Bioenergetics has emerged as a critical lens for understanding health promotion and disease pathogenesis, thus offering potential biomarkers for various energy-related diseases and crafting innovative interventional strategies. This article comprehensively covers the significant role of bioenergetic processes in health, focusing on the systemic implications of cellular energy dynamics, such as adenosine triphosphate production, mitochondrial efficacy, redox balance, and metabolic adaptability. Through highlighting the complexity of these processes, this article underscores the collective impact on health, suggesting that deeper insight into bioenergetic flux can inform both diagnostic and therapeutic advancements. Moreover, this article explores how diets can modulate energy balance and bioenergetic flow, offering innovative approaches for health promotion through precision nutrition and food-based therapeutic strategies.

The integration of artificial intelligence (AI) in precision exercise nutrition is reshaping how athletes optimize their dietary intake for performance, recovery, and overall well-being. This article discusses the intersection of AI technologies in formulating precision nutrition strategies tailored to distinct physiological and metabolic requirements of athletes. AI-based mechanisms, such as real-time diet monitoring, continuous glucose monitoring, and nutrient optimization systems, offer unique insights into the impact of AI on advancing precision nutrition applications through the involvement in analyzing complex datasets, merging genetic, metabolic and environmental factors, thereby contributing precise dietary recommendations that adjust to evolving necessities of an athlete. However, the obstacles presented by AI in this domain, including ethical considerations, data confidentiality, and the necessity for uniformity across diverse populations are also confronted. By using AI, athletes can attain greater precision in their nutrition plans, ultimately enhancing exercise performance and promoting fatigue or injury recovery in ways that traditional methods cannot rival. This article further culminates with an address on future trends, emphasizing the role of AI in boosting precision nutrition engagement for athletes, even common exercise enthusiasts.

Oligospermia (OA) represents a significant contributor to male infertility, with a pressing need for effective and low-side-effect therapeutic strategies. This study aims to investigate the ameliorative effects of mangiferin (MG) on OA and its underlying molecular mechanisms. To this end, an OA rat model was induced using busulfan (BU), wherein the effects of MG on sperm quality, testis histopathology, and serum hormone levels were assessed. Furthermore, an in vitro model of testicular Sertoli cells was prepared using benzimidazole (DRB) to evaluate the impact of MG on cell viability and apoptosis. Integrative bioinformatics approaches predicted targets and pathways associated with MG, supplemented by molecular docking and validation experiments employing Western blot and RT-qPCR techniques to elucidate the regulation of the NLRP3-ASC-Caspase-1-GSDMD signaling pathway. Results demonstrated that MG significantly enhanced sperm quality and rescued testicular tissue damage in OA rats while restoring hormonal balance. In vitro experiments corroborated these findings by showing increased Sertoli cell viability and reduced apoptosis. Network pharmacology and enrichment analysis indicated that MG exerts its effects primarily by inhibiting NLRP3 inflammasome activation. Mechanistic investigations revealed that MG downregulated the expression of NLRP3, ASC, Caspase-1, and GSDMD, thereby suppressing pyroptosis while mitigating oxidative stress (lowering MDA and enhancing SOD) and inflammatory responses (reducing TNF-α and IL-1β). In conclusion, MG regulates cell pyroptosis via the NLRP3-ASC-Caspase-1-GSDMD axis, thereby mitigating oxidative stress and modulating the inflammatory microenvironment in OA, suggesting its potential as a promising therapeutic agent for male infertility.

Chronic diseases, with a focus here on non-cancerous conditions including cardiovascular, metabolic, neurological, and musculoskeletal disorders, as well as other relevant conditions, share pathological characteristics, such as persistent oxidative stress, reduced metabolic flexibility, and progressive tissue degeneration. Ferroptosis, an iron-dependent cell death triggered by lipid peroxidation, is now recognized as a critical factor in these pathological processes. Natural polyphenols, derived from plant sources, exhibit antioxidant and anti-inflammatory properties and demonstrate potential in regulating ferroptosis-related signaling pathways. This review systematically explores the molecular crosstalk between ferroptosis and polyphenols across major chronic diseases, highlighting their therapeutic and translational potential. Specifically, it elucidates the regulatory role of polyphenols in iron homeostasis, the inhibition of lipid peroxidation, and the restoration of redox balance, thus uncovering novel opportunities for dietary or pharmacological interventions targeting ferroptosis. Elucidating this interaction underscores the therapeutic potential of natural polyphenols as an innovative strategy for the prevention and treatment of chronic diseases.

Nutrigenomics is an emerging research field to investigate the interactions between food components and genes and elucidate their impacts on health and diseases. Exercise, another critical factor influencing human health, is intricately linked with nutrition and genetics, and is influenced by a combination of genetic background, lifestyle choice, and environmental factors. The high-throughput sequencing technologies and advanced bioinformatic tools have offered researchers to delve deeper into how individual genetic expression responses to exercise and how dietary interventions can enhance exercise performance and recovery through the gene expression changes and modifications. Among these mechanisms, gene expression emerges as the primary focus, highlighting its role in linking nutrients and exercise to metabolic pathways, muscle synthesis, and inflammation. While epigenetic modifications are briefly considered, the emphasis remains on how direct and indirect influences on gene expression drive physiological adaptations. Herein, the article reviews recent advancements in nutrigenomics within the context of exercise science, exploring gene-regulating mechanisms affected by specific nutrients and dietary patterns on exercise capacity, muscle synthesis, and damage repair. It also outlines the potential applications of personalized nutrition plans in athletic training and general fitness. In addition, this article addresses current challenges and potential issues in the practical implementation of nutrigenomics in exercise-induced health promotion. Future studies should emphasize interdisciplinary collaboration to unravel the intricate gene-nutrition-exercise interaction networks, thereby providing a solid theoretical foundation and technological support for the advancement of precision exercise nutrition.

Alzheimer’s disease (AD), a common aging-related neurodegenerative diseases, is an important inducement of cognitive, memory and mental disorders in the elderly. The major pathological characteristics of AD include amyloid β-protein (Aβ), neurofibrillary tangles, neuroinflammation, impaired autophagy, and mitochondrial dysfunction and decreased synaptic plasticity and function. The pharmacological treatment strategies for AD are focused on acetylcholinesterase inhibitors and N-methyl-D-aspartic acid (NMDA) receptor antagonists. However, most medications for AD can only alleviate symptoms, not substantially delay the development of AD. With the in-depth studies of natural products, it is found that resveratrol (RSV), which is an activator of silent mating type information regulation 2 homolog-1 (Sirt1), can activate autophagy in nerve cells, improve mitochondrial quality and inhibit neuroinflammation by regulating Sirt1-related signaling pathways, thereby having the potential prevent and treat AD. In this article, the studies on the role and mechanism of action of RSV in the prevention and treatment of AD are summarized, which will provide a reference for follow-up studies on RSV in the targeted prevention and treatments of AD, and the development of new anti-AD agents.

It is well known that appropriate aerobic exercise can effectively alleviate fatty liver and enhance brain function. The concept of multi-organ crosstalk coordinating disease progression has become the current research hot topic. However, there remains an urgent need to elucidate its specific mechanisms. This study aimed to explore the impact of a high-fat diet (HFD) on liver health and cognitive function, and to further uncover the regulatory effect of aerobic exercise by liver-specific activating transcription factor 3 (Atf3) knockout (ATF3^cKO) mice in a “liver-brain” axis mode. The 5-week-old C57BL/6 and ATF3^cKO mice were fed with HFD for 32 weeks, and sequentially subjected to aerobic exercise intervention at the 20^th week for another 12 consecutive weeks. Meanwhile, C57BL/6 mice were provided with a normal diet as the control group. The functional parameters of liver and brain of all mice were assessed. Cognitive capacity of all mice was assessed by the Morris water maze (MWM). Inflammatory factors in the serum and brain of mice were quantified using enzyme-linked immunosorbent assay (ELISA), and the expression of inflammasomes was detected by immunohistochemistry (IHC). Additionally, the activation of nuclear factor-κB (NF-κB) and phosphoinositide 3-kinase (PI3K) signal pathways was analyzed by Western blotting. In this study, HFD impaired hepatic and brain functions, while aerobic exercise and liver-specific Atf3 knockout suppressed inflammatory factors in the peripheral circulation through hepatoprotective mechanisms, thereby attenuating cerebral inflammation and preserving neurological integrity, as well as mitigating HFD-induced cognitive decline.

Obesity, caused by excessive energy, leads to body weight gain and various diseases, including cognitive impairment. Current studies suggest that diet restriction such as optimal fasting and regular exercise are crucial for improving cognitive capacity. However, further exploration is needed to understand the specific mechanisms of high fat diet (HFD)-induced cognitive decline in obesity. In the present study, 4-month-old mice were subjected to HFD feeding for 18 weeks, followed by aerobic exercise and high-intensity intermittent exercise, regular diet feeding, and intermittent fasting for 8 weeks, and then used to evaluate cognitive capacity, inflammation, compromised insulin signaling pathway, and apoptosis in hippocampal tissue, as well as AMPK/SIRT1 and TLR4 signal pathways. Obese mice revealed impaired cognitive capacity as compared with mice fed with regular diets. In contrast, aerobic exercise, high-intensity intermittent exercise, regular diet, and intermittent fasting could inhibit apoptosis caused by inflammation-mediated compromised insulin signaling pathway in hippocampal tissues through activating the AMPK/SIRT1 signal pathway and suppressing the TLR4 signal pathway, thereby rescuing the cognitive impairment of obese mice. Therefore, diet restriction and exercise interventions may play a positive role in reverting obesity-induced cognitive impairment.

Resveratrol (RSV), as a functional food component extracted from natural plants, has been widely studied and recognized in preventing and treating various diseases, with major mechanisms including executing anti-inflammation and anti-oxidation functions, and improving mitochondrial quality. Chronic diseases as non-communicable diseases are mainly caused by multiple factors, such as physiological decline and dysfunction in the body, and have become a significant challenge on public health worldwide. It is worth noting that chronic diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), muscle atrophy, cardiovascular disease, obesity, and cancer are accompanied by abnormal mitochondrial function. Therefore, targeted regulation of mitochondria may be a meaningful way to prevent and treat chronic diseases. Increasing evidence has confirmed that RSV is actively involved in regulating mitochondria, and it has become an essential consideration to prevent and treat chronic diseases through targeting mitochondria and improving corresponding functions. In this article, current studies on RSV to optimize mitochondrial quality for preventing and alleviating chronic disease are systematically summarized, which can provide a theoretical reference for the development of functional foods or drugs to combat chronic diseases.

Cases of foodborne doping are frequently reported in sports events and can cause severe consequences for athletes. The foodborne doping can be divided into natural endogenous and artificially added foods according to the sources, including anabolic agents, stimulants, diuretics, β-blockers, β2 agonists and others. In order to control foodborne doping, chromatographic technique, immunoassay, nuclear magnetic resonance, biosensor technology, pyrolytic spectroscopy, comprehensive analysis and electrochemical analysis have usually used as analytical and inspection strategies. Meanwhile, the legislation of anti-doping, the improvement of testing standard and technology, and the prevention and control of food safety, as well as the improvement of risk perception of athletes are highly necessary for achieving the effective risk control and supervision of foodborne doping, which will be beneficial for athletes, doctors and administrators to avoid the risks of foodborne doping test and reduce foodborne doping risks for the health of athletes.