Background: Sarcopenia is an age-related condition characterized by progressive loss of muscle mass, strength, and function. The occurrence of sarcopenia has a huge impact on physical, psychological, and social health. Therefore, the prevention and treatment of sarcopenia is becoming an important public health issue. Method: 35 six-week-old male C57BL/6 mice were randomly divided into five groups, one of which served as a control group, while the rest of the groups were constructed as a model of sarcopenia by intraperitoneal injection of D-galactose. The intervention with lactoferrin, creatine, and their mixtures, respectively, was carried out through gavage for 8 weeks. Muscle function was assessed based on their endurance, hanging time, and grip strength. The muscle tissues were weighed to assess the changes in mass, and the muscle RNA was extracted for myogenic factor expression and transcriptome sequencing to speculate on the potential mechanism of action by GO and KEGG enrichment analysis. Result: The muscle mass (lean mass, GAS index), and muscle function (endurance, hanging time, and grip strength) decreased, and the size and structure of myofiber was smaller in the model group compared to the control group. The intervention with lactoferrin and creatine, either alone or combination, improved muscle mass and function, restored muscle tissue, and increased the expression of myogenic regulators. The combined group demonstrated the most significant improvement in these indexes. The RNA-seq results revealed enrichment in the longevity-regulated pathway, MAPK pathway, focal adhesion, and ECM–receptor interaction pathway in the intervention group. The intervention group may influence muscle function by affecting the proliferation, differentiation, senescence of skeletal muscle cell, and contraction of muscle fiber. The combined group also enriched the mTOR-S6K/4E-BPs signaling pathway, PI3K-Akt signaling pathway, and energy metabolism-related pathways, including Apelin signaling, insulin resistance pathway, and adipocytokine signaling pathway, which affect energy metabolism in muscle. Conclusions: Lactoferrin and creatine, either alone or in combination, were found to inhibit the progression of sarcopenia by influencing the number and cross-sectional area of muscle fibers and muscle protein synthesis. The combined intervention appears to exert a more significant effect on energy metabolism.

The efficacy of functional lipids with antioxidant properties in reducing cardiovascular risk has not been consistent. Randomized controlled trials (RCTs) reporting estimates for the effects of antioxidant functional lipid supplementations on cardiometabolic risk factors were searched up to 1 May 2024. Overall, antioxidant lipid supplementations, compared with placebo, had favorable effects on systolic blood pressure (lycopene: −1.95 [−3.54, −0.36] mmHg), low-density lipoprotein cholesterol (n6 fatty acid: −0.39 [−0.71, −0.06] mmol/L; astaxanthin: −0.11 [−0.21, −0.01] mmol/L), high-density lipoprotein cholesterol (n3 fatty acid: 0.20 [0.13, 0.27] mmol/L; n6 fatty acid: 0.08 [0.01, 0.14] mmol/L; astaxanthin: 0.13 [0.05, 0.21] mmol/L), total cholesterol (n6 fatty acid: −0.24 [−0.37, −0.11] mmol/L; astaxanthin: −0.22 [−0.32, −0.12] mmol/L; beta-carotene: −0.13 [−0.23, −0.04] mmol/L), triglyceride (n3 fatty acid: −0.37 [−0.47, −0.28] mmol/L; astaxanthin: −0.46 [−0.83, −0.10] mmol/L), and fasting blood insulin (astaxanthin: −2.66 [−3.98, −1.34] pmol/L). The benefits of antioxidant lipid supplementations appeared to be most evident in blood pressure and blood lipids in participants with different cardiometabolic health statuses. Notably, n9 fatty acid increased triglyceride and hemoglobin A1C in the total population, which increases CVD risk. Antioxidant lipid supplementations ameliorate cardiometabolic risk factors, while their effect may depend on type and cardiometabolic health status. Long-term RCTs are needed to corroborate risk–benefit ratios across different antioxidant functional lipid supplementation settings.

Background: Durative exercise-induced fatigue influences muscle structure and exercise performance. Dietary supplements combining bioavailable proteins with essential vitamins and minerals may help reduce fatigue. Compared with proteins, whey peptides, as easily absorbed energy sources, are regarded as better promoting the utilization of vitamins and minerals. This study investigated whether the combination of whey peptides and micronutrients could synergistically improve exercise-induced fatigue and exercise performance. Methods: Four-week-old male C57BL/6J mice were forced to exercise using a treadmill for four weeks to evaluate the supplemental effects of whey peptides and/or micronutrients on exercise performance. Results: Compared with mice receiving whey peptides or micronutrients alone, mice receiving a combination of whey peptides and micronutrients displayed increased muscle mass, muscle fiber cross-sectional area, muscle strength, and exercise performance, including running exhausting time and swimming exhausting time. Consistent results were obtained in detecting fatigue-associated serum metabolites and markers reflecting muscle injury. To elucidate the anti-fatigue mechanisms of whey peptides and micronutrients, RNA transcriptome in the muscle tissues were analyzed. Enrichment analysis results suggest that micronutrients and/or whey protein alleviate exercise-induced fatigue, not only via reducing oxidative stress but also repressing excessive immune activation in muscle tissue, thereby decreasing the tissue injury caused by strenuous exercise. Conclusions: Overall, the current study indicates that the combination of whey peptides and micronutrients produces a synergistic effect on promoting exercise performance. Our findings provide scientific evidence for the development of novel and efficient anti-fatigue functional foods using whey peptides and micronutrients.

Sarcopenia is an age-related condition with a slow and prolonged decrease in muscular mass, strength, and function. As the population ages, the frequency of sarcopenia rises, and aggressive prevention methods and effective treatment options are in urgent need. Here, we explore the hypothesis that nutritional interventions can ameliorate skeletal muscle aging in mice affected by sarcopenia, and the aforementioned hypothesis was validated through histopathological characterization and behavioral experiments. The model group exhibited reduced muscle mass (Lean Mass, GAS Index), muscular strength (Maximum Limb Muscle Strength), and muscular function (Exhaustion Time, Inverted Grid Time), along with increased fat content and smaller myofiber size compared to the control group. Treatments with lactoferrin and CoQ10, both individually and in combination, enhanced muscle indices and facilitated muscle tissue regeneration, with the combined treatment showing the most significant improvement. Research further shows that Lactoferrin and CoQ10, whether administered alone or in combination, were discovered to restrain the progression of sarcopenia by inhibiting both protein metabolism and mitochondrial energy metabolism, and compared to groups treated with lactoferrin or CoQ10 alone, the combined treatment demonstrated varying degrees of improvement across all evaluated metrics, such as Lean Mass (2.273 ~ 5.365%), Fat Mass (−1.058 ~ −0.359%), GAS index (0.259 ~ 0.335%), Maximum Limb Muscle Strength (6.83 ~ 53.498 g), Inverted Grid Time (563 ~ 859 s), Exhaustion Time (386 ~ 468 s).

Background: Sarcopenia is an age-related disorder characterized by loss of muscle mass, strength, and function, driven by oxidative stress, chronic inflammation, and protein imbalance. Broccoli-derived peptides (BDP) exert anti-inflammatory and myofiber-protective effects, while leucine regulates energy metabolism and redox balance. Methods: We established a D-galactose aging mouse model and treated mice with BDP alone, leucine alone, or their combination for 8 weeks. Lean mass, muscle index, grip strength, endurance, and treadmill capacity were detected, and atrophic, disorganized myofibers were observed through histology. RNA-seq was applied to screen differential signaling pathways, and qPCR was used to verify related gene expression levels. Results: D-galactose caused marked deficits in lean mass, muscle index, grip strength, endurance, and treadmill capacity, accompanied by atrophic and disorganized myofibers. Single BDP or leucine partially reversed these deficits, but the combination produced the most robust improvements. RNA-seq revealed that BDP enriched actin, chemokine, and TNF pathways; leucine enriched Apelin and ECM pathways; while the combination uniquely regulated MAPK signaling. qPCR confirmed that co-administration optimally upregulated myogenic drivers (Myod1, Myog, Mef2c), suppressed catabolic/inflammatory mediators (Mstn, Tnf, Cxcl10), and restored metabolic/adhesive regulators (Sirt3, Aplnr, Icam1). Conclusions: BDP and leucine show superior efficacy in ameliorating sarcopenia, through multimodal regulation of multiple signaling pathways, offering a promising plant-based nutritional strategy against age-related muscle decline.