Sergey A. Bondarev

Endurance training induces significant cardiac remodeling, with evidence suggesting that prolonged high-intensity exercise may increase the risk of atrial fibrillation (AF). However, physiological responses differ by event type. This review compares AF-related markers in marathon and ultramarathon runners, focusing on structural adaptations, inflammatory and endothelial biomarkers, and the incidence of arrhythmias. A systematic analysis of 29 studies revealed consistent left atrial (LA) enlargement in marathon runners linked to elevated AF risk and fibrosis markers such as Galectin-3 and PIIINP. In contrast, ultramarathon runners exhibited right atrial (RA) dilation and increased systemic inflammation, as indicated by elevated high-sensitivity C-reactive protein (hs-CRP) and soluble E-selectin levels. AF incidence in marathoners ranged from 0.43 per 100 person-years to 4.4%, while direct AF incidence data remain unavailable for ultramarathon populations, highlighting a critical evidence gap. These findings suggest distinct remodeling patterns and pathophysiological profiles between endurance disciplines, with implications for athlete screening and cardiovascular risk stratification.

Ultramarathon running elicits a profound inflammatory response, characterized by significant increases in interleukin-6 (IL-6) and C-reactive protein (CRP), with comparatively modest changes in tumor necrosis factor-alpha (TNF-α). We reviewed approximately 80 field studies of ultramarathon events (distances >42.2 km) that measured IL-6, CRP, and TNF-α before and after races. IL-6 typically spiked immediately post-race—often rising dozens or even thousands of times above baseline—then rapidly declined, usually returning to near baseline within 24–48 h. CRP, an acute-phase protein, exhibited a slower, sustained elevation, peaking 24–72 h after race completion and remaining above baseline for 2–3 days before gradually returning to normal. TNF-α responses were variable: some studies reported small but significant post-race increases (roughly 1.2–1.7-fold above baseline), while others found no significant change in circulating TNF-α despite the extreme effort. Longer race durations and distances generally correlated with higher peak IL-6 and CRP levels. Experienced ultramarathon runners tended to exhibit attenuated inflammatory responses compared with less-trained individuals, and anti-inflammatory cytokines (e.g., IL-10) increased in tandem with IL-6 in well-trained athletes, helping to mitigate TNF-α elevations. In total, 28 studies were included in the final synthesis, and their quality was assessed using the Newcastle–Ottawa Scale. Visual synthesis tools, including a PRISMA flowchart and time course plots, are provided to enhance the narrative’s interpretability. In summary, ultramarathon running elicits a robust systemic inflammatory response with distinct temporal patterns for IL-6, CRP, and TNF-α. These findings have important implications for athlete recovery, monitoring, and understanding the physiological limits of the inflammatory response to extreme endurance stress.

Background: Sinus bradycardia and first-/second-degree atrioventricular (AV) block in athletes are traditionally considered secondary to increased vagal tone and therefore reversible. However, recent studies have suggested that they may persist even after the cessation of physical activity, and combined with the effects of aging, lead to the earlier onset of clinically significant bradyarrhythmias. Methods: We evaluated the correlation between lifetime sport practice and the age of the onset of premature (≤70 years old) idiopathic sinoatrial node or AV node dysfunction requiring pacemaker (PM) implantation. Results: Of the 1316 patients followed up with at our PM clinic in 2024, we included 79 (6%) who received a PM when they were ≤70 years old for bradyarrhythmias in the absence of secondary causes. Nineteen (24%) had engaged in at least 6 h of sports/week for ≥20 years and were classified as former athletes. For comparison, former athletes who received a PM for idiopathic bradycardia at >70 years old were 6% (p < 0.001). In the group ≤70 years old, the average age of PM implantation was 62.8 years in non-athletes versus 57.9 years in former athletes (p = 0.03). The main reason for PM implantation was AV block in both subgroups. Among former athletes, the correlation between the lifetime volume of sports activity and the age of PM implantation reached borderline statistical significance (p = 0.08). Echocardiography at the time of implant did not reveal significant differences between former athletes and non-athletes. Conclusions: In a cohort of patients who received a PM for bradyarrhythmia before the age of 70 years old in the absence of secondary causes, former athletes were implanted on average ≈5 years before non-athletes. This may suggest a contributing role of cumulative sports activity volume in the development of idiopathic sinus/AV node dysfunction.

Ventricular pre-excitation (VP) is a cardiac disorder characterized by the presence of an accessory pathway (AP) that bypasses the atrioventricular node (AVN), which, although often asymptomatic, exposes individuals to an increased risk of re-entrant supraventricular tachycardias and sudden cardiac death (SCD) due to rapid atrial fibrillation (AF) conduction. This condition is particularly significant in sports cardiology, where preparticipation ECG screening is routinely performed on athletes. Professional athletes, given their elevated risk of developing malignant arrhythmias, require careful assessment. Early identification of VP and proper risk stratification are crucial for determining the most appropriate management strategy and ensuring the safety of these individuals during competitive sports. Non-invasive tools, such as resting electrocardiograms (ECGs), ambulatory ECG monitoring, and exercise stress tests, are commonly employed, although their interpretation can sometimes be challenging. This review aims to provide practical tips and electrocardiographic clues for detecting VP beyond the classical triad (short PR interval, delta wave, and prolonged QRS interval) and offers guidance on non-invasive risk stratification. Although the diagnostic gold standard remains invasive electrophysiological study, appropriate interpretation of the ECG can help limit unnecessary referrals for young, often asymptomatic, athletes.

Athletes with heart disease are at increased risk of malignant ventricular arrhythmias and sudden cardiac death compared to their sedentary counterparts. When athletes have symptoms or abnormal findings at preparticipation screenings, a precise diagnosis by differentiating physiological features of the athlete’s heart from pathological signs of cardiac disease is as important as it is challenging. While traditional imaging methods such as echocardiography, cardiac magnetic resonance, and computed tomography are commonly employed, nuclear medicine offers unique advantages, especially in scenarios requiring stress-based functional evaluation. This article reviews the use of nuclear medicine techniques in the diagnostic work-up of athletes with suspected cardiac diseases by highlighting their ability to investigate myocardial perfusion, metabolism, and innervation. The article discusses the application of single photon emission computed tomography (SPECT) and positron emission tomography (PET) using radiotracers such as [99mTc]MIBI, [99mTc]HDP, [18F]FDG, and [123I]MIBG. Several clinical scenarios are explored, including athletes with coronary atherosclerosis, congenital coronary anomalies, ventricular arrhythmias, and non-ischemic myocardial scars. Radiation concerns are addressed, highlighting that modern SPECT and PET equipment significantly reduces radiation doses, making these techniques safer for young athletes. We conclude that, despite being underutilized, nuclear medicine provides unique opportunities for accurate diagnosis and effective management of cardiac diseases in athletes.

Background: Sinus bradycardia and first degree or second degree Mobitz type I atrioventricular (AV) block in an athlete are considered adaptive and reversible phenomena; however, some evidence suggests that they may persist after detraining and become pathological. The aim of the study was to investigate the characteristics of a group of former professional athletes who required pacemaker (PM) implantation for intrinsic (idiopathic) sinus node (SN) dysfunction or AV block in comparison to control groups of sedentary individuals. Methods: We included all patients who underwent PM implantation during 2022. Three groups were compared: group 1 including 18 former professional athletes who received a PM for SN dysfunction/AV block in the absence of heart disease; group 2 including the first 20 sedentary individuals without heart disease who underwent PM implantation; and group 3 including all other 323 patients who received PM, the majority with underlying heart diseases. Results: Compared to the non-athlete control group 2, the mean age at diagnosis and at the time of PM implantation of former professional athletes did not show statistically significant differences. However, subgroup analysis revealed significant differences depending on the type of sports discipline: the age at diagnosis and at PM implantation was significantly lower in former endurance athletes than former strength/mixed athletes, control non-athletes, and all other patients. Moreover, former endurance professional athletes exhibited a higher prevalence of second or third degree AV block (78%) as the reason for PM implantation compared to power/mixed athletes (44%). The other clinical characteristics, including echocardiographic parameters, did not differ between former athletes and non-athletes. Conclusions: Former professional endurance athletes with idiopathic SN dysfunction/AV block manifested the disease earlier in the life course compared to former power/mixed athletes and non-athletes. This suggests that bradycardia/AV block caused by intense and prolonged endurance sports may not always be benign and adaptive phenomena.

Polycystic ovarian syndrome (PCOS) can cause infertility in females due to hyperandrogenism and neuroendocrine abnormalities. The aim of this study is to decipher the impact of endocrine variables, hyperandogenism, insulin resistance, oxidative stress, and dietary conditions in PCOS conditions, subsequently to depict the role of epigenetic factors relative to phenotypic manifestations in PCOS conditions. We have reviewed several metabolic milieus pertinent to PCOS conditions. Comparative efficacies of various PCOS therapies, and recent clinical recommendations for the effective management of PCOS and role of metabolic/endocrine variables in PCOS conditions were described. Comparative therapeutic effects were vividly delineated according to the variable pathophysiology and internal variables during PCOS syndrome on the female body through the formation of cascade of endocrine pathology, which affects working capacity and fosters redox stress-induced cardiovascular, neural, and liver abnormalities. GLP-1 agonists, insulin sensitizers (metformin), and diet and exercise regimens efficacy were explained in enhancing the fertility outcomes among the overweight or obese females with PCOS. Comprehensive appraisal of DNA methylation as epigenetic changes and the manifestations of methylated genes in PCOS conditions were discussed particularly to screen novel molecular targets for developing efficient diagnostic indicators for predicting PCOS risk or its progression. Due to the reversible nature of epigenetic modifications, it is possible to screen the “druggable” regions to target or to correct abnormalities in the gene expression subsequently to develop chromatin-modifying therapies against PCOS.

Background — Recurrent upper airway obstruction during the sleep is a key feature of obstructive sleep apnea (OSA). In patients with OSA, an intermittent upper airway obstruction yields an increase in inspiratory effort and, consequently, an augmented impact on inspiratory muscles (IM). However, the issue of IM fatigue development in OSA patients is still controversial. Objective — to investigate the functional condition of IM in patients with OSA of various degrees of severity. Material and Methods — Were examined 82 men (30-65 years old), who were distributed among four groups depending on the OSA severity. Cardiorespiratory monitoring was performed to detect OSA. IM electrical activity was detected via surface electromyography (EMG) while holding the breath (during the inhalation). Results — In the course of our study, we detected a reduction in the frequency of EMG of accessory IM, specifically sternocleidomastoid muscle (SCMM) and external intercostal muscles (EIM), accompanied by a simultaneous increase in the amplitude of EMG of SCMM, EIM, and diaphragm (D), while holding the breath (during the inhalation), in the group of patients without OSA. In patients with mild OSA, when holding the breath during the inhalation, the frequency of EMG of SCMM and EIM decreased, while the amplitude of SCMM and EIM increased. In patients with moderate OSA, when holding the breath during the inhalation, a decrease in the frequency of SCMM EMG with a simultaneous increase in the amplitude of the EIM EMG were revealed. Same maneuver in the group of patients with severe OSA yielded no significant changes in the frequency and amplitude of EMG of respiratory muscles. Conclusion — Periodic obstruction of the upper airways with OSA leads to the development of fatigue resistance in accessory IM.