Mecanismos cardiovasculares del declive del rendimiento longitudinal en atletas veteranos:

A Revisión narrativa del Envejecimiento, Enfermedad de las arterias coronarias, Miocardio silencioso Isquemia, y No reconocido Infarto de miocardio

Resumen

Esta revisión narrativa sintetiza evidencia seleccionada y revisada por pares sobre los mecanismos cardiovasculares y fisiológicos subyacentes al declive del rendimiento longitudinal en atletas masters de entre 50 y 80 años. Los temas abordados incluyen (1) la trayectoria natural de la capacidad física del estudio de la Cohorte de Población Sueca para la Actividad Física y la Aptitud Física (SPAF)[1]; (2) el contraste entre el atleta entrenado y el sedentario V̇O₂caída máxima2][3][4]; (3) mecanismos cardiovasculares centrales y periféricos del V̇O₂erosión máxima; (4) la paradoja de la coronaria subclínica ateroesclerosis en atletas de resistencia de larga duración; (5) isquemia miocárdica silenciosa e infarto de miocardio no reconocido —incluyendo epidemiología, mecanismos, pronóstico y enfoque diagnóstico; (6) coronaria disfunción microvascular como posible contribuyente a la intolerancia al ejercicio en atletas mayores seleccionados; y (7) consideraciones contemporáneas de detección en cardiología deportiva basadas en el Guía de cardiología deportiva de la ESC 2020. La síntesis es interpretativa más que exhaustiva; la estrategia de búsqueda específica y el alcance se describen en la sección Identificación de Literatura.

1. Introducción

El proceso de envejecimiento en los seres humanos está inexorablemente vinculado a una disminución progresiva de la capacidad fisiológica; sin embargo, la velocidad y la trayectoria de esta disminución están influenciadas significativamente por la actividad física habitual. Entre los individuos que mantienen altos niveles de entrenamiento de resistencia en sus décadas sexta, séptima y octava —comúnmente denominados atletas máster—, la disminución de la capacidad aeróbica máxima (V̇O₂máx) y el rendimiento de resistencia proporciona un modelo biológico único para estudiar los límites del envejecimiento humano2Mientras que los atletas veteranos demuestran consistentemente una superioridad condición cardiorrespiratoria (FCR) en comparación con sus pares sedentarios, no son inmunes a los procesos biológicos fundamentales que erosionan la función cardiovascular con el tiempo3][4].

La disminución del rendimiento longitudinal entre los 50 y los 80 años está regida por una compleja interacción de limitaciones cardíacas centrales, deterioro vascular periférico y mitocondrial, y la aparición paradójica de patologías cardiovasculares subclínicas. Estas incluyen coronarias arteria enfermedad en atletas de resistencia de por vida13][14][15] y, en la población de mayor edad en general, isquemia miocárdica silenciosa, infarto de miocardio no reconocido, y disfunción microvascular coronaria (DMC)[21][22]. Para comprender estos mecanismos en su contexto, resulta útil primero establecer una línea de base a nivel poblacional de la cohorte longitudinal del SPAF[1] y luego contrastar esa línea base con las adaptaciones fisiológicas específicas —y los riesgos patológicos— observados en atletas de resistencia de toda la vida.

2. Identificación de la literatura

Este artículo es una revisión narrativa. La literatura se identificó principalmente mediante búsquedas en PubMed y Embase (1990–2026) y mediante la revisión de referencias retrospectivas de estudios primarios relevantes, metaanálisis y documentos de orientación de las principales sociedades que abordan a los atletas veteranos, el deterioro de la capacidad aeróbica relacionado con la edad, la aterosclerosis coronaria en atletas de resistencia, la isquemia miocárdica silenciosa, el infarto de miocardio no reconocido, la disfunción microvascular coronaria y el cribado en cardiología del deporte. Se dio prioridad a los estudios de cohortes originales, los ensayos aleatorizados, revisiones sistemáticas, metaanálisis y declaraciones de guías oficiales. Debido a que esta no fue una revisión sistemática basada en protocolos, la selección de estudios fue cualitativa y la síntesis debe interpretarse como interpretativo en lugar de exhaustivo. No se realizó ninguna agrupación metanalítica formal; los valores cuantitativos se reproducen de las fuentes primarias citadas sin reanálisis.

3. La línea base de la población general: Perspectivas del estudio SPAF de Westerståhl

El estudio longitudinal SPAF de 47 años informado por Westerståhl y sus colegas ofrece una de las evaluaciones más integrales de cómo cambia la capacidad física desde la adolescencia hasta la vejez temprana en una cohorte representativa de la población general[1]. Al hacer un seguimiento de 427 personas nacidas en 1958, el estudio utilizó evaluaciones objetivas repetidas de la capacidad aeróbica, la resistencia muscular y la potencia explosiva desde los 16 hasta los 63 años[1]. El conjunto de datos es informativo porque identifica la tasa natural de disminución en una población donde la actividad física no está estandarizada, destacando la naturaleza acelerada del envejecimiento biológico independientemente del estatus de atleta de élite.

El rendimiento físico máximo generalmente se alcanzaba entre los 26 y los 36 años tanto en la capacidad aeróbica absoluta como en la resistencia muscular1]. Específicamente, los hombres alcanzaron su capacidad aeróbica absoluta máxima a los 35 años (3.26 L·min⁻¹), mientras que las mujeres alcanzaron su punto máximo a los 36 años (2.61 L·min⁻¹)[1]. Tras estos picos, el descenso comenzó a un ritmo aproximado de 0,3 a 0,61 TP9T por año y se aceleró hasta alcanzar aproximadamente 2,0 a 2,51 TP9T por año a medida que los participantes se acercaban a los 60 años[1]. A los 63 años, la disminución acumulada de la capacidad aeróbica absoluta con respecto al valor máximo fue de aproximadamente 33% en los hombres y de 30% en las mujeres[1].

Tabla 1. Trayectorias de la capacidad física de la cohorte longitudinal SPAF de 47 años.

Parámetro	Hombres (edad máxima 35–36 años)	Mujeres (edad máxima 36 años)	Disminución total de 63
Capacidad aeróbica absoluta (L·min⁻¹)	3.26	2.61	30–33%
Capacidad aeróbica relativa (mL·kg⁻¹·min⁻¹)	42.2 a los 26 años	39.7 a los 31 años	37–40%
Salto vertical (cm)	45.5 a los 27 años	33,0 a los 19 años	41–48%
Resistencia muscular (press de banca, repeticiones)	52.7 a los 36 años	39.7 a los 34 años	32–35%

Westerståhl M, et al. J Cachexia Sarcopenia Músculo. 2025[1]. Los valores son las medias de las cohortes a la edad indicada. SPAF = Cohorte de Población Sueca para la Actividad Física y la Aptitud Física.

Los datos del SPAF también subrayaron el papel de los factores del estilo de vida en la modificación de estas trayectorias. Una mayor actividad física en el tiempo libre a los 16 años y un estilo de vida activo durante la adultez se asociaron con un rendimiento superior en todas las métricas a lo largo de la vida1]. Un mayor nivel educativo se asoció con una mayor capacidad aeróbica absoluta y resistencia muscular, posiblemente a través de conductas de búsqueda de salud. Sin embargo, incluso con estos factores protectores, la aceleración del deterioro después de los 40 años fue un hallazgo consistente, lo que refuerza el concepto de que el envejecimiento biológico impone una limitación fisiológica progresiva sobre la capacidad funcional que comienza a operar mucho antes de volverse clínicamente significativa.

4. Disminución comparativa: atletas masters vs. población general

Al contrastar la línea base del SPAF con datos longitudinales de atletas veteranos, surge una clara distinción en la altitud inicial y la pendiente del V̇O₂disminución máxima. Los atletas de resistencia de élite representan una cohorte que ha maximizado su potencial adaptativo y puede portar un V̇O₂máximo a los 60 años que supera la mediana de una persona sedentaria de 40 años2]. A pesar de esta ventaja, el inevitable declive del V̇O₂max sigue siendo el principal mecanismo fisiológico asociado con la reducción del rendimiento de resistencia en atletas que envejecen[3][4].

Las evaluaciones longitudinales indican que los atletas veteranos que mantienen un entrenamiento de alta intensidad y gran volumen reducen la tasa de V̇O₂una disminución máxima de aproximadamente 5–71 TP9T por década, en comparación con los 10–121 TP9T por década observados en personas sedentarias de la misma edad[2][3][4]. Sin embargo, esta disminución atenuada por el entrenamiento es frágil; los análisis de regresión indican que una proporción sustancial de la varianza en el V̇O₂La disminución máxima en los atletas de la categoría «master» se debe directamente a la reducción del volumen y la intensidad del entrenamiento, y las disminuciones más pronunciadas (15–46% por década) se observan en los atletas que reducen sustancialmente su entrenamiento[3][4].

Tabla 2. Tasas decadales de V̇O₂descenso máximo por grupo.

Grupo	Disminución decenal	Motivación principal
Adultos sedentarios	10–12%	Sarcopenia, inactividad, declive cardíaco central
Atletas veteranos (entrenamiento constante)	5–7%	Disminución intrínseca de la máxima frecuencia cardíaca
Atletas veteranos (entrenamiento reducido)	15–46%	La pérdida de condición física superpuesta al envejecimiento

Fuentes: refs [2][3][4].

5. Mecanismos cardiovasculares de la disminución de la capacidad aeróbica

La erosión de V̇O₂máximo se describe matemáticamente por el Principio de Fick: V̇O₂max = Q̇ × (a–v)O₂ diferencia, donde Q̇ es el gasto cardíaco y (a–v)O₂ es la diferencia en el contenido de oxígeno entre las arterias y las venas. En los atletas de la categoría «master», la contribución relativa de los factores cardíacos centrales (frecuencia cardíaca y volumen sistólico) frente a factores periféricos (extracción de oxígeno) cambia con la edad[8][9].

5.1 Mecanismos centrales: la «bomba del envejecimiento»

El factor determinante más constante y en gran medida inmodificable del V̇O₂La disminución máxima es la reducción de la frecuencia cardíaca máxima (FC) relacionada con la edad_máx.). El ampliamente citado Ecuación de Tanaka — RR. HH._máx. ≈ 208 − 0,7 × edad — lo que implica una disminución promedio de aproximadamente 0,7 latidos·min⁻¹ al año[7]. Esto se debe principalmente a cambios en la electrofisiología intrínseca del nodo sinuatrial y mediante la reducción de Respuesta β-adrenérgica con la edad. Si bien el entrenamiento de resistencia puede reducir la frecuencia cardíaca en reposo y mejorar el tono parasimpático, tiene una capacidad limitada para mantener la frecuencia cardíaca máxima durante un esfuerzo al máximo.

Derrame cerebral El volumen sistólico (VS) ofrece una perspectiva más matizada. En las personas sedentarias, el VS disminuye debido al aumento de la rigidez miocárdica, la reducción de la complacencia ventricular y el deterioro del llenado diastólico[10]. En los atletas de categoría máster, el entrenamiento crónico de resistencia induce una remodelación ventricular excéntrica caracterizada por mayores dimensiones de la cavidad y una mayor distensibilidad miocárdica[10][11]. Esta adaptación permite a los atletas mantener un volumen sistólico (VS) más alto durante el mecanismo de Frank-Starling. No obstante, los atletas veteranos pueden experimentar una reducción del volumen sistólico (VS) en el ejercicio máximo debido al acortamiento anormal del tiempo de llenado diastólico a frecuencias cardíacas muy elevadas, donde el intervalo diastólico es demasiado corto para un llenado ventricular completo.

5.2 Mecanismos periféricos: extracción de oxígeno y deterioro mitocondrial

Si bien las limitaciones centrales predominan en las primeras etapas del deterioro, los factores periféricos se vuelven cada vez más limitantes a medida que los atletas se acercan a los 80 años[9]. Tres procesos periféricos son los más importantes:

• Arteriovenoso O₂ (a–v)O máximo₂ La diferencia disminuye ligeramente con la edad en los atletas veteranos, debido principalmente a escasez capilar — adelgazamiento de las redes capilares que irrigan el músculo individual fibras — lo que aumenta la distancia de difusión del oxígeno9].
• Función mitocondrial. El envejecimiento se asocia con reducciones en densidad mitocondrial y en la actividad de enzimas oxidativas clave como la citrato sintasa y la succinato deshidrogenasa2El mantenimiento del entrenamiento de alta intensidad en atletas veteranos preserva la calidad mitocondrial, pero las reducciones en el volumen de entrenamiento producen una caída rápida y casi lineal en la capacidad oxidativa.
• La atrofia selectiva de las fibras de tipo II (de contracción rápida) y la pérdida general de masa muscular reducen la demanda metabólica y el rendimiento en el ejercicio, un efecto documentado en la cohorte SPAF y en otros estudios[1].

6. Aterosclerosis coronaria en atletas máster: la paradoja de la calcificación

Uno de los hallazgos más desafiantes en la cardiología deportiva moderna es la aparente paradoja de la alta calcio en las arterias coronarias (CAC) puntuaciones en atletas de resistencia de por vida. Los datos transversales, incluida la cohorte Master@Heart, han demostrado que los atletas de resistencia de por vida (predominantemente hombres) a menudo presentan una mayor prevalencia de coronariopatía placas y puntajes de CAC más altos que sus pares sedentarios con un perfil de riesgo similar13][14][15][16][17].

6.1 Morfología y distribución de la placa

El Estudio Master@Heart por De Bosscher y sus colaboradores incluyó a 191 atletas de toda la vida, 191 atletas de inicio tardío y 176 no atletas sanos (todos hombres) y demostró que los atletas de toda la vida tenían la mayor cantidad de coronarias carga de placa[15]. La carga incluía no solo placas calcificadas — generalmente consideradas estables —, pero también placas no calcificadas y mixtas en segmentos coronarios proximales[15].

Tabla 3. Hallazgos de placa coronaria de la cohorte Master@Heart.

Grupo	≥1 placa coronaria (OR)	≥1 placa proximal (OR)	≥50% luminal estenosis
No atletas (referencia)	1.00	1.00	≈ referencia
Atletas de inicio tardío	intermedio	intermedio	bajo
Atletas de resistencia de toda la vida	1.86	1.96	poco común, pero elevado en comparación con los controles

De Bosscher R, et al. Eur Heart J. 2023[15]. OR = razón de probabilidades frente a la referencia de no deportistas; los valores son estimaciones ajustadas. Todos los participantes eran hombres; edad promedio ≈ 60 años. La estenosis obstructiva (≥50%) fue poco frecuente en términos absolutos en todos los grupos; la prevalencia exacta reportada en el grupo de deportistas de toda la vida debe contrastarse con la publicación original antes de la composición tipográfica final.

En Master@Heart, los atletas de toda la vida también tenían una probabilidad desproporcionada de presentar placas no calcificadas en segmentos proximales en comparación con los no atletas15]. La ubicación proximal es clínicamente relevante porque dichas placas controlan el flujo hacia grandes territorios miocárdicos. Si bien una mayor aptitud cardiorrespiratoria se asocia con una morfología de placa estable en algunos análisis, la presencia absoluta de estas lesiones sugiere que el entrenamiento de resistencia de alto volumen puede interactuar con el convencional factores de riesgo para acelerar la progresión de la enfermedad subclínica preexistente16][17].

6.2 Impulsores mecanísticos propuestos

El desarrollo de la enfermedad coronaria en atletas veteranos sigue sin explicarse por completo. La literatura observacional actual plantea varias mecanismos propuestos, las cuales deben interpretarse como hipótesis plausibles más que como vías causales establecidas:

• Esfuerzo cortante hemodinámico. El ejercicio vigoroso produce un flujo coronario hiperdinámico. En los sitios de flujo perturbado o turbulento, las fuerzas mecánicas pueden contribuir a disfunción endotelial[13][17].
• Estrés oxidativo. Las extremas demandas metabólicas del entrenamiento de ultraresistencia pueden generar transitoriamente especies reactivas del oxígeno más de antioxidante capacidad, con posibles efectos posteriores en función endotelial y lipoproteína retención17].
• Inducido por el ejercicio hipertensión. En una cohorte reciente de atletas masculinos veteranos de resistencia, la hipertensión oculta en reposo y la inducida por el ejercicio fue frecuente y se asoció con una mayor carga de placa coronaria18]. Ejercicio exagerado presión arterial sistólica las respuestas se reconocen cada vez más como un fenotipo clínicamente procesable.
• Interacciones con los factores de riesgo convencionales. Even in athletes, conventional risk factors — LDL-cholesterol, apolipoproteína B, lipoproteína(a), hypertension, historial familiar — remain the dominant drivers of atherosclerosis[49][50].

7. Silent Myocardial Ischemia and Unrecognized Myocardial Infarction

7.1 Definitions and key distinction

Silent myocardial ischemia (SMI) refers to objective evidence of transient inducible ischemia — typically ST-segment depression on ambulatory or exercise ECG, or inducible perfusion abnormality on stress imaging — in the complete absence of anginal symptoms[21][22]. Unrecognized myocardial infarction (UMI) refers to a completed infarction that was not clinically diagnosed at the time it occurred[28][29][30][31]. Late gadolinium enhancement (LGE) on resonancia magnética cardíaca (RMC) characterizes prior myocardial injury — scar, fibrosis, or completed infarction — and is therefore the reference standard imaging modality for UMI rather than a primary test for active ischemia[30][36]. This distinction is preserved throughout the remainder of this section.

7.2 Epidemiology of silent ischemia and unrecognized MI

Silent or unrecognized MIs account for a substantial fraction of all myocardial infarctions in epidemiological cohorts. The original Framingham Heart Study reported that approximately one-quarter of MIs were unrecognized when first detected during routine biennial examination[28]. The Atherosclerosis Risk in Communities (ARIC) study found that the proportion of MIs that were silent and detected only by ECG was approximately 22%, with substantial sex and race differences in detection[29]. In the Cardiovascular Health Study of older community-dwelling adults, the prevalence of UMI rose with age[31].

The advent of resonancia magnética cardíaca with LGE has substantially raised estimates of UMI prevalence. The ICELAND-MI study by Schelbert and colleagues found that UMI detected by CMR-LGE was more than twice as common as UMI detected by ECG in an older community cohort, and that ECG-detected UMI represented only a fraction of all CMR-detected events[30]. En el MESA cohort, CMR-detected myocardial scar was identified in approximately 7.9% of asymptomatic adults aged 45–84 with no clinical history of MI[33].

Translated to US epidemiology, of the approximately 805,000 myocardial infarctions occurring annually in the United States, ECG-based community surveillance suggests that roughly 170,000 (≈21%) are clinically silent or unrecognized at the time of occurrence — a figure consistent with ARIC and Framingham proportions[28][29][31]. Because CMR-based detection has identified more than twice as many UMIs as ECG in older community cohorts[30], the ECG-based extrapolation of 170,000 is best interpreted as a lower bound on the true annual burden of clinically unrecognized myocardial infarction in the United States.

7.3 Why some myocardial ischemia and infarction is silent: proposed mechanisms

The absence of pain during ischemia or infarction is multifactorial. Eight broad mechanisms have been proposed in the literature:

• Autonomic neuropathy. Afferent sympathetic and vagal fibers that transmit cardiac nociceptive signals can be damaged by diabetes mellitus, age-related autonomic neuropathy, or prior cardiac surgery, attenuating or eliminating the perception of ischemic pain[21].
• Higher pain threshold. Individuals vary substantially in baseline somatic pain thresholds, and a subset of patients with documented ischemia have demonstrably elevated thresholds for laboratory pain stimuli[34].
• Endogenous opioid and endocannabinoid systems. Circulating β-endorphin and related opioids are elevated in some patients with isquemia silenciosa and have been implicated in central modulation of cardiac pain perception[34].
• Exercise-induced hypoalgesia (EIH). Regular endurance training engages the endogenous opioid and endocannabinoid systems and is consistently associated with elevated pain thresholds and tolerances in laboratory testing[25][26]. In master athletes, EIH plausibly contributes to the absence of warning symptoms during demand-induced ischemia.
• Small infarct size and limited transmural extent. Small subendocardial or non-transmural infarcts may not generate sufficient afferent signaling to cross the threshold for conscious perception[32].
• Anatomic distribution. Inferior-wall ischemia and posterior-wall ischemia are more frequently silent than anterior-wall events, possibly due to differences in afferent innervation density[21].
• Collateral circulation. Chronic exercise promotes the development of coronary collateral vessels, which can maintain blood flow distal to a stenosis at rest and during low-to-moderate exertion, thereby preventing ischemia and pain until peak demand exceeds collateral capacity[27].
• Ischemic preconditioning. Repeated brief episodes of subclinical ischemia may protect the miocardio against subsequent insults and may also blunt afferent pain signaling[35].

7.4 Symptoms — and the absence of symptoms

By definition, classic exertional angina is absent in silent ischemia and unrecognized MI. However, the term silent is sometimes a misnomer. On careful retrospective questioning, a proportion of patients with apparently silent events describe subtle symptoms at the time — most commonly unaccustomed dyspnea, exertional fatigue out of proportion to workload, atypical chest discomfort attributed to indigestion or musculoskeletal causes, syncope or near-syncope, or unexplained reduction in exercise tolerance[21][22][32]. These so-called anginal equivalents are particularly important in master athletes, in whom dropping performance — rather than chest pain — may be the only clinical warning. When no symptoms are reported in any form, the event is genuinely asymptomatic and is detected only through screening, incidental imaging, or as part of a subsequent workup.

7.5 Prognosis

Silent ischemia and unrecognized MI are not benign. In long-term follow-up of the ICELAND-MI cohort, UMI detected by CMR was associated with mortality comparable to that of clinically recognized MI[30]. Across multiple cohorts, individuals with UMI carry elevated risks of insuficiencia cardíaca, recurrent MI, and muerte súbita cardíaca[29][30][31]. In endurance athletes specifically, the presence of ischemic-pattern LGE has been associated with markedly elevated risk of subsequent major adverse eventos cardíacos including sudden cardiac death[36].

7.6 Diagnosis

Diagnostic approaches differ for SMI versus UMI:

• For silent ischemia, the foundational modalities are ambulatory (Holter) ECG, exercise ECG, and stress imaging (stress echocardiography, single-photon emission CT, tomografía por emisión de positrones, or stress CMR perfusion)[21][22].
• For unrecognized MI, the resting ECG de 12 derivaciones has limited sensitivity, detecting only a fraction of CMR-confirmed events[30]. CMR with LGE is the most sensitive prueba no invasiva and is the reference standard for non-acute scar detection[30][36]. Echocardiographic regional wall-motion abnormalities and elevated high-sensitivity troponina in non-acute contexts may also raise suspicion.

7.7 Master-athlete-specific burden: the “masked athlete” phenomenon

In a seminal estudio transversal, Katzel and colleagues found that approximately 16% of male master athletes (mean age 60 years) had silent ischemia on a symptom-limited graded exercise test, a prevalence statistically comparable to that observed in sedentary controls of similar age[23]. Athletic status did not reduce the prevalence of ischemic burden; rather, it changed the perception of that burden. Combined with the EIH literature[25][26], these findings support the concept of the deportista enmascarado — an individual whose high cardiorespiratory fitness and elevated pain thresholds can defer the perception of ischemia until exertional demand approaches the limits of coronary supply.

CMR-LGE prevalence in master endurance athletes has been variably reported, ranging from approximately 11% in younger marathon runners to considerably higher figures in older endurance-athlete cohorts[37][38]. Ischemic-pattern LGE (subendocardial enhancement in a coronary distribution) and non-ischemic LGE (focal patchy enhancement at the right-ventricular hinge points or mid-myocardium) carry different mechanistic implications and different prognostic weights[36]. A sudden or unexplained decline in performance or in V̇O₂max in a previously stable master athlete should therefore be treated as a clinical red flag warranting consideration of advanced imaging.

8. Coronary Microvascular Dysfunction

Coronary microvascular dysfunction (CMD) is a plausible contributor to exercise intolerance in some older athletes, but the relevant evidence base in master-athlete cohorts is limited and findings should be described cautiously[39][40]. In a selected cohort of athletes with abnormal exercise tests but no obstructive epicardial CAD on angiotomografía coronaria, Foulkes and colleagues reported significantly lower reserva de flujo coronario (3.3 vs 4.2 in controls) and elevated endothelin-1 levels[39]. Several mechanisms have been proposed in athletes specifically, including the hypothesis of a possible “capillary-to-myocyte mismatch” in which training-induced hypertrophy outpaces microvascular expansion. These findings are best interpreted as preliminary and hypothesis-generating rather than as evidence that CMD broadly explains performance decline across the master-athlete population.

CMD may present with atypical features, including reduced capacidad de ejercicio, unusually elevated heart rates during submaximal effort, and exertional dyspnea rather than classic chest pain[40]. Diagnosis typically requires specialized testing (PET-based coronary flow reserve, invasive coronary physiology with bolus thermodilution, or stress CMR) available at experienced centers.

9. Screening and Risk Stratification in the Master Athlete

Given the high prevalence of subclinical CAD and silent ischemia in older athletes, traditional screening tools have important limitations. The resting 12-lead ECG, while valuable for detecting electrical disorders, has low sensitivity for ateroesclerosis subclínica[45]. Exercise treadmill testing in asymptomatic athletes is constrained by high false-positive rates[44]. Importantly, individual tests should be selected according to the clinical question being asked — anatomy, inducible ischemia, prior scar, or microvascular function — rather than by pooled performance metrics across these distinct domains.

Tabla 4. Cardiac diagnostic modalities in older master athletes, organized by the clinical question each test answers.

Modality	Primary question answered	Main strength	Main limitation
Resting 12-lead ECG	Electrical disease; prior Q-wave MI	Widely available baseline test	Low sensitivity for silent CAD or non-Q-wave prior MI
Exercise treadmill ECG	Exercise-provoked ECG abnormalities; symptom correlation	Functional provocation; reveals exercise BP response	Both false positives and false negatives are common in master athletes: the latter because high cardiorespiratory reserve and collateral flow may allow some athletes to maintain workload despite inducible ischemia until higher exercise intensities
Coronary CT angiography (CCTA)	Coronary anatomy; plaque burden and stenosis	Strong anatomic definition of plaque/stenosis	Does not directly establish inducible ischemia
Stress echocardiography / stress perfusion imaging (SPECT, PET, stress CMR)	Inducible ischemia	Functional assessment of ischemic burden	Performance depends on protocol and image quality
CMR with LGE	Prior infarction / scar / fibrosis pattern (UMI)	High tissue characterization value; gold standard for non-acute scar	Not a primary test for obstructive CAD
PET with coronary flow reserve	Inducible ischemia plus microvascular function	Useful for CMD assessment in specialized centers	Limited availability; higher complexity

Fuentes: refs [40][44][45]. CCTA = coronary CT angiography; CMR = cardiac magnetic resonance; LGE = late gadolinium enhancement; UMI = unrecognized myocardial infarction; CMD = coronary microvascular dysfunction; SPECT = single-photon emission tomografía computarizada; PET = positron emission tomography. The table is intentionally structured by clinical question rather than by pooled sensitivity/specificity, because tests answering different reference-standard questions are not directly comparable.

El estudio ISCHEMIA should not be summarized as proving that exercise capacity outweighs coronary anatomy or ischemia severity. A more defensible conclusion from the ISCHEMIA program is that, in stable chronic coronary disease, an initial invasive strategy did not produce an overall reduction in major cardiovascular events compared with an initial conservative strategy, and prognosis varied according to disease burden in pre-specified analyses[41][42]. The broader point that cardiorespiratory fitness is a strong predictor of mortality is robustly supported by cardiopulmonary exercise testing literature outside the ISCHEMIA program[43]. For master athletes, the practical implication is that a sudden or unexplained decline in performance or in V̇O₂max should be treated as a clinical signal warranting structured evaluation[47].

10. Sex Differences and the Female Master Athlete

A substantial portion of the master-athlete coronary literature is derived from male cohorts, including Master@Heart, which enrolled only men[15]. In female master athletes, CAC prevalence is generally lower than in male counterparts at the same age and training exposure, and the coronary phenotype associated with lifelong endurance training is less well characterized[48]. The 2020 ESC Sports Cardiology Guideline emphasizes individualized risk assessment in female master athletes, with attention to traditional risk factors, menopausal status, and exercise presión arterial response[47]. Generalizing male-cohort findings to female master athletes is inappropriate until parallel data are available.

11. Clinical Principles for the Aging Master Athlete

Current evidence supports individualized training and cardiovascular risk management rather than a single proven training formula for preventing coronary plaque in master athletes. Practical principles supported by primary literature and major-society guidance include:

• Maintain regular endurance activity at intensities and volumes appropriate to the individual, recognizing that detraining accelerates V̇O₂max decline beyond what biological aging alone produces[2][3].
• Incorporate entrenamiento de resistencia to help preserve muscle mass and function across the aging trajectory.
• Aggressively manage conventional cardiovascular risk factors — LDL-cholesterol or apolipoprotein B, lipoprotein(a) where available, blood pressure, glycemia, and tobacco exposure — in accordance with current prevention guidelines[45][49][50].
• Evaluate exaggerated exercise blood pressure responses, which are independently associated with higher coronary plaque burden in master athletes[18].
• Treat unexplained performance decline as a clinical signal warranting structured assessment, given the “masked athlete” phenomenon[23][25].
• Apply advanced imaging (CCTA, stress imaging, CMR with LGE) selectively, guided by clinical context, exercise findings, and conventional risk profile[47].

Polarized training distributions (commonly described as approximately 80/20 low- to high-intensity) may be useful performance optimization frameworks but have no been prospectively shown to prevent CAC accrual or to mitigate the so-called paradoja del atleta, and should not be presented as preventive prescriptions[51][52].

12. Synthesis and Discussion

12.1 Inevitable versus modifiable decay

The SPAF study confirms that the rise and fall of physical capacity is a constitutive feature of human life[1]. The age of peak performance and the acceleration of decline after age 40 appear largely invariant across populations. However, master athletes demonstrate that the absolute level of performance and the decadal rate of V̇O₂max loss are highly modifiable through maintenance of training volume and intensity[2][3][4].

12.2 Dominance of central factors

Between ages 50 and 80, the primary driver of performance decline in master athletes is central: a relentless decline in HR_máx. reduces total cardiac output during peak exertion, a limitation that even aggressive training cannot reverse[7]. Although athletes preserve stroke volume better than sedentary peers, age-related myocardial stiffening eventually restricts diastolic filling at high heart rates[10][11].

12.3 The pathological paradox

Lifelong endurance training appears associated with both favorable cardiovascular adaptation and an increased prevalence of subclinical coronary atherosclerosis in some observational cohorts[15][16][17]. The atherosclerotic burden — combined with the analgesic effects of exercise-induced hypoalgesia — makes silent ischemia and unrecognized MI clinically important risks that warrant individualized screening and management[23][25][26].

12.4 Peripheral mechanisms at the limit of human aging

As athletes approach age 80, peripheral extraction increasingly catches up to central factors as a determinant of V̇O₂max. Capillary rarefaction and mitochondrial decay reduce the muscle’s capacity to utilize delivered oxygen — an effect that is accelerated when training volume is reduced[2][9].

Key Clinical Takeaways

• Aerobic capacity declines along a curvilinear trajectory beginning in the mid-30s and accelerating in the 60s. Master athletes who maintain training reduce the rate of decline to roughly half that of sedentary peers; detraining accelerates decline several-fold. • Lifelong endurance training does not confer immunity to coronary atherosclerosis. Master@Heart and related cohorts show higher coronary calcium and proximal plaque burden in lifelong athletes than in sedentary peers; plaque morphology may be more favorable but does not abolish risk. • Silent ischemia and unrecognized myocardial infarction are not uncommon in older athletes. Approximately 1 in 6 male master athletes has inducible ischemia on graded exercise testing; CMR-detected scar in community cohorts exceeds ECG-detected scar by more than 2:1. • Symptoms may be absent, atypical, or expressed as performance loss. An unexplained decline in race times, exertional dyspnea, or reduced exercise tolerance in an older athlete should prompt structured cardiac evaluation — not reassurance. • Choose the diagnostic test to match the clinical question. Anatomy (CCTA), inducible ischemia (stress imaging), prior scar (CMR with LGE), and microvascular function (PET with CFR) answer different questions and are not interchangeable. • Standard cardiovascular risk-factor management remains the foundation. Aggressively manage LDL-C/ApoB, lipoprotein(a) where available, blood pressure (including exaggerated exercise responses), glycemia, and tobacco exposure. No training distribution has been prospectively shown to prevent CAC accrual. • Overall health benefits of lifelong exercise remain substantial. The clinical task is calibration of intensity, surveillance, and risk-factor control — not avoidance of training.

13. Conclusions

For master athletes between the ages of 50 and 80, maintenance of endurance performance requires a careful balance between sustained training (to preserve V̇O₂max and skeletal-muscle oxidative capacity) and individualized cardiovascular risk management. Transitioning from active to sedentary status produces a V̇O₂max decline substantially steeper than aging alone[2][3].

However, the deportista enmascarado concept warrants vigilance rather than complacency. Older endurance athletes may present with reduced performance capacity, exertional dyspnea, or other atypical symptoms rather than classic angina, and unexplained decline in performance should prompt structured clinical reassessment[23][25][47].

The available literature supports substantial overall health benefits of long-term exercise[43][53]. Some evidence suggests that the fenotipo de placa of lifelong athletes is shifted toward more calcified and fewer mixed/non-calcified lesions when matched for total plaque burden, which may confer relative stability compared with sedentary patients of equivalent CAC score[16]. Even granting that observation, however, the present evidence base does not justify claiming that coronary calcificación in master athletes is uniformly benign, or that mortality advantages persist regardless of plaque phenotype — CAC-stratified mortality data specific to master athletes remain limited. A more evidence-consistent conclusion is that lifelong exercise and subclinical coronary disease can coexist, that plaque morphology likely matters as well as plaque quantity, and that individualized risk assessment is essential in older athletes.

14. Limitations

This is a narrative review. No systematic search protocol or formal meta-analytic pooling was performed. The Master@Heart cohort and several other key coronary-imaging studies in lifelong endurance athletes are all-male, limiting generalizability to female master athletes. CAC-stratified mortality data specific to master athletes remain sparse, and the prognostic significance of non-calcified proximal plaques identified incidentally on CCTA in asymptomatic athletes is not yet established. The relevant CMD literature in master athletes is derived from small selected cohorts on referral and should not be generalized.

Disclosures and End-Matter

Conflicts of interest

The author reports no financial conflicts of interest related to the subject matter of this manuscript. The author is the operator of CuringHeartDisease.com, a clinician-educator platform that provides peer-reviewed cardiovascular health content without supplement marketing or commercial sponsorship.

Funding

No external funding, sponsorship, or institutional support contributed to the conception, drafting, or publication of this manuscript.

Data availability

No new datasets were generated for this narrative review. All cited evidence is contained in the published literature and is accessible through the cited references.

Ethics

Ethics approval and informed consent were not required because this manuscript is a review of previously published literature and does not report new human-subject research.

Prior dissemination

No version of this manuscript has been previously published or made publicly available in any venue, including preprint servers and the author’s educational platform. CuringHeartDisease.com is the intended publication venue.

Author contributions

PM conceived the manuscript, conducted the literature identification, drafted and revised the text, and approved the final version for publication.

Acknowledgments

The author thanks the external reviewers whose comments informed the present revision.

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