In part 1 of this series I made the following points:
1. Barring
extenuating circumstances, older folks can sustain muscle strength and muscle
mass well into “old age.”
2. Protein
synthesis appears to be sustained throughout life, perhaps to the same extent
as found in young people;
3. This
is counter to the prevailing paradigm, which holds that muscle wasting is an
inevitable consequence of aging.
4. Resistance
exercise is rarely recommended for old folks; generally they are urged to “go
walk in the mall for 30 minutes” as if that is all they are capable of.
5. Muscle
wasting in older adults may occur primarily because of their sedentary
lifestyle.
Pretty exciting stuff, no?
But there is emerging evidence that “too much” exercise, at
least exercise that gets the heart rate up to a “high” level for extended
periods, may not be good for you—whether you are young OR old. Further, data indicates that there are
“optimal” levels of exercise. Scientists
have not, however, zeroed in on how often and how hard we should exercise to
achieve maximum health benefits.
In a medical-screening study published in 2011*, researchers
surveyed 416,175 Taiwanese individuals about their level of exercise upon
enrollment in the study and then repeated this survey each year for the next 8 years. Based on their answers to the survey
questions, each subject was placed into one of five exercise categories: “inactive,” “low volume,” “medium
volume,” “high volume,” and “very high volume.” During the course of the study, the researchers recorded deaths
as well as the incidence of cancer, diabetes, cardiovascular disease, heart
attack, and stroke .
Simply put, here is what they found: As the participants’ level of activity
increased, the rate of overall mortality decreased, as well as rates of death
from cancer, diabetes, and cardiovascular disease. All statistically significant. The same results were found for every tested category, whether
male or female, young or old. Surprisingly,
the results held true even for individuals with chronic kidney disease, metabolic
syndrome, hypercholesterolemia, obesity, diabetes, or high blood pressure. The conclusion is that exercise,
even in very moderate amounts, helps EVERYONE at any age, regardless of the
state of their health.
In fact, exercising for only 92 minutes PER WEEK decreased all-cause
mortality and resulted in an increased life expectancy of 3 years. Amazingly, all-cause mortality was
further reduced by each additional15 minutes of exercise beyond a minimal 15 minutes
per day.
BUT the benefit maxed out at 90 minutes of exercise per
day. So the authors concluded that
exercising beyond this amount has no additional benefit as far as mortality is
concerned. And for those in
the “vigorous” group, the maximum benefit was achieved after about 45 minutes.
Similar results were found in a 15-year study of 52,000 people,
14,000 of whom runners. Overall,
the runners had a 19% lower rate of mortality than non-runners, but the benefit
was NOT seen in those who ran the fastest or the farthest. For example, those who ran at 7 mph had
the least mortality (17% reduction compared with non-runners), but those who
ran faster than 8 mph had the same mortality as those who ran 1-5 mph (~10%
reduction). Similarly, those
who ran the greatest distances (over 25 miles per week) had mortality
reductions of 5-10%, while those who ran 0.1-19.9 miles per week had reductions
of about 25%.
So this study indicates that there is an “optimal” level of
running for fitness—and too much may be, well, too much.
Finally, the really big news in this area is the recent
evidence that athletes who do EXTREME amounts of running may be damaging their
cardiovascular systems. The issue
at hand is reminiscent of the legend of Pheidippides, the famous Greek runner who
ran 150 miles in 48 hours to
deliver the message “Victory is ours!” after the Battle of Marathon in 490 BC—and
then dropped dead. Read on.
Dr. James O’Keefe, professor of medicine at the University
of Missouri-Kansas City, has published several articles concerning the effects
of extreme running on heart health.
His publications have been pretty radical, prompting lots of discussion
in exercise physiology circles. In
fact, they have sent a tremor through the exercise world.
Here are some examples:
1. A
2012 study reports that sudden cardiac death in marathoners who run the full 26.2
miles is 1/100,000. I could not
find statistics for the expected rate of sudden cardiac death among
non-marathoners. However, between
the year 2000 and 2010, 11 million people ran in full and half marathons. 59 experienced cardiac arrest
(0.54/100,000). For half marathons
(13.1 miles)), the rate of sudden cardiac death was 0.27/100,000, and for full
marathons the rate was 1/100,000.
Although these numbers are really low, they do suggest that something is
going on.
2. In
a 2010 study, 60 male patients with cardiovascular disease were divided into
two groups. One group exercised
for 30 minutes, and the other for 60 minutes. The researchers took blood pressure measurements and
performed an EKG (electrocardiogram) on each of the participants. They found that the two groups did not
differ with regard to blood pressure (rather counter to the idea that exercise
decreases blood pressure). More
importantly, they also found that the 30-minute group had MORE favorable EKG
results than the 60-minute group.
3. A
2010 study looked at a particular chemical that is generally considered to be
associated with cardiac damage—troponin.
(Troponins are molecules that help with muscle contraction, and when
they leak out of muscle fibers, it may be an indication of muscle damage. So, finding cardiac troponins in blood
plasma may be diagnostic of several types of heart damage, including heart
attacks.) The authors reviewed 18
studies involving various types of exercise: walking (18 to 30 miles), running (full and half marathons),
cycling (124 miles), and one iron man triathlon (swim 2.2 miles, cycle 112
miles, run 26.2 miles). Although 0%
to 100% of the participants in a given event showed elevated cardiac troponin,
the shorter the duration of the event, the HIGHER the troponin levels. This suggests that shorter events,
which are more intense and require greater cardiac output, result in the
production of more troponin—and possibly more heart damage.
The hearts of athletes are different from those of normal
people. Overall an athlete’s heart
is larger—which makes sense, since a larger heart can do more work. The concern is that the hearts of some athletes
involved in endurance events may show signs of “strain,” such as scarring
(fibrosis), diastolic dysfunction, large-artery wall stiffening, and coronary
artery calcification (plaque build up). And in particular, the right ventricle may have decreased
functionality.
Here are some more studies comparing the cardiovascular
systems of endurance athletes to those of “normal” people:
1. A
2008 study looked at forty athletes who participated in marathons (7),
triathlons (11), ultra-triathlons (13), or alpine cycling events (9). 90% were males, their average age was
37, they had an average of 10 years in training, and they exercised an average
of 16 hours per week. Each
athlete was examined before a race, immediately after a race, and one week
later. What the researchers found
is that the function of an athlete’s right ventricle immediately following a race
was reduced in comparison to its function before the race, and after one week
it was almost back to baseline. However,
5 of the 40 athletes showed areas of tissue damage in the septum (tissue separating left and right ventricles),
and those athletes also had hearts that pumped less blood. The authors concluded that (a) intense
endurance exercise caused dysfunction of the right ventricle (but not the left),
(b) eventual recovery was nearly total, and (c) reduced right ventricle
function was most evident in some of the most “practiced” athletes.
2.) A
2009 study looked at 102 runners, age 50 or older, who had completed at least
five full marathons in the last three years and had no history of heart disease. It showed that 12% of them had heart tissue damage; this
compared to 4% of a “normal” population.
3.) A
2010 study looked at 49 marathon runners who were, on average, 38 years old. It showed that these athletes had
significantly higher blood pressure than a group of “normal” people did.
I could go on and on, but it seems that
a consistent story is emerging: very intense aerobic exercise such as running, cycling, and rowing
over a long period of time may lead to damaged heart and arterial tissues.
These studies also suggest that, at
least in some individuals, there is an optimal level of exercise and exceeding it
may be harmful, or at least provide no benefit. This may be genetic, and it may be true in only a “small”
percentage of the population. So
unfortunately there are no rules here—and few recommendations, except that some
is good and too much may be bad.
It may behoove us, as we age, to
have our cardiovascular system checked out more thoroughly than is possible
with a family doctor’s stethoscope.
As we enter our “golden” years, and especially if we are beating
ourselves up with lots of exercise, perhaps it is worth having an
echocardiogram every 5-10 years, just as a status check.
Finally, I’d like to point out that
the “intensity” of exercise is measured by one’s heart rate, regardless of the
type of exercise. (After all, the
heart does not know if it is beating fast because we are running or lifting
weights. I personally find my
highest heart rates occur when wall climbing, and weight lifting gets my rate
as high as if I were running.) There
is growing interest in highly-intense exercise of short duration—this is the regime
advocated by the increasingly popular “Crossfit” program, which is designed to maximize heart rate
through running, weight lifting, and various body-weight
exercises. In light of recent
studies, is it possible that there are negative consequences to a lifetime of causing
our hearts to beat wildly, even if only for 10 minutes at a time? No one knows.
Useful References:
*http://vivafit.eu/pdf/Pang_Wen_minimum_amount_PA_reduced_mortality_Lancet_2011.pdf
http://eurheartj.oxfordjournals.org/content/early/2011/12/05/eurheartj.ehr397.full
http://ajh.oxfordjournals.org/content/23/9/974.long
No comments:
Post a Comment