Physicians often face patients with cardiovascular
risk factors or different kinds of heart disease.
They prescribe statins, ACE inhibitors or ß-blockers,
but also (should) encourage patients to engage in
regular physical activity to reduce cardiovascular
disease burden. Physical exercise, as a part of
cardiac rehabilitation or a primary prevention
programme, is seemingly one of a kind.
For most health outcomes, additional benefits occur
as the amount of physical activity increases through
higher intensity, greater frequency, and/or longer
duration. No other known therapy offers such
advantageous characteristics.
This even led some researchers to speculate, some 40
years ago, that marathon runners were immune to
atherosclerosis. Running a marathon was quite
unusual at that time, and cardiovascular adaptation
to such a high load of exercise had been scarcely
explored.
Since then, the late 70s, the number of
non-professional runners finishing a marathon has
increased 20-fold, and current observational studies
are jeopardising the notion of exercise as risk-free.
Increased sudden death risk during exercise bouts is
well established but extremely rare.
An evolving core of evidence supports the hypothesis
that regular exercise increases the risk of atrial
fibrillation (AF), ventricular arrhythmias or even
ischaemic heart disease.
How do these findings fit with the well-known
benefits of exercise? Two papers explore this
subject, and provide important insights.
By assessing outcomes such as AF incidence and
cardiovascular or total mortality, both groups
elegantly suggest in two large cohorts that exercise
intensity and duration are key players in this
association. They describe a similar U-shaped or
reverse J-shaped pattern for the dose–response
effect of exercise: maximum cardiovascular benefits
are obtained if performed at moderate doses, while
these benefits are lost with (very) high-intensity
and prolonged efforts.
For more information
Heart
Exercise and the heart: unmasking Mr Hyde
MDN |