How Much Exercise Is Too Much Exercise?

A twenty-six-year-old man is running a race. The terrain is tough and mountainous. The weather is hot and humid; the mid-day sun is beating down on him. Despite the hard conditions, the man doesn’t stop for a break; he must reach the finish line. Finally, his goal is in sight as he sprints towards and crosses the finish line. When he has achieved his objective, he shouts “Victory!” then collapses and dies.

The man, of course, is Pheidippides, the legendary runner who sprinted from Marathon to the city of Athens in 490 BC to relay the news of the Greeks’ victory over the Persians.  The Persians outmanned the Greeks by four to one, so winning the battle on the plain of Marathon was newsworthy, but just as important, Pheidippides had to warn the Athenians that the Persians were heading their way. While the story of Pheidippides may or may not be true, the distance between Marathon and Athens, 26.2 miles, is now legendary.  When the modern Olympics were resurrected in 1896, the organizers wanted to stage a final event based on Greek history. They conceived a race from Marathon to the Olympic Stadium in Athens and the marathon was born. Since the first marathon was run in 1896, long distance racing has taken off. Many cities now stage marathons and there were  approximately 541,000 marathon finishers in 2013. Two of the most famous marathons include the New York City Marathon with 50,000 participants and the Athens Marathon- The Authentic, featuring the original course run by Pheidippides.

Why would an athlete, a runner in prime physical shape, die during or after a marathon?  In Pheidippides case, it may have been from sheer exhaustion as he ran to Sparta and back (a distance of 140 miles each way) two days prior and he ran in the hot Greek August heat.  In general, the risk of dying from a marathon is about 0.8 runners per 100,000 runners, a far lower risk of death than in the majority of daily activities.  One would expect that being a runner should have protected Pheidippides from a cardiac related death, but did he overexert himself? Did he exercise too much?

In general, regular exercise is good. The recommended amount of exercise for adults is 150 minutes per week of moderate intensity or 75 minutes per week of vigorous intensity exercise.  Moderate intensity exercise includes walking at 3 miles per hour, bicycling less than 10 mile per hour, water aerobics, doubles tennis, and general gardening. Vigorous exercise is walking uphill, race walking, bicycling faster than 10 miles per hour, singles tennis and heavy gardening.  The highest risk of cardiac death is in the sedentary individual. Any exercise will decrease the risk of dying from heart disease compared to the couch potato. Just standing for more than two hours per day decreases the risk of dying by 10% compared to those who are sedentary.   People performing moderate to vigorous physical activity below the recommended amounts were still able to reduce their rate of cardiac death by 20%. For maximal reduction in cardiac death, 45% compared to those who are sedentary, one needs approximately 547 minutes per week of moderate intensity exercise or 289 minutes per week of vigorous activity.  Interestingly, increasing levels of moderate intensity exercise continues to reduce the risk of cardiac death while the curve flattens or may go up for vigorous activity.  Two large studies recently reported a U shaped curve comparing cardiac death and the volume of exercise.  In people who exercised ten times or more than the recommended amount, the risk of dying stopped going down and trended upward. These studies did have limitations and it cannot be concluded that high volume exercise increases cardiac death. Most studies including both amateur and elite athletes who exercised at high volumes demonstrate a 3 to 6 year increase in life expectancy compared to the general population.

While elite athletes exercising at a high volume may not be dying at a higher rate, they do experience heart problems.  Athletes involved in marathons, endurance cycling events or triathalons have been shown to have elevated levels of troponin right after events. Troponin is a blood enzyme that goes up during a heart attack. While elevation in troponin in athletes does not equate to a heart attack, it suggests that there may be some heart damage due to excessive exercise.  Surprisingly, high volume exercisers have been shown to have excess calcium in the heart arteries, a measure of plaque in the artery.  Excess exercise may paradoxically accelerate heart artery disease, although other traditional risk factors such as diet may also play a role. Athletes are also at a higher risk for atrial fibrillation, an irregular rhythm from the upper chambers of the heart, compared to the general population. Lastly, athletes are prone to sudden cardiac death due to an irregular rhythm from the lower chamber of the heart. Pheidippides was the first report of sudden cardiac death in a long distance runner. In fact athletes who have sudden cardiac arrest without any other underlying heart problem, are said to have Pheidippides cardiomyopathy (disease of the heart muscle). It is felt that chronic high-level exercise causes enlargement of the heart chambers in response to the demand for extra oxygen. This enlargement can cause patchy areas of scarring in the heart. If the scars are in the atria (the upper chambers) the athlete is at risk for atrial fibrillation. If the scars are in the ventricles (the lower chambers) they act as foci for ventricular rhythms and sudden cardiac death.  Chronic high volume exercise can cause excessive wear and tear on the heart and appears to erase the benefits gained by moderate exercise.

While there may such a thing as too much exercise, it must be emphasized that regular exercise is good and will lower the risk for cardiac death. The average exerciser occasionally pushes his or her heart rate to the maximum. The elite endurance athlete pushes the heart rate well beyond the maximum, for days, years and decades.  These athletes can and do experience heart complications. For the average person seeking optimal heart health, too much exercise is less of a consideration than too little exercise. The benefits of exercise clearly outweigh the risks. So start training for that marathon.

A look at TRIALs in FIBRILLATION

Atrial fibrillation (Afib) is the most common heart rhythm disturbance with about 5.6 million diagnosed cases in the United States. Afib is a major health problem and a growing epidemic with increased death, stroke and health care costs associated with it.

Recent studies have advanced our knowledge of the causes of Afib and have helped direct treatment.

Afib is a rapid, irregular rhythm in the upper chambers of the heart (the atria).  Instead of a regular, coordinated beat, the atria are rapid and disorganized. When the atria are not beating in a coordinated fashion, the blood in these chambers does not drain effectively into the lower chambers of the heart. When blood is not draining well, it sits in the atria and can form a blood clot. A clot, or a small part of a clot, can break loose, go to the brain and cause a stroke.  Afib is a major cause of stroke. If left untreated, Afib leads to stroke in 5 out of 100 people per year. To prevent blood clots and strokes, Coumadin (warfarin) has been prescribed for many decades. Coumadin will decrease the risk for stroke to less than 1 in 100 patients per year. Coumadin however is difficult to take; requiring frequent blood draws to ensure that the blood is not “too thin” (leading to bleeding) or “too thick” (leading to stroke). In addition, eating green leafy foods will interfere with the level of blood thinning provided by Coumadin (green leafy foods have Vitamin K which reverses the effect of Coumadin). Many common medications interfere with Coumadin’s effect as well. Lastly, there is a significant risk for major bleeding on Coumadin, especially bleeding in the brain.  Since 2011, newer blood thinners including Dabigatran (Pradaxa), Rivaroxaban (Xarelto) and Apixaban (Eliquis) have been used with increasing frequency.   These newer agents reduce the risk of stroke to a greater degree than Coumadin and they are generally safer with lower risk for major bleeding and bleeding into the brain. Other advantages include no dietary restrictions, less interactions with other medications and a consistent blood thinning effect, so blood drawing to test levels is not needed. Until recently, one major disadvantage of these agents had been the lack of an “antidote”, an agent that could reverse the blood thinning effect if a patient presents with life threatening bleeding or needed emergency surgery.  Fortunately within the past year, two new reversing medications have been developed, with one already approved for use. A different approach to preventing blood clots and strokes is the use of a device called the Watchman, which was recently approved for use in the U. S.  The Watchman is an umbrella like device that plugs an outpouching in the left atrium, the left atrial appendage, the most likely source for blood clots.  The Watchman is an invasive procedure done in the heart catheterization lab and may be an alternative for patients who cannot take blood thinners. Its place in Afib management is evolving as doctors develop more experience with the device.

Since Afib is a major cause of stroke, can we predict who is at risk? The risk factors for stroke in Afib patients have been known for a long time. In 2014, a risk calculator was endorsed by the national guidelines for Afib. The risk calculator is called CHA2DS2VASc: Congestive heart failure, Hypertension, Age > 75, Diabetes, Stroke, Vascular disease (ex, heart attack), Age 65-74 and Sex (female).  One point is assigned for each risk factor except age over 75 and stroke, those categories are given two points.  The risk for stroke rises with rising risk score (1.3% per year for a score of 1, 2.2% for a score of 2, 4%  for a score of 4, etc).  In general, blood thinners are recommended for a score greater than two.

We now know who is at risk for Afib and how to protect these patients from having a stroke. What about patients with no history of Afib who present to the hospital with a stroke? There are several reasons why a patient may have a stroke but even after being hospitalized and after testing, no cause may be found in 20-30% of stroke patients. These types of stroke are called cryptogenic, or cause unknown.  Afib can cause cryptogenic stroke but capturing the Afib on a rhythm strip can be difficult.  Recently it was shown that long term monitoring (wearing a heart monitor for one month) increased the ability to diagnose Afib in cryptogenic stroke patients. Once Afib is diagnosed, blood thinners can be prescribed and a future stroke prevented.

The management of Afib patients on Coumadin who need surgery can be a problem. The Coumadin must be held before surgery, but the proper approach is not known. A recent study looked at two options: holding Coumadin several days before surgery and exposing the patient to the risk of a stroke while off the medication or holding Coumadin and bridging the patient with an injectable blood thinner, holding the injection 12-24 hours before the surgery.  The study found that in low risk patients (those without mechanical heart valves or a prior stroke) holding the Coumadin and not bridging did not result in an increase in strokes and was safer with less bleeding during and after the surgery.  These results have greatly simplified the approach to managing Afib patients who require procedures.

Patients often ask, “What caused my Afib? What can I do to prevent it from happening again?” Some of the most exciting new information comes from risk factor modification for Afib. There are several modifiable risk factors for Afib including hypertension, diabetes, obesity, sleep apnea, and lack of exercise.  Obesity (body mass index greater than 27 kilograms per meter squared) can increase the size of the atria and cause scarring in the atria, predisposing the patient to Afib. In obese Afib patients, it has been shown that weight loss of 10% of body weight is associated with a six-fold reduction in Afib. Cardiorespiratory fitness is also a modifiable risk factor. There is a lower incidence of Afib in patients who regularly perform light to moderate exercise compared to those who are sedentary.  Afib patients who were entered into a tailored exercise program were able to dramatically decrease their risk for Afib.

Recent trials, new medications, devices and risk scores have helped manage the consequences of Afib but the more we learn about Afib, the more obvious it is that we must treat the risk factors. If Afib occurs because of hypertension, blood pressure medication should be given. If Afib occurs due to obesity and low cardiorespiratory fitness, weight loss and exercise should be prescribed. The best way to prevent Afib is to identify and treat the underlying causes.

Screening Student Athletes: Controversies and Benefits

Sudden cardiac death (SCD) is caused by ventricular fibrillation (an irregular heart rhythm from the lower chambers of the heart) and is almost always fatal.  Sudden cardiac death does occur in athletes. Young athletes have an increased risk of SCD compared to their non-athlete peers. The combination of physical exercise and an underlying heart disorder in an athlete can trigger cardiac arrest. The incidence of SCD in athletes varies widely, from about 1 in 150,000 in high school athletes to 1 in 53,000 in college athletes. The rate of SCD in NCAA athletes is highest in males, black athletes and in basketball players.  Screening athletes for their risk for SCD has been shown to reduce the rate of SCD, but the best method of screening remains controversial.

The American Heart Association (AHA) recommends a 14-point history and physical examination to be used for athletes prior to participation in sports. In Europe and in other parts of the world, screening is performed using a questionnaire plus an electrocardiogram (EKG), a test that detects the electrical activity of the heart. The AHA does not recommend an EKG. In both cases if the athlete is felt to be at risk, further cardiac testing including an echocardiogram (an ultrasound of the heart) is performed.  The biggest controversy in screening is therefore whether to include an EKG or not.  This controversy centers on the ability of an EKG to accurately detect heart abnormalities known to cause SCD in athletes.  Intense athletic conditioning changes the structure of the heart and these changes may be reflected in the EKG.  An athlete’s EKG can mimic the EKG of a patient with significant heart disease. Therefore, accurate interpretation of EKGs requires extra training and lots of experience reading athletes’ EKGs.  The reader must be able to discern whether findings on an EKG are normal for the athlete or whether it points to heart disease. False positive testing occurs when a test (such as an EKG) is abnormal but the patient does not have a disease and in fact is normal.  The screening questionnaire has never been shown to accurately identify heart conditions that put an athlete at risk for SCD.  It may have a false positive rate of 30%,  which is considered quite high. The EKG false positive rate is around 11-22%. The Seattle criteria, introduced in 2012, tightened up the guidelines for reading EKGs in athletes and have decreased the false positive rate to 2.5-6%. By using the Seattle criteria an athlete’s EKG can be correctly identified and can lessen the need to do further cardiac testing. Adding the EKG to the screening process has resulted in other controversies as well, including the cost of doing the EKG (and the subsequent cost of cardiac testing for false positive EKGs), the emotional cost of an abnormal EKG (being disqualified from playing sports) and the financial cost if a scholarship or professional contract is forfeited.

Additional controversies in screening include the fact that not all heart diseases that can cause SCD can be identified (even with the addition of an EKG and echo). Having a normal screening might provide a false sense of security.  In addition, the screening generally targets young adults.  The athlete may be genetically programmed to have a disease causing SCD, but it cannot yet be detected by screening since the athlete is still growing and maturing.  Lastly, it is not known how often to do cardiac screening, whether it is a one-time event or whether it should be repeated every few years until the athlete has finished growing.

Certainly the biggest benefit to screening is the correct identification of a heart abnormality associated with SCD. In this case, the athlete is held out from competition and appropriate treatment is begun, both potentially life-saving moves. The incidence of heart disease associated with SCD in the general population is about 1 in 500 to 1 in 1000, so the vast majority of athletes undergoing screening are not identified with disease. Despite that, screening is still beneficial to the athlete. Just by participating in the screening, the athlete and the family are educated about the signs and symptoms which may precede SCD.  Heightening the awareness of SCD in the community can potentially be life-saving as well. Lastly and most surprisingly, many athletes are identified with an elevated body mass index (obesity) or an elevated blood pressure (hypertension), both measured at screening. Since the majority of these young adults would likely not see a doctor for many years, the screening can identify potential future problems for them, allowing them to make lifestyle changes early on in their lives and well before heart disease begins to manifest.

Music, Inflammation and Holiday Stress

Can listening to music decrease inflammation and stress? Can music be beneficial to heart patients? To answer these questions, we have to understand inflammation and it role in heart disease.

What is inflammation?

Inflammation is the body’s protective response to a harmful agent.  The purpose of inflammation is to eliminate the initial cause of an injury to the body, clear out the dead cells caused by the injury and repair the damaged tissue.  The inflammatory process involves the vascular system, the immune system and specialized cells in the blood used to fight injury.  In addition, with inflammation, a variety of proteins are released to help break down a foreign body. Unfortunately, these proteins may also break down healthy tissue and increase the blood clotting ability of the body.  Acute inflammation occurs in response to specific injury, such as an infection by a virus or trauma to a body part.  This inflammatory response is quick and of a short duration. For example in a bacterial infection, the body sends cells to fight the bacteria, a fever is produced to help kill the bacteria, and there is swelling and redness in the area of the infection. Chronic inflammation occurs over years in a long running cycle of tissue destruction and healing. An example of chronic inflammation is rheumatoid arthritis.

Is heart disease an inflammatory process?

Atherosclerosis (plaque or blockage in the heart arteries) is now felt to be a type of chronic inflammatory process.  Inflammation has a key role in atherosclerosis, from the initiation of plaque, through the build up of blockage to the blood clotting that occurs with an acute heart attack. When the inner lining of the heart artery is damaged by high blood flow or biochemical stimuli (smoking, high blood pressure, diabetes or high cholesterol) it permits cholesterol and inflammatory cells to enter and be deposited in the wall of the artery, thus forming plaque. Once the body realizes that there is damage to the artery wall, more cholesterol and inflammatory cells are deposited to try to repair the damaged wall causing the plaque to grow over time.  Ultimately, the plaque starts to limit the blood flow through the artery, causing chest pain (angina) or the plaque breaks open stimulating blood clotting and an acute heart attack. The effect of inflammation can be measured via a simple blood test. Elevation in the inflammatory marker called C reactive protein (CRP) has been shown to increase the risk of heart artery disease.

How is inflammation in the heart arteries treated?

Aspirin is used to reduce the risk for a heart attack.  It does this by reducing the body’s ability to clot, but it is also a powerful anti-inflammatory agent. Interestingly, other popular anti-inflammatories such as ibuprofen (Motrin, Advil) and naprosyn (Aleve) don’t reduce the risk for a heart attack and may in fact increase the risk. They should not be used in place of aspirin to reduce heart risks.  The cholesterol lowering agents called statins have been shown to reduce the risk for heart attack and stroke. These medications lower total cholesterol and LDL (the bad cholesterol) and raise the good cholesterol (HDL). However there are many other medications which lower cholesterol, but have not been shown to reduce the risk of heart disease. It is felt that statins have anti-inflammatory properties. In patients with an elevated CRP treating with a statin reduces the risk for cardiac events by 50%. It is this anti-inflammatory effect, along with the cholesterol lowering properties, that gives statins their edge over other medications and their power to reduce heart attacks and stroke.  There are many non-pharmacologic therapies that are anti-inflammatory. These include foods such as fruits, vegetables and fish high in omega3 fatty acids.  Other anti-inflammatory therapies include exercise, yoga, meditation and music.

Is music anti-inflammatory? Can music be used as therapy?

Sounds in nature, such as a babbling brook or ocean waves on the shore, are known to be soothing and are promoted as a method to relax and to fall asleep.  Many musical pieces can produce the same sense of calmness.  When his biographer asked Steve Jobs, the inventor of ITunes, what music he listened to, the answer revealed the anti-inflammatory power of music.  Aside from songs by Bob Dylan and the Beatles, his favorites included a Gregorian chant, "Spiritus Domini" performed by Benedictine monks and the "Goldberg Variations", by J.S. Bach and performed by Glenn Gould.  The interview took place during Jobs third medical leave for treatment of pancreatic cancer. He felt the first piece was so calming it almost put him in a trance and the later he felt was deep and reflective. After listening to those pieces, Jobs insight is certainly supported.  The data supporting music therapy comes from diverse medical fields.  In patients with pregnancy or schizophrenia, listening to music provided clear-cut psychological benefits. In patients on respirators, music reduced the breathing rate and blood pressure.  Surgical patients who listen to music, even under general anesthesia, have less anxiety and less need for pain medication during recovery.  A large review of twenty-three trials with more than 1000 participants looked at music therapy in heart attack patients. It concluded that music reduced anxiety, heart rate, respiratory rate and blood pressure in these patients, suggesting a psychological relaxation response.

Certainly what is good and soothing for one listener is cacophony to another listener. Everyone should find their own anti-inflammatory songs as music therapy has no side effects or risks, assuming of course that the decibel level is reasonable. So, after a day of battling the world and increasing your inflammatory markers, go home, slip on a pair of headphones, find some good relaxing music and engage in your own form of anti-inflammatory therapy. Perhaps sing or listen to some holiday tunes to reduce the stress and increase the enjoyment of the holiday season.