Our cells and, therefore, our organism, need energy to function at their best, which is mainly produced by mitochondria. These intracellular organelles generate energy from food macromolecules across the Krebs cycle by oxidative phosphorylation. Energy is developed by converting adenosine triphosphate (ATP) to adenosine diphosphate (ADP). It is essential, for adequate mitochondrial energy production in the form of ATP, to have the right number of well-functioning mitochondria and the right amount of oxygen (O2) available. Unfortunately, the aging process and the chronic diseases that arise over the years are associated with a reduction in the number of mitochondria and their insufficient functioning. Among the chronic diseases related to significant damage of the arteries with a reduction in the supply of O2, there is atherosclerosis, where the process of atherothrombosis occurs. To keep our organs well-functioning despite aging, we must therefore protect our mitochondria and arteries. This can be achieved by intervening early in prevention with a lifestyle correction and diet integration with effective natural substances or, in some cases, with drugs. Among the many natural substances that have good scientific support, we have chosen four that have demonstrated benefits in the absence of side effects and that we know best: quercetin and pyrroloquinoline quinone to stimulate mitochondrial biogenesis and mitophagy, while L-arginine and nattokinase to protect the arteries from atherothrombosis.

Scientific evidence seems to indicate that, in males, intense and prolonged endurance sport can favor the onset of atrial fibrillation. A plausible explanation may be the impact that intense endurance sports produce on the three vertices of Coumel’s triangle. However, genetics is probably also involved in translating this impact into an arrhythmic phenotype. On a management level, the first task of the cardiologist is to exclude the presence of structural heart disease, channelopathy, endocrine and/or electrolyte disorders, and substance use. As for the treatment of arrhythmia, the “CARE” paradigm proposed by the latest ESC guidelines should probably be accompanied by detraining, although this suggestion is often rejected by the athlete. Anticoagulant therapy, where indicated, must take into account the risk of trauma that the sport entails, even if the particular pharmacodynamics/pharmacokinetics of DOACs should allow training/competition to take place when the anticoagulant effect of the previous administration has completely or almost completely worn off.

L-Carnitine (LC) is integral to energy production and fatty acid metabolism, facilitating the transport of long-chain fatty acids into mitochondria for β-oxidation. It modulates metabolic pathways, including pyruvate dehydrogenase activity, proteolysis, and protein synthesis, while also having anti-inflammatory and antioxidant characteristics. LC can be commonly applied to win the battle against HIV and cancer cachexia. Also, it can be recruited with the aim of improving physical and cognitive functions in athletes and the elderly. Despite these benefits, long-term LC administration has been associated to cardiovascular risks due its conversion to trimethylamine-N-oxide (TMAO) by the gut microbiota. Elevated TMAO levels are linked to atherosclerosis, oxidative stress, and an increased risk of cardiovascular disease, diabetes, and chronic kidney disease. Managing TMAO levels using dietary treatments and gut microbiota-targeting techniques, such as probiotics, may reduce these risks. This comprehensive review presents the state-of-the-art information on LC’s dual role, emphasizing the balance between its therapeutic potential and the risks of prolonged supplementation. It aims to guide clinicians and researchers in optimizing LC’s benefits while addressing its long term cardiovascular safety concerns.