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Exercise and Sports Cardiology
Additional content is available online at Elsevier eBooks for Practicing Clinicians
This chapter presents basic exercise physiology, describes cardiovascular (CV) adaptations to exercise training, and addresses common clinical issues among physically active individuals. The goal is to help clinicians evaluate symptoms produced by exercise, manage questions and clinical problems in athletes and physically active people, and assess the risks and benefits of exercise for individual patients. The reader is referred to Chapter 15 for a discussion of Exercise Testing.
Historical Perspective
Clinicians have long been interested in the CV risks and benefits of exercise. Herodicus (480 bc ) was a Greek physician who advocated exercise in the practice of medicine, whereas F.C. Sky, a London surgeon, in 1867 equated the Oxford-Cambridge crew race to cruelty to animals and opined that such extreme exertion would cause heart disease. Concern about rowers’, runners’, and bicyclists’ hearts emerged in the late 19th century, when these activities migrated from being occupational competitions among only the working classes to being sporting activities for the social elite. The normal CV adaptations to exercise training include resting bradycardia, global cardiac enlargement, and functional pulmonic and aortic valve flow murmurs. Evaluation of these normal adaptations by auscultation and cardiac percussion, the diagnostic tests of the day, led to their interpretation as signs of pathologic conduction disease, dilated cardiomyopathy, and valvular obstruction, respectively. Concerns about the risks associated with prolonged and vigorous exercise were commonplace in the 19th and early 20th centuries. Clarence DeMar, seven-time winner of the Boston Marathon, took a 5-year hiatus from competition during the peak of his competitive years, in part because, according to DeMar, “The frequent warnings of the doctors and fans of the danger to one’s heart had left their impression.” Current concerns about the risks and benefits of exercise include the risk of exercise-related acute cardiac events, the effects of exercise training on cardiac structure, and whether or not long-term endurance exercise training has deleterious CV effects.
Cardiovascular Response to Exercise And Exercise Training
Physical activity acutely increases systemic oxygen (O 2 ) demand, which prompts the CV system to increase cardiac output (Q) and the arterial-venous (A-V) O 2 difference. The increase in Q is coupled to the energy required such that there is a 5- to 6-liter increase in Q for each 1-liter increase in oxygen consumption (V̇ o 2 ) . Q is increased by augmentation of both the heart rate (HR) and stroke volume (SV). Several mechanisms increase the A-V O 2 difference, including shunting of blood from non-exercising tissue to working muscle, increased O 2 extraction by exercising muscle, and hemoconcentration. Myocardial oxygen (MO 2 ) demand depends in part on HR and systolic blood pressure (SBP) and therefore increases with exertion because both HR and SBP increase. This increase in MO 2 can produce ischemia in individuals with flow-limiting coronary artery lesions. In addition, the coronary arteries dilate in response to the myocardial metabolic demands of exertion, but inadequate vasodilation or frank vasoconstriction develops with exercise in some individuals with coronary atherosclerosis because of endothelial dysfunction. Cardiac ischemia, induced by exercise, can contribute to cardiac events during exercise, as discussed later.
The CV response to exercise has both an external and internal work rate. The external work rate is the V̇ o 2 required by the exercise task and, as mentioned, is a direct determinant of Q. V̇ o 2 can also be crudely estimated from treadmill speed and grade or from a stationary bicycle watt requirement. The internal work rate refers to the myocardial oxygen consumption (MO 2 ) required for the exercise task and relates directly to increases in HR. In contrast to Q, the HR response to exercise, and therefore MO 2 , is not determined by the external work rate or V̇ o 2 max but by the V̇ o 2 required relative to the individual’s maximal exercise capacity, or V̇ o 2 . Individuals with higher exercise capacity and a greater V̇ o 2 max have a larger SV at any given external work rate, such that any exercise task, and V̇ o 2 demand, requires a slower HR to generate the same externally determined Q.
Repetitive aerobic exercise sessions and aerobic exercise training increase maximal exercise capacity, measured physiologically by an increase in V̇ o 2 max. This increase in healthy individuals results from increases in both maximal Q and the maximal A-V O 2 difference. Because maximal HR is largely immutable, determined by age, and minimally affected by exercise training, the increase in maximal Q results from an increase in maximal SV. The increase in SV means that performing the same exercise task or external work rate, which requires the same V̇ o 2 max, can be performed at a slower HR and a lower MO 2 or internal work rate. The reduction in HR and thereby MO 2 contributes to the increase in exercise capacity in patients with angina pectoris after exercise training. In addition to the increase in maximal exercise capacity, exercise training also increases endurance capacity, the ability to perform submaximal effort for a prolonged period. This effect contributes critically to the exercise training response because few work or recreational tasks require maximal CV effort.
Intense and prolonged aerobic exercise training produces an array of CV adaptations, commonly referred to as “athlete’s heart” ( Fig. 32.1 ). Such changes include an increase in resting SV and a decrease in resting HR. The physiologic mediators of training-induced reductions in resting HR are related in part to increased resting vagal tone and reduced resting sympathetic tone. However, the bradycardia persists in trained mice after autonomic blockade or sinus node denervation, suggesting that autonomic changes alone cannot explain the training effect on HR. Indeed, trained mice show widespread remodeling of pacemaker ion channels, including downregulation of the I f , or funny channel, mediated by microRNAs (miR-423-5p) and blockade of I f abolishing the reduced HR. Highly trained endurance athletes often develop resting bradycardia, which may be associated with marked sinus arrhythmia, first-degree heart block, Mobitz I second-degree atrioventricular (AV) block, or even third-degree AV block during sleep. The reduced AV conduction velocity may make accessory conduction pathways, such as those of Wolff-Parkinson-White syndrome, more apparent. Athletes also have an increased prevalence of an early-repolarization ST-segment pattern and ST-T wave abnormalities, findings also historically attributed to increased vagal tone ( Fig. 32.2 ).
Four-chamber cardiac enlargement, often exceeding the standard upper limits of normal (ULN), develops in response to routine aerobic exercise training, whereas left ventricular (LV) wall thickness usually increases only mildly. Small increases in aortic root dimensions also occur, but increases in aortic size greater than expected for body size seldom occur in young athletes, even among those playing in the National Basketball Association. The long-term effect of vigorous exercise on aortic dimensions is less clear. The aortic root diameter exceeded 40 mm in 41% of 152 asymptomatic, predominantly retired, Australian rugby players, and 58% had effacement of the sinotubular junction. Similarly, among older runners and rowers (mean age ± SD of 61 ± 6 years) 31% of the men and 6% of the woman had an aortic diameter ≥40 mm. Consequently, the possibility and significance of aortic enlargement in older, lifelong athletes requires additional study. In contrast to the extensive cardiac changes reported in endurance-trained athletes, strength exercise training produces modest increases in LV wall thickness with little change in chamber dimensions. Among 1300 elite Italian athletes, 45% exceeded the upper limit of normal (ULN) of 55 mm, with the most marked increases in LV size occurring in the largest athletes and those with the slowest HR. In contrast, LV wall thickness rarely exceeds ULN among trained athletes. For example, among 947 national-caliber and international-caliber Italian athletes, only 16 had LV wall thickness greater than 12 mm. Trained athletes usually have normal resting LV systolic function, most frequently measured as LV ejection fraction (LVEF), but may be near the lower limit of the normal range because large ventricles can meet resting metabolic demands with a lower LVEF.
Cessation of exercise training, or “detraining,” may help in clinically differentiating adaptations to exercise training from hypertrophic cardiomyopathy (HCM). Several studies have examined the effect of detraining in endurance athletes with eccentric LV hypertrophy (LVH), a geometric pattern characterized by concomitant LV wall thickening and chamber dilation. Regression of eccentric LVH can occur in highly trained athletes after 6 to 34 weeks (mean, 13 weeks) of abstinence from exercise. A detraining study of 40 Italian male athletes with eccentric LVH and peak fitness LV dimensions (mean ± SD) of 61.2 ± 2.9 mm and LV wall thickness of 12.0 ± 1.3 mm reported complete normalization of wall thickness and a significant but incomplete reduction in cavity dilation after 5.8 ± 3.6 years of detraining. Because the LV wall thickening and concentric LVH common in strength-trained athletes can regress partially after 3 months and completely after 6 months of detraining, such diagnostic trials should last 6 months.
Effects of Habitual Physical Activity on Cardiovascular Risk
Multiple epidemiologic, cross-sectional studies examining the frequency of CV events in healthy individuals demonstrate that the more active participants have lower CV risk than their more sedentary counterparts. The reduction in risk in the most active versus the least active individuals is approximately 40%. Even small amounts of physical activity reduce CV risk. CV risk falls progressively with increasing physical activity until approximately 9.1 hours per week of moderate-intensity activity, such as brisk walking. After this level of exertion, there appears to be little additional benefit and, possibly diminution, of the beneficial effects.
Cross-sectional studies, however, cannot prove that the reductions in CV risk result from physical activity alone. Individuals who engage in physical activity may inherit greater exercise capacity, thereby leading them to select active lifestyles and lower their CV risk. Physical activity contributes to the improvement in multiple CV risk factors including SBP, body weight (BW), blood glucose, and triglycerides. Nevertheless, there are no randomized clinical trials (RCTs) comparing the effects of physical activity or exercise training on CV outcomes in previously sedentary, healthy individuals, but there are multiple RCTs examining CV outcomes of exercise-based cardiac rehabilitation in patients with established disease. None of these studies was large enough to provide conclusive results alone, but a meta-analysis of 63 RCTs including 14,486 patients demonstrated a 26% decrease in CV mortality in the patients assigned to the exercise-based programs. Such results, plus the plethora of epidemiologic and experimental evidence linking increased physical activity with lower CV risk have led to the acceptance of physical inactivity as a major modifiable CV risk factor. Epidemiologic data suggest that the largest reduction in CV risk with physical activity occurs at low levels of activity. Consequently, current American guidelines recommend 150 to 300 minutes weekly of moderate aerobic activity such as brisk walking or 75 to 100 minutes weekly of vigorous activity such as jogging, plus some resistance exercise twice weekly.
Support for the possibility that habitual exercise and lower CV disease are genetically linked is provided by studies that have selected and bred rats over multiple generations for superior or reduced exercise performance. The animals that result from breeding for higher exercise capacity also developed lower CV “risk” profiles including less evidence of the metabolic syndrome, fewer CV complications, and greater longevity than rats bred for reduced exercise capacity even though CV risk factors were not considered in the breeding selection process. Consequently, the same physiologic factors associated with increased exercise capacity may also be associated with reduced CV risk, and individuals choosing an active lifestyle may have lower CV risk independent of their exercise habits.
Cardiovascular Risks of Exercise
The Pathology of Exercise-Related Cardiovascular Events
Despite the putative benefits of habitual physical activity, vigorous physical activity transiently increases the risk for sudden cardiac death (SCD) and acute myocardial infarction (AMI). This conclusion is based on studies comparing the hourly cardiac event rate during vigorous exertion with rates during more sedentary activities. The pathologic substrate associated with these acute cardiac events varies by age, because the prevalence of cardiac conditions responsible for SCD also varies by age. Exercise-related SCD in young individuals, defined as age less than 30 or 40 years, has historically been attributed to inherited and congenital conditions, including HCM (see Chapter 54, Chapter 70 ) and anomalous origin of the coronary arteries (AOCA), although acquired conditions such as myocarditis and cardiomyopathy can also cause exercise-related SCD in this group.
Recent studies, however, have questioned the role of HCM as the leading cause of SCD in athletes. Autopsy data reveal no structural abnormality in up to 40% of SCDs in young athletes, suggesting that many of these such deaths are due to the sudden arrhythmic death syndrome (SADS). Further, HCM and AOCA were found in only 6% and 5% of these cases respectively, thereby suggesting that other conditions, such as inherited channelopathies, may be more prevalent. Each of these 357 cases was evaluated in a cardiac pathology referral center raising the possibility that definitively diagnosed cases of HCM and AOCA may have not been referred. Similar findings were generated by an analysis of SCD among National Collegiate Athletic Association (NCAA) athletes over a 10-year period in which HCM and AOCA were responsible for only 15% (79) of 514 deaths. There was no structural abnormality in 25% of the 64 autopsied cases, whereas only 5% and 11% were due to HCM and AOCA, respectively. Similarly, a meta-analysis of 34 studies of SCD reported normal hearts in 23% of nonathletes and 18% of the athletes and HCM in 8% and 14% of the nonathletes and athletes, respectively. These studies are difficult to compare because some included all SCDs in athletes, whereas others included only exercise-related SCDs. Consequently, it is not clear if this apparent shift in the causes of SCD during exertion is due to previous selected case ascertainment (because the earliest studies often originated from HCM centers), a true change in the causes of SCD because of more effective screening, diagnosis, and care of athletes with HCM, or to the inclusion of both exercise- and nonexercise-related SCDs in the analyses.
Atherosclerotic cardiovascular disease (ASCVD) causes most exercise-related AMI and SCD in adults, although there are rare reports of spontaneous coronary artery dissection with vigorous exertion (more often in young, but occasionally in older individuals). AMI in previously asymptomatic adults during exercise is usually associated with acute coronary arterial plaque disruption. However, malignant ventricular arrhythmias and SCD triggered by myocardial ischemia attributable to stable but obstructive coronary lesions also occur. Several triggering mechanisms for plaque disruption may pertain, including increased flexing and bending of atherosclerotic coronary arteries. Approximately 33% of SCDs in adults caused by ASCVD are associated with clinicopathologic findings of an acute coronary syndrome (ACS), whereas the remainder show evidence of nonacute ASCVD.
The Relative and Absolute Risk of Exercise
Vigorous exercise increases the relative risk of cardiac events, but the absolute risk of exercise-related cardiac events is low, particularly among people who are habitually highly active. Among young individuals, the increase in risk relative to SCD during exercise is greatest in the youngest age groups. Approximately 14% of SCD in individuals less than 35 years old in Portland, OR, were related to sport activity. In this cohort, SCDs occurred during sports in 39% of cases among individuals less than 18 years old, 13% of those aged 19 to 25, and 7% of those aged 25 to 34.
This observed decline with increasing age is likely attributable to decreasing exercise intensity with increasing age, the rarity of non-exertion deaths in the youngest group, and the decrease in overall sport activity with increasing age. Importantly, the risk of exercise-related SCD appears higher in athletes than in nonathletes as evidenced by the fact that SCDs or cardiac arrests were ≈4.5-fold greater in French competitive athletes aged 10 to 35 than among recreational athletes of similar age.
Estimates of the absolute risk of death among young competitive athletes are highly variable and depend on study design and the groups studied. The most consistent estimate for the absolute risk of sports-related SCD in the young is one death per year for every 200,000 athletes. However, rates as high as one death per year for every 5100 Division 1 male NCAA basketball players and every 14,704 male adolescent, elite soccer players (mean age ± SD; 16.4 ± 1.2 years) have been reported. These rates are high compared to historical data, so additional studies are required to clarify this variability.
Between 4.4% and 13.6% of AMIs are associated with physical exertion and approximately 5% of all SCDs are sports related. Vigorous exertion increases the risk of SCD in adults between 3 and 17 times that of more sedentary activities. Historical estimates of the absolute risk suggested that one exercise-related death occurred per year for every 15,000 to 18,000 previously healthy adult men, but more recent estimates are markedly lower at between one death per year for every 50,000 to 300,000 individuals. Most studies suggest that both young and older women have a much lower risk for exercise-related events.
Approach to Common Clinical Problems in Sports Cardiology
Athletes and active individuals may seek CV evaluation for a multitude of reasons, but the following section discusses several common clinical complaints in athletic patients and the clinical approach to their management.
Decreased Exercise Capacity
Athletes with decreased exercise capacity are frequently referred to CV specialists for evaluation. SV contributes critically to Q and therefore to exercise capacity, but V̇ o 2 max also requires maximal performance from its other CV components, HR and A-V O 2 difference, as well as from the central nervous system, lungs, and skeletal muscle. Decrements in any of these components can compromise exercise performance. An inappropriately fast HR at low levels of exertion as a result of hyperthyroidism or stimulant use can decrease exercise performance, as can exercise-induced asthma, diseases of skeletal muscle, and reduced O 2 -carrying capacity from anemia (often resulting from iron deficiency in female endurance athletes who eat a vegetarian diet). Atrial fibrillation (AF) or frequent premature contractions during exercise can reduce exercise capacity. Recurrent pulmonary emboli are often not suspected in athletes because of their overall health and atypical presentation, but prolonged travel to competition, tissue trauma and immobility from injury, and factors such as genetic predisposition, birth control use, and dehydration can increase athletes’ thrombotic risk. Other conditions not directly related to the CV system, including viral illnesses (e.g., mononucleosis, hepatitis), hematologic malignancies, and autoimmune conditions, can initially be manifest in athletes as decreased exercise capacity or exercise intolerance.
These same issues can reduce exercise performance in older athletes but occult coronary disease with atypical symptoms always requires consideration first in older patients. Many adult athletes with reduced exercise capacity referred for expert evaluation have LV diastolic dysfunction because prior encounters have eliminated the more obvious diagnoses. This scenario often presents as a lifelong endurance athlete with “borderline hypertension” who avoided antihypertensive treatment. These patients frequently have mild-resting hypertension but exhibit an exaggerated blood pressure response to exercise.
Psychological factors and overtraining can cause decreased exercise capacity in athletes. Psychological issues generally occur in young athletes who have lost their desire to compete before their parents have lost interest in the child’s sport. This diagnosis often becomes clear if parents or other key adults are included in the patient’s assessment. Some athletes appear to find it easier to use a medical excuse for stopping sports participation rather than to admit that they have lost interest, want to pursue other interests, or “just aren’t good enough” to continue.
Evaluation of athletes complaining of decreased exercise performance requires listening to the athlete’s history carefully. Practitioners may dismiss many complaints in athletes because their exercise performance remains superior to that of nonathletes, but important cardiac conditions may present sooner in athletes because of the physical demands of their sport. Evaluating performance times, training diaries, and training/performance data captured by GPS-enabled wearable technology in endurance athletes often helps plot the time course of the complaint. The conditions mentioned earlier must be excluded, as must obvious cardiac disease. Exercise testing using protocols designed to mimic the athlete’s sport frequently helps document the complaint and its cause. Exercise echocardiography and cardiopulmonary exercise testing with specific attention to the oxygen pulse curve are useful when the history suggests diastolic dysfunction. The oxygen pulse can be calculated by dividing V̇ o 2 by HR, and assuming no important change in the A-V O 2 difference, reflects SV. It can help determine when cardiac performance becomes a limiting factor during exercise. Long-term electrocardiographic monitoring, increasingly done using adhesive ambulatory monitoring patches and occasionally performed with implanted monitoring devices, can detect cardiac rhythm disorders in athletes with infrequent symptoms. Psychological and emotional issues should be diagnosed only after the exclusion of other medical conditions and require frank discussions with the athlete and family. Depression can frequently cause otherwise unexplained fatigue.
Overtraining is a complex interaction of psychological and physiologic fatigue in athletes that can occur after prolonged high-intensity training. The diagnosis of overtraining is made by careful history because there is no diagnostic test for this condition. Diminished exercise tolerance (sometimes with an elevated resting HR), the sensation of nocturnal fevers, and insomnia all characterize overtraining. The insomnia appears paradoxical because the athletes often experience extreme fatigue but find it difficult to sleep as a result of restlessness and sometimes involuntary muscle contractions. Overtraining should be diagnosed only when other conditions are excluded and frequently requires a therapeutic trial of markedly reduced training to see whether the symptoms resolve and performance improves. The optimal duration of prescribed detraining for overtrained athletes has yet to be defined but may be weeks to months depending on the duration and severity of the overtraining symptoms.
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