrosis in athletes . Mayo Clin Proc 2016,2016

3)Abdullah, Sm Lifelong Physical Activity regardless of does is not associated with myocardial
fibrosis. Circ Cardiovas Imaging. 2016 9,:e005511 (ful text)

4)Chan R, et al Significance of late gadolinium enhancement at right ventricular attachment to ventricular septum in patients with hypertrophic cardiomyopathy. Am J cardiol. 2015:116 436

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