Vigorous Exercise—Too Much of a Good Thing, Continued: Studies on Atrial Fibrillation

More than a year ago I wrote an earlier blog titled “Exercise, part 2: Moderation in all things?”  I reviewed studies that indicated that intense aerobic exercise may lead to damaged heart and arterial tissues.  Pretty scary for those of us that do long duration exercise.

This topic continues to evolve, and I thought I’d bring this topic up to date, and focus at this time on one aspect of heart damage: atrial fibrillation. 

Many, many studies support the thesis that exercise is beneficial to people of all ages.  Beneficial to one’s physical as well as mental health.  And I, too, believe that.

And many believe, logically, that if a little exercise is good for you then more is better.  And much more would logically be much better. 

Indeed we have become a culture of long distance runners and cyclists.  Well, not quite a “culture,” but the statistics on the number of people running marathons (full marathon is 26 miles) have gone up dramatically since the 1970’s.  In 1976 there were an estimated 25,000 who ran a marathon; in 2012 there were 500,000, an increase of 20 times.

                          

I suppose everyone has heard of The Complete Book of Running, published in 1977.  It was a best selling book, authored by Jim Fixx (actual name James Fuller).  And probably Jim Fixx can be credited with starting the running craze that is still with us.

And so it was ironic when Jim Fix died in 1984, after his daily run, at the age of 52.  I think the world did a pause and said…ummmm.  But it soon came out that Fix had a genetic predisposition to heart problems, and we all went happily back to running.

Fast forward to 2009.  At that time another book was published, Born to Run, by Christopher McDougall.   I thought it was over all a fine book, especially when it stuck to “the science.” In it he prominently featured an ultramarathon runner, Micah True (aka Caballo Blanco).

But, Caballo Blanco died in 2012, aged 59, during a run. 

An autopsy showed that True was suffering from cardiomyopathy (general word covering a deterioration of the heart) for no known cause. 

It turns out that scientists have been studying the effects of “extreme” exercise on heart health for several years now.  And I think I’m safe in saying that the science is not yet “settled”, but there are some patterns emerging….I think.

Now some heart-vocabulary.  First there is “atrial fibrillation” (called here AF).  It results when the two small chambers on top of the heart (the atria) don’t beat in unison.  It affects 0.4 to 1% of the general population, and its incidence increases with age, going up to 8% for those over the age of 80.  Next we have the ventricles—the two large chambers forming the bottom of the heart. There are right and left ventricles—the right being the largest, but the walls of the left are thicker.

It seems the first studies on exercise and the heart concerned AF.  Back in the mid to late 1990’s some studies suggested that extreme exercise may be associated with AF.  For example a 1998 study of competitive Finnish Orienteers, average age of 47.5 years, had AF at 5.5% over controls.

Since that time there have been two large studies—The Physicians’ Health Study and the Cardiovascular Health Study.

The Physicians’ Health Study was reported in 2009.  It was based on the exercise habits of 16,921 men (Physicians) who ranged from doing no exercise to those who exercised 5-7 days per week.  After 12 years of follow up they found that the incidence of AF was about 1%, and that there WAS a relation between AF and amount of exercise: men who jogged 5 or more days per week had a 53% increase in AF.  Further, this trend was only found in men younger than 50 years old.  Interestingly, for men over the age of 50 there has no correlation between AF and exercise.

Let’s stop there and keep these numbers in perspective.   So this 2009 study found that in the worst case scenario the incidence of AF went up to 1.53% of the population studied.  That is, 1.53 men out of 100 men developed AF. And, this occurred only in younger men.

In 2008 the results of the Cardiovascular Health Study were published.  Here they looked at “walkers” only, and placed them into categories of how far and fast they walked.  They found that the faster and longer they walked, the lower the incidence of AF.

The 2008 and 2009 studies are not really comparable—the 2009 study included runners, while the 2008 only had walkers.  But, both of them together may imply that “light/moderate” exercise reduces AF while more intense exercise increases AF (though still at a low percentage).

A 2013 study that looked at ~45,000 walkers and runners and ranked them in energy expenditure.  Their average age was greater than 50 years, and they all had run or walked for greater than 9 years.  After studying this population for an average of 6.2 years they found 1.) the incidence of AF was 2.3%, and 2.) the greater the exercise intensity then the LESS incidence of AF.

A very recent study looked at 44,410 Swedish men who were AF free at the start of the study in 1997.  They ranged in age from 45-79, and were asked to rank themselves on levels of exercise throughout their lifetimes. There were a couple interesting results: 1.) after 12 years of follow-up there were 4,568 cases of AF, or 10.2%; 2.) for those men who had the greatest levels of exercise by the time they were 30 years old, they had 19% more AF by the time they were averaged 60 years old.  And, if they had no intense exercise AFTER the age of 30 they had a rate of 49% greater than controls. 

Wow.  These results suggest that greater physical activity when young resulted in greater AF when old. Even if they stopped exercising.  What?

And so, generally, that’s where we seem to be.  It does look like a muddle. Some studies say yes, and some say no—but the preponderance of the evidence is, yes—that the highest levels of exercise will increase the frequency of AF.  Is exercise uncovering or “forcing” a predisposition to AF?  Many are now recommending that we engage in more moderate amounts of exercise.  The problem is, no one knows how much is “moderate,” and overall, I think many agree, the benefits of moderate to extreme exercise outweigh the “low” frequency of AF.

There are other studies that have reported on plaque, left and right ventricle changes, and other modifications to the heart as a result of exercise. 

A 2014 editorial in the American College of Sports Medicine essentially concludes that “extreme or obsessive exercisers…are at more risk than for those that practice moderation.”

Of course managing risk is something we do through out our lives, in all sectors.  Balancing risk and reward is always a problem. Understanding the level of risk is often a challenge, and often editorials, such as the above 2014 editorial, don’t seem willing to attach a number to “risk.”  I can’t fathom how anyone can manage risk without knowing the basic statistics behind “risk” statements.

Anyway, I will  continue  on exercise and heart issues in my next blog.

Useful References

1.) 2008; 118(8): 800-807

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133958/

2.) 2014 Annual Marathon Report

Date: March 23, 2014

http://www.runningusa.org/index.cfm?fuseaction=news.details&ArticleId=332&returnTo=annual-reports.%20Retrieved%2027%20May%202013.

3.) 2009 Am J Cardiol. Jun 1;103(11):1572-7. doi: 10.1016/j.amjcard.2009.01.374. Epub 2009 Apr 22.

Relation of vigorous exercise to risk of atrial fibrillation.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687527/

4.) 2013. doi:  10.1371/journal.pone.0065302

Reduced Incidence of Cardiac Arrhythmias in Walkers and Runners

Paul T. Williams^1,* and Barry A. Franklin²

5.) Heart 2014;100:1037-1042 doi:10.1136/heartjnl-2013-305304

Atrial fibrillation is associated with different levels of physical activity

Drca, N. et al.

http://heart.bmj.com/content/100/13/1037.long

 

6.) 2014. ACSM'S Health & Fitness Journal:

July/August 2014 - Volume 18 - Issue 4 - p 47-49

doi: 10.1249/FIT.0000000000000047

Have a Heart: Can Too Much Exercise Be Bad?

Asplund, Chad A. M.D., M.P.H., FACSM

 

Vigorous Exercise: Not Only for the Young—Part 3

As anyone that has read my blogs knows, I’m very interested in exercise and training, with a particular interest in geriatrics—I guess that’s because I am one!

I’ve written before that the amount of literature reporting on exercise and old folks is dwarfed by that reported on in the young; however, there have been several very interesting, recent reports regarding older adults.

The need for studies on the effect of exercise on older adults is urgent.   34% of US adults over the age of 70 have walking limitations; those reporting such limitations have a  four times higher risk of needing nursing home placement and are three times more likely to die than those with no walking difficulty.

That exercise lowers medical costs has been shown.  Studies have demonstrated that ON AVERAGE exercise improves physical function.  However, there are some niggling little facts associated with studies on older adults that are not generally known: not all participants in studies show improvement from exercise.  What??

For example, in a small 2005 study of adults over the age of 60 who were overweight had knee osteoarthritis, and who participated in exercise training for 6 months (aerobic and resistance exercise), 7.5% showed no increase in walking distance and 58% showed no increase in muscle strength.  Ouch. 

What’s going on here? Exercise is hard enough, let alone if you get no benefit out of it.

A study published in 2012 came up with related similar results looking at changes in insulin as well as high density cholesterol: an analysis of 1,687 adults over six studies concluded that 8.3% of participants had worse insulin numbers, and 13.3% had worse cholesterol results.

The point being that a portion of the population does not respond to exercise.  Or they may even get worse.

So, what accounts for this variation from individual to individual? Well, there are of course environmental reasons—but there are potentially genetic reasons, too.

The exercise literature has been examining one particular gene for more than a decade—the ACE gene (“angiotensin-converting enzyme”).  Everyone has an ACE gene, and there are two different types (alleles), called the “I” gene and the “D” gene. 

Therefore, people can be either II, ID, or DD for the ACE gene.

There have been many many studies on the ACE gene and athletic performance in young athletes.  IN GENERAL the I gene is found in elite endurance athletes—long distance runners, cyclists, rowers, and mountaineers.  The D gene is associated with “power” athletes such as sprinters or those that excel in strength related events.  I should add that there are studies that show the opposite results—however, the preponderance of the evidence is as I state above.   This seems to be an emerging pattern with respect to the genetics of athletic ability.

It may not be surprising, therefore, that ACE genotypes have been looked at with respect to how old folks respond to exercise—the question being,  “is some of the variability in older adults responses to exercise dependent on their ACE genes?”

There are at least two long-term studies involving oldsters and exercise.  One is the Health ABC study and the other is the Lifestyle Intervention and Independence for Elders  Pilot (LIFE-P).

The Health ABC study started in 1997 and 1998.  It enrolled about 3,000 people, males and females, whites and blacks, ages 70-79.  They had to be “normal,” with no limitation in their ability to walk a quarter mile or go up 10 steps without resting.

In 2005 a study analyzed these folks.  They found that at the initial start of the study there was NO difference between II, ID, and DD genotypes for a wide variety of characteristics such as weight, diabetes, hypertension, physical activity, etc. (Further, as points of reference, the frequency of the II type was 19.2%, 33.6% were DD, and 47.2% were ID). 

However, after 4 years they classified the people according to their level of physical activity, genotype, AND degree of “mobility limitation” (difficulty in walking a quarter mile or going up 10 steps without resting).  What they found was 1) the group that was most active had 18% less mobility limitation than the inactive group (providing more evidence that activity is good); 2)  that within the group that  had very low physical activity over the 4 years there was no difference between the genotypes; and 3) in the most active group the II, ID, and DD genotypes differed.

So, of interest here is point 3 above: in the most active group the II, ID, and DD genotypes differed in their response to exercise.  The II having the most mobility limitation and the ID and DD having the least; the difference between the II and ID OR DD being 45%.

Wow.  A 45% difference in mobility limitation.  The II genotype had HALF of the benefit of exercise compared with either ID or DD genotypes, and those that did weight lifting the greatest benefit.  Also, the II genotype had a higher percentage of body fat.

So, although exercise reduced mobility limitation, the II genotype had the poorest response. And remember they represent 19% of the population. 

The LIFE-P study is smaller than the Health ABC study, and started in in 2004.  It enrolled around 400 men and women who were 70-85 years old, who were able to walk 400 meters within 15 minutes, had a sedentary life style (spent less than 20 minutes per week on regular physical activity), and scored less than 10 on the SPPB test (discussed  below).  Persons with physical infirmaries, cardiac issues, and diseases of various types were excluded. 

The SPPB test (Short Physical Performance Battery) has become a kind of gold standard for quickly assessing physical capability for old folks.  The test includes determining how long it takes to get up and down out of a chair 5 times, how long one balances one’s self with the feet side by side or positioned heel to toe, and how long it takes to walk EIGHT (8) FEET, with a maximum score being  less than 3.1 seconds.  (Just reading these requirements almost makes me cry!).

An SPPB score of 10 or less (maximum of 12), means that there were “some” strength and balance issues

So in other words, these are older people who were pretty “normal” without major health issues.

There are around 400 people enrolled in the LIFE-P study.  Since 2006 there have been several studies published on this group of people.  A very early study, conducted after the program had been started for a little more than a year, showed that indeed, and unsurprisingly, individuals subjected to a combination of strength, aerobic, balance, and flexibility exercises performed better on SPPB test one year later than another group that only received exercise instruction. 

A study published in 2014 on 283 individuals enrolled in the LIFE-P study looked at those that were subjected to exercise vs. no exercise, and who were further classified into II, ID, and DD genotypes.  Exercise consisted of walking, strength, flexibility, and balance training. The strength exercises consisted of standing chair squats, toe stands, leg curls, knee extensions, and side hip rises with ankle weights.

So, first they found that those enrolled in the exercise group (E), maintained their SPPB score, while those that did not exercise (NE) significantly declined in their score.  Once again showing that exercise maintains performance.  But, of importance to this blog, in the E group there was a wide variation in SPPB score, with 33% experiencing a DECLINE in performance compared to 37% who showed a 2-point improvement in their score. 

So, with exercise, as with the Health ABC, a significant percentage of those had NO BENEFIT.  I suppose you can guess what comes next: they also looked at II, ID, and DD genotypes.

And what they found was, you guessed it (!), the II genotype had no or decreased performance—again like the Health ABC study. 

If this is borne out by future studies, then this is huge, in my opinion.  It may totally change how older adults are counseled with respect to exercise.  It is possible that some genotypes benefit most by, for example, walking, while others benefit most by doing strength exercises.

Helpful Resources:

http://jama.jamanetwork.com/article.aspx?articleid=201372

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0037887

http://link.springer.com/article/10.2165/00007256-200838120-00008/fulltext.html

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2657174/

https://www.google.com/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=effects%20of%20a%20physical%20activity%20intervention%20on%20measures%20of%20physical%20performance

http://aginginmotion.org/the-key-to-fighting-physical-decline-the-short-physical-performance-battery-sppb/

http://pps.sagepub.com/content/5/5/575

The Obesity Epidemic (part 6): The Effects of Diet

The previous blog in this series discussed some of the genetics surrounding obesity.  More than 20 genes have been discovered that may be involved. 

I’m sure there are more. 

The next issue I’d like to examine is the effects of diet on weight loss.  But interestingly, there is evidence that the type of diet one has is influenced to some degree by the types of genes you have.

First, there are generally four types of diets: low fat, low carbohydrate, low calorie, and very low calorie.

The low-fat diet, as the name implies, reduces the percentage of fat in one’s diet. Concurrently, calories are reduced because energy-dense fat is reduced.

The low carbohydrate diet is higher in protein and fat, since carbohydrates are reduced. These include the Atkins and Protein Power diets; the new Paleo diet would also fit in this category.  

Low calorie diets are what their name suggests—they typically produce a deficit of 500-1,000 calories/day. The DASH diet and Weight Watchers are low calorie diets.

Finally, the very low-calorie diet is a near-starvation diet, providing 200-800 calories/day. 

Well, all of these diets will cause you to lose weight.  An interesting question is, which is better?

Guess what—there is NO scientific evidence that one diet is better than the other.  They all cause weight loss—and perhaps weight loss is observed because they all result in a reduction in calories—a conclusion reached by almost all the studies.  Let me repeat: there is no evidence that having high or low carbohydrates, high or low protein, or high or low fat confers a diet that has any more superiority over another for weight loss.

Such was a 2012 report of 424 men and women who had BMI’s of over 30, tracking fat as well as muscle loss.  Tracking muscle loss makes this study different from most weight studies, who only look at waist circumference and/or total weight.   Further, this study looked at total fat, visceral fat, subcutaneous abdominal fat, as well as hepatic fat, using X-ray analysis.

Simply, visceral fat is “deep fat” that wraps around organs, resulting in a large belly and waist, and is considered the most dangerous of the types of fat.  Subcutaneous abdominal fat is fat found directly under the skin, and is typically measured by a “pinch test.” Hepatic fat is fat leading to “fatty liver disease” wherein fat accumulates in liver cells.

This 2012 paper looked at the effects of four weight loss diets that all had reduced calories (the following percentages are amount of energy provided by the nutrients): 1.) low fat (20% fat), average protein (15% protein), high carbohydrate (65%); 2.) low fat (20% fat), high protein (25%), high carbohydrate (55%); 3.) high fat (40% fat), average protein (25% protein), low carbohydrates (35%).

They found that after 6 months on the diets participants lost an average of 9.3 pounds of total fat and 4.6 pounds of muscle.  Of the fat, 5.0 pounds were abdominal fat, 3.3 pounds were visceral fat.  There was no significant difference for hepatic fat.  Further, as stated above, there was no significant difference between the diets.  Finally, after two years, participants gained back 40% of their weight loss. There was also apparent “cheating” on the diets, as, for example, urinary nitrogen levels were the same between the low and the high protein groups (it is expected that as protein in the diet is increased, then there is more excretion of nitrogen).

In recent years there has been a lot of interest shown in high protein diets.  A 2013 paper reported a meta-analysis of 15 studies involving 1,990 male and female subjects, all obese, and lasting for a year or more. The dietary protocol of all studies was high or low protein, low fat, variable carbohydrates, and 11 studies had energy restriction and 4 did not.

What did they find? No effects of either high or low protein diets on weight, waist circumference, or fat mass. Nor were there effects on total cholesterol, high density lipoprotein (HDL) ,though HDL was near statistical significance, and total triglycerides, or blood pressure.  However, high protein diets DID result in statistically lower fasting insulin levels. And finally, for those of you on high protein diets (like myself sometimes!), there was no difference in renal (kidney) function.

HOWEVER, all may not be so simple—which seems to be a general conclusion in dietary studies. A 2013 meta-analysis of “all-cause mortality” which looked at 17 studies covering 272,216 people, the largest such analysis to date, concluded that low carbohydrate diets had a statistically significant increase in mortality, and there was no effect one way or the other on cardiovascular disease. The authors conclude:

“Given the facts that low-carbohydrate diets are likely unsafe and that calorie restriction has been demonstrated to be effective in weight loss regardless of nutritional composition…it would be prudent not to recommend low-carbohydrate diets for the time being.”

Now, to turn to the point I introduced at the beginning of this blog: the types of genes you have may influence the effectiveness of weight loss diets as well as where on your body you lose weight.

As mentioned in the Obesity-5 blog, some FTO genes have been associated with obesity.  Actually, I glossed over the point that there are different kinds of FTO genes—some are associated with obesity and some are not.  Of relevance here is that one of these genes is known by scientists as rs1558902.   Let’s call it gene “A” for this discussion.  Further, let’s call the normal FTO gene (not causing obesity), “T.”

In a study published in 2012, 742 obese adults were classified as having the “A” gene or “T” gene.  They next randomly divided these individuals into four diets: 20% fat, 15% protein, 65% carbohydrate; 20%, 25%, 55%; 40%, 15%, 45%; and 40%, 25%, 35%.    Interestingly, the found that HIGH PROTEIN diets showed the most impact on weight loss parameters amongst those that that the “A” gene.   So in other words, if you only had the “T” gene you did not respond to a high protein diet. 

This constitutes proof that your response to a particular diet depends on the types of genes you have—or to say it differently, people that do not respond to high vs. low protein diets may do so for innate reasons.

I can only assume that given the large number of genes that influence obesity, many other such interactions would be found—leading to the conclusion that not one diet fits all people. 

But, the question is NOT just which diet causes weight loss, but HOW sustainable is the diet? That is, is the diet one that folks will stay on for years? The rest of their life?  How about other life-style changes that are incorporated in to some diets, such as exercise—is it sustainable?  A rather shocking observation in all of the diet studies that I looked at is that the drop out rates were discouraging. The 2012 study above had 20% drop out rates; the 2013 meta-analysis of 15 studies had dropout rates ranging from 8% to 55%, with most around 30%.  Plus, there is evidence of dietary cheating in some studies—which must raise questions about some conclusions.

In summary, there is no scientific consensus as to which diet is best for weight loss.  The ONLY consensus (so far) is that calorie reduction has the greatest impact, and even that may depend on they types of genes you have. 

And now I’m done with Obesity!! On to other subjects. 

Useful References:

http://www.cmaj.ca/content/174/1/56.full

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3041737/

http://www.nejm.org/doi/full/10.1056/NEJMoa0804748#t=articleBackground

http://ajcn.nutrition.org/content/95/3/614.long

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636027/         

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646098/