Mitochondrial damage is implicated as a major contributing factor for a number of noncommunicable chronic diseases such as cardiovascular diseases, cancer, obesity, and insulin resistance/type 2 diabetes. Here, we discuss the role of mitochondria in maintaining cellular and whole-organism homeostasis, the mechanisms that promote mitochondrial dysfunction, and the role of this phenomenon in noncommunicable chronic diseases. We also review the state of the art regarding the preclinical evidence associated with the regulation of mitochondrial function and the development of current mitochondria-targeted therapeutics to treat noncommunicable chronic diseases. Finally, we give an integrated vision of how mitochondrial damage is implicated in these metabolic diseases.

Among multiple mechanisms, low-grade inflammation is critical for the development of insulin resistance as a feature of type 2 diabetes. The nucleotide-binding oligomerization domain-like receptor family (NOD-like) pyrin domain containing 3 (NLRP3) inflammasome has been linked to the development of insulin resistance in various tissues; however, its role in the development of insulin resistance in the skeletal muscle has not been explored in depth. Currently, there is limited evidence that supports the pathological role of NLRP3 inflammasome activation in glucose handling in the skeletal muscle of obese individuals. Here, we have centered our focus on insulin signaling in skeletal muscle, which is the main site of postprandial glucose disposal in humans. We discuss the current evidence showing that the NLRP3 inflammasome disturbs glucose homeostasis. We also review how NLRP3-associated interleukin and its gasdermin D-mediated efflux could affect insulin-dependent intracellular pathways. Finally, we address pharmacological NLRP3 inhibitors that may have a therapeutical use in obesity-related metabolic alterations.

Caffeine is a popular ergogenic aid that has a plethora of evidence highlighting its positive effects. A Google Scholar search using the keywords "caffeine" and "exercise" yields over 200,000 results, emphasizing the extensive research on this topic. However, despite the vast amount of available data, it is intriguing that uncertainties persist regarding the effectiveness and safety of caffeine. These include but are not limited to: 1. Does caffeine dehydrate you at rest? 2. Does caffeine dehydrate you during exercise? 3. Does caffeine promote the loss of body fat? 4. Does habitual caffeine consumption influence the performance response to acute caffeine supplementation? 5. Does caffeine affect upper vs. lower body performance/strength differently? 6. Is there a relationship between caffeine and depression? 7. Can too much caffeine kill you? 8. Are there sex differences regarding caffeine's effects? 9. Does caffeine work for everyone? 10. Does caffeine cause heart problems? 11. Does caffeine promote the loss of bone mineral? 12. Should pregnant women avoid caffeine? 13. Is caffeine addictive? 14. Does waiting 1.5-2.0 hours after waking to consume caffeine help you avoid the afternoon "crash?" To answer these questions, we performed an evidence-based scientific evaluation of the literature regarding caffeine supplementation.

Overweightness and obesity can negatively influence many activities, including postural balance and locomotion, increasing predisposition to injury and risk of falls due to limitations on the biomechanics of daily living. The present study aimed to determine the influence of the anthropometric profile and physical activity level (PAL) on the postural balance of overweight and obese children. The sample included 387 schoolchildren (216 boys and 171 girls). The variables of the anthropometric profile studied were body mass, biped height, BMI, waist circumference, waist-to-hip ratio (WHR), summation of folds, body composition, and somatotype. PAL was measured using the PAQ-C questionnaire. Static and dynamic postural balance were measured through an open-eye (OE) and closed-eye (CE) posturographic test and the SEBTm, respectively. For static balance, the significant models were for mediolateral velocity (R² = 0.42 in OA; R² = 0.24 in OC), anteroposterior velocity (R² = 0.21 in OA; R² = 0.27 in OC), and mean velocity (R² = 0.27 in OA; R² = 0.46 in OC), where the predictors of low performance were younger age, male sex, overweight/obese nutritional status, greater thickness of skin folds, less tendency to mesomorphy, and greater fat mass. On the other hand, for dynamic postural balance, the significant models were observed in the previous direction (R² = 0.39), posteromedial (R² = 0.57), and posterolateral (R² = 0.56), where the variables that predict a low performance were low PAL, overweight/obese nutritional status, and high WHR. Overweight and obese children presented a deficit in static and dynamic postural balance, enhanced by variables such as gender, age, PAL, and anthropometric characteristics related to adiposity.