The revised European consensus defined sarcopenia as a progressive and generalized skeletal muscle disorder that is associated with an increased likelihood of adverse outcomes including falls, fractures, physical disability and mortality. The aim of this study was to determine the prevalence of sarcopenia and analyse the influence of diet, physical activity (PA) and obesity index as risk factors of each criteria of sarcopenia. A total of 629 European middle-aged and older adults were enrolled in this cross-sectional study. Anthropometrics were assessed. Self-reported PA and adherence to the Mediterranean diet were evaluated with the Global Physical Activity Questionnaire (GPAQ) and Prevention with Mediterranean Diet questionnaire (PREDIMED), respectively. The functional assessment included handgrip strength, lower body muscle strength, gait speed and agility/dynamic balance. Of the participants, 4.84% to 7.33% showed probable sarcopenia. Sarcopenia was confirmed in 1.16% to 2.93% of participants. Severe sarcopenia was shown by 0.86% to 1.49% of participants. Male; age group ≤65 years; lower body mass index (BMI); high levels of vigorous PA; and the consumption of more than one portion per day of red meat, hamburgers, sausages or cold cuts and/or preferential consumption of rabbit, chicken or turkey instead of beef, pork, hamburgers or sausages (OR = 0.126–0.454; all p < 0.013) resulted as protective factors, and more time of sedentary time (OR = 1.608–2.368; p = 0.032–0.041) resulted as a risk factor for some criteria of sarcopenia. In conclusion, age, diet, PA, and obesity can affect the risk of having low muscle strength, low muscle mass or low functional performance, factors connected with sarcopenia.

Background: Frailty syndrome (FS) is one of the most common noncommunicable diseases, which is associated with lower physical and mental capacities in older adults. FS diagnosis is mostly focused on biological variables; however, it is likely that this diagnosis could fail owing to the high biological variability in this syndrome. Therefore, artificial intelligence (AI) could be a potential strategy to identify and diagnose this complex and multifactorial geriatric syndrome. Objective: The objective of this scoping review was to analyze the existing scientific evidence on the use of AI for the identification and diagnosis of FS in older adults, as well as to identify which model provides enhanced accuracy, sensitivity, specificity, and area under the curve (AUC). Methods: A search was conducted using PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) guidelines on various databases: PubMed, Web of Science, Scopus, and Google Scholar. The search strategy followed Population/Problem, Intervention, Comparison, and Outcome (PICO) criteria with the population being older adults; intervention being AI; comparison being compared or not to other diagnostic methods; and outcome being FS with reported sensitivity, specificity, accuracy, or AUC values. The results were synthesized through information extraction and are presented in tables. Results: We identified 26 studies that met the inclusion criteria, 6 of which had a data set over 2000 and 3 with data sets below 100. Machine learning was the most widely used type of AI, employed in 18 studies. Moreover, of the 26 included studies, 9 used clinical data, with clinical histories being the most frequently used data type in this category. The remaining 17 studies used nonclinical data, most frequently involving activity monitoring using an inertial sensor in clinical and nonclinical contexts. Regarding the performance of each AI model, 10 studies achieved a value of precision, sensitivity, specificity, or AUC ≥90. Conclusions: The findings of this scoping review clarify the overall status of recent studies using AI to identify and diagnose FS. Moreover, the findings show that the combined use of AI using clinical data along with nonclinical information such as the kinematics of inertial sensors that monitor activities in a nonclinical context could be an appropriate tool for the identification and diagnosis of FS. Nevertheless, some possible limitations of the evidence included in the review could be small sample sizes, heterogeneity of study designs, and lack of standardization in the AI models and diagnostic criteria used across studies. Future research is needed to validate AI systems with diverse data sources for diagnosing FS. AI should be used as a decision support tool for identifying FS, with data quality and privacy addressed, and the tool should be regularly monitored for performance after being integrated in clinical practice.

Childhood cancer survivors are at risk of developing important adverse effects, many of which persist for years after the end of treatment. The implementation of interventions aiming at attenuating tumor/treatment-associated adverse effects is therefore a major issue in pediatric oncology, and there is growing evidence that physical exercise could help in this regard. The present review aims to summarize the main milestones achieved in pediatric exercise oncology. For this purpose, we conducted a systematic review of relevant studies written in English in the electronic database PubMed (from inception to 14 August 2021). This review traces the field of pediatric exercise oncology throughout recent history based on three fundamental pillars: (i) exercise during childhood cancer treatment; (ii) exercise during/after hematopoietic stem cell transplantation; and (iii) exercise after childhood cancer treatment. Accumulating evidence––although still preliminary in many cases––supports the safety and potential benefits of regular exercise (with no major contraindications in general) in the childhood cancer continuum, even during the most aggressive phases of treatment. Exercise can indeed represent an effective coadjuvant therapy for attenuating cancer-related adverse effects.

Physical activity (PA) in the form of aerobic exercise (AE) preserves and improves neurocognitive function across the lifespan. However, a mechanistic understanding of the pathways by which aerobic exercise impacts brain health is still lacking, particularly with respect to stress-related pathways. One mechanistic hypothesis is that AE improves neurocognitive health in part by modifying circulating levels of stress-related hormones and signaling factors associated with the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS), as commonly measured by the biomarkers cortisol (CORT) and salivary α-amylase (sAA). Thus, this hypothesis predicts that changes in stress biomarkers, such as CORT and sAA, are possible explanatory pathways mediating the positive effects of AE on neurocognitive health. In the present review article, we provide a summary of available studies examining the possibility that exercise-induced changes to stress biomarkers could partly account for exercise-related improvements in neurocognitive health. Our review indicates that despite the intuitive appeal of this hypothesis, there is insufficient evidence available to conclude that chronic and habitual AE affects neurocognitive health by altering stress biomarker pathways. The cross-sectional nature of the majority of reviewed studies highlights the need for well-controlled studies to adequately test this hypothesis.

There is controversy about the relationship between ACE I/D polymorphism and health. Seventy-four healthy adults (n = 28 women; 22.5 ± 4.2 years) participated in this cross-sectional study aimed at determining the influence of ACE I/D polymorphism, ascertained by polymerase chain reaction, on cardiometabolic risk (i.e., waist circumference, body fat, blood pressure (BP), glucose, triglycerides, and inflammatory markers), maximal fat oxidation (MFO), cardiorespiratory fitness (maximal oxygen uptake), physical activity and diet. Our results showed differences by ACE I/D polymorphism in systolic BP (DD: 116.4 ± 11.8 mmHg; ID: 116.7 ± 6.3 mmHg; II: 109.4 ± 12.3 mmHg, p = 0.035) and body fat (DD: 27.3 ± 10.8%; ID: 22.6 ± 9.7%; II: 19.3 ± 7.1%, p = 0.030). Interestingly, a genotype*sex interaction in relativized MFO by lean mass (p = 0.048) was found. The DD polymorphism had higher MFO values than ID/II polymorphisms in men (8.4 ± 3.0 vs. 6.5 ± 2.9 mg/kg/min), while the ID/II polymorphisms showed higher R-MFO values than DD polymorphism in women (6.6 ± 2.3 vs. 7.6 ± 2.6 mg/kg/min). In conclusion, ACE I/D polymorphism is apparently associated with adiposity and BP, where a protective effect can be attributed to the II genotype, but not with cardiorespiratory fitness, diet and physical activity. Moreover, our study highlighted that there is a sexual dimorphism in the influence of ACE I/D gene polymorphism on MFO.

The present study aimed to investigate the effects of a 12-week concurrent training intervention on cardiometabolic health in obese men. Twelve obese men (42.5 ± 5.3 years old) participated in the current 12−week randomized controlled trial with a parallel group design. The participants were randomly assigned to a concurrent training group or to a no-exercise control group. Anthropometry and body composition assessment were determined by electrical bio-impedance. Blood samples were obtained and a cardiometabolic risk Z-Score was calculated. Energy metabolism-related parameters [i.e., resting metabolic rate (RMR), respiratory quotient (RQ), and substrate oxidation in both resting conditions and during exercise] were determined by indirect calorimetry. Echocardiographic studies were performed using an ultrasound system equipped with a transducer to measure cardiac function. A significant decrease of weight (Δ = −4.21 kg; i.e., primary outcome), body mass index (Δ = −1.32 kg/m²), fat mass (FM; Δ = −3.27 kg), blood pressure (BP; Δ = −10.81 mmHg), and cardiometabolic risk Z-Score (Δ = −0.39) was observed in the exercise group compared with the control group (allP< 0.05), while no significant changes were noted in waist circumference (WC), lean mass (LM), bone mineral content, glycemic and lipid profiles, liver function, nor in energy metabolism-related parameters (allP> 0.1). Moreover, a significant increment of left ventricular (LV) end diastolic diameter (Δ = −4.35 mm) was observed in the exercise group compared with the control group (P= 0.02). A 12-week concurrent training intervention is an effective strategy to induce weight and fat loss with simultaneous reductions of BP and cardiometabolic risk, and improving cardiac function in obese men.