Search Results (268)

Background: Vitamins are micronutrients involved in multiple physiological processes critical for athletic performance. Because athletes are often exposed to increased oxidative stress, higher metabolic turnover, and greater nutritional demands, which can potentially lead to deficiencies in vitamins, understanding vitamin supplementation as a function of sport discipline is of fundamental importance. Methods: This narrative review synthesizes research findings from the past decade, supplemented with earlier studies where necessary, focusing on vitamins A, C, D, E, and the B-complex vitamins. Peer-reviewed literature was evaluated for evidence on the prevalence of deficiencies in athletes, physiological mechanisms, supplementation strategies, and their effects on performance, injury prevention, and recovery. Results: Vitamin D deficiency is highly prevalent among athletes, particularly in indoor sports and during the winter months. Supplementation has been shown to improve musculoskeletal health and potentially reduce injury risk. The antioxidant vitamins C and E can attenuate exercise-induced oxidative stress and muscle damage; however, excessive intake may impair adaptive responses such as mitochondrial biogenesis and protein synthesis. Vitamin A contributes to immune modulation, metabolic regulation, and mitochondrial function, while B-complex vitamins support energy metabolism and red blood cell synthesis. Conclusions: Vitamin supplementation in athletes should be individualized, targeting confirmed deficiencies and tailored to sport-specific demands, age, sex, and training intensity. Dietary optimization should remain the primary strategy, with supplementation serving as an adjunct when intake is insufficient. Further high-quality, sport-specific, and long-term studies are needed to establish clear dosing guidelines and to assess the balance between performance benefits and potential risks associated with over-supplementation. Full article

Iron is an essential trace element that participates in multiple physiological processes, including oxygen transport, electron transfer, DNA synthesis, and red blood cell production. Iron loss is particularly severe among athletes, so maintaining iron homeostasis is crucial for sports nutrition and health. Excess iron, iron deficiency, and ferroptosis can lead to muscle disorders and health issues, including sarcopenia, muscular atrophy, myocardial fibrosis, skeletal muscle injury, cardiovascular disease, and metabolic disorders. Maintaining iron homeostasis within physiological limits is essential for athletes to sustain high-intensity performance and accelerate recovery. Therefore, a comprehensive review of the effects of iron homeostasis and ferroptosis on muscle health is significant for identifying potential therapeutic targets and developing new disease treatment and prevention strategies. This paper systematically reviews research progress on targeted therapies for iron overload and ferroptosis in muscle diseases, clarifies the impact of iron on athletes’ physiological functions and competitive performance, and explores the potential application of iron in precision nutritional regulation. It aims to provide new insights for preventing exercise-induced muscle injury, myocardial damage, and overtraining syndrome in athletes. Full article

Exercise-induced fatigue involves oxidative stress and metabolic dysregulation. While the anti-aging protein α-Klotho regulates metabolism and oxidative stress, its role in exercise fatigue is unexplored. This study investigated whether α-Klotho supplementation mitigates cumulative exercise-induced fatigue and elucidated the underlying tissue-specific mechanisms. Male C57BL/6J mice were divided into three groups (n = 10 per group), the control group, fatigue treated with saline, or α-Klotho (0.2 mg/kg, i.p. daily) group. Fatigue was induced by a 6-day exhaustive swimming protocol (5% body weight load). Tissues were collected 24h post-final exercise. Assessments included daily exhaustion time, grip strength, serum creatine kinase (CK), urea nitrogen (BUN), oxidative stress markers (H₂O₂, MDA, SOD, GSH/GSSG), tissue glycogen, and pathway protein expression (Western blot). α-Klotho supplementation prevented exercise-induced weight loss and restored grip strength. While exhaustive exercise markedly increased serum CK and BUN levels, α-Klotho selectively normalized CK without effecting serum BUN. α-Klotho attenuated oxidative damage by reducing hydrogen peroxide levels while enhancing antioxidant capacity, accompanied by activation of the NRF2/HO-1 pathway and further upregulation of PGC-1α. Notably, α-Klotho induced striking hepatic glycogen supercompensation through activation of the AKT/GS signaling pathway and upregulation of GLUT4, whereas muscle glycogen levels remained unchanged. In conclusion, α-Klotho ameliorates cumulative exercise-induced fatigue through dual recovery-phase mechanisms: NRF2/HO-1-mediated antioxidant protection in skeletal muscle and AKT/GS-triggered hepatic glycogen supercompensation, thereby facilitating oxidative stress resolution and enhancing energy reserve restoration. Full article

Astaxanthin (AX), a naturally occurring xanthophyll carotenoid, has attracted growing scientific interest due to its potent antioxidant, anti-inflammatory, and metabolic-regulatory properties. This review provides a critical appraisal of the current evidence regarding the nutraceutical potential of AX in muscle metabolism, exercise adaptation, and obesity management. Preclinical and clinical findings indicate that AX enhances lipid utilization, promotes mitochondrial biogenesis through AMPK activation, and improves endurance and muscle strength, particularly among older adults. Moreover, AX mitigates exercise-induced oxidative stress and muscle damage, thereby supporting recovery and physiological adaptation. In obesity models, AX reduces adipose tissue inflammation, improves insulin sensitivity, and modulates adipokine secretion, suggesting a multifaceted role in metabolic syndrome prevention. Despite robust preclinical data, human trials remain limited and often yield inconsistent outcomes, highlighting the need for well-designed, long-term clinical studies. Emerging evidence highlights the importance of optimized delivery strategies to enhance AX bioavailability and mitochondrial targeting. Nanoemulsions, liposomes, and lipid-based carriers improve stability, absorption, and tissue distribution, thereby potentiating AX’s effects on mitochondrial function and exercise adaptation. Overall, AX emerges as a promising nutraceutical candidate for enhancing muscle function, supporting exercise performance, and managing obesity-related metabolic disease, with delivery innovations representing a critical frontier for future translational applications. Full article

The present study examined the prophylactic effects of far-infrared-emitting fabric (FIR) on exercise-induced muscle damage and investigated its influence on neuromuscular parameters during eccentric exercise. FIR and placebo garments were worn for 1 h prior to and throughout a knee extension eccentric exercise protocol consisting of 10 sets of 15 maximal contractions performed at 210°·s⁻¹, using a randomized, counterbalanced, double-blind, placebo-controlled crossover design. Twenty-one physically active individuals (age: 24 ± 1 years; body mass: 69.7 ± 2.3 kg; height: 1.73 ± 0.02 m) participated in this two-phase study. In the first phase (FIR effects on muscle damage; n = 9), eccentric peak torque (EPT) and total work (TW) were assessed during exercise, while maximal voluntary isometric contraction (MVIC) and creatine kinase (CK) were measured before and 24, 48, and 96 h after the protocol. No fabric × time interaction was observed for MVIC or CK. However, FIR use suggested an increased EPT and TW during exercise. To further investigate this effect and explore potential neuromuscular mechanisms, a second phase was conducted (FIR effects on eccentric exercise; n = 12) using the same exercise protocol. EPT, TW, and electromyographic root mean square (EMG-RMS) activity of the vastus lateralis (VL) and vastus medialis (VM) were assessed. Combined results from both phases (n = 21) demonstrated significant increases of 11% in mean EPT and 18.6% in mean TW, along with greater VL and VM EMG-RMS activity (n = 12), under FIR compared with placebo conditions. These findings indicate that FIR use enhances neuromuscular performance during eccentric exercise. Full article

Exercise-induced muscle damage (EIMD) is characterized by structural muscle tissue damage and elevated biochemical markers following high-intensity or unaccustomed exercise. This study evaluated the utility of a small animal grip strength measurement device as a model for EIMD. Thirty-four male mice were divided into four groups: one control and three experimental groups, and sacrificed at 2, 4, and 7 days post-exercise. The exercise protocol involved 50 tail-pull contractions at 60 Hz using a forelimb grip strength device. Biochemical biomarkers, inflammatory gene expression, and oxidative stress markers from blood and muscle tissue were assessed at each sacrificial time point. Muscle damage marker, plasma aldolase activity, showed significant elevation at 4 days post-exercise (p < 0.01). Inflammatory gene expression in triceps brachii showed no significant changes. Oxidative stress analysis revealed significantly decreased biological antioxidant potential (BAP) at 7 days and a trend toward a significant increase in Diacron-reactive oxygen metabolites (d-ROMs) at 4 days. NF-kB expression showed a trend toward significance increase. The grip strength exercise model induced modest biochemical alterations suggesting possible involvement of oxidative stress. The early release of aldolase and subsequent oxidative stress suggest that this model replicates EIMD and may serve as a valuable tool for quantitative loading on muscles, studying EIMD mechanisms and facilitating EIMD-based interventions. Full article

(1) Background: This study aims to explore the changes in urinary metabolomic profile among trained young males following acute intermittent rowing training (AIRT), and to identify potential urinary biomarkers associated with exercise-induced muscle damage (EIMD). (2) Methods: 22 trained young males were recruited to perform AIRT. The changes in blood biochemical indexes associated with EIMD were analyzed. EIMD occurrence was evaluated using blood biochemical indexes, muscle function, and pain assessment. The changes in urinary metabolites were determined using untargeted metabolomic analysis. (3) Results: Four blood biochemical indices, including creatine kinase, lactate dehydrogenase, creatine kinase-MB, and hydroxybutyrate dehydrogenase, were significantly elevated immediately after AIRT. Furthermore, an obvious immune response appeared, and countermovement jump performance significantly decreased. Among 384 urinary metabolites, 33 were significantly upregulated, and 12 were downregulated immediately after AIRT. Upregulated metabolites were mainly involved in phenylacetate metabolism, ammonia recycling, the urea cycle, and glutathione metabolism. Four potential urinary biomarkers were identified, including 2′-Deoxycytidine, cytosine, Phenylacetaldehyde, and Pyridoxamine. (4) Conclusions: AIRT induced EIMD in all participants and significantly altered urinary metabolite profiles. The changes in urinary metabolites and pathways were due to the metabolic adaptation to oxidative stress, inflammatory responses, and ammonia metabolism imbalance. The selected four potential urinary biomarkers provide important evidence for the further development of a non-invasive, urine-based method for the immediate assessment of EIMD. Full article

Various non-pharmacological practices have been reported to enhance overall health. The molecular effects of exercise have been shown to involve the upregulation of enzymes and transcription factors that enhance antioxidative and anti-inflammatory activity, boost mitochondrial function and growth, and promote a parasympathetic tone. These beneficial changes occur as an adaptive/hormetic response to an initial increase in oxygen radical and nitric oxide production in working muscles. The redox-sensitive nuclear factor erythroid 2-related factor 2 (Nrf2) was identified as the key mediator of the cellular defense response. A similar adaptive response appears to occur in response to exposure to heat or cold, hyperbaric or hypobaric oxygen, cupping therapy, acupuncture, caloric restriction, and the consumption of polyphenol-rich plant-based foods or spices, and there is direct or indirect evidence for the involvement of Nrf2. In many cases, additional stress signaling pathways have been observed to be upregulated, including the nicotinamide adenine dinucleotide (NAD+)-sirtuin and the adenosine monophosphate (AMP)-activated protein kinase pathways. We conclude that while several traditional health practices may share a hormetic mechanism—mild radical-induced damage triggers a defense response through upregulation of antioxidative, anti-inflammatory, and repair activities, which may impact body-wide tissue function. Full article

Exercise and physical training induce diverse physiological responses that can be modulated by functional foods. This article examines how different exercise models—from moderate exercise to intense training—can be applied to evaluate food functionality in preventing inflammation, oxidative stress, and enhancing athletic performance. We discuss the paradoxical nature of exercise, where moderate physical activity promotes health through anti-inflammatory and antioxidant effects, while intense exercise can induce muscle damage, inflammation, and immunosuppression. Through analysis of recent research, including studies on polyphenols, amino acid derivatives, and novel delivery systems, we highlight the importance of appropriate exercise model selection, timing, and dosage of nutritional interventions. Emerging approaches such as nano-processed compounds, gut microbiota modulation, and synergistic combinations offer promising strategies. This review provides guidance for researchers and practitioners in selecting suitable exercise models to evaluate functional foods, emphasizing the need for personalized approaches that balance performance enhancement with health protection. Full article

Dietary supplementation is commonly used by athletes to gain muscle mass, enhance performance, and improve recovery. Most adults engage in insufficient physical activity. Yet healthy muscles are also critical for activities of daily living (ADLs), maintaining a good quality of life and positive ageing. There is growing interest in whether dietary supplementation is of value, particularly among subgroups such as the occasionally active, the ill and elderly, and peri- and menopausal women. By focusing on function, performance, mass and strength, ADLs, exercise-induced muscle damage and delayed onset muscle soreness, this review sought to examine muscle health through a nutritional lens. Further, to look at the potential benefits and harms of some commonly proposed dietary supplements in non-athlete adults, while exploring the emerging role of the gut–muscle axis. Inflammation appears central to cellular events. Several supplements were identified that, alone or in combination, may help optimise muscle health, particularly when combined with exercise or where a deficit may exist. Although supportive evidence is emerging, real-world clinical benefits remain to be substantiated. Though dietary supplements are generally safe, their regulation is less stringent than for medicines. Adherence to recommended dosage, seeking medical advice regarding possible side effects/interactions, and obtaining supplies from reliable sources are recommended. Full article

Purpose: The primary aim of this study was to determine the efficacy of acute fish oil (FO) supplementation on indices of exercise-induced muscle damage (EIMD) in young healthy adults. Methods: Twenty-two healthy young male and females were randomly assigned to two experimental groups: fish oil (FO) or placebo control (CON). Participants performed a muscle damage protocol consisting of 10 sets of 10 plyometric drop jumps. Vertical jump height, isometric maximal voluntary contraction (MVC) torque, and systemic inflammation markers were assessed at pre-exercise, immediately post (post-0), post-24, post-48, and post-72 h. Results: Vertical jump performance and quadriceps peak torque significantly decreased in the CON group at post-0, 24, and 48 h (p < 0.05), while FO group recovered to baseline levels by post 48 h. Hamstring peak torque reductions recovered in the FO group at post-48 h but remained suppressed in the CON group until post-72 h (p < 0.05). Muscle soreness was significantly higher in the CON group compared to the FO group at post-48 h (p < 0.05). Systemic TNF-α levels significantly increased from baseline to post-0, 24, and 48 h in both groups (p < 0.05), with the CON group showing a trend toward incomplete recovery (p = 0.065). Conclusions: Our findings indicate that acute FO administration may modestly aid muscle recovery and reduce muscle soreness following EIMD in healthy young adults while the overall impact may be limited. Full article

Objectives: This study assessed the influence of oral and topical sodium bicarbonate (SB) on recovery and soccer-specific performance after exercise-induced muscle damage (EIMD). Methods: In a randomized, double-blind, placebo-controlled, parallel group design, 24 soccer players were allocated to oral SB, topical SB (PR Lotion, Momentous), or placebo (PLA) (n = 8 per condition) and attended six laboratory sessions: (i) familiarization, (ii) baseline measures, and (iii) four experimental trials on consecutive days. Muscle damage was induced on day 1 using 40 × 15 m sprints, after which either 0.3 g·kg⁻¹ body mass (BM) SB (SB-ORAL), 0.9036 g·kg⁻¹ BM PR Lotion (SB-LOTION), or an equivalent PLA was given. Recovery outcomes were measured post-EIMD, 1 d, 2 d, and 3 d post (day 1–4). Soccer-specific performance was repeated 3 d post, with supplements administered again 2 h pre-exercise. Recovery measures included muscle soreness, vertical jump height, and maximal voluntary isometric contraction. Illinois agility test (IAT), 8 × 25 m repeated sprints, and Yo-Yo Intermittent Recovery Test Level 2 (Yo-Yo IR2) were assessed as soccer-specific performance. Results: Neither SB-ORAL nor SB-LOTION accelerated indices of recovery but decline in soccer-specific performance from baseline to 3 d post was attenuated for SB-ORAL, with significant effects for IAT (p = 0.032, g = 1.69) and Yo-Yo IR2 (p = 0.026, g = 1.61) compared with PLA. Conclusions: SB did not accelerate recovery following EIMD but prescribing oral SB before subsequent exercise might rescue key performance indicators. These findings offer implications for practitioners working with soccer players during periods where full recovery is not achieved. Full article

Light therapy has been shown to produce several beneficial physiological effects in a wide range of tissues. The musculoskeletal system can be irradiated with deeply penetrating wavelengths in near infrared (NIR) regions. Photobiomodulation therapy (PBMT) reduces pain and inflammation and enhances physical performance. However, the mechanism(s) of cellular responses to PBMT in muscle is not clearly understood. Therefore, the goal of this study is to improve our understanding of the mechanism(s) of action of PBMT effects in exercised and sedentary muscle. In sedentary mice, PBMT using a wavelength of 830 nm increased the gene expression for muscle tissue development, including cFos, which is critical for activating interstitial and satellite cells that repair muscle. Immunostaining for cFOS expression confirmed an increase in the number of activated cells in PBMT-treated muscle. We observed that PBMT-treated mice showed increased performance on the treadmill, reduced muscle fiber damage, and altered mitochondrial structure. RNA sequencing from fatigued TA tissue suggested that PBMT treatment increased the gene expression of tissue regeneration and remodeling, suggesting tissue adaptation and muscle repair after exercise with PBMT. In conclusion, our study suggests that the 830 nm wavelength may have altered the muscle by activating regenerative genes that protect the tissue from exercise-induced cellular stress. Full article

Cisplatin is a widely used chemotherapy drug for the treatment of various cancers; however, its clinical use is often accompanied by skeletal muscle atrophy, which not only impacts patients’ physical health but also significantly diminishes their quality of life. The mechanisms underlying cisplatin-induced muscle atrophy are complex and involve a series of molecular biological processes, including oxidative stress, inflammation, protein degradation, and muscle cell apoptosis. Recent studies have suggested that exercise intervention can significantly alleviate cisplatin-induced muscle damage by modulating exercise-induced myokines. Myokines, such as muscle-derived cytokines (e.g., IL-6, irisin) and other related factors, can mitigate muscle atrophy through anti-inflammatory, antioxidative, and muscle-synthesis-promoting mechanisms. This review explores the molecular mechanisms of cisplatin-induced skeletal muscle atrophy, examines the potential protective effects of exercise intervention, and highlights the role of exercise-induced myokines in this process. The findings suggest that exercise not only alleviates chemotherapy-induced muscle atrophy by improving metabolic and immune status but also activates myokines to promote muscle regeneration and repair, offering a promising adjunctive therapy for cisplatin-treated patients. Full article