Editor comment: Focus on sport cardiology and exercise prescription

Exercise and competitive sports are linked to a wide range of health benefits, with the potential to leave a good community health legacy. The reputation of sports, on the other hand, is under assault from an ever-expanding arsenal of agents with actual or perceived benefits in performance improvement. Aside from the immorality of unfair advantage for dishonest athletes, performance-enhancing substances pose major potential health concerns. In fact, these medications can have an impact on the cardiovascular system by directly affecting the heart, vasculature, and metabolism. This impact is determined by the type of drug, the dose, the length of use, and the individual reaction to the substances, considering the wide range of responses. This Position Paper evaluated new material and serves as an update to the last Position Paper, which was released in 2006.1 The goal is to educate physicians, players, coaches, and individuals who participate in sports for health reasons about the negative cardiovascular consequences of doping drugs, routinely prescribed pharmaceuticals, and ergogenic aids when used in conjunction with sport and exercise. In the last few years, comprehensive assessment of low-molecular-weight compounds in bodily fluids for metabolic phenotyping has emerged as a viable approach for better understanding the processes underlying cardiovascular disease (CVD) and improving risk stratification. In this issue of the journal, the connections between physical activity (PA), metabolites, and atherosclerosis markers were evaluated in 2160 heart research participants, looking at the presence of any mediation effects.2 In a targeted metabolomic approach, 61 metabolites (amino acids and acylcarnitines) were quantified using liquid chromatography–tandem mass spectrometry. Intended athletic participation, but not daily PA, was associated with a reduced degree of atherosclerosis. Twelve amino acids, free carnitine, and five acylcarnitines were linked to PA. Eight of these metabolites were also linked to the degree of atherosclerosis. In the mediation analyses, a group of amino acids (arginine, glutamine, pipecolic acid, and taurine) were investigated as potential athero-protective mediators. In contrast, a set of carnitine metabolism members (free carnitine, acetyl carnitine, and octadecenoyl carnitine) were linked to inactivity and a larger atherosclerotic load. A recent paper states that PA before, during, and after cancer treatment can counteract the negative effects of therapies on the cardiovascular system. In addition, it can relieve symptoms such as nausea and fatigue and help prevent unwanted changes in body weight.3 In the current issue of the journal, a systematic review investigated the role of exercise in preventing cancer therapy-related cardiac dysfunction. Four databases were searched.4 Studies that assessed global longitudinal strain (GLS) or ejection fraction (EF) prior to and after any period of exercise intervention in breast cancer patients undergoing chemotherapy and were published in English from 2000 onwards were eligible for inclusion. Even though GLS and EF changes were similar in the exercising and non-exercising groups, the authors confirmed that exercise enhanced peak oxygen consumption. Cardiovascular disease and cancer are the two major causes of death worldwide. Although they are frequently regarded as separate entities, there is rising scientific interest in a putative link between the two, owing to common risk factors (such as cigarette use, obesity, and diabetes) and pathogenic mechanisms (chronic inflammation, free radical pathways). Treatment and malignancy-related factors contribute to this relationship. For example, there is a doubling of CVD risk in patients with clonal haematopoiesis, and childhood cancer survivors have a 2- to 12-fold risk of developing a myocardial infarction (MI), depending on the malignancy subtype. Here, Jain et al.5 explored the association between atherosclerotic CVD and the risk of cancer in 28 522 young adults with a history of premature CVD. They confirmed that premature CVD patients were more likely to be diagnosed associated with any type of cancer. This association remained consistent in multivariable models where it was significant for head and neck and genitourinary cancer. Exercise-based cardiac rehabilitation (exCR) improves aerobic capacity and outcomes in CVD individuals and is highly recommended: however the effects on overall mortality have long been a source of controversy. To address this issue, Ekblom et al.6 investigated the relationship between participation in exCR post-MI and total mortality in a nationwide real-world cohort from the SWEDEHEART registry. Out of 20 895 patients, 1000 individuals died throughout the course of an average of 4.55 years of follow-up. ExCR involvement was associated with significantly decreased overall mortality, and the results were unaffected by excluding individuals who had a shorter follow-up than 2 years. Furthermore, women’s risk decreased more than men’s. In post-MI patients, low- to moderate-intensity continuous training (MICT) has been demonstrated to be beneficial and is currently recognized as a safe and effective strategy for enhancing exercise capacity and avoiding adverse cardiac events. In recent years, there has been mounting evidence that high-intensity interval training (HIIT) may be more beneficial than MICT in increasing cardiorespiratory fitness. However, there is currently inadequate clinical evidence to support HIIT’s benefits in post-MI patients. In this review, Qin et al.7 investigated the effects of HIIT on post-MI patients: HIIT increased peak oxygen uptake (peak VO2) compared to MICT and/or routine PA. The occurrence of adverse events was comparable among groups. Physical activity can help you live longer by lowering your risk of death from any cause. Adults should engage in at least 150 min of moderate-intensity aerobic PA per week or 75 min of vigorous-intensity aerobic PA per week, according to expert guidelines. More survival advantages are obtained by continuing frequent PA as suggested throughout time. Maintaining a healthy body weight has also been linked to a higher chance of survival. As a result, keeping a healthy body weight and continuing to engage in regular PA are essential variables in enhancing survival. These two elements are inextricably linked. Weight gain is linked to future physical inactivity, and PA plays a crucial role in body weight regulation. However, it is unclear how maintaining body weight and keeping a regular PA interact, and only a few studies have looked at the combined effects of PA and body mass index on mortality. A study presented here aimed to elucidate whether continuing regular PA and maintaining body weight have interactions in terms of all-cause mortality risk.8 During a median 7.4-year follow-up, 91 347 people died out of a total of 6 572 984 people. Compared with the remaining active and stable weight group, most other groups had a higher mortality risk. The weight loss and remaining inactive groups and the weight gain and remaining inactive groups showed the highest mortality risk. Remaining active and maintaining a stable body weight had a synergistic effect on decreasing all-cause mortality risk. Chronic kidney disease (CKD) is associated with an increased risk of end-stage renal disease (ESRD), major adverse cardiovascular events (MACE), and mortality. Chronic kidney disease is characterized by increased oxidative stress, inflammation, and uraemic toxins, which result in skeletal muscle degeneration and atrophy. The latter promotes insulin resistance and visceral fat build-up, which increases the risk of CVD. Systemic inflammation, proatherogenic adipokines, and endothelial dysfunction have all been demonstrated to be reduced by regular PA. The majority of prior research in CKD patients supports the notion that PA is effective in lowering all-cause mortality. Nonetheless, the precise dose–response relationship between PA and mortality is unknown, as is the influence of PA on MACE. To fill this knowledge gap, Kuo et al.9 evaluated a longitudinal cohort of 4508 Taiwanese CKD patients between 2004 and 2017. Physical activity was assessed by a questionnaire and quantified in metabolic equivalent-hours per week (MET-h/week). During a median follow-up of 686 days, there were 739 deaths, 1059 ESRD, and 521 MACE episodes. The very active group had the lowest risk of all study outcomes, followed by the low-active and sedentary groups. Only the very active group was independently linked with decreased risks for all-cause mortality and MACE compared with the sedentary group. Interestingly, MACE risks were not reduced further if PA exceeded 15 MET-h/week, showing a U-shaped connection. Cardiopulmonary exercise testing (CPET) is a dynamic, non-invasive assessment of the cardiopulmonary system at rest and during exercise. Gas exchange measurements during exercise have been shown to improve decision-making in a variety of clinical settings, by providing functional capacity assessment, prognostic stratification, training prescription, treatment efficacy evaluation, diagnosis of causes of unexplained reduced exercise tolerance, and exercise pathophysiology evaluation in a wide range of clinical scenarios, from heart failure patients to athletes. In this issue of the journal, four papers are dedicated to this test. In their meta-analyses, Wadey et al.10 assessed the prognostic role of CPET among congenital heart disease patients, while Pane et al.11 showed the feasibility of upper limb CPET in assessing exercise tolerance in Friedreich ataxia patients. The interpretation and clinical use of CPET data necessitates the use of reference standards that define the usual range of exercise response. For this objective, general population-based reference criteria that account for the influence of age and gender on exercise physiology have been devised. However, normative CPET reference standards that are applicable to endurance athletes are lacking, so Petek et al.12 provided new externally validated VO2peak prediction equations for this group of athletes, incorporating age, gender, and height for both treadmill and cycle ergometer CPET. One of the most important CPET parameters is the anaerobic threshold (AT), which is used to estimate preoperative surgical risk and post-surgery need for critical care, as well as in the prognosis of chronic heart failure or respiratory patients, both for exercise prescription and training programme. During CPET, AT is often detected using one of three methods: the V-slope technique, the ventilatory equivalent method, or the end-tidal method. When a VO2 difference >15 mL/min is detected between the V-slope technique (meet AT) and the other two methods, a double threshold (DT) is present. Rovai et al.13 examined 476 healthy patients who performed CPET. Of those, 51 were found to have DT. Data from CPET at rest and during activity were not different between participants with DT and those without. Patients with DT had decreased carbon dioxide output (VCO2), end-tidal carbon dioxide tension (PetCO2), respiratory exchange ratio (RER), and greater ventilatory equivalent for carbon dioxide (VE/VCO2) when compared with subjects without DT. Conflict of interest: none declared.