This is an excerpt from Science and Application of High-Intensity Interval Training by Paul Laursen & Martin Buchheit.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity "high-stress"training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
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