Environmental factors such as extreme temperatures, humidity, wind, pollution, altitude, and diving can significantly impact athletes’ cardiovascular systems, potentially hindering their performance, particularly in outdoor sports. The urgency of this issue is heightened by the increasing prevalence of climate change and its associated conditions, including fluctuating pollution levels, temperature variations, and the spread of infectious diseases. Despite its critical importance, this topic is often overlooked in sports medicine. This narrative review seeks to address this gap by providing a comprehensive, evidence-based evaluation of how athletes respond to environmental stresses. A thorough assessment of current knowledge is essential to better prepare athletes for competition under environmental stress and to minimize the harmful effects of these factors. Specifically, adaptative strategies and preventative measures are vital to mitigating these environmental influences and ensuring athletes’ safety.

Dyslipidemia is a major risk factor for atherosclerosis. Identification of dyslipidemia in athletes has raised interest in establishing preventive strategies and reducing cardiovascular (CV) events. Nowadays, targets or “scores” for athletes are undefined. The aim of our study was to create a “Lipid Athlete Score” based on lipid parameters and derive score indexes to identify high-risk athletes. We retrospectively enrolled 957 Olympic athletes practicing different sporting disciplines (power, skills, endurance, and mixed), analyzing their CV profiles and anthropometrics; 55.4% were male, the mean age was 27.1 ± 5 years, and the mean body mass index (BMI) was 23.1 ± 3.2 kg/m². Three hundred and forty-three athletes (35.8%) were dyslipidemic (LDL ≥ 115 mg/dL or LDL/HDL ≥ 1.90). Multivariate analysis revealed the following: male p = 0.001, OR 1.88 [0.41–2.51], familiarity for dyslipidemia p = 0.001, OR 2.82 [1.72–4.59], BMI ≥ 30 kg/m² p = 0.001, OR 2.53 [1.46–4.38], and fat mass p = 0.001, OR 2.29 [1.38–3.80] were significant. Endurance athletes presented the lowest CV risk. We proposed a lipid athlete score including major (LDL ≥ 115 mg/dL and LDL/HDL ≥ 1.90) and minor criteria (male, BMI > 30 kg/m² or fat mass >22% for males and 32% for females, familiarity for dyslipidemia, and conventional CV risk factors). Twelve athletes (1.2%) were at high risk, 150 athletes (15.7%) at medium risk, 171 athletes (17.9%) at low risk, and 624 (65.2%) were at no risk. Dyslipidemia is very common in elite athletes. We have defined a specific lipid athlete score based on lipid parameters and derived score indexes for the stratification of risk. In accordance with this tool, a substantial proportion of athletes (16.9%) were at medium-to-high risk and need early preventive strategies to improve their lipid profiles and reduce the future development of atherosclerotic CV diseases.

Background: Previous studies demonstrated that variations of fT3, even within the euthyroid range, can influence cardiac function. Our aim was to investigate whether thyroid hormones, even within the euthyroid range, are associated with the magnitude of exercise-induced cardiac remodeling in Olympic athletes. Methods: We evaluated 1342 Olympic athletes (mean age 25.6 ± 5.1) practicing different sporting disciplines (power, skills, endurance, and mixed). Athletes underwent blood testing (thyroid stimulating hormone, fT3, and fT4), echocardiography, and exercise-stress testing. Athletes taking thyroid hormones, affected by thyroiditis, or presenting TSH out of ranges were excluded. Results: The level of thyroid hormones varied according to the type of sporting discipline practiced: endurance athletes presented the lowest TSH (p < 0.0001), fT3 (p = 0.007), and fT4 (p < 0.0001) in comparison to the remaining ones. Resting heart rate (HR) was positively correlated to fT3 in athletes of different disciplines (power: p = 0.0002, R2 = 0.04; skill: p = 0.0009, R2 = 0.05; endurance: p = 0.007, R2 = 0.03; and mixed: p = 0.04, R2 = 0.01). The same results were seen for peak HR in the exercise-stress test in athletes engaged in power, skill, and endurance (respectively, p < 0.0001, R2 = 0.04; p = 0.01, R2 = 0.04; and p = 0.005, R2 = 0.02). Moreover, a positive correlation was observed with cardiac dimensions, i.e., interventricular septum (power: p < 0.0001, R2 = 0.11; skill: p = 0.02, R2 = 0.03; endurance: p = 0.002, R2 = 0.03; mixed: p < 0.0001, R2 = 0.04). Furthermore, fT3 was directly correlated with the left ventricle (LV) end-diastolic volume in skills (p = 0.04, R2 = 0.03), endurance (p = 0.04, R2 = 0.01), and mixed (p = 0.04, R2 = 0.01). Conclusions: Thyroid hormones, even within the euthyroid range, are associated with cardiac adaptive response to exercise and may contribute to exercise-induced cardiac remodeling.

Background: Various creatinine-based equations are used to estimate the glomerular filtration rate (eGFR) in athletes, but each has limitations. The aim of our study was to identify the most suitable formula for use in athletes. Methods: We evaluated 490 Olympic athletes (27 ± 5.3 yo) with normal values of serum creatinine and no history of kidney diseases. Athletes were divided into those practicing skills and endurance disciplines. The EGFR was calculated with Cockcroft–Gault (CG), MDRD, MCQE and CKD-EPI, and classified as stages G1–G5 according to the Kidney Disease Improving Global Outcomes (KDIGO) GFR categories. Results: Endurance athletes showed higher serum creatinine (0.91 ± 0.14 mg/dL vs. 0.88 ± 0.13 mg/dL in skills, p = 0.014). The eGFR calculated with the CKD-EPI and MCQE formulas showed no differences between the groups. The CG formula produced a lower eGFR for endurance athletes (113.6 ± 27 mL/min/1.73 m²) compared to skills athletes (122.6 ± 30.8, p = 0.008), while MDRD produced higher values for endurance athletes (129.3 ± 25.8 vs. 122.6 ± 24 mL/min/1.73 m², p = 0.004). According to CKD-EPI, all athletes were in G1, while with MCQE, 0.5% of skills athletes and 1% of endurance athletes were in G2. With the CG formula, a significant percentage of athletes were in G2 (13.2% of skills athletes and 18.5% of endurance athletes, p = 0.125). With the MDRD formula, 29 athletes (5.9%) were in G2 (6% for skills athletes and 5.8% for endurance athletes, p = 0.927). Conclusions: CKD-EPI and MCQE showed better stability and reliability, making them the most suitable for kidney function evaluation in athletes.

Atrial fibrillation (AF) is the most common sustained supraventricular arrhythmia, affecting 2–3% of the adult population and contributing significantly to morbidity, mortality, and healthcare burden. Catheter ablation has become a cornerstone in the treatment of symptomatic, drug-refractory AF, with pulmonary vein isolation (PVI) established as the standard approach, especially in paroxysmal AF. Over the past three decades, ablation technologies have evolved considerably—from radiofrequency and cryoballoon to the recent advent of pulsed field ablation—enhancing procedural safety, efficiency, and lesion durability. Despite these technological advancements, long-term outcomes have plateaued, suggesting that success may depend not just solely on the energy source used, but also on a more individualized, mechanism-based approach. The classification of AF based on duration alone fails to capture the complexity of its underlying pathophysiology. Tailored strategies that consider arrhythmic mechanisms, electrophysiological triggers, and patient-specific substrates—especially in persistent AF—are increasingly recognized as essential for durable results. Tools such as high-density mapping, autonomic modulation, and substrate-targeted ablation are expanding therapeutic horizons. Moreover, special populations, such as athletes, present unique arrhythmic profiles influenced by structural and autonomic remodeling, requiring nuanced management. The integration of lifestyle interventions, neuromodulation techniques, and emerging genetic and pharmacological insights further supports a comprehensive, personalized approach. In this paper, we explore whether future success in AF ablation lies more in refining technology or in advancing our understanding of arrhythmic mechanisms to guide patient-specific therapy.