Sports cardiology is a burgeoning field encompassing a wide range of topics involving the care of patients across various activity levels and fitness abilities.¹ From competitive athletes and highly active people (CAHAP) to patients with ischemic heart disease participating in cardiac rehabilitation, understanding cardiac and exercise physiology are essential skills for any sports cardiologist. This brief review focuses on the basic concepts of exercise physiology that should serve as a foundation for trainees interested in pursuing a career in sports cardiology.

Exercise Physiology: The Basics

Physical activity produces substantial increases in oxygen consumption (VO₂), which is achieved through increases in cardiac output (CO) and arterial-venous O₂ (AVO₂) difference.² At rest, VO₂ is 3.5 mL O₂/kg/min, which is equal to one metabolic equivalent (MET). With increasing levels of activity, VO₂ is increased to meet the energy expenditure required for a particular level of activity (external work rate), which is achieved through augmentation of CO and AVO₂ difference. Internal work rate, which depends on heart rate (HR) and blood pressure (the so-called "double product"), refers to the myocardial oxygen demand that occurs at a given level of activity. With increasing aerobic capacity, the myocardial oxygen demand required to perform a particular activity can decrease as fitness levels improve.

Exercise and sports disciplines have classically been divided as involving primarily dynamic or static exercise components. Dynamic exercise (e.g., running, cycling) is characterized by repetitive contraction and relaxation of large skeletal muscle groups, which require increases in oxidative metabolism and is achieved primarily through increases in CO to ensure oxygen delivery to actively contracting muscle.³ In dynamic exercise, systolic blood pressure increases mostly due to the rise in CO, while diastolic blood pressure either remains constant or falls as a result of reduction in the peripheral vascular resistance. Static exercise (e.g., weight lifting), involves short, forceful skeletal muscle contractions resulting in increased afterload and blood pressure.³ The primary role of the cardiovascular system during static exercise is to maintain CO in the face of increased left ventricular (LV) afterload.³ While this paradigm is helpful to understand isolated physiological changes during exercise, the reality is that most sporting disciplines involve both dynamic and static components.

Increased VO₂-Max during exercise is achieved through an augmented CO (stroke volume x HR) and AVO₂ difference. CO can increase up to four to five times resting values in highly conditioned individuals.⁴ With repetitive aerobic exercise training, maximal stroke volume (SV) and AVO₂ difference can be augmented, while maximum HR is largely immutable and dependent on various factors such as age, sex, BMI, etc.² Aerobic training does, however, result in a decrease in resting HR.

SV during exercise increases in a hyperbolic fashion compared with VO₂.⁵ In untrained individuals, SV during exercise increases by less than 50% and up to 100% with training.⁵ The rise in SV during exercise is achieved through multiple mechanisms including increased LV contractility,⁶ increased LV filling by capacitance venoconstriction and increased venous return, greater negative intrathoracic pressure, and the pumping action of exercising limbs.⁷ This increase in LVEDV promotes increased SV through Frank-Starling mechanisms.⁸ HR augments during exercise in a relatively linear fashion with VO₂ and occurs through an increase in sympathetic tone with concomitant withdrawal of vagal tone to achieve a two- to threefold increase in HR during maximum exercise.^9,2 Increased AVO₂ difference during exercise is achieved through the redistribution of blood flow from renal, splanchnic and cutaneous circulation to the exercising muscles, which increases oxygen extraction as much as three-fold in the periphery, and hemoconcentration as a result of plasma fluid losses into the interstitial space.²

The "Athlete's Heart:" Cardiac Adaptations to Meet the Demands of Exercise

Given the physical and metabolic demands of repetitive exercise, athletes are known to experience physiological remodeling of their cardiac structure and function. This exercise-induced cardiac remodeling (EICR) allows their hearts to meet the increased demands of their particular sport. A critical skill for the sports cardiologist is the ability to distinguish EICR from pathological remodeling, and the foundation for this training consists of understanding the anticipated physiologic remodeling of an "athlete's heart" based on the chosen sport.³

Sports are classified by the relative intensities of two major characteristics: 1) the static component; and 2) the dynamic component.¹⁰ An increasing static component (e.g., bodybuilding and rowing) results in exposing the LV to an augmented pressure load. An increasing dynamic component (e.g., cycling and ice hockey) exposes the LV and the rest of the cardiac chambers to an increased volume load due to the increased CO required to meet the higher oxygen consumption of the muscle mass that is engaged in dynamic exercise. While sports do not necessarily fit neatly into this paradigm, and while there may be significant heterogeneity within each sport (e.g., defensive lineman versus wide receiver in American-style football), this classification system helps to reiterate the importance of understanding the key components of cardiovascular demands during sporting activity.

Therefore, cardiac structural and functional changes that result from long-term training in a given sport should be reflective of its particular combination of static and dynamic components. In athletes who participate in sports with relatively higher static components, the increased wall tension on the LV myocardium promotes concentric remodeling or LV wall thickening with no concomitant increase in LV chamber size. However, the other three chambers are spared and relatively unaffected, with no significant changes in chamber size. Conversely, in athletes who participate in sports with higher dynamic components, the increased volume load leads to 4- chamber cardiac remodeling and enlargement. Eccentric remodeling of the LV, in which the LV internal diameter is increased with no concomitant increase in LV wall thickness, is seen, and dilation of both atria and the right ventricle (RV) can also be seen. In athletes who participate in sports with high intensity static and dynamic components (e.g., rowers, triathletes), a combination of these cardiac adaptations can be seen.

Regarding cardiac function, a key concept to remember is that SV, not the left ventricular ejection fraction (LVEF), is the hemodynamic parameter regulated by the body's metabolic demands.³ LVEF can be found to be in the low-normal to borderline depressed range in healthy athletes,¹² but SV remains preserved due to eccentric remodeling. However, one functional measurement that should be preserved, if not augmented, in the healthy athlete is diastolic function and any evidence of diastolic dysfunction should prompt further evaluation.^3,13

Despite an understanding of these basic concepts of EICR, there are many "gray zones," which describe the overlap between expected dimensions based on EICR and actual pathology. The sports cardiologist should be aware of threshold dimensions, including sport-specific data, and understand the concept of symmetrical changes in chamber sizes that should be observed in athletes.^3,14,15

Cardiopulmonary Exercise Testing for the Athlete

Patients presenting with exercise intolerance have become an increasingly common cause of referral to cardiovascular specialists. Cardiopulmonary exercise testing (CPET) is used to measure the extent of physical capacity and endurance in healthy athletes and to evaluate the cause of unexplained symptoms in others.¹⁶ CPET is a robust tool that integrates spirometric analyses such as the volume of oxygen uptake (VO₂) and exhaled carbon dioxide to the traditional parameters obtained from incremental exercise-testing such as exercise duration, HR and blood pressure (BP) response. Hence, CPET yields a holistic view of oxygen transport to the inspired air to the alveoli, then to the mitochondria and eventually its utilization during exercise.¹⁷

The seeds of CPET application in cardiology were planted over three decades ago when systolic heart failure functional status was categorized based on VO₂.¹⁸ Here, we aim to delineate the indications of CPET in athletes, the physiological basis of different variables tested, and the expected responses in athletes.

Technical Considerations

Indications

In athletes, CPET can be used as a screening tool to diagnose latent diseases in asymptomatic athletes. In addition, it can provide a baseline physical performance assessment before the initiation of a training regimen. In symptomatic patients, CPET can help in delineating the etiology of symptoms. Furthermore, another application of CPET lies in the ability to recommend the intensity of training in patients with pre-existing cardiovascular conditions based on their response to standard testing.¹⁶ Indications for CPET in athletes are summarized in Table 1.

Table 1: Indications of CPET in Sports Cardiology

Subset	Indication
Asymptomatic athletes	Screening for latent conditions
	Assessment of conditioning and physical performance before initiating an exercise regimen
	Assessment of performance capacity for specific sports. For example marathon training
	Follow-up assessment during training to prescribe recommendations on exercise and intensity of training19
	Prognostic characterization for future cardiovascular, metabolic or even psychiatric events20
Symptomatic athletes	Evaluation of symptoms of chest pain, dyspnea, palpitations, presyncope, syncope
	Assessment of known medical conditions such as hypertrophic cardiomyopathy in controlled conditions before enrolling in certain sports

Test Protocols

Detailed history, physical examination and a resting 12-lead electrocardiogram (ECG) should be performed before initiating CPET. Continuous HR, BP and ECG monitoring are mandated so that the test can be terminated if any complications arise. Appropriately trained technicians well-versed with cardiopulmonary resuscitation and an experienced physician must be present for testing to be conducted.¹⁶ Spirometric parameters are collected using a facemask or a mouthpiece, depending on laboratory and patient preferences. The exercise tests can be incremental in intensity or constant work rate protocols. Different kinds of ergometers can be used to perform CPET – treadmill or bicycle ergometer (Table 2). The main advantages of the latter are less ECG artifact, a higher degree of safety, ability to use it in the supine position and less patient anxiety.¹⁶ On the other hand, the treadmill involves a larger muscle mass and more anti-gravity work which leads to a 5-10% higher peak VO₂.²¹

Table 2: Comparison of Treadmill and Bicycle Ergometry

Factor	Treadmill ergometer	Bicycle ergometer
Higher peak VO2	X
Leg muscle training	X
Less EKG artifact		X
Work rate measurement		X
Blood gas measurement		X
Less noise		X
Higher safety		X
Use in the supine position		X
Experience in Europe		X
Experience in the US	X

Interpretation of Findings

CPET interpretation can be challenging owing to the wide range of normal physiologic measurements. Studies have shown individual normal variation of 7-15% for HR and arterial BP during exercise.²² Due to this unpredictability, multiple meta-analyses have been unsuccessful in generating definitive reference values.²³ Furthermore, the stress testing protocol can profoundly influence measurements. For example, a change in stress increments at 2 minutes leads to higher peak performance as compared to 3-minute increments.¹⁶ Some key parameters of CPET are described below (Table 3):

Table 3: CPET Variables in Healthy Individuals

VARIABLE	VALUE
Peak oxygen consumption (pVO2)	> 84% predicted
Blood pressure	< 220/90
Respiratory rate	< 60/minute
Maximum heart rate	> 90% age predicted
Ventilatory anaerobic threshold (VAT)	> 40% pVO2 (40-80%)
Expired ventilation (VE)/VCO2 at VAT	< 34
Oxygen pulse (VO2/HR)	> 80% predicted

Peak VO₂: Peak oxygen uptake (pVO₂) or VO₂-max is the highest volume of oxygen consumed averaged over a 20- to 30-second period, achieved at maximal effort during incremental CPET. VO₂ is defined by the Fick principle: VO₂ = CO x C(a-v)O₂ where C(a-v)O₂ is the arteriovenous oxygen content difference. CO is determined by HR x SV.

Heart rate: Conditioned athletes have a lower resting HR and lower HR at each stage of exercise; however, the maximum HR is a function of age (approximately 220 – age in years) and does not depend as much on conditioning.²⁴

Stroke volume (SV): Response curve with exercise is curvilinear, rising early in exercise with little change subsequently. Trained athletes have higher resting SV and higher SV at each stage of the exercise test.

Arteriovenous oxygen content difference (AVO₂): In healthy subjects, the arterial oxygen content does not change with exercise. Conversely, exercise leads to vasodilation in skeletal muscle leading to more oxygen extraction and lower venous oxygen content. Trained individuals have a higher AVO₂ difference leading to higher pVO₂.

Peak VO₂: Considered to be the most important criterion of peak performance ability. The VO₂ max response curve to exercise is linear until peak VO₂ is achieved after which it begins to plateau. Limiting factors include SV, HR or tissue extraction. Some of the factors that determine pVO₂ are genetic factors, age, sex, body size and recruitment of exercising muscle. pVO₂ declines about 10% per decade after the age of 30 due to decreasing maximal HR, SV, skeletal muscle blood flow and decreasing aerobic potential.²⁵ Within the same age group, men have 10-20% higher pVO₂ owing to higher hemoglobin concentration, greater SV and muscle mass.²⁶ Healthy people without specific training can achieve pVO₂ values of 30-45 ml/kg/min. Elite endurance athletes can attain values of close to 80 ml/kg/min.²⁷

Ventilatory anaerobic threshold (VAT): Originally referred to as the anaerobic threshold, the VAT is used to measure exercise capacity. In the initial phase of exercise, which is until 50-60% of pVO₂, metabolism is primarily aerobic. Hence, the expired ventilation (VE), which reflects CO₂ produced in muscles, increases linearly with VO₂. Muscle lactic acid production at this point is low, and consequently, serum lactate levels are normal.

With the progression of exercise stages, at around 60-70% of pVO₂, anaerobic metabolism takes over as the metabolic demands of the muscle surpass the oxygen supply. Lactic acid is produced in muscle and serum lactate concentration rises. The point at which VE increases disproportionately relative to VO₂ is defined as the VAT. Serum lactate measurements can be used to calculate VAT invasively, and VE/VO₂ ratio can be used for non-invasive estimation. To summarize, VAT is the VO₂ at which VE/VO₂ begins to rise without an immediate increase in VE/VCO₂.¹⁷ In conditioned athletes, the nadir of VE/VO₂ occurs distinctly sooner (first VAT), as compared to the nadir of VE/VCO₂ (second VAT) and this distinction may be lost in patients with impaired exercise tolerance predicting poor prognosis. A nadir VE/VCO₂ of < 34 reflects adequate ventilatory efficiency.

Respiratory exchange ratio (RER): The ratio of VCO₂/VO₂ is the RER. With increasing exercise intensity beyond 60-70% of pVO₂, anaerobic metabolism takes over leading to more CO₂ production. RER, as a result, rises to values over one after the first VAT. After the second VAT, hyperventilation occurs which further increases RER. Hence, RER can be used to objectively classify patient motivation and maximal effort achievement.

Oxygen pulse: Oxygen pulse is defined as the amount of oxygen consumed per heartbeat (VO₂/HR). Since VO₂ = SV x HR x AVO₂; oxygen pulse can be rearranged as SV x AVO₂. Since both SV and AVO₂ rise with incremental exercise, oxygen pulse should rise in healthy athletes. A drop in oxygen pulse during exercise can indicate impaired SV during exercise, such as in myocardial ischemia or conditions such as hypertrophic obstructive cardiomyopathy. Lack of peripheral perfusion can also lead to low oxygen pulse due to lack of oxygen extraction and a higher venous O₂ content.

Conclusion

A deep understanding of cardiac exercise physiology and CPET is a vital tool in the arsenal of sports cardiologists to determine which athletes may be presenting with pathology, to diagnose latent cardiopulmonary diseases in athletes and to assess fitness and endurance before or after specific exercise regimens. CPET has yet to achieve full potential, which could be due to lack of standardization of parameters and the knowledge-gap in the majority of physicians in grasping the nuances of CPET interpretation.¹⁷ Trainees in sports cardiology should seek opportunities to deepen their knowledge of exercise physiology and CPET, as these opportunities tend to be limited in general cardiology fellowships.

References

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Keywords: Athletes, Anxiety, Anaerobiosis, Anaerobic Threshold, Artifacts, Blood Pressure, Body Mass Index, Carbon Dioxide, Body Size, Cardiac Rehabilitation, Cardiomyopathy, Hypertrophic, Cardiopulmonary Resuscitation, Energy Metabolism, Electrocardiography, Dilatation, Exercise, Exercise Test, Exercise Tolerance, Fellowships and Scholarships, Healthy Volunteers, Heart Failure, Systolic, Heart Rate, Heart Ventricles, Hemoglobins, Hyperventilation, Lactic Acid, Metabolic Equivalent, Midazolam, Mitochondria, Motivation, Muscle Contraction, Myocardial Ischemia, Oxidative Stress, Myocardium, Muscle, Skeletal, Patient Preference, Prognosis, Oxygen, Referral and Consultation, Reference Values, Specialization, Stroke Volume, Supine Position, Tissue Extracts, Vascular Resistance, Vasodilation, Sports

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