The second in a series of posts about what makes runners uniquely equipped to run. This discussion attempts to explain the physiological changes to the runner’s heart and address the endurance athlete’s normal anxieties as to whether these changes cause permanent damage.
Updates: There’s a 2021 update near the end of this post reflecting the outcomes of more recent studies of the endurance athlete’s heart. Spoiler alert: the conclusion is there’s no new conclusion from what we knew at the time this post was first written, but the data are more extensive and interesting.
The heart’s four chambers function as a double-sided pump to circulate oxygen-rich blood to the body through a coordinated and normal rythym. It normally beats about 100,000 times in one day — about 35 million times in a year.
Blood enters the heart on the right – the right atrium to the right ventricle. Leaving the right ventricle, blood travels to the lungs to gather oxygen before entering the left atrium and finally to the left ventricle, which pumps the oxygen-rich blood through a maze of arteries to every cell in the body.
A normal resting heart rate (heart beats per minute while sitting or lying down) is around 60-100 beats per minute. Moderately active humans will likely have a resting heart rate similar to the rest of the population: 60-100 bpm. Professional Athletes and the very fit may have a resting heart beat as low as 40 bpm.
1) The resting heart rate of five-time Tour de France winner Miguel Indurain was once recorded at 28 beats per minute.
2) A sudden increase in the athlete’s resting heart rate is a sure sign of working too hard: over-training, which will inevitably lead to injury, decreases in immune function, and increases the risk of disease.
3) When training is completely stopped the resting heart rate returns to your untrained heart rate within three to four weeks.
4) Factors that have little to do with your level of fitness will impact your heart rate, such as dehydration, heat, or pain. Medications, such as beta-blockers and some migraine medicines, caffeine, and stress will also affect heart-rate. Studies have shown that running by feel and doing the talk test is well correlated with target paces rather than relying on a heart rate monitoring device that can be frustratingly inaccurate in reporting data.
What happens to the body during exercise?
In strenuous exercise, just about every system in your body either focuses its efforts on helping the muscles do their work, or it shuts down.
For example, your heart beats faster during strenuous exercise so that it can pump more blood to the muscles, you breathe faster and deeper, and your stomach shuts down so it does not waste energy the muscles can’t use. (In addition to the stomach, blood is also diverted from the kidneys and liver in favor of the skeletal muscles.)
If you are going to be exercising for more than a couple of minutes, your muscles need oxygen or they stop working. Just how much oxygen is used depends on how well your body gets blood to the muscles and how well the muscles extract oxygen from the blood.
During exercise, active muscles require as much as 20 times more oxygen instantaneously while the inactive muscles’ oxygen demands remain unchanged. Also, working muscles can take oxygen out of the blood three times better than resting muscles.
There is a limit, however, to how deeply you can breathe, the number of times you can breathe per minute, and the speed and frequency with which your heart muscle can contract and pump blood.
So the body’s response to exercise is: lung capacity increases (they become more efficient), heart chambers grow bigger, and heart muscles stronger. This means the blood carries more oxygen, and a greater volume of blood is pumped per beat (the stroke volume).
Runner’s Note: avoid non-steroidal anti-inflammatory (NSAIDS) medications, such as ibuprofen and naproxen, prior to races. These drugs work by inhibiting the function of prostaglandins, compounds that plays a role in inflammation but also protects blood flow to the kidneys. Because blood flow is already decreased to the kidney during running, NSAIDS could further decrease blood flow, placing the kidneys at risk of potential injury. Tylenol or acetaminophen is a better choice since it relieves pain via a different mechanism.
The Athlete’s Heart
A consequence of exercising more than an hour a day (or in excess of 5 hours per week) is Athlete’s Heart, a normal, physiological adaptation of the body to the stresses of physical conditioning and aerobic exercise.
Static training, such as strength training, is mostly anaerobic (the body does not rely on oxygen for performance), and only moderately taxes the heart.
Dynamic (aerobic) exercises, such as running, swimming, skiing, rowing, and cycling, rely on oxygen from the body and taxes the heart to produce the oxygen needed.
People diagnosed with athlete’s heart commonly display three signs that would indicate the condition: a slower than normal heartbeat (bradycardia) along with irregular rhythms, an enlarged heart (cardiomegaly), and the thickening of the muscular wall of the heart (Cardiac Hypertrophy), specifically the left ventricle (by approximately 15-20%), which pumps oxygenated blood to the aorta.
Both static and dynamic exercises cause the thickening of the left ventricular wall, however weight-lifting or resistance training causes the muscle to thicken to increase blood pressure necessary for anaerobic exercise, but does not create a more efficient stroke volume or lower the pulse rate. Combining a form of aerobic exercise and resistance training will, of course, show the benefits of an enlarged heart and lower pulse rate.
Athlete’s heart is not dangerous for athletes – although a nonathlete with the same symptoms may be found to have a serious cardiovascular disease. Nor is athlete’s heart the cause of sudden cardiac death during or shortly after a workout, which has instead been linked to a genetic disorder (hypertrophic cardiomyopathy).
The athlete’s heart will return to its normal size and all symptoms disappear with detraining, usually within 3-6 months.
The Athlete’s Heartbeat Anomaly
Up to 69 percent of aerobically trained athletes demonstrate Phasic Sinus Arrhythmia, a pulse that speeds and slows with respiration (what feels like a skip between beats).
Skipped heartbeats are usually premature heartbeats – one beat quickly follows another, and the resulting pause in the rhythm of your normal heartbeat is assumed to be a “skipped” beat. This benign rhythm discrepancy becomes more common as you become more fit, and temporarily disappears when you increase your heart rate with exercise.
Phasic Sinus Arrhythmia usually doesn’t indicate a problem unless accompanied by chest pain, light-headedness or other symptoms.
(Click here for more information on the Athlete’s Heart.)
Athletes = Heart Problems?
A significant number of heart attacks or sudden death in marathon runners have been reported over the years and it’s probably safe to say the news is unsettling to runners everywhere.
Subsequent studies have shown that unlike an enlarged heart caused by stress, heart disease or high blood pressure, the physiological remodeling of the athlete’s heart is generally beneficial and does not progress to heart failure.
What we hear most are that athletes show right ventricular dysfunction and elevated levels of cardiac troponin – biomarkers typically found in left ventricular failure – immediately following a race or long training run. Symptoms generally disappear, however, within 1 week post race.
A study of 114 world-class endurance athletes who had undergone uninterrupted exercise training over a 4- to 17-year period and competed in two to five consecutive Olympic Games demonstrated that long-term, high-intensity exercise training does not lead to cardiac dysfunction, or adverse clinical events (although one study found substantial heart chamber enlargement persisted in 20% of retired and deconditioned former elite athletes after 5 years, which has opened the question as to whether certain individuals experience permanent physiological changes. It is generally considered that more research is needed to determine possible predisposing factors for these individuals.)
Twenty amateur long-distance runners between the ages of 18 and 60, who were going to run in the Quebec City Marathon were evaluated for heart damage post-marathon. In half of the runners, researchers observed that the marathon prompted a decrease in left and right ventricular function with some experiencing swelling and reduced blood flow in the heart. All symptoms were temporary.
Dr. Eric Larose, of the Institut universitaire de cardiologie et de pneumologie de Québec (IUCPQ) in Canada, says that the heart muscle changes they observed were more common in runners who had lower fitness levels and who trained less – reaffirming that being less prepared or undertrained for the marathon has the potential to cause more damage to the body than for those who have adequately prepared through proper training for the distance.
Click here for more information about sudden cardiac arrest in athletes and for the American Heart Association (AHA) 12 point sudden cardiac death screening guidelines.
Are you at risk? A 2019 study of young athletes suggests snoring and sleep apnea are linked to sudden cardiac arrest. Read more….
The first sentence in a 2006 comprehensive review on training (Midgley and McNaughton) reads, “The maximal oxygen uptake (VO2max) has been suggested to be the single most important physiological capacity in determining endurance running performance.”
Numerous training programs for distance runners (and other endurance sports) have become fixated on the VO2max concept, leaving us with the assumption that it must be directly tied to performance and fatigue. Some would say it is not.
VO2max is a measure of the maximum volume of oxygen that an athlete can use. It is measured in millilitres per kilogramme of body weight per minute (ml/kg/min), and has been used as a traditional measurement of endurance since the 1920s.
The amount of oxygen consumed to produce energy (and hence the rate at which you exhale carbon dioxide) increases as exercise continues. However, there is a maximum level of oxygen that can be consumed and even when exercise continues, oxygen consumption plateaus. At least this has been the thinking for many years.
Studies suggest this plateau phenomenon can only be identified in about 30% of tested subjects (Noakes 1998b; M. Doherty tell al 2002), and is seldom identified in children at all (Rowland 1993; Rowland and Cunningham 1992).
Nonetheless, some training programs focus almost exclusively on improving VO2max to improve performance even though studies show that VO2max does not change in elite runners and does not correlate with performance.
In one study by Smith and Donnell of untrained individuals, changes in VO2max over a 36 week training period substantially increased by 13.6%, but all of those gains were seen in the first 24 weeks of the study with no further increases during the final 12 weeks.
Paula Radcliffe’s VO2max was monitored from 1992 – 2003 (Jones 2006). Her training increased from 25-30 miles per week (with a VO2max of 72 at the time) to 120-160 miles per week, yet her VO2max did not change despite the change in volume and intensity of training.
Meanwhile, the study of a female Olympic level runner showed that while the athlete’s 3,000m time improved by 46 seconds, VO2max actually decreased from 72 ml/kg/min to 66 ml/kg/min (Jones, 1998).
Training Note: studies show VO2max values can improve with training but independently decrease with age. However, the degree of trainability affects VO2max widely; for example, conditioning may double VO2max in some individuals, and will never improve it at all in others (Bouchard, 1999). Also it has been shown that respiratory muscle training does not improve VO2max of triathletes and marathon runners (Amonette & Dupler 2002).
(On-line Calculators will determine VO2max using age, body mass, max and resting heart rates, or recent exercise times.)
Dr. Timothy Noakes is a highly decorated and respected South African scientist, professor, runner and author (notably Lore of Running now in its fourth edition).
Dr. Noakes has challenged paradigms in the discipline of exercise physiology, including VO2max, where he introduced the concept of a central governor (located in the brain) that prevents the muscles from working at their maximum level for extended periods to protect the body (and more specifically the heart) from permanent damage or death.
The central governor regulates power output so that the task, or exercise is completed in the quickest, most efficient manner while maintaining a reserve of physical and mental capacity. In other words, Noakes contends the central governor acts as a regulator for exercise rather than exercise being limited by a person’s VO2max.
The concept that the central governor would be located in the brain, or concluding that it is actually the brain that restricts endurance has been one of the more contentious of Noakes’ conclusions (a topic we’ll cover extensively when this series reaches the brain).
But for the argument presented here, consider French free diver Stéphane Mifsud, who stayed underwater unaided for 11 minutes and 35 seconds in 2009 – a world record for breath-holding at the time, and one of several world records he holds. His lung capacity was measured at 10.5 litres, twice the capacity of most men.
He attributes his success in part to ignoring the overwhelming distress signals that force us to gasp long before we’re out of oxygen.
A quote from his website says, “Our minds have the power to destroy or push us beyond our limitations.”
Do the muscles fatigue and reduce their output because the body has reached its maximum potential to deliver oxygen? Does the heart force the muscles to reduce output because it senses a lack of blood flow (oxygen) and works to protect itself? Or, does the brain anticipate when the blood and oxygen supply to the heart is about to become inadequate and reduce the recruitment of the muscles causing exercise to diminish or cease (fatigue) before damage is incurred to the heart or skeletal muscles? Is our training dependent on the final answer to these questions?
To be a successful endurance athlete requires muscles with superior contractility that allows them to run very fast despite the limiting output of the heart.
Obviously oxygen is the universal currency of every athletic endeavor. Muscles require oxygen for the chemical reaction that converts food energy into motion, and the best athletes are those who use oxygen best.
If we agree that Noakes’ Central Governor Model is the accepted de facto model (in the absence of another indisputable approach), VO2max is not the only factor determining exercise performance.
Noakes suggests that VO2max is the result of two distinct physiological processes:
- the maximum pumping capacity of the heart, which determines the peak rates that blood and oxygen can be transported to the exercising muscles, and
- the athlete’s exercising muscles – where the best athletes are those whose muscles have superior contractility (the capacity of the muscle to contract or shorten forcefully).
The ability to process oxygen (VO2max) as a measurement of how fast you can run is not useful in isolation. How efficiently you put that oxygen to use is equally important.
Noakes offers a useful analogy: “supplying fuel at the same maximum rate to the engines of a Formula 1 racer and a family sedan would not eliminate the performance difference between the two. This would be due to limitations, not in the rate of fuel (oxygen) supply to the engine, but in other factors inherent in the engine (muscle) itself.”
Athletes with superior athletic ability have muscles with a superior capacity to generate force, which is essentially independent of the oxygen or fuel supply. Just as we suspected in our last discussion of the upper leg, it’s all about that bass.
UPDATE: A few years before I wrote this post, studies began to report that even modest amounts of exercise might actually be bad rather than good for your heart. The controversy launched new studies that have since been concluded.
An Outside Online August 2021 article reviewed what’s new from these studies and concluded there’s still no real conclusion. Although endurance exercise definitely changes the heart in ways that would typically be considered negative, these changes are not always equal among athletes and non-athletes.
For example, as the article states: “The most solid evidence for potentially negative heart changes associated with long-term serious endurance training relates to elevated coronary artery calcium (CAC) scores. The gradual build-up of calcium-rich plaques causes narrowing and stiffening of the coronary arteries, which supply blood to your heart muscles. These plaques can also rupture, blocking the artery completely and causing a heart attack. The CAC score measures how much calcium has accumulated in your arteries, so anything that increases it seems like bad news.
What’s new is how we interpret those scores in runners. When Sharma’s group studied 152 masters endurance athletes with an average age of 54, 11 percent of them had a CAC score of greater than 300 (which is considered very high), compared to none of the 92 people in the age-matched control group. That’s concerning, and other studies have reached similar conclusions. Not all plaques are equal, though. Some are smooth, hard, and calcified, and these are considered stable and less likely to rupture. Others are a softer mix of cholesterol, fats, calcium, and other substances, and these mixed plaques are more dangerous and likely to rupture. The athletes, it turns out, had 72 percent stable calcified plaques, while the controls had just 31 percent.”
Maybe running ultramarathons adds a few months of life expectancy for 99% of us, but shortens it by a decade for the unlucky few that have an under lying issue or genetic predisposition. The research will continue, but for now the advice is to “keep running to your heart’s content.” Read that article here.
Next up: Wooly Chaps and the Big Joint (the knee).
High-intensity exercise may not lower blood pressure as effectively as moderate-intensity exercise. In one study, moderate exercise (jogging 2 miles a day) controlled high blood pressure so well that more than half the patients who had been taking drugs for the condition were able to discontinue their medication.
Studies show that yoga and tai chi, an ancient Chinese exercise involving slow, relaxing movements, may lower blood pressure almost as well as moderate-intensity aerobic exercises.
Experts recommend at least 30 minutes of exercise on most — if not all — days.
Benefits of aerobic exercise include cancer prevention (including colon, breast and prostate cancers), reduces the risks & symptoms associated with osteoporosis, diabetes, depression, cardiovascular disease, and helps improve cognitive function.
Everyone, especially people with high blood pressure, should breathe as normally as possible through exercise. Holding the breath increases blood pressure.
There is such a thing as a broken heart. Takotsubo cardiomyopathy (TC), or broken heart syndrome, revolves around the weakening of the muscular portion of the heart that’s triggered by emotional stress presenting with the same symptoms as a heart attack: chest pain, shortness of breath, and sweating – although the arteries are completely clean, no blockages.
Patients respond to supportive care and to the same types of medicines used for patients with weak hearts. Typically the heart function begins to improve and is back to normal within six weeks.
Experts say the best recovery for a broken heart also includes yoga, meditation, talking to and socializing with friends, and exercise.
Endurance athletes, especially those with a family history of heart disease and other coronary risk factors, should not consider themselves immune to either sudden death or to coronary heart disease and should seek medical advice immediately if they develop any symptoms suggestive of ischemic heart disease. Physicians should not assume that “physically fit” marathon runners cannot have serious, life-threatening cardiac disease.
This post is meant for informational purposes only.
References not previously linked within this post:
Athletic Heart Syndrome, Wikipedia
Central Governor Model: A review of Professor Noakes’ Revolutionary Model of Performance, TrainingScience.net
The Fallacy of Vo2max and %VO2max, Science of Running
The Heart of Trained Athletes, AHA Journals
Mitochondrial adaptations to physiological vs. pathological cardiac hypertrophy, Oxford Academic