The differentiation of the competitive athlete with physiologic cardiac remodeling from the athlete with cardiomyopathy

Henning, Robert J.

doi:10.1016/j.cpcardiol.2024.102473

Cited by 1 publication

(1 citation statement)

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“…If conditions like hypertrophic cardiomyopathy, dilated cardiomyopathy, or arrhythmogenic ventricular cardiomyopathy are not correctly diagnosed in athletes, it can lead to sudden cardiac arrest and death during training or sports competition. On the other hand, unnecessary restrictions on athlete training and competition can have disastrous consequences for the athlete [ 36 ].…”

Section: Reviewmentioning

confidence: 99%

Meldonium Supplementation in Professional Athletes: Career Destroyer or Lifesaver?

Pușcaș,

Buț,

Vari

et al. 2024

Cureus

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Meldonium is a substance with known anti-anginal effects demonstrated by numerous studies and human clinical trials; however, it does not possess marketing authorization within the European Union, only in ex-Soviet republics. Since 2016, meldonium has been included by the World Anti-doping Agency (WADA) on the S4 list of metabolic modulators. In performance athletes, meldonium is now considered a doping agent due to its capacity to decrease lactate production during and after exercise, its capability to enhance the storage and utilization of glycogen, and its protective action against oxidative stress. Together, these attributes can significantly improve aerobic endurance, cardiac function, and capacity as well as shorten recovery times (allowing higher intensity training), thereby enhancing performance. The purpose of this review is to highlight the most important mechanisms underlying the protective effect of meldonium against mitochondrial dysfunction (MD), which is responsible for oxidative stress, inflammation, and the cardiac changes known as "athletic heart syndrome." Meldonium acts as an inhibitor of γ-butyrobetaine hydroxylase (BBOX), preventing the de novo synthesis of carnitine and its absorption at the intestinal level via the organic cation/carnitine transporter 2 (OCTN2) and directing the oxidation of fatty acids to the peroxisomes. The decrease in mitochondrial β-oxidation of fatty acids leads to a reduction in lipid peroxidation products that cause oxidative stress and prevent the formation of acyl/acetyl-carnitines involved in numerous pathological disorders. Given the recent findings of the potentially detrimental effects of prolonged high-intensity exercise on cardiovascular health and coronary atherosclerosis, there may be legitimate arguments for the justification of the use of substances like meldonium as protective supplements for athletes.

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Section: Reviewmentioning

confidence: 99%