Hypertrophic Cardiomyopathy: What the Strength Athlete Needs to Know

TAGS: heart health, John Giandonato, EliteFTS Q&A, athletic performance, cardiorespiratory health, strength athletes, Mike Robertson, smitty

Hypertrophic Cardiomyopathy

What the Strength Athlete Needs to Know

The majority of the elitefts readership consists of hardcore lifters and serious athletes. Each day, we toil in the gym, busting our asses off to achieve a bigger pull, squat, or bench or increased athletic performance. We dedicate a few hours or more each week to keeping our bodies healthy, engaging in the usual round of corrective and restorative modalities such as self-myofascial release and stretching. We seek out knowledgeable sources to keep our musculoskeletal health in check, regularly perusing the elitefts Q&A thread to see what solutions and suggestions Mike Robertson, Smitty, and Dr. Smith have provided to banged up athletes.

Knowledge

Lifters nowadays are far more knowledgeable than they ever were before. I’ve encountered and worked with athletes whose knowledge of functional anatomy rivaled that of a physical therapist or an athletic trainer. Competent strength coaches have embraced the vast field of sports medicine, borrowing assessment and screening tools and corrective modalities to better serve their athletes. However, an overwhelming majority of athletes, coaches, and sports medicine professionals overlook cardiorespiratory health.

At the literal center of cardiorespiratory health is the heart, a powerful muscle that consists of four distinct chambers—the right atrium, the right ventricle, the left atrium, and the left ventricle. The heart is supplied oxygenated blood by the coronary arteries, which encapsulate the myocardium sitting on its surface. The flow of blood through the heart is dictated by the differing pressures of the chambers. Venous blood is deposited in the right atrium through the superior and inferior vena cava before passing through the tricuspid valve where it then flows into the right ventricle. From there, the blood pumps through the pulmonary valve into the lungs where the blood becomes oxygenated. The blood is now returned to the heart where it enters the pulmonary veins and then the left atrium, passing through the mitral valve before flowing into the left ventricle.

The left ventricle, which is the chamber that is most active, pushes the oxygenated blood into the aorta and coronary arteries where it is utilized by the body. Increased oxygen demands via physical exertion require a greater quantity of oxygen enriched blood. The heart responds by working to meet those demands, contracting more forcefully and/or pumping more rapidly.

Exercise

As we know, exercise is a stressor culminating in adaptations, many of which we consider favorable. Exercise, which includes both cardiovascular exercise and resistance exercise, provides the heart with a stimulus to get stronger and more efficient. Cardiovascular exercise, conducted at lower intensities, imposes a volume load on the heart whereas resistance exercise, which is conducted at higher intensities, and other forms of anaerobic training such as sprinting and bouts of exertion interspersed with brief periods of rest (interval training), imposes a pressure load on the heart. Either way, the heart is getting stronger. However, the left ventricle is being taxed disproportionately.

Cardiovascular exercise and resistance training have been proven to remodel the myocardium, which includes altering the dimensions of the ventricles and the atrial cavity size (1). Alarmingly, studies have indicated marked enlargement of the left ventricle in highly trained athletes (2). Greater mean left ventricular wall increases were noted in athletes who competed in sports which largely consist of intervals carried out at higher intensities (2). Rowing, basketball, swimming, and tennis netted the greatest increases. A group tabbed as “other” consisted of 43 athletes from various sports including baseball, diving, and motor racing and ten strength athletes (seven weightlifters and three bodybuilders). They also showed comparable increases in left ventricular wall thickness (2).

Heavy Resistance Training

Heavy resistance training, which generally includes the practice of the Valsalva maneuver, sharply elevates both diastolic and systolic blood pressure. Weightlifters and powerlifters, who regularly use 90 percent of their 1RM in training, often utilize the Valsalva maneuver as do Strongman competitors when engaging in event training and bodybuilders who sometimes hold their breath to squeak out a few extra repetitions. However, bodybuilders have lower resting blood pressures than do their aforementioned strength training counterparts likely due to regular participation in cardiovascular exercise. They also don’t regularly eclipse 90 percent of their 1RM in training (3). Increased blood pressure during exercise induces a great pressure on the myocardium, which over time contributes to left ventricular wall thickness and an overall enlargement of the left ventricle.

Sympathetic Activity

Sympathetic activity, which increases prior to the onset of physical activity and continues to increase during physical activity, has been proven as a contributing factor in HCM (4). The heart consists of a conduction system comprised of nodes and bundles that are governed by the autonomic nervous system. The atria is comprised of numerous sympathetic and parasympathetic neurons that influence heart rate. When activity is anticipated and commenced, whether sudden or gradual, the sympathetic neurons are stimulated, accelerating the depolarization of the sinoatrial node and triggering the heart to beat faster.

Who is Most Susceptible to HCM?

Individuals who are larger and taller might be more susceptible to HCM, as the heart has to work harder to supply oxygenated blood ensuring that it travels further. Large body size, regardless of body composition, coupled with regular vigorous exercise potentially spells a recipe for disaster. It’s crucial that athletes, active larger bodied individuals, and younger athletes be properly screened. Family history must be thoroughly pored over to reveal or rule out congenital influences. Personal history must also be meticulously evaluated. Recurrent or singular episodes of chest pain, shortness of breath following comparatively mild exertion, and irregular heartbeat or palpitations warrant medical intervention. Usually, a cardiologist will administer a 12 lead ECG to examine the heart rate, rhythm, and conduction pathways to reveal or rule out underlying issues such as ischemia or infarction. ECG tests have been proven helpful in reducing sudden cardiac events in athletic populations (1).

Scaring you or boring you wasn’t my intention. I wanted to shed some light on a problem that could be potentially fatal or life altering. This is a problem that I have faced professionally and personally. Recently, one of my athletes who is a Division 1 caliber baseball player was diagnosed with HCM. A few weeks after his diagnosis, a close relative of mine, who is a non-athlete but commutes by bike to work fifteen miles each way, was also diagnosed with HCM. I urge both sport coaches and strength and conditioning coaches to gain more knowledge about the cardiorespiratory system and its adaptations to competitive demands and exercise. Additionally, because these coaches are on the front lines, they must keep an open line of communication with their athletes and pay attention to their health status every day during practices, games, and workouts. Serious lifters and athletes must not neglect odd feelings of chest pain and the inability to fully catch their breath during or after training sessions or practice. As it pertains to your health, especially your cardiovascular health, intervention is critical.

References

  1. Maron BJ, Pelliccia A (2006) The heart of trained athletes: Cardiac remodeling and the risk of sports, including sudden death. Circulation 114:1633–44.
  2. Pelliccia A, Culasso F, DiPaolo FM, et al (1999) Physiologic left ventricular cavity dilatation in elite athletes. Ann Inten Med 130:23–31.
  3. Fleck SJ, Dean LS (1987) Resistance-training experience and the pressor response during resistance exercise. J App Physiol 63:116–20.
  4. Rowland T (2009) Sudden unexpected death in young athletes: Reconsidering “hypertrophic cardiomyopathy.” Pediatrics 123–217.
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