It is an extremely urgent problem that physical fitness promotion must face not only the increasing air pollution but also the decline of physical activity level of children and adolescents worldwide at present, which is the major reason that forms an inactive lifestyle and does harm to adolescents’ health. Thus, it is necessary to focus on the exposure factor in environmental health risk assessment (EHRA) which conducts supervision of environmental pollution and survey of adolescents’ activity patterns according to the harmful characteristics of air pollutant and relationship between dose and response. Some countries, such as USA, Canada and Australia, regard both respiratory rate and physical activity pattern as main exposure factors for adolescents in both air pollution health risk assessment and exercise risk assessment to forecast a safe exposing condition of pollutant for adolescents while they are doing exercise outdoors. In addition, it suggests that the testing indexes and testing methods of these two exposure factors, such as investigating the time of daily physical activity, strength, and characteristic of frequency, help to set up the quantitative relationship between environmental pollution index and the time, strength, frequency of daily activities, and formulate children’s and adolescents’ activity instructions under different levels of environmental pollutions. As smog becomes increasingly serious at present, it is meaningful to take physical activity as a critical composition of exposure factor and establish physical activity guideline, so as to reduce the risk of air pollution, and promote physical health of children and adolescents effectively.

Resveratrol (RSV) has various pharmacological effects; however, few studies have directly addressed the possible antifatigue effects of long-term endurance exercise. The clinical use of RSV is limited by its poor water solubility and extremely short plasma half-life. Solid lipid nanoparticles (SLNs) are considered as reasonable drug delivery systems to overcome some of these drawbacks and expand its applications. In this study, RSV-SLNs were successfully prepared through emulsification and low-temperature solidification. Results showed that RSV-SLN supplementation effectively enhanced endurance performance. RSV-SLN supplementation might enhance mitochondrial function by ameliorating mitochondrial quality control (QC), which was superior to RSV application. These results revealed an unexpected role of RSV-SLN compared with RSV in terms of linking nutrient deprivation to mitochondrial oxidant production through mitochondrial QC. A mitochondrion-mediated pathway was likely involved in RSV-SLN, thereby improving endurance performance. Overall, this study highlighted new possibilities for anti-physical-fatigue strategies.

Background/Aims: The role of the β3-adrenergic receptor (β3-AR) agonist BRL37344 in atrial fibrillation (AF) structural remodeling and the underlying mechanisms as a therapeutic target were investigated. Methods: Four groups of dogs were evaluated: sham, pacing, β3-AR agonist BRL37344 (β3-AGO), and β3-AR antagonist L748337 (β3-ANT) groups. Dogs in the pacing, β3-AGO and β3-ANT groups were subjected to rapid atrial pacing for four weeks. Atrial structure and function, AF inducibility and duration, atrial myocyte apoptosis and interstitial fibrosis were assessed. Atrial superoxide anions were evaluated by fluorescence microscopy and colorimetric assays. Cardiac nitrate+nitrite levels were used to assess nitric oxide (NO) production. Protein and mRNA expression of β3-AR, neuronal NO synthase (nNOS), inducible NO synthase (iNOS), endothelial NO synthase (eNOS) and guanosine triphosphate cyclohydrolase-1 (GCH-1) as well as tetrahydrobiopterin (BH4) levels were measured. Results: β3-AR was up-regulated in AF. Stimulation of β3-AR significantly increased atrial myocyte apoptosis, fibrosis and atrial dilatation, resulting in increased AF induction and prolonged duration. These effects were attenuated by β3-ANT. Moreover, β3-AGO reduced BH4 and NO production and increased superoxide production, which was inhibited by the specific iNOS inhibitor, 1400w β3-AGO also increased iNOS but decreased eNOS and had no effect on nNOS expression in AF. Conclusions: β3-AR stimulation resulted in atrial structural remodeling by increasing iNOS uncoupling and related oxidative stress. β3-AR up-regulation and iNOS uncoupling might be underlying AF therapeutic targets.

The possible role of fatty acid translocase (CD36) in the treatment of obesity has gained increasing research interest since researchers recognized its coordinated function in fatty acid uptake and oxidation. However, the effect of CD36 deficiency on intracellular insulin signaling is complex and its impact may depend on different nutritional stresses. Therefore, we investigated the various effects of CD36 deletion on insulin signaling in C2C12 myotubes with or without palmitic acid (PA) overload. In the present work, we reported the upregulated expression levels of CD36 in the skeletal muscle tissues of obese humans and mice as well as in C2C12 myotubes with PA stimulation. CD36 knockdown using RNA interference showed that insulin signaling was impaired in CD36-deficient C2C12 cells in the absence of PA loading, suggesting that CD36 is essential for the maintenance of insulin action, possibly resulting from increased mitochondrial dysfunction and endoplasmic reticulum (ER) stress; however, CD36 deletion improved insulin signaling in the presence of PA overload due to a reduction in lipid overaccumulation. In conclusion, we identified differential roles of CD36 in regulating muscle insulin response under conditions with and without PA overload, which provides supportive evidence for further research into therapeutic approaches to diabetes.

Whether physical activity can offset the health risks of a pro-inflammatory diet is a compelling question, but it becomes conceptually misleading when interpreted as simple behavioral compensation. This narrative review integrates evidence on dietary inflammatory potential, movement-related physiological capacity, and chronic disease vulnerability, with particular attention to the Dietary Inflammatory Index, biological translation pathways, and emerging joint diet–activity evidence. Pro-inflammatory dietary exposure may be translated into disease vulnerability through immune activation, oxidative stress, adipose tissue inflammation, metabolic dysfunction, endothelial impairment, and gut-related inflammatory signaling. Habitual movement and exercise training may influence many of these same pathways through skeletal muscle signaling, improved insulin sensitivity, reduced visceral adiposity, redox adaptation, vascular regulation, and higher cardiorespiratory fitness. Taken together, current human evidence is more consistent with partial buffering and joint risk stratification than with full compensation. We therefore propose an Inflammatory Resilience Framework in which physical activity, cardiorespiratory fitness, skeletal muscle function, adiposity, metabolic flexibility, vascular function, and baseline health status are positioned as modifiers of the biological translation from dietary inflammatory exposure to disease vulnerability. This framework shifts the research question from whether exercise cancels dietary risk to how movement-related physiological capacity modifies inflammatory risk expression across individuals, pathways, and outcomes.

How physical activity may modify the health consequences of a pro-inflammatory diet remains an important but unresolved question. This hypothesis-generating narrative review examines this question by integrating evidence on dietary inflammatory potential, physical activity, physiological capacity, and inflammation-related health outcomes, and by proposing an Inflammatory Resilience Framework to guide future research. Current evidence strongly supports systemic inflammation, adiposity, insulin resistance, and vascular dysfunction as relevant pathways linking dietary inflammatory exposure to disease vulnerability, while redox- and gut-related mechanisms remain more indirect. Physical activity and higher physiological capacity may influence several of these pathways through metabolic, vascular, muscular, and inflammatory regulation. Preliminary human joint-association evidence suggests that physical activity may partially attenuate selected consequences of pro-inflammatory dietary exposure, but it does not establish a consistent modifying effect or full compensation. The proposed framework positions physical activity, cardiorespiratory fitness, skeletal muscle function, adiposity, metabolic flexibility, vascular function, and baseline health status as factors that may modify the association between dietary inflammatory exposure and disease vulnerability. Rather than asking whether exercise cancels dietary risk, the framework provides a testable structure for future studies integrating objective physical activity, fitness, physiological reserve, inflammatory and metabolic markers, and longitudinal interaction analyses to determine when, how, and in whom physical activity modifies diet-related inflammatory risk.