While the struggle for most people is getting enough exercise, a small proportion of adults are endurance athletes, exercising far beyond the minimum recommended exercise of at least 2.5 hours per week.
While it may seen reasonable to think that more exercise can only be good to reduce the risk of cardiovascular disease, more recent studies have reported an increased prevalence of coronary atherosclerosis (plaques in the arteries supplying the heart) amongst highly trained athletes, compared to non athletes. Prior studies have suggested that the plaques seen in athletes were calcified, which are more stable and less worrisome than non-calcified or mixed plaques, but data on the prevalence of each type of plaque compared to nonathletes were lacking.
The Master@Heart Study, published in the European Heart Journal, looked at the prevalence and types of plaques in coronary arteries of endurance athletes compared to non athletes.
This was was a cross sectional study of three groups of white men age 45-70, with no cardiovascular risk factors and BMI ≤27.2:
- 191 lifelong endurance athletes (cycling ≥8h or running ≥6h per week, or triathlon (combo swim/cycling/running) ≥8h per week , starting at age <30 (average 11h/week, average 36 years of endurance exercise)
- 191 late onset endurance athletes (same as above but starting at age >30) (average 10h/week, average 14 years of endurance exercise), or
- 176 healthy nonathletes (≤3h of activity per week) (average 1h/week; 77% of whom exercised up to 3h per week, 23% of whom did not exercise regularly at all; average 5 years of prior endurance exercise)
All participants underwent CT coronary angiography to evaluate the heart’s arteries.
Cardiovascular risk factors and and family history of cardiovascular disease were similar between groups. Nonathletes had a higher body fat percent (19.4%) than lifelong athletes (13.9%) or late onset atletes (15%) (all in healthy range). Lifelong athletes had a higher VO2peak (a measure of aerobic fitness) (48 mL/min/kg) than late onset athletes (46 mL/min/kg) than nonathletes (37 mL/min/kg). All groups including the control group had higher than predicted VO2peak, suggesting that the ‘nonathletes’ were actually quite fit as a group.
They found that compared to the healthy nonathletes, lifelong endurance athletes had a higher risk of having more than one coronary plaque, proximal plaque, calcified plaque, calcified proximal plaque, noncalcified plaque, noncalcified proximal plaque, and mixed plaque. Compared to late onset endurance athletes, lifelong athletes had a higher risk of having ≥50% stenosis (narrowing) in any coronary segment and any proximal segment.
These findings don’t jive with other data showing that endurance exercises reduces the risk of actual cardiovascular events (eg heart attacks). While there was an increased plaque burden in this study in lifetime endurance athletes, the overall plaque burden remained low. Endurance athletes also have larger coronary arteries and a greater capacity to vasodilate those arteries, meaning the plaque:vessel ratio in athletes could be lower, and their vessels have the capacity to become larger and allow blood flow around the plaques.
This study was limited to white men. Data is needed in diverse populations.
BOTTOM LINE: This study suggests that endurance athletes are not ‘immune’ to cardiovascular disease as some may think, and that lifelong endurance athletes may in fact have a higher risk of cardiovascular disease. Longitudinal data are needed to know how this may (or may not) translate to actual cardiovascular events, and this study is following these patients over time to look at this. Exercise is definitely powerful to reduce cardiovascular risk, but at some point, more may not be better.
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