cycling reduce heart disease risk
A study conducted by the Purdue University, Indiana, United States concluded that regular cycling can cut your risk of heart disease by a whopping 50 percent.
Similarly, the Copenhagen Heart Study, which monitored over 5000 people over a period of 14 years, found a major association between high intensity cycling and reduced risk of coronary heart disease death.
Cardiovascular diseases are responsible for over 30 percent of the global deaths annually.
In India too, cardiovascular disease is the leading cause of deaths today, accounting for more than a quarter of all mortalities.
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Interestingly, as many as 50 percent of heart disease related deaths can be prevented by adopting healthy habits and a hygienic lifestyle.
Much like smoking, physical inactivity is also a significant risk factor for heart disease.
In fact, physical inactivity is associated with many of the leading causes of lifestyle diseases like obesity, diabetes, hypertension, cardiac ailments and even some forms of cancer.
According to the World Health Organization, insufficient physical activity is one of the 10 leading risk factors for death worldwide.
While we count smoking as a serious health hazard, physical inactivity is hardly considered a life risk.
The WHO recommends that adults between the ages of 18-64 years should indulge in at least 150 minutes of moderate-intensity physical activity throughout the week.
Regular cycling has multiple benefits, from a healthy heart to fit muscles to a better metabolism.
(Shutterstock)
Counting on the benefits of cycling, Singal explained, “Cycling is one of the best cardio exercises for people of all age groups and all body types. It not only helps burn calories and keeps weight under control, but also helps build stamina and increase muscle and bone strength. Being a low impact exercise, it is also soft on the joints and unlike hard gym training sessions, it doesn’t put you at risk of overuse injuries or sprains. This is why it can also be taken up by elderly people who have arthritic joints.”
“At the same time, cycling is also a major stress relieving exercise, especially when undertaken in a congenial environment such as a park or a non-congested road. Regular cycling stimulates and improves your heart, lungs and circulation, reducing your risk of cardiovascular diseases,” he added.
Persistently elevated levels of blood pressure have the potential to damage the blood vessels which causes heart attacks. Exercise helps keep blood pressure under check and cycling is the most potent cardio exercise.
Cycling also reduces the risk of type 2 diabetes.
The rise in incidence of type 2 diabetes is a major cause of concern in India.
Physical inactivity and obesity are considered to be the leading risk factors for type 2 diabetes.
“Yet again, cycling is a very good way of keeping your weight under check and preventing diabetes. Keeping body weight under control: Obesity is today the key driver of hypertension, diabetes and cardiovascular diseases in India. Rise in the obesity epidemic including in young children is again attributed to physical inactivity,” he said.
The people, who cycle regularly, will tell you that it is a wonderful stress busting exercise.
There is no other workout as calming as riding a bicycle in a green environment. Keeping stress under control is also important to check the risk of cardiovascular disease and stroke.
Cycling when done regularly helps raise the levels of heart-protecting HDL cholesterol and reduce the levels of dangerous triglycerides. Cycling can be adopted in daily life without actually demarcating time for exercise as it can be incorporated as a mode of transport.
Switching from driving to cycling to work may lower the risk of heart disease.
For many, walking and cycling not only contribute to daily health-enhancing physical activity levels, but also provide cost- and time-effective alternatives to commuting by car or public transport - while reducing traffic congestion and air and noise pollution.
Though active commuting has been previously linked to a lower risk of heart disease and premature death, few studies have specifically assessed the cardiovascular health benefits of commuting by bike - or investigated the impact of changing modes of commuting to work, from car and public transport to active commuting.
The aim of the Circulation study was to examine the association between cycling, changes in cycling habits, and risk of coronary heart disease in Danish men and women.
Findings showed that the 45,000 Danish adults aged 50-65 years who regularly cycled to work or for leisure had between 11-18 percent fewer heart attacks over the course of a 20-year follow-up.
The analysis indicated that some protection against heart disease was achieved with as little as 30 minutes of biking per week. Participants who changed their behavior and took up cycling in the first 5 years of follow-up had a 25 percent reduced risk of developing heart disease, compared with men and women who remained non-cyclists in the subsequent 15-year period.
While the findings are promising, the researchers say they do not prove that cycling for commuting or leisure prevents heart attacks. The results do highlight, however, that the participants who cycled on a regular basis had fewer cardiovascular events and is, therefore, a strong indicator that cycling is beneficial for cardiovascular health.
Regular cycling could have prevented over 7 percent of heart attacks
"Finding time for exercise can be challenging for many people, so clinicians working in the field of cardiovascular risk prevention should consider promoting cycling as a mode of transportation," advises Anders Grøntved, M.Sc., M.P.H., Ph.D., senior study author and associate professor of Physical Activity Epidemiology at the University of Southern Denmark.Participants were questioned about their cycling habits at the start of the study and then again 5 years later. Additionally, Grøntved and colleagues recorded the exercise habits, physical activity levels, and frequency of bicycle riding of all participants as well as heart disease risk factors, such as blood pressure, weight, cholesterol, smoking, diet, and alcohol consumption.
Overall in the 20-year follow-up, there were 2,892 heart attacks, of which, cycling on a regular basis could have avoided more than 7 percent, the team says.
"Because recreational and commuter biking is an easy way to make physical activity part of one's routine in a non-structured and informal fashion; based on the results, public health authorities, governments, and employers ought to consider initiatives that promote bicycle riding as a way to support large-scale cardiovascular disease prevention efforts," says Kim Blond, M.Sc., lead author and research assistant at the University of Southern Denmark.
In the Journal of the American Heart Association study, similarly, researchers examined the potential relationships of cycling to work at the start of the research with a change in commuter cycling, with 10-year incidence of obesity, hypertension, hypertriglyceridemia, and impaired glucose tolerance in men and women from Northern Sweden.
The team also assessed whether genetic and other factors modified the relationships, and they examined the percentage of these risk factors for cardiovascular disease that could be prevented if all participants continued to cycle or switched to commuting by bicycle to work, during a 10-year follow-up period.
Switching from passive to active commuting reduced all risk factors
Over a decade, more than 20,000 individuals in their 40s, 50s, and 60s had their commuting habits, weight, cholesterol levels, blood glucose, and blood pressure assessed.At the study onset, compared with passive commuters - who drove to work or used public transport - participants who cycled to work were found to be 15 percent less likely to be obese, 13 percent less likely to have high blood pressure, 15 percent less likely to have high cholesterol, and 12 percent less likely to have pre-diabetes or diabetes.
The researchers revealed that after 10 years, the individuals who switched from passive to active commuting were also less likely to be obese, have hypertension, have elevated cholesterol levels, or develop diabetes, when compared with the inactive commuters.
"We found active commuting, which has the additional advantages of being time-efficient, cheaper and environmentally friendly is also great for your health. The multiple advantages of active commuting over structured exercise may help clinicians convey a message that many patients will embrace more readily than being told to join a gym, go for a jog, or join a sports team."The researchers note that while individuals who cycled for a longer duration or more frequently experienced small additional gains in risk reduction, there was no minimum amount of time or distance required to reduce the risk of cardiovascular risk factors.
Paul Franks, Ph.D.
According to the study authors, it is estimated that switching from passive to active commuting may have prevented 24 percent of obesity cases, 6 percent of hypertension diagnoses, 13 percent of high cholesterol diagnoses, and 11 percent of the diabetes cases.
"The really good news here is that it's never too late to benefit from an active lifestyle. People who switched from passive to active commuting saw considerable gains in their cardiovascular health," Franks concludes.
Read about how fitness, not physical activity, may ward off the effects of a sedentary lifestyle.
From the viewpoint of a keen athlete, I would like to first address the “who cares?” factor. The lay press and medical journals like to focus on the stats. Do athletes live a year longer or a year less? Are they 0.1% more or less likely to suddenly die of a heart attack? These are important scientific questions but will the answers influence my decision as to whether I go running in the forest this Sunday? All athletes know that their motivations for sport practice are not based on statistics but from the immediate satisfaction that comes from it. You are more likely to be killed by a car when riding than you are of dying of a heart attack and yet cyclists do not spend all of their cycling hours avoiding this risk on a wind trainer.
On the other hand, my job is to assess athletes who have developed heart problems and so the question as to whether sport may have contributed becomes important. With current evidence, I would not advise that any level of exercise is unhealthy. At the same time, I think that it is important to recognize that some things remain unanswered.
What is strenuous exercise?
Here is the first major problem with the medical literature. Numerous studies report improved health outcomes as a result of regular strenuous exercise. For example, in a widely quoted study (Blair et al., 1989) longer overall survival was attributed to “high levels of fitness” but it was also concluded that these benefits may not be seen in those performing exercise above a level of 10 metabolic equivalents (METS). So, what is 10 METS? This is the equivalent of exercising at an oxygen consumption of 35 ml/kg/min which is about 50% intensity for a well-trained athlete, jogging, riding a bike at 20km/h etc. Put simply, it is way below that which competitive athletes do in training on a regular basis. This same problem is true of nearly all of the large studies that have assessed exercise benefit – they all set maximal exercise at a level way below that appropriate for athletes. Thus, the current evidence base can be summarized as follows:
Figure 1: The benefit of exercise is likely to extend to high levels of exercise but is there a point where the benefits start to plateau or even reverse? Note, however, that it is unlikely that any level of exercise will increase risk to the level of a sedentary person.
It is likely that the benefits of exercise extend beyond the fairly conservative range which has been studied but the controversy involves whether there is a point where ‘extreme’ amounts of exercise may increase the risk of some heart problems.
There are some well-conducted studies from Scandinavia which have looked at health outcomes in ex-Olympic athletes and the results have been very reassuring (Sarna, Sahi, Koskenvuo, & Kaprio, 1993) Olympic athletes live longer and develop fewer health complaints. However, they are also wealthier, smoke and drink less and are likely to have better diets etc. – all of which may account for the differences in health that were reported. Thus, whilst it seems clear that being an athlete is healthy, these studies do not enable analysis as to whether benefits are due to lifestyle factors, exercise, or a combination of both.
What evidence is there to suggest that extreme exercise may have unwanted effects on the heart?
- Exercise causes heart enlargement
Mostly the heart enlargement that occurs is quite mild and goes away completely if the athlete stops training. This is called ‘physiological remodeling’ and simply reflects enlargement of the muscle just as your biceps enlarge with curls.
However, in more extreme endurance exercise, the heart enlargement can be dramatic (see figure below) and it may not resolve when the athlete stops training. For example, in a study of nearly 150 Tour de France riders (Abergel et al., 2004), hearts size was greatly increased and, when studied 3 years later, the riders’ hearts were larger still. In a recent study from Switzerland (Baldesberger et al., 2008), ex-professional cyclists had persisting enlargement of the heart despite having retired from sport 30+ years earlier. This would suggest that something other than simple muscle enlargement was occurring because otherwise it would have returned to normal size once the load of exercise ceased. This might not seem a big deal but there are only a few things in the heart – muscle, the connective tissues which hold the muscle in place and the electrics of the heart. If there is an increase in the connective tissue part then it can interfere with muscle or electric function. Therefore, the failure of heart size to return to normal MAY be a cause for concern.
Figure 2: Comparison of the heart size in two 23 year olds – a non-athlete and a young professional cyclist. Note the 10cm marker as a reference. The non-athlete’s heart is approximately 15 x 12cm vs. 25 x 18 for the athlete!
- Enlargement of the heart in athletes may cause scarring
In one recent high profile case, Ryan Shay died during the 2008 US marathon trials and the cause of this death was never established. His autopsy result was stated as “Cardiac arrhythmia due to cardiac hypertrophy with patchy fibrosis of undetermined etiology. Natural causes.” In other words, he had heart muscle enlargement (completely expected for an elite athlete) with small areas of scar (definitely abnormal in athletes) and the conclusion…natural causes. It is surprising that this finding did not stimulate debate as to why a fit young athlete had patches of scar in his heart. Was exercise the cause? We do not know. But, we will never know if the question is not asked. This is shaky ground, however, because a balance has to be struck between investigating issues such as these and yet not creating disproportionate hysteria within the media and wider community. We must always remember that the death of a young athlete is very, very rare.
- Some heart rhythm problems are more common in athletes
Summary
This is a lot of information and may well seem somewhat confusing. I will try to summarise all of this information in some simple points.
Are endurance athletes hurting their hearts by repeatedly pushing beyond what is normal?
His life was about to change forever.
When his heart began to flop like a fish in his chest, and his heart
rate jumped from 155 to 218 beats per minute and stayed pegged there,
his first reaction was simple: “I went into denial.”
He arrived to the ER that afternoon and was later brought via ambulance to the main cardiac unit for an overnight stay. Though he trusted the cardiologists and the ER doctor, he doubted their warnings. His denial was strong.
After following their recommendations for rest, he returned to training; the electrodes glued to his chest and the telemetric EKG unit dangling around his neck didn’t disrupt his routine. But the annoying episodes happening with increasing frequency during his more intense rides did. The flopping fish would return as his heart rate spiked. More upsetting was the phone call in the middle of the night from a faraway nurse who had been watching his EKG readings and had some shocking news: His heart had stopped for a few seconds.
By October, Zinn received an official diagnosis: multifocal atrial tachycardia. Normally, the heart rate is controlled by a cluster of cells called the sinoatrial (SA) node. When a number of different clusters of cells outside the SA node take over control of the heart rate, and the rate exceeds 100 beats per minute, this is called multifocal atrial tachycardia (AT).
“That’s when I decided to take the warning I’d been given and quit racing,” he said.
Zinn was instantaneously downgraded from thoroughbred to invalid. He has had to back off from riding with intensity, or duration. He has had to alter his life, in more ways than one. He has had to face the fact that he can never do what he used to do, in the same way that he used to do it. Life has changed. Forever.
Was his bike trying to kill him?
Zinn is not alone. When he began his arduous reconciliation with his life-changing condition, he began reaching out to others from his generation that were fabulous athletes in their day, and who continued to push themselves well into their 40s and 50s.
The number of friends and former teammates that had similar or more severe heart issues was disconcerting. Far from being an outlier, Zinn was one among many.
Mike Endicott was one of those friends. He had been interested in endurance sports since he was a teenager.
“By nature I’m a person who likes to train,” Endicott said. “I race to train; a lot of people train to race. That was kind of anti-climactic. I use racing as kind of a gauge as to where you’re at, but I much prefer to be just out doing stuff. I just like the movement and activity, being outside.”
He arrived to the ER that afternoon and was later brought via ambulance to the main cardiac unit for an overnight stay. Though he trusted the cardiologists and the ER doctor, he doubted their warnings. His denial was strong.
After following their recommendations for rest, he returned to training; the electrodes glued to his chest and the telemetric EKG unit dangling around his neck didn’t disrupt his routine. But the annoying episodes happening with increasing frequency during his more intense rides did. The flopping fish would return as his heart rate spiked. More upsetting was the phone call in the middle of the night from a faraway nurse who had been watching his EKG readings and had some shocking news: His heart had stopped for a few seconds.
By October, Zinn received an official diagnosis: multifocal atrial tachycardia. Normally, the heart rate is controlled by a cluster of cells called the sinoatrial (SA) node. When a number of different clusters of cells outside the SA node take over control of the heart rate, and the rate exceeds 100 beats per minute, this is called multifocal atrial tachycardia (AT).
“That’s when I decided to take the warning I’d been given and quit racing,” he said.
Zinn was instantaneously downgraded from thoroughbred to invalid. He has had to back off from riding with intensity, or duration. He has had to alter his life, in more ways than one. He has had to face the fact that he can never do what he used to do, in the same way that he used to do it. Life has changed. Forever.
Was his bike trying to kill him?
Zinn is not alone. When he began his arduous reconciliation with his life-changing condition, he began reaching out to others from his generation that were fabulous athletes in their day, and who continued to push themselves well into their 40s and 50s.
The number of friends and former teammates that had similar or more severe heart issues was disconcerting. Far from being an outlier, Zinn was one among many.
Mike Endicott was one of those friends. He had been interested in endurance sports since he was a teenager.
“By nature I’m a person who likes to train,” Endicott said. “I race to train; a lot of people train to race. That was kind of anti-climactic. I use racing as kind of a gauge as to where you’re at, but I much prefer to be just out doing stuff. I just like the movement and activity, being outside.”
His interests evolved so that six months of the year he would be
Nordic skiing, and the other six months would be devoted to riding road
and mountain bikes. It was non-stop. Meanwhile, he was expanding his
business as an independent sales representative across the Rocky
Mountain West.
“I was burning the candles at both ends,” Endicott said. “I was having a ball. I was working, I was making a good living, but boy was I burning it and I didn’t realize it.”
Then, one day in 2005, he headed to a Nordic ski race at Devil’s Thumb Ranch, an area in the Fraser Valley of Colorado. In a familiar tale, Endicott’s life was about to change forever.
“I had created the perfect storm over a good 20-year period, but it all came to a head here because of the week or two prior to this race,” he said.
With a stressful week of travel leading up to the event, Endicott hadn’t slept well the night before. But, like so many of us, he just enjoyed being out there. He didn’t eat much before the race except for two big coffees, and an hour before the race downed a few caffeinated energy gels. The temperature was around zero degrees, overcast, with light snows falling and a bit of a breeze swirling around. The conditions for the perfect storm had fallen into place.
“I’m having a good race, I was having fun, going after it,” he recalled. “I punched up over this rise and all of a sudden, I don’t feel good, something’s not right. Something was beating inside my chest. No pain, no discomfort, but I was a little dizzy.”
He felt like he was drunk. He could hardly stay up on his legs. He would collapse and get back up, his heart still doing something strange inside his chest. By the time the last skiers of the field passed by, Endicott was done. He collapsed in the snow and began to die. He was on his back, barely maintaining consciousness, in a skin suit, in the snow, in zero-degree weather. There was no pain, but he couldn’t catch his breath. He tried to yell for help, but he’d barely make a noise. He could only wave his pole.
“Fairly quickly I learned I’m in deep shit here. Basically, I figured I was done, this was it,” he said. “It’s interesting; at the time, my emotions were… I was frustrated. It was not on my list of things to do because I was kind of a type-A. My dog was in my truck, we were going to go out and do a ski when I was done, I had work to do that afternoon, phone calls. It just wasn’t on my list of things to do, to die on the ski trails. I was pissed [laughs]. I was beating on my chest with my hands saying, ‘Come on, something’s got to work here.’ So I struggled in and out of consciousness out there in the snow for about an hour. I don’t know how long I was out, and then I’d come back again, and then I’d try to look around and then I’d get dizzy again. It was ugly.”
“I was burning the candles at both ends,” Endicott said. “I was having a ball. I was working, I was making a good living, but boy was I burning it and I didn’t realize it.”
Then, one day in 2005, he headed to a Nordic ski race at Devil’s Thumb Ranch, an area in the Fraser Valley of Colorado. In a familiar tale, Endicott’s life was about to change forever.
“I had created the perfect storm over a good 20-year period, but it all came to a head here because of the week or two prior to this race,” he said.
With a stressful week of travel leading up to the event, Endicott hadn’t slept well the night before. But, like so many of us, he just enjoyed being out there. He didn’t eat much before the race except for two big coffees, and an hour before the race downed a few caffeinated energy gels. The temperature was around zero degrees, overcast, with light snows falling and a bit of a breeze swirling around. The conditions for the perfect storm had fallen into place.
“I’m having a good race, I was having fun, going after it,” he recalled. “I punched up over this rise and all of a sudden, I don’t feel good, something’s not right. Something was beating inside my chest. No pain, no discomfort, but I was a little dizzy.”
He felt like he was drunk. He could hardly stay up on his legs. He would collapse and get back up, his heart still doing something strange inside his chest. By the time the last skiers of the field passed by, Endicott was done. He collapsed in the snow and began to die. He was on his back, barely maintaining consciousness, in a skin suit, in the snow, in zero-degree weather. There was no pain, but he couldn’t catch his breath. He tried to yell for help, but he’d barely make a noise. He could only wave his pole.
“Fairly quickly I learned I’m in deep shit here. Basically, I figured I was done, this was it,” he said. “It’s interesting; at the time, my emotions were… I was frustrated. It was not on my list of things to do because I was kind of a type-A. My dog was in my truck, we were going to go out and do a ski when I was done, I had work to do that afternoon, phone calls. It just wasn’t on my list of things to do, to die on the ski trails. I was pissed [laughs]. I was beating on my chest with my hands saying, ‘Come on, something’s got to work here.’ So I struggled in and out of consciousness out there in the snow for about an hour. I don’t know how long I was out, and then I’d come back again, and then I’d try to look around and then I’d get dizzy again. It was ugly.”
By chance, two of his friends who had gone out for a cool down after
their race saw Endicott wave his arm out of the corner of their eyes,
and skied to find a fallen friend dying in the snow.
Endicott was in ventricular tachycardia (VT or V-tach); the result was sudden cardiac death, an immediate, unexpected loss of heart function, breathing, and consciousness. Just 50 at the time, Endicott miraculously survived, resuscitated on the scene. But his life is very different now.
Endicott was in ventricular tachycardia (VT or V-tach); the result was sudden cardiac death, an immediate, unexpected loss of heart function, breathing, and consciousness. Just 50 at the time, Endicott miraculously survived, resuscitated on the scene. But his life is very different now.
THE HEART OF THE MATTER
Cycling is an endurance sport like no other. Long rides can be a
standard component of the diet, something that devotees look forward to
all week. In any case, as a cyclist, you likely love the weekend
rampage, the six-hour tour of the mountains, or the endless training
sessions that are the only way to develop fitness for races that last as
long as a workday. But fit for racing doesn’t necessarily equal
healthy.
Stories abound that undermine the notion that elite athletes are healthy. From the running world, marathoner Alberto Salazar, at the age of 48, suffered a heart attack and lay dead for 14 minutes before a cardiologist placed a stent in a blocked artery, saving his life. Micah True, the ultra-marathoner and protagonist of the bestselling book Born to Run, went for a 12-mile run in the New Mexico wilderness and was later found dead.
Of course, these tragic tales are preceded by the origin story of an endurance athlete running himself, literally, to death. An enlarged, thickened heart with patchy scar tissue is common in long-term endurance athletes and is dubbed “Pheidippides cardiomyopathy” after the 40-year-old running messenger (and prototypical masters endurance athlete) who died after bringing the news of Greek victory at the battle of Marathon to Athens. Pheidippides was a hemerodrome, (an all-day running courier in Ancient Greece), and he had run 240km over two days to request help from Sparta against the Persians at Marathon, before expiring after running the additional 42km (26.2 miles) back from the battlefield. We celebrate his death by running marathons.
Stories abound that undermine the notion that elite athletes are healthy. From the running world, marathoner Alberto Salazar, at the age of 48, suffered a heart attack and lay dead for 14 minutes before a cardiologist placed a stent in a blocked artery, saving his life. Micah True, the ultra-marathoner and protagonist of the bestselling book Born to Run, went for a 12-mile run in the New Mexico wilderness and was later found dead.
Of course, these tragic tales are preceded by the origin story of an endurance athlete running himself, literally, to death. An enlarged, thickened heart with patchy scar tissue is common in long-term endurance athletes and is dubbed “Pheidippides cardiomyopathy” after the 40-year-old running messenger (and prototypical masters endurance athlete) who died after bringing the news of Greek victory at the battle of Marathon to Athens. Pheidippides was a hemerodrome, (an all-day running courier in Ancient Greece), and he had run 240km over two days to request help from Sparta against the Persians at Marathon, before expiring after running the additional 42km (26.2 miles) back from the battlefield. We celebrate his death by running marathons.
These deaths are even more alarming when you consider the subjects —
highly trained athletes in what many would consider peak physical
condition. Isn’t exercise supposed to prevent us from falling to a heart
attack?
In recent years, cardiologists who have studied extreme exercise and its side effects have proposed a hypothesis that suggests these tragedies may not be so shocking after all. There can be too much of a good thing when it comes to your heart.
That organic metronome in your chest, rhythmically coordinating 100,000 beats per day without pause, takes the brunt of the abuse in endurance athletes. When you’re seated, it pumps about five quarts of blood per minute. When you’re running, that figure bounds to 25 to 30 quarts. The human heart wasn’t designed to handle that load for hours on end, day after day.
In the case of endurance athletes who have competed for years — whose hearts have exceeded the threshold of normal heart rates for decades — going above what is normal defines them. But it may also be killing them.
To understand why, it helps to know the mechanisms of the heart. There are two systems at play: the plumbing and the electronics. We’ll begin with the pipes.
The heart’s right side pumps deoxygenated blood from the body to the lungs, and the left side pumps oxygenated blood from the lungs to the body. Each side has two chambers, a small one called the atrium and a large one called the ventricle. When the heart contracts, everything moves in a coordinated fashion, with the atria contracting first and the ventricles following. The blood is pushed through the heart into either the vascular system in the lungs or the body.
For one out of every five people with heart disease, the first sign is sudden cardiac death. However, sudden cardiac death during an athletic undertaking is, in general, very rare. In some cases it can be due to heart attack — myocardial infarction — caused by lifestyle diseases such as atherosclerosis, which can lead to blockages.
But various forms of arrhythmia (abnormal heart rhythms) are trickier. This is where the electronics come in. They may have a genetic component, but they can also be influenced by stress and intense training. Arrhythmia is a generic label for a condition in which the heart rhythm is altered from its common pattern in various parts of the heart. These episodes can be more or less dangerous depending on their speed, how long they last, and which part of the heart they affect.
In recent years, cardiologists who have studied extreme exercise and its side effects have proposed a hypothesis that suggests these tragedies may not be so shocking after all. There can be too much of a good thing when it comes to your heart.
That organic metronome in your chest, rhythmically coordinating 100,000 beats per day without pause, takes the brunt of the abuse in endurance athletes. When you’re seated, it pumps about five quarts of blood per minute. When you’re running, that figure bounds to 25 to 30 quarts. The human heart wasn’t designed to handle that load for hours on end, day after day.
In the case of endurance athletes who have competed for years — whose hearts have exceeded the threshold of normal heart rates for decades — going above what is normal defines them. But it may also be killing them.
To understand why, it helps to know the mechanisms of the heart. There are two systems at play: the plumbing and the electronics. We’ll begin with the pipes.
The heart’s right side pumps deoxygenated blood from the body to the lungs, and the left side pumps oxygenated blood from the lungs to the body. Each side has two chambers, a small one called the atrium and a large one called the ventricle. When the heart contracts, everything moves in a coordinated fashion, with the atria contracting first and the ventricles following. The blood is pushed through the heart into either the vascular system in the lungs or the body.
For one out of every five people with heart disease, the first sign is sudden cardiac death. However, sudden cardiac death during an athletic undertaking is, in general, very rare. In some cases it can be due to heart attack — myocardial infarction — caused by lifestyle diseases such as atherosclerosis, which can lead to blockages.
But various forms of arrhythmia (abnormal heart rhythms) are trickier. This is where the electronics come in. They may have a genetic component, but they can also be influenced by stress and intense training. Arrhythmia is a generic label for a condition in which the heart rhythm is altered from its common pattern in various parts of the heart. These episodes can be more or less dangerous depending on their speed, how long they last, and which part of the heart they affect.
When we train intensively for an endurance event, several adaptations
occur in our hearts. The most common is that our resting heart rate
goes down due to improved heart function. Many endurance athletes will
experience what they think is the sensation of their hearts skipping a
beat. Actually, this is most often due to premature beats — a premature
ventricular contraction (PVC) if it originates in the ventricle or a
premature atrial contraction (PAC) if it originates in the atrium. Both
PACs and PVCs are quite common in well-trained athletes and often are
not dangerous.
The heart adapts to this by growing larger, contracting with more strength, and responding more vigorously to adrenaline. We call this fitness. Whether or not it’s also healthy is up for debate.
Does the scientific community have a solid definition for what an endurance athlete is? How many hours it takes per week or month to go from part-time participant to all-out endurance junkie? “Hell no,” said Dr. John Mandrola, a heart-rhythm doctor from Louisville, Kentucky, who takes a keen interest in the hearts of endurance athletes, and who is himself a cyclist with atrial fibrillation (AF). “What’s too much? That’s the $64,000 question. Though I will say it’s a little like what the judge said about indecency: ‘I know it when I see it.’”
Endurance athletes push so far beyond what has historically been considered normal that their hearts can show signs that mimic disease. Abnormal heart rhythms would usually be cause for concern. But trained athletes experience a host of benign irregularities, including premature beats, those PACs and PVCs. Most of them remain simple nuisances, and, more often than not, rest increases their frequency.
As for electrical abnormalities, the data speaks for itself. Long-term endurance exercise results in a five-fold increase in the risk of developing AF. A review of the relevant research finds many small studies that correlate long-term sports activity with AF (incidentally, Robert Gesink of Lotto-JumboNL had surgery in May 2014 for atrial fibrillation and has returned to the sport). Though none is conclusive, collectively they indicate a pattern: “Younger patients with a lower cumulative dose of exercise have lower AF risk. Older patients with higher dosages of exercise have higher AF risk,” Mandrola said.
“[People] criticize the studies that have been done that make this association. And they have a point: Each of the studies, individually, has flaws. They’re from one center, they include small numbers of athletes, and there’s selection bias. But taken together — there’s maybe ten to 20 single-center studies that show this association. If you put all that evidence together, there’s reason to believe that endurance athletes can develop AF.”
Perhaps the most influential study on mechanisms of AF in athletes comes from the study of rats and the effects of endurance exercise on the atria, conducted by a group of Spanish researchers and published in the journal Circulation in 2010. Rats were run one hour per day, five days a week, for up to 16 weeks. And they paid. Compared with sedentary controls, the exercised rats displayed evidence of damage, things such as enhanced vagal tone, atrial dilation, atrial fibrosis, and vulnerability to pacing-induced AF. Detraining the rats quickly led to a reduction in the vulnerability of AF, but not structural changes. Fibrosis and left atrial dilation remained after the rats stopped exercising. Is this what is happening inside your chest when you repeatedly go out and ride your bike, before work, after work, and every weekend in the summer?
“Look at some of the science that’s been done and think about what an endurance athlete has to go through,” Mandrola said. “They have a high cardiac output, their heart is exposed to high volume, high pressure, intense electrical and adrenaline stimulation, but then they also develop slow heart rates. So it’s this combination of spikes in adrenaline and pushing through that red zone combined with always having a slow heart beat. If you look at the plausibility side, it is plausible. When you have the experience I have as a physician, as a heart rhythm doctor, there are definite patterns of Zinn-like people, and me, and others who get this, and they have nothing else that could have caused it. They don’t have high blood pressure, they don’t have diabetes, they’re not fat, and most don’t drink alcohol excessively. So most of these things that lead to heart rhythm problems, the endurance athlete doesn’t have. The only thing is the endurance exercise — too much endurance exercise over too long of a time period.”
The more you ride, the harder you ride, the faster you ride, the better athlete you might become today. But over decades of exertion, the myocardial cells of the heart begin to simply fall apart, and you’re left with an unhealthy ticker. Or so these new studies suggest. When you’re 20, or even 30, this can lead to acute reversible injuries — temporary damage that can be relieved with correct rest. In a 50-year-old, repeated hard doses of the sport you love, the rides you cherish — since complete recovery doesn’t occur as efficiently — could be leading to accelerated aging, or hypertrophy — in layman’s terms, a stiff muscle in your chest. That probably wasn’t what you were looking for when you bought your last bike. One of the more telling research papers on the subject, published in 2011 in the Journal of Applied Physiology, studied the structure and function of the heart in lifelong competitive endurance veteran athletes, ranging in age from 50 to 67. MRI studies revealed that some 50 percent of the veteran athletes had myocardial fibrosis, a condition that involves the impairment of the heart’s muscle cells, called myocytes, through hardening or scarring of tissue. In age-matched controls — people of the same age who didn’t compete — and young athletes, there were zero cases of the disease. Furthermore, the fibrosis was significantly associated with the number of years spent training, and the number of marathons and ultra-endurance marathons they had completed.
OVERDOSE
With the growth of endurance sports (the number of licensed bike racers in the U.S. increased by 15 percent between 2009 and 2013, according to USA Cycling; the number of runners has grown 70 percent over the past decade, according to the National Sporting Goods Association), there has been an increase in interest to the potential adverse acute effects of long and intense training and racing on the heart. Endurance athletes endure fluid shifts, changes in pH and electrolytes, and fluctuations in blood pressure. Their atria are exposed to chronic volume and pressure overload. The athlete’s heart lurches from extreme to extreme — from spikes approaching 200bpm to long periods of ultra-low resting heart rates below 60bpm, a condition called bradycardia.The heart adapts to this by growing larger, contracting with more strength, and responding more vigorously to adrenaline. We call this fitness. Whether or not it’s also healthy is up for debate.
Does the scientific community have a solid definition for what an endurance athlete is? How many hours it takes per week or month to go from part-time participant to all-out endurance junkie? “Hell no,” said Dr. John Mandrola, a heart-rhythm doctor from Louisville, Kentucky, who takes a keen interest in the hearts of endurance athletes, and who is himself a cyclist with atrial fibrillation (AF). “What’s too much? That’s the $64,000 question. Though I will say it’s a little like what the judge said about indecency: ‘I know it when I see it.’”
Endurance athletes push so far beyond what has historically been considered normal that their hearts can show signs that mimic disease. Abnormal heart rhythms would usually be cause for concern. But trained athletes experience a host of benign irregularities, including premature beats, those PACs and PVCs. Most of them remain simple nuisances, and, more often than not, rest increases their frequency.
As for electrical abnormalities, the data speaks for itself. Long-term endurance exercise results in a five-fold increase in the risk of developing AF. A review of the relevant research finds many small studies that correlate long-term sports activity with AF (incidentally, Robert Gesink of Lotto-JumboNL had surgery in May 2014 for atrial fibrillation and has returned to the sport). Though none is conclusive, collectively they indicate a pattern: “Younger patients with a lower cumulative dose of exercise have lower AF risk. Older patients with higher dosages of exercise have higher AF risk,” Mandrola said.
“[People] criticize the studies that have been done that make this association. And they have a point: Each of the studies, individually, has flaws. They’re from one center, they include small numbers of athletes, and there’s selection bias. But taken together — there’s maybe ten to 20 single-center studies that show this association. If you put all that evidence together, there’s reason to believe that endurance athletes can develop AF.”
Perhaps the most influential study on mechanisms of AF in athletes comes from the study of rats and the effects of endurance exercise on the atria, conducted by a group of Spanish researchers and published in the journal Circulation in 2010. Rats were run one hour per day, five days a week, for up to 16 weeks. And they paid. Compared with sedentary controls, the exercised rats displayed evidence of damage, things such as enhanced vagal tone, atrial dilation, atrial fibrosis, and vulnerability to pacing-induced AF. Detraining the rats quickly led to a reduction in the vulnerability of AF, but not structural changes. Fibrosis and left atrial dilation remained after the rats stopped exercising. Is this what is happening inside your chest when you repeatedly go out and ride your bike, before work, after work, and every weekend in the summer?
“Look at some of the science that’s been done and think about what an endurance athlete has to go through,” Mandrola said. “They have a high cardiac output, their heart is exposed to high volume, high pressure, intense electrical and adrenaline stimulation, but then they also develop slow heart rates. So it’s this combination of spikes in adrenaline and pushing through that red zone combined with always having a slow heart beat. If you look at the plausibility side, it is plausible. When you have the experience I have as a physician, as a heart rhythm doctor, there are definite patterns of Zinn-like people, and me, and others who get this, and they have nothing else that could have caused it. They don’t have high blood pressure, they don’t have diabetes, they’re not fat, and most don’t drink alcohol excessively. So most of these things that lead to heart rhythm problems, the endurance athlete doesn’t have. The only thing is the endurance exercise — too much endurance exercise over too long of a time period.”
The more you ride, the harder you ride, the faster you ride, the better athlete you might become today. But over decades of exertion, the myocardial cells of the heart begin to simply fall apart, and you’re left with an unhealthy ticker. Or so these new studies suggest. When you’re 20, or even 30, this can lead to acute reversible injuries — temporary damage that can be relieved with correct rest. In a 50-year-old, repeated hard doses of the sport you love, the rides you cherish — since complete recovery doesn’t occur as efficiently — could be leading to accelerated aging, or hypertrophy — in layman’s terms, a stiff muscle in your chest. That probably wasn’t what you were looking for when you bought your last bike. One of the more telling research papers on the subject, published in 2011 in the Journal of Applied Physiology, studied the structure and function of the heart in lifelong competitive endurance veteran athletes, ranging in age from 50 to 67. MRI studies revealed that some 50 percent of the veteran athletes had myocardial fibrosis, a condition that involves the impairment of the heart’s muscle cells, called myocytes, through hardening or scarring of tissue. In age-matched controls — people of the same age who didn’t compete — and young athletes, there were zero cases of the disease. Furthermore, the fibrosis was significantly associated with the number of years spent training, and the number of marathons and ultra-endurance marathons they had completed.
Other studies have shown that Tour de France riders and other former
professional athletes live lon- ger than average, and often have lower
rates of heart issues later in life. Maybe that sounds counterintuitive,
because often these athletes are riding in volumes that far exceed even
those of the most addicted masters endurance athlete. But there’s a key
difference. The pro athletes did it, then quit and didn’t continue to
do it later in life. Masters athletes? They just keep plugging away,
with the mindset that if they train like Contador, they’ll be able to
ride like Contador. Year after year, decade after decade, it adds up.
Still, there is no arguing that physical activity is an effective, efficient, and virtually incomparable way to care for your heart, fight cardiovascular disease, and prolong your life. For every journal article that says endurance athletics is hurting their heart, there is one that says the opposite. Or maybe two.
But, like many other medicines, more isn’t always better. Research is honing in on the issue of dosage in exercise. If you think of exercise as a drug, there is a certain threshold at which good becomes bad, when benefit becomes detriment. When is too much? Is everyone the same, or are some predisposed to risks of extreme exercise? Is intensity as bad as duration, or duration as bad as intensity? Is it only bad if repeated over years or decades? The science is new when it comes to the science of overdosing on exercise.
Still, there is no arguing that physical activity is an effective, efficient, and virtually incomparable way to care for your heart, fight cardiovascular disease, and prolong your life. For every journal article that says endurance athletics is hurting their heart, there is one that says the opposite. Or maybe two.
But, like many other medicines, more isn’t always better. Research is honing in on the issue of dosage in exercise. If you think of exercise as a drug, there is a certain threshold at which good becomes bad, when benefit becomes detriment. When is too much? Is everyone the same, or are some predisposed to risks of extreme exercise? Is intensity as bad as duration, or duration as bad as intensity? Is it only bad if repeated over years or decades? The science is new when it comes to the science of overdosing on exercise.
THE PERFECT STORM
Doctors immediately ruled out any plumbing issues in Endicott’s
heart. Had he gone to the Mayo Clinic the day before the race, it’s more
than likely that nothing would have ever shown up on paper, on any
test, that would have led the doctors to stop him from racing.
“They would have pronounced me healthy as a horse,” he said. “The EKG would have been perfect because I wasn’t having any symptoms. Nothing was symptomatic whatsoever. No PVCs, no weird rhythms. Everything on paper [was fine], with the exception of a little bit of artery disease — not much more than a lot of people that age.”
“They would have pronounced me healthy as a horse,” he said. “The EKG would have been perfect because I wasn’t having any symptoms. Nothing was symptomatic whatsoever. No PVCs, no weird rhythms. Everything on paper [was fine], with the exception of a little bit of artery disease — not much more than a lot of people that age.”
After looking at a lot of different cases and talking to a lot of
different doctors, Endicott has concluded that this was all his fault.
“Yeah, I did all this to myself — by personality. And if someone would
have gone to me before this happened — and this is a key part of reality
— and said you need to back off because this is your future, would I
have changed anything? Probably not. I would likely do the same
activities, but I would rest and recover more. Just because that’s the
nature of a lot of us. We enjoy doing it, we’re probably doing it too
much, we’re selfish about it, and we’re going to be in denial, and
that’s a problem that a lot of these electrophysiologists have when we
ask ‘Why me?’”
The most difficult component to life after heart malfunction, at least for many, is the psychological struggle.
One of the problems with a lot of athletes — the problem with Endicott — is that they can’t stop asking “why.” How could this happen to someone who has built his life around being active? It just doesn’t make sense.
Patients naturally want to find out what went wrong when they’re meeting with their cardiologist. They want the doctor to help solve the puzzle. But physicians don’t like to speculate. The doctor’s job is to stabilize a patient, keep them alive, and try to give them quality of life. Nowhere in the patient-doctor relationship is there an agreement that the patient won’t go out and race again, or compete in gran fondos, marathons, or triathlons.
But going to the hospital again and again for repeated invasive procedures until doctors settled on a long-term — and uncomfortable — solution. In Endicott’s case, that meant having not one, but three failed ablations (four in total).
Cardiac arrhythmias can be mapped by stimulating the heart with adrenaline in the operating room and following the aberrant circuitry with a catheter electrode. The tissue through which that current is flowing can then sometimes be destroyed with RF radiation or cryogenics from another catheter; this is called cardiac ablation.
One of the problems with a lot of athletes — the problem with Endicott — is that they can’t stop asking “why.” How could this happen to someone who has built his life around being active? It just doesn’t make sense.
Patients naturally want to find out what went wrong when they’re meeting with their cardiologist. They want the doctor to help solve the puzzle. But physicians don’t like to speculate. The doctor’s job is to stabilize a patient, keep them alive, and try to give them quality of life. Nowhere in the patient-doctor relationship is there an agreement that the patient won’t go out and race again, or compete in gran fondos, marathons, or triathlons.
But going to the hospital again and again for repeated invasive procedures until doctors settled on a long-term — and uncomfortable — solution. In Endicott’s case, that meant having not one, but three failed ablations (four in total).
Cardiac arrhythmias can be mapped by stimulating the heart with adrenaline in the operating room and following the aberrant circuitry with a catheter electrode. The tissue through which that current is flowing can then sometimes be destroyed with RF radiation or cryogenics from another catheter; this is called cardiac ablation.
Because Endicott’s tachycardia was exercise-induced, he would not
only need to be awake for the procedure, but would be caffeinated and
given intravenous adrenaline so as to improve the chances of inducing
arrhythmia while he was on the table.
The first attempt failed to stabilize him after an eight-hour session. The next time he spent 16 hours on the table. Still, physicians couldn’t induce tachycardia. Eventually, it was determined that he was too high risk not to have an implantable cardioverter defibrillator (ICD) since he was going out and still doing the things he loved to do, which was leading to more episodes of VT.
The ICD can be a beautiful device, shocking the heart back into rhythm, saving a life from the inside out. But it isn’t without its discomforts. It is, according to Endicott, like getting hit by lightning. If you’re on a bike when it happens, it’s going to knock you off. When the device determines that the rhythm is out of synch, it establishes what kind of rhythm is needed, and then it momentarily re-boots you. Your heart stops, so it can restart with the correct rhythm.
It may sound like a miracle, and it can be. But it can also lead to catastrophe, in what is called an electrical storm. Endicott suffered such a storm when he was performing as a member of a band at a retirement community. His instrumental solo bumped his level of adrenaline, and he went into V-tach.
The first attempt failed to stabilize him after an eight-hour session. The next time he spent 16 hours on the table. Still, physicians couldn’t induce tachycardia. Eventually, it was determined that he was too high risk not to have an implantable cardioverter defibrillator (ICD) since he was going out and still doing the things he loved to do, which was leading to more episodes of VT.
The ICD can be a beautiful device, shocking the heart back into rhythm, saving a life from the inside out. But it isn’t without its discomforts. It is, according to Endicott, like getting hit by lightning. If you’re on a bike when it happens, it’s going to knock you off. When the device determines that the rhythm is out of synch, it establishes what kind of rhythm is needed, and then it momentarily re-boots you. Your heart stops, so it can restart with the correct rhythm.
It may sound like a miracle, and it can be. But it can also lead to catastrophe, in what is called an electrical storm. Endicott suffered such a storm when he was performing as a member of a band at a retirement community. His instrumental solo bumped his level of adrenaline, and he went into V-tach.
“I would go into V-tach, I would get the shock [from the ICD], and
the adrenaline, the shock, would convert me into sinus rhythm for a
couple of beats, but there was so much adrenaline that I would get
thrown right back into V-tach. This is a cycle, and it was brutal. [The
ICD] is going to do its job until I’m dead,” Endicott recalled. “We’re
talking about something that feels like 1,000 volts. It happens quickly
but you’ll see a flash… It was basically like being tortured,” he said.
He had only one to one and a half minutes between shocks. When the paramedics arrived he was still convulsing. He had suffered through 32 consecutive shocks from the ICD. The result was an acute case of post-traumatic stress disorder (PTSD).
Finally, in 2009, Endicott was referred to the cardiology department at Brigham and Women’s Hospital in Boston. Their top electrophysiologist, Dr. William Stevenson, reviewed the case and decided to try one more ablation. It worked in four hours, after it was discovered that the bad circuitry was on the outside of the heart, rather than inside, which is most typical.
Zinn hasn’t been so lucky. His first — and so far only — ablation attempt failed. Despite the best efforts of doctors to elicit an episode of AT, which involved elevating his heart rate to 300bpm for four hours, they were unable to detect the location of the abnormal circuitry.
“Today’s masters endurance athletes are guinea pigs; we are the first generation to be training so hard past age 50 in large numbers,” he said.
After two years of coming to grips with the way he must now live, the 55-year-old Zinn has found that, while he misses doing hard workouts, epic rides, and races on both bikes and cross-country skis, he prefers the person he has become.
“I’m easier to be around,” he said. “I can go on vacations with my wife and be perfectly happy with whatever we do; I’m not pacing around hoping to get out and get some exercise. Rather than being out training or out of town at races, I now enjoy fixing my wife’s breakfast and lunch before her early-morning drive to her job. This new lifestyle is a work in progress, but I think I will be healthy longer.”
He had only one to one and a half minutes between shocks. When the paramedics arrived he was still convulsing. He had suffered through 32 consecutive shocks from the ICD. The result was an acute case of post-traumatic stress disorder (PTSD).
Finally, in 2009, Endicott was referred to the cardiology department at Brigham and Women’s Hospital in Boston. Their top electrophysiologist, Dr. William Stevenson, reviewed the case and decided to try one more ablation. It worked in four hours, after it was discovered that the bad circuitry was on the outside of the heart, rather than inside, which is most typical.
Zinn hasn’t been so lucky. His first — and so far only — ablation attempt failed. Despite the best efforts of doctors to elicit an episode of AT, which involved elevating his heart rate to 300bpm for four hours, they were unable to detect the location of the abnormal circuitry.
“Today’s masters endurance athletes are guinea pigs; we are the first generation to be training so hard past age 50 in large numbers,” he said.
After two years of coming to grips with the way he must now live, the 55-year-old Zinn has found that, while he misses doing hard workouts, epic rides, and races on both bikes and cross-country skis, he prefers the person he has become.
“I’m easier to be around,” he said. “I can go on vacations with my wife and be perfectly happy with whatever we do; I’m not pacing around hoping to get out and get some exercise. Rather than being out training or out of town at races, I now enjoy fixing my wife’s breakfast and lunch before her early-morning drive to her job. This new lifestyle is a work in progress, but I think I will be healthy longer.”
TAKING IT TO HEART
The complexities of the heart, the body, human physiology, and
genetics make it extremely difficult to predict when and in which heart
something catastrophic will take place. Why did this happen to Endicott
when it did?
There are 50 years of cumulative variables that would need to be
considered to fully understand what went wrong on that cold, crisp day
at Devil’s Thumb.
Much of it would be genetic. Did he have a tendency toward higher blood pressure? Yes. What about cholesterol? He was always well below average for that, like many typical athletes, with a sound diet that was verging on vegetarian. Plaque build up? A little, but nothing out of the ordinary. These are the little clues that would be easy to dismiss, but put in combination with his stressful lifestyle, filled with epic endurance events and a somewhat frantic employment schedule, sketch a pastel watercolor of an impending storm on the distant horizon. Add stress, caffeine, cold weather, and that watercolor quickly became an IMAX feature film on dying in the woods alone.
“For years it was like the hints were there in all the studies, and [researchers] always conclude that more research needs to be done. And they’re still saying that,” Endicott said. “I’ve done the research, folks. It happened to me. I’ve had friends that are either dead or alive that it happened to. The research is out there; listen to it.”
Have you ever felt that flutter in your chest? Ever thought, “That’s odd. What was that?”
Maybe you dismissed it. I couldn’t possibly have something wrong with my heart — I’m an athlete. I’m fit. I’m invincible. You wouldn’t be the first, or last, to disregard that subtle blip on the radar screen. Chances are it’s nothing, after all.
But how much is too much? Where is that line? If you have a heart rhythm problem, then perhaps you’ve already crossed that line. Is there any turning back?
“Everyone asks where that line is, and how much is too much,” Mandrola said. “It will never be a yes or no thing. It will always be this gray zone. But one of my takes on the evidence is if you have a heart rhythm problem, then perhaps you are over that line for you. Still, number one: Exercise is good. The endurance athlete who gets this stuff is often over-cooked or over-done.”
For Zinn and Endicott, two of thousands who may have ridden and run their way to a contracted lifestyle, the lesson is clear.
“Few people sharing our mentality will make much of a change based on reading an article like this,” Zinn said. “But if the takeaway is that they can keep doing the things they do but with a much higher prioritization of rest, that stands the most chance of actually saving some people from veering off down the path of becoming a cardiac patient.”
We might know what is too little exercise; we have a good idea what is too much; but there’s a large space in between. And you can never rest too much. Embrace it.
Sometimes, cycling can take us too far.
Much of it would be genetic. Did he have a tendency toward higher blood pressure? Yes. What about cholesterol? He was always well below average for that, like many typical athletes, with a sound diet that was verging on vegetarian. Plaque build up? A little, but nothing out of the ordinary. These are the little clues that would be easy to dismiss, but put in combination with his stressful lifestyle, filled with epic endurance events and a somewhat frantic employment schedule, sketch a pastel watercolor of an impending storm on the distant horizon. Add stress, caffeine, cold weather, and that watercolor quickly became an IMAX feature film on dying in the woods alone.
“For years it was like the hints were there in all the studies, and [researchers] always conclude that more research needs to be done. And they’re still saying that,” Endicott said. “I’ve done the research, folks. It happened to me. I’ve had friends that are either dead or alive that it happened to. The research is out there; listen to it.”
Have you ever felt that flutter in your chest? Ever thought, “That’s odd. What was that?”
Maybe you dismissed it. I couldn’t possibly have something wrong with my heart — I’m an athlete. I’m fit. I’m invincible. You wouldn’t be the first, or last, to disregard that subtle blip on the radar screen. Chances are it’s nothing, after all.
But how much is too much? Where is that line? If you have a heart rhythm problem, then perhaps you’ve already crossed that line. Is there any turning back?
“Everyone asks where that line is, and how much is too much,” Mandrola said. “It will never be a yes or no thing. It will always be this gray zone. But one of my takes on the evidence is if you have a heart rhythm problem, then perhaps you are over that line for you. Still, number one: Exercise is good. The endurance athlete who gets this stuff is often over-cooked or over-done.”
For Zinn and Endicott, two of thousands who may have ridden and run their way to a contracted lifestyle, the lesson is clear.
“Few people sharing our mentality will make much of a change based on reading an article like this,” Zinn said. “But if the takeaway is that they can keep doing the things they do but with a much higher prioritization of rest, that stands the most chance of actually saving some people from veering off down the path of becoming a cardiac patient.”
We might know what is too little exercise; we have a good idea what is too much; but there’s a large space in between. And you can never rest too much. Embrace it.
Sometimes, cycling can take us too far.
Understanding heart arrhythmias with Dr. John Mandrola
What are the warning signs for heart arrhythmias?
A lot of the time in athletes, atrial fibrillation begins as
premature beats, as just shorter periods of irregularity and you feel
something in your heart. If you’re an endurance athlete and you get
those warning signs, that’s when it’s time to start thinking about going
in and getting your heart looked at; if you’re feeling stuff like skips
or jumps of your heart rhythm, you don’t really know if it’s V-tach or
AF. The majority of the time, those are not dangerous or life
threatening, but that’s the time to get it looked at and at least raise
your hand and say, ‘Okay, what is this?’ The problem, though, with an
evaluation for an endurance athlete — they go to the doctor, and the
doctor has no idea what they do [as an athlete]. It’s tough because 999
out of 1,000 patients he sees don’t do the stuff that Velo
readers do. Your reader has to be wise to the fact that a lot of doctors
don’t really understand what they do [as an endurance athlete].
What do you tell people that do develop AF?
The first thing that a person with AF ought to do is figure out what
company that it keeps, because the first thing we ask as doctors is,
‘What else is going on?’ Is AF associated with heart failure or valve
disease, or is their thyroid out of whack, or is there something really
wrong medically? So a basic medical checkup and a basic heart check up
is the first step.
Then they have to be armed with the knowledge that their lifestyle likely may be playing a role. I’m not saying they have to stop exercising. I would never say they couldn’t do this. But if you’re in AF or having AF, you really don’t have a lot of good options if you want to continue doing what you’re doing; drugs really take away what makes you good at what you do. All the drugs for AF slow you down. They affect your cardiac output and some of the procedures for AF are scarier than the disease itself. [Patients] have to know that.
Then they have to be armed with the knowledge that their lifestyle likely may be playing a role. I’m not saying they have to stop exercising. I would never say they couldn’t do this. But if you’re in AF or having AF, you really don’t have a lot of good options if you want to continue doing what you’re doing; drugs really take away what makes you good at what you do. All the drugs for AF slow you down. They affect your cardiac output and some of the procedures for AF are scarier than the disease itself. [Patients] have to know that.
Why are physicians reluctant to speculate as to why someone develops a heart arrhythmia?
Doctors are trained to see problems in a silo. A doctor will see a
patient, but will see him or her as the heart rhythm problem. And that
heart rate problem probably came from a part of the heart that had a
scar and that needed to be fixed. But one of the things we’ve learned
from AF is that you can’t ignore the context — chronic stress and
endurance exercise, but it might be high blood pressure or obesity or
alcohol. If we ignore that and just try to deal with the problem in a
silo rather than as a human being, then that’s one of the reasons why
we’re struggling with heart rhythm problems, specifically AF. Whatever
we use to treat AF — drugs or ablation — AF can come back. New research
is showing that if you look for the factors that are leading to the
problem, the patients do better. So I don’t completely think it’s a code
of medicine, it’s just the way we’re trained. We’re trained in systems:
heart problems, kidney problems, brain problems. And we’re not trained —
and I know this is a goofy word — holistically. Specialists see their
organ but they don’t see the whole person.
As bike riders and racers, we train extensively, we eat right, we
don't smoke and we're not obese. Heart-wise, this should put us way
ahead of the curve. Recently, however, there are increasing reports of
competitive athletes experiencing major cardiac events.
How can a heart that sustains a major aerobic effort be vulnerable to a heart attack?
Sudden, unexpected cardiac events in athletes are usually caused by "acquired" heart disease. That is, the same heart disease present in sedentary overweight truck drivers. Here we'll explore how these events occur, how one "acquires" the disease and ways you can safeguard against sudden cardiac failure.
"Acquired" heart disease involves the build up of
cholesterol, fat and scar tissue inside these blood vessels. Less
appreciated, but more important, are the reactivity of the coronaries
and the stickiness of the blood passing through them. The sensitivity of
the vessel and the stickiness of blood are both inherited and affected
by lifestyle.
Inflammatory stimuli like adrenaline (racing), trans-fats, poor sleep and tobacco make the inner lining of the coronary vessel more reactive and thus more likely to fissure. These same stimuli activate blood platelets, making the blood stickier.
A fissure exposes the vessel to the sticky platelets. Platelets then attract more platelets and, similar to a cut on the skin, a clot forms. A clot inside the coronary stops the flow of nutrients to the muscle. A "heart attack" occurs and may cause electrical chaos leading to sudden death.
The answer is the 20-percent blockage, which is more "irritable." It is less stable and more likely to fissure, causing blood to clot on it. An 80-percent blockage is older, has a "smoother" cap and is less likely to expose the sticky parts of blood to an adhesive surface.
Unlike a chronic heart disease patient, whose heart is in a constant state of compromised blood flow ("pre-conditioning"), an athlete's heart is accustomed to perfect blood flow. Abrupt disruption of nutrients to a heart unaccustomed to compromise creates an electrically unstable situation. In the event of a complete coronary obstruction, this lack of "preconditioning" makes an athletic heart more susceptible to cardiac problems.
Generally, this is true, but here are four facts of an athletic lifestyle that may contribute to irritable blood vessels and stickier blood.
1. Statistically, bike racers are more likely to have the "minor" 20-percent blockage rather than the more obstructive, but less irritable 80-percent blockage. These non-symptomatic, undetectable blockages are repeatedly exposed to the spiking adrenaline levels of a typical athlete's life—a potentially risky scenario.
2. Bike racing is intense. A criterium, a 'cross race and even a century are different endeavors than most structured 30-minute aerobic workouts. Intense race-like efforts result in high adrenaline levels and marked cardiac stress. Much like an argument spikes adrenaline levels, so do intense physical efforts.
3. Bike racers are often "Type A", high-adrenaline, overachiever personality types.
4. Racers often over train and are poorly rested. Lack of rest can result in stickier blood and inflammation of the blood vessels.
Interestingly, in nearly three in 10 people, their first symptom of heart disease is sudden death. For the most part, bike riders and racers have "fitter" hearts than the general public. However, our lifestyle has specific stressors. Understanding and managing the life factors responsible for inflammation of blood vessels and the stickiness of blood will help reduce sudden cardiac events.
In
some ways, we health and fitness reporters are a bit to blame for
misconceptions about our favorite topics. We get so excited about all
the health benefits of cycling, and all the ways riding a bike
strengthens and protects your heart
and prolongs your life, that it’s easy to think riding makes you immune
to heart problems. That assumption can lead you to brush off some
serious symptoms.
“You see it all the time: Men and women in their 40s and 50s who are healthy and recreationally active, like cyclists and triathletes, make the assumption that because they’re active, heart disease won’t happen to them. That’s not necessarily true,” says Larry Creswell, MD, a triathlon enthusiast, heart surgeon, and author of the Athlete’s Heart Blog. Creswell admits to having had similar thoughts when he took up endurance sports. “I was really surprised when I started swimming and running and cycling in my 40s how many of the folks I trained with either had a heart problem or knew someone with one—pretty much everyone! Exercise helps strengthen your heart and is good for cardiovascular health. That is a certainty. But there’s obviously no guarantee that everyone who exercises will be forever immune to heart disease."
Mysterious shortness of breath. If you’re a
cyclist—no matter what your level—you know what your breathing pattern
is like when you’re riding. When it doesn't feel normal for the exertion
level you're at, particularly if you’re cruising along fairly easily
and suddenly working to catch your breath, something is wrong. This is
another easy one to blow off as something else, says Creswell, and
indeed it might be. “You could be fatigued or coming down with a cold or virus. But it’s a warning sign and if it’s unexplained, you need to get it checked out,” he says.
Unexplained fatigue. This one generally shows up off the bike. You’re just run down and hunting for a quiet place to nap for no good reason. “It also can show up as a performance decrement that is unexplained,” says Creswell. “If for no good reason, you’re tired on the bike and not progressing or you’re even regressing, it’s a warning sign.”
RELATED: 7 Signs You're Overtraining
Nearly blacking out. This is a big red warning flag. If you are nearly blacking out—or worse, actually blacking out—while you’re exerting yourself, it’s really dangerous for a few reasons. One, you could crash. Two, you could suddenly die from a serious underlying heart problem. Get it checked pronto.
One last crucial heart care tip: Get a regular check-up from a primary care doctor. “This is where women are often at an advantage. They tend to go to an OB/GYN regularly, so they get their blood pressure checked; they get some blood work done," says Creswell. But guys? "There are men who are healthy and in their 40s, maybe even their 50s and they don’t have a primary care doctor. They’ve never had their blood work done, and can’t remember last time they had their blood pressure checked. If you’re going to spend all that money on a nice bike and bike computer and maybe even a power meter and a coach, get yourself a doctor, too! It’ll cost a fraction of all that and take less than an hour out of your year!”
How can a heart that sustains a major aerobic effort be vulnerable to a heart attack?
Sudden, unexpected cardiac events in athletes are usually caused by "acquired" heart disease. That is, the same heart disease present in sedentary overweight truck drivers. Here we'll explore how these events occur, how one "acquires" the disease and ways you can safeguard against sudden cardiac failure.
The Science of an Attack
The heart is a large muscle that pumps 100,000 times daily. The muscle requires blood to contract. Blood is delivered to the beating heart muscle by the coronary arteries, which are on the surface of the heart.Check Out Today's Most Popular Articles
Inflammatory stimuli like adrenaline (racing), trans-fats, poor sleep and tobacco make the inner lining of the coronary vessel more reactive and thus more likely to fissure. These same stimuli activate blood platelets, making the blood stickier.
A fissure exposes the vessel to the sticky platelets. Platelets then attract more platelets and, similar to a cut on the skin, a clot forms. A clot inside the coronary stops the flow of nutrients to the muscle. A "heart attack" occurs and may cause electrical chaos leading to sudden death.
Two Paradoxes
Blockages in blood vessels most likely to fissure are young, immature and not obstructive. For example, a common medical board question is, which lesion is more likely to cause a heart attack, an 80-percent blockage or a 20-percent blockage?The answer is the 20-percent blockage, which is more "irritable." It is less stable and more likely to fissure, causing blood to clot on it. An 80-percent blockage is older, has a "smoother" cap and is less likely to expose the sticky parts of blood to an adhesive surface.
Unlike a chronic heart disease patient, whose heart is in a constant state of compromised blood flow ("pre-conditioning"), an athlete's heart is accustomed to perfect blood flow. Abrupt disruption of nutrients to a heart unaccustomed to compromise creates an electrically unstable situation. In the event of a complete coronary obstruction, this lack of "preconditioning" makes an athletic heart more susceptible to cardiac problems.
Isn't Exercise Healthy?
A common sentiment among the endurance sports community regarding cardiovascular health sounds something like this: "I am an athlete. I thought exercise made my heart healthier."Generally, this is true, but here are four facts of an athletic lifestyle that may contribute to irritable blood vessels and stickier blood.
1. Statistically, bike racers are more likely to have the "minor" 20-percent blockage rather than the more obstructive, but less irritable 80-percent blockage. These non-symptomatic, undetectable blockages are repeatedly exposed to the spiking adrenaline levels of a typical athlete's life—a potentially risky scenario.
2. Bike racing is intense. A criterium, a 'cross race and even a century are different endeavors than most structured 30-minute aerobic workouts. Intense race-like efforts result in high adrenaline levels and marked cardiac stress. Much like an argument spikes adrenaline levels, so do intense physical efforts.
3. Bike racers are often "Type A", high-adrenaline, overachiever personality types.
4. Racers often over train and are poorly rested. Lack of rest can result in stickier blood and inflammation of the blood vessels.
Interestingly, in nearly three in 10 people, their first symptom of heart disease is sudden death. For the most part, bike riders and racers have "fitter" hearts than the general public. However, our lifestyle has specific stressors. Understanding and managing the life factors responsible for inflammation of blood vessels and the stickiness of blood will help reduce sudden cardiac events.
A Bike Racer's Checklist for a Healthy Heart
- Be informed and engaged in your heart health. Know that athletes are not immune to heart disease.
- Know your genetics. A strong family history of heart disease mandates extreme vigilance. Genetics are the strongest risk factor.
- Food is important. Nuts, fish, berries and vegetables are soothing to blood vessels. Man-made foods, especially "white" foods, are inflammatory.
- Keep your blood pressure less than 130/85.
- LDL ("Bad cholesterol") should be lower than 100 or preferably <70.
- Sleep well consistently. Quality sleep decreases inflammation and blood stickiness.
- Manage stress and anger. For competitive athletes, this is an especially pertinent issue.
- Do not ignore warning symptoms like chest pain, excessive shortness of breath or fainting.
- Seek out a doctor who exercises, competes or has experience with an athletic lifestyle
“You see it all the time: Men and women in their 40s and 50s who are healthy and recreationally active, like cyclists and triathletes, make the assumption that because they’re active, heart disease won’t happen to them. That’s not necessarily true,” says Larry Creswell, MD, a triathlon enthusiast, heart surgeon, and author of the Athlete’s Heart Blog. Creswell admits to having had similar thoughts when he took up endurance sports. “I was really surprised when I started swimming and running and cycling in my 40s how many of the folks I trained with either had a heart problem or knew someone with one—pretty much everyone! Exercise helps strengthen your heart and is good for cardiovascular health. That is a certainty. But there’s obviously no guarantee that everyone who exercises will be forever immune to heart disease."
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Unexplained fatigue. This one generally shows up off the bike. You’re just run down and hunting for a quiet place to nap for no good reason. “It also can show up as a performance decrement that is unexplained,” says Creswell. “If for no good reason, you’re tired on the bike and not progressing or you’re even regressing, it’s a warning sign.”
RELATED: 7 Signs You're Overtraining
Nearly blacking out. This is a big red warning flag. If you are nearly blacking out—or worse, actually blacking out—while you’re exerting yourself, it’s really dangerous for a few reasons. One, you could crash. Two, you could suddenly die from a serious underlying heart problem. Get it checked pronto.
One last crucial heart care tip: Get a regular check-up from a primary care doctor. “This is where women are often at an advantage. They tend to go to an OB/GYN regularly, so they get their blood pressure checked; they get some blood work done," says Creswell. But guys? "There are men who are healthy and in their 40s, maybe even their 50s and they don’t have a primary care doctor. They’ve never had their blood work done, and can’t remember last time they had their blood pressure checked. If you’re going to spend all that money on a nice bike and bike computer and maybe even a power meter and a coach, get yourself a doctor, too! It’ll cost a fraction of all that and take less than an hour out of your year!”
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