Search Results (317)

Objectives: This study aimed to evaluate the effects of photomodulation therapy (PMT) on delayed onset muscle soreness (DOMS). Methods: Controlled studies investigating PMT for DOMS were identified through systematic searches of PubMed and EMBASE databases. Selected articles were reviewed for the effects of PMT, and the outcome data were extracted according to specific assessments and time points for meta-analysis. Results: A total of 14 studies met the inclusion criteria, all of which evaluated the effects of PMT following the induction of DOMS. The wavelength of PMT ranged from 660 to 950 nm and was applied to one to six points on the affected muscles. Four studies provided sufficient data for quantitative synthesis, comparing PMT with the placebo in terms of visual analog scale (VAS) scores and muscle strength at 24, 48, 72, and 96 h after the induction of DOMS. The results demonstrated a statistically significant reduction in VAS scores at 72 h (pooled SMD = −0.55) and 96 h (pooled SMD = −0.56), indicating a moderate effect. Muscle strength showed significant improvement at 24 h (pooled SMD = 0.97) and 48 h (pooled SMD = 0.99), reflecting a large effect size. Conclusions: These findings suggested that PMT may be an effective intervention for managing DOMS, with potential effects on reducing pain, enhancing muscle strength, and decreasing biochemical markers of muscle damage. Full article

The prognosis of sarcopenia is poor in cancer patients. Recently, urinary titin, a biomarker of muscle damage, has been suggested as a potential marker for sarcopenia. However, its utility in patients with unresectable digestive malignancies remains unclear. In addition, sex differences have been reported in the association between sarcopenia and urinary titin levels. This study aimed to evaluate urinary titin as a diagnostic marker for unresectable digestive malignancies, focusing on sex differences. This retrospective study enrolled 96 patients (58 males, 38 females; median age 70), and urinary titin was evaluated as a diagnostic biomarker in relation to clinical factors (e.g., age, Eastern Cooperative Oncology Group performance status [ECOG PS], albumin [Alb]) and muscle indicators (e.g., psoas muscle index [PMI], handgrip strength). In male patients, urinary titin levels were significantly higher in the sarcopenia subgroup (5.78 vs. 2.79 pmol/mgCr, p = 0.008), and multivariate analyses identified urinary titin as an independent predictor of sarcopenia (odds ratio 13.4, p = 0.028). The receiver operating characteristic (ROC) analysis demonstrated fair diagnostic performance (area under the curve [AUC] 0.729), with an optimal cutoff value of 3.676 pmol/mgCr. Urinary titin may serve as a useful non-invasive diagnostic biomarker for sarcopenia in patients with unresectable digestive malignancies, particularly in males. These findings suggest that sex-specific approaches are required for sarcopenia assessment with urinary titin. Full article

Objective: This study aimed to evaluate the effects of cold-water immersion (CWI) on post-training recovery in Kung Fu athletes. Methods: In a 3-week crossover design, 16 Kung Fu athletes (22.00 ± 5.95 years, 76.90 ± 9.74 kg) were divided into two conditions: CWI and passive recovery as a control (CON) measure. Through the study, muscle damage markers (creatine kinase [CK], lactate dehydrogenase [LDH], aspartate aminotransferase [AST] and alanine aminotransferase [ALT]), physical performance tests (upper limbs power, SJ and CMJ), skin temperature (from lower and upper limbs), and skin temperature asymmetries were measured. Results: CWI resulted in a higher reduction of CK concentration than CON 24 h after the intervention (−21.32%; p < 0.001). The SJ height 24 h after the intervention was higher in the CWI than in the CON (p < 0.001). Both CWI and CON resulted in skin temperature returning to baseline levels 24 h after intervention. Conclusions: CWI was effective in restoring muscle power, reducing muscle damage and reducing body temperature (BT) in Kung Fu athletes. Cold water recovery showed better muscle power and strength 24 and 48 h after training when compared to the passive method. CK and skin temperature were better 24 h after cold water recovery. Full article

Aim of the study: Idiopathic inflammatory myopathies (IIM) are autoimmune diseases with a low prevalence and incidence worldwide. The levels of IFN-γ production by T-lymphocytes are related to disease activity. IFN-γ +874 T/A (rs2430561) has been shown to alter the serum levels of IFN-γ in different pathologies. The aim of this work is to explore the role of IFN-γ +874 T/A polymorphism in IIM. Methods: Using a specific sequence primer-polymerase chain reaction (SSP-PCR), the genotype was defined for normal healthy controls (HC) and patients with IIM. Markers of muscle damage, clinical features and treatment were collected from chart at the time of diagnosis and at recruitment point. All the data were analyzed by demographic characteristics, genotype, type of IIM, treatment, clinical features, and enzymatic levels. Results: No association was found comparing the genotypes or alleles of the IIM patients vs. HC. On the other hand, the TT genotype, previously described as a high producer of INF γ, showed higher levels of CPK at diagnosis in IIM patients, whereas females at diagnosis and males in remission presented higher levels. Conclusions: Even with a limited number of patients due to the rarity of this disease, no association was found between the disease development. Further, the TT genotype promoted muscle damage due to CPK elevation in the sera compared to the TA/AA genotype in patients with IIM. This could be genetic evidence of the impact of IFN-γ in the disease activity of IIM patients. A larger cohort is needed to confirm these results. Full article

Resistance training (RT) has emerged as an effective strategy to counteract the deleterious effects of aging, improving metabolic health, and preserving functional capacity. However, the impact of low-volume RT on older adults, particularly those with cognitive impairment, remains underexplored. This study investigated the effects of an eight-week low-volume RT program on muscle health, liver function, lipid profile, glycemic control, and oxidative stress markers in individuals with cognitive decline. Twenty-eight participants were assigned to a low-volume RT group (81.0 ± 9.66) and a control group (90.0 ± 10.39 years). The low-volume RT group performed an 8-week RT program (two sessions per week) comprised of one set of 6–12 repetitions at 40–70% 1RM. The control group did not receive the intervention. Before and after the 8 weeks, the biomarkers of muscle health, metabolic profile, and oxidative stress were assessed. The results showed no significant differences between the groups in any biomarker at the baseline or post-test. The intervention group showed a significant increase in serum lactate dehydrogenase, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) activities, all of which remained within normal ranges. No changes were observed in serum creatine kinase activity or the AST/ALT ratio in the intervention group, suggesting that acute-phase responses were occurring rather than tissue damage. Additionally, the intervention group showed a significant increase in high-density lipoprotein cholesterol levels, accompanied by a reduction in the atherogenic index, indicating potential cardiovascular benefits. No significant alterations were detected in the glycemic control and lipid peroxidation markers. These results suggest that low-volume RT can elicit modest, yet clinically meaningful metabolic improvements in individuals with cognitive impairment. Future studies should focus on identifying the minimal effective RT dose needed to optimize the health benefits in this vulnerable population, facilitating long-term adherence to exercise interventions. Full article

Background: Quasipaa spinosa crude extract (QSce), a natural source rich in proteins such as parvalbumin (PV), has been traditionally used to promote physical recovery. However, its mechanisms in mitigating exercise-induced fatigue remain unclear. Methods: Using a murine treadmill exhaustion model, we evaluated the effects of QS-derived Parvalbumin (QsPV) (30 and 150 mg/kg/day) on endurance capacity, oxidative stress, tissue injury, and muscle function. Indicators measured included time to exhaustion, intracellular calcium levels, antioxidant enzymes [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px)], lipid peroxidation (malondialdehyde, MDA), injury markers [creatine kinase (CK), lactate dehydrogenase (LDH), cardiac troponin I (cTnI)], renal function (blood urea), and muscle force. Results: QsPV-150 significantly increased time to exhaustion by 34.6% compared to the exercise-only group (p < 0.01). It reduced MDA by 41.2% in skeletal muscle and increased SOD and GSH-Px levels by 35.4% and 28.1%, respectively. Serum CK, LDH, and cTnI were reduced by 39.5%, 31.7%, and 26.8%, respectively, indicating protection against muscle and cardiac injury. QsPV also decreased blood urea by 22.3% and improved renal histology, with reduced glomerular damage and tubular lesions. At the molecular level, QsPV restored calcium balance and downregulated calpain-1/2 and atrophy-related genes (MuRF-1, MAFbx-32). Muscle contractile force (GAS and SOL) improved by 12.2–20.3%. Conclusions: QsPV attenuates exercise-induced fatigue through multi-organ protection involving calcium buffering, oxidative stress reduction, and anti-atrophy effects. These findings support its potential as a natural recovery-enhancing supplement, pending further clinical and pharmacokinetic studies. Full article

Aging is a significant risk factor for various conditions, including neurodegeneration, cardiovascular disease, and type 2 diabetes. The accumulation of reactive oxygen species (ROS) and a decline in antioxidant defense are mechanisms that are widely acknowledged as causing the acceleration of both aging and the onset of age-related diseases. To promote longevity and reduce the risk of the development of aging-related disorders, it is essential to prevent or minimize oxidative stress and enhance antioxidant defense. It has been shown that Anoectochilus burmannicus (AB), a jewel orchid rich in phenolic compounds, can impact various biological activities associated with aging prevention. These activities include antioxidant, anti-inflammation, anti-insulin resistance, and anti-obesity effects. The aim of this study was to explore whether AB extract (ABE) could serve as an anti-aging agent using a Sod1-deficient Drosophila model, which accelerates the process of aging through ROS production. The results demonstrated that ABE, at a concentration of 2.5 mg/mL, significantly extended the lifespan of the flies and helped maintain their locomotor activity as they aged. ABE also reduced the age-related accumulation of damaged proteins in the muscle of the flies by inhibiting the expression of Gstd1, a genetic marker for oxidative stress. This finding agrees with those from in vitro experiments, which have shown the potential for ABE to reduce the production of ROS induced by H₂O₂ in myoblasts. ABE has been shown to attenuate insulin resistance, an age-related disorder, by inhibiting the pro-inflammatory cytokine TNF-α, which in turn increased insulin-stimulated glucose uptake in adipocytes. These findings suggest a promising role of ABE as an ingredient in functional foods or nutraceuticals aimed at promoting health, preventing oxidative stress, and potentially managing age-associated diseases. Full article

Purpose: Although chronic resting hormonal changes were traditionally considered to modulate muscle tissue remodeling and growth, our knowledge of exercise on the acute post-exercise hormonal response is limited. Moreover, the type of exercise protocol may trigger different hormonal profiles. The aim of this study was to evaluate changes in muscle damage, as well as hormonal and inflammatory markers following the response to three different resistance training protocols. Methods: A crossover study was conducted in which 33 recreationally active men were randomly assigned to three different training groups: high-intensity interval training (HIIT), concurrent training (CT), and high-intensity resistance circuit (HRC) training. Blood biomarkers were measured by standard procedures at rest, after exercise (P0), 30 min (P1), 24 h (P24), and 48 h (P48) after exercise. Results: Regarding testosterone, the Friedman test detected a significant time × group interaction (p = 0.004), and Durbin–Conover showed higher levels in HRC compared to HIIT at P1 (p = 0.006) and P48 (p = 0.021). However, CT showed higher levels than HIIT (p = 0.008) at P1. Concerning myostatin, there was a trend in the time × group interaction (p = 0.056) with lower values in HRC compared to CT in P1 (p = 0.003), and a trend between HRC and HIIT in P1 (p = 0.056). Conclusions: HRC generates higher levels of testosterone than HIIT in the acute (P1) and late (P48) phases of recovery and produces lower levels of myostatin than CT and HIIT (P1) in the acute phase of recovery. Full article

Background: Sprinting, a high-intensity, short-duration exercise, induces oxidative stress. This causes molecular and ultrastructural alterations. Antioxidant supplementation may mitigate side effects of near or complete exhaustion. Methods: Twenty-eight healthy male adult rats received orally normal saline, carboxymethylcellulose (vehicle), artificial, N-acetylcysteine or a natural antioxidant, Rutin. Rats were subjected to treadmill sprinting at increasing speeds for 5 days/week. After 26 days, samples were collected to measure oxidative stress (malondialdehyde, MDA; the ratio of reduced-to-oxidized glutathione, GSH/GSSG), inflammation markers (enzymatic level of inducible nitric oxide synthase, iNOS; cytokine level of tumor necrosis factor alpha, TNFα) and for transmission electron microscopy (TEM) analysis. Results: Rutin attenuated MDA levels and increased antioxidant protection in all tissues, while NAC decreased the lipid peroxidation in all tissues except the lungs. NAC increased aortic inflammation, with higher TNF-α and iNOS. Sprinting caused intimal detachment in the heart and aorta. Rutin and NAC minimized endocardium alterations. Additionally, Rutin prevented myocardial disorganization. Conclusions: Rutin mitigated the oxidative stress damage of sprinting in the heart, aorta, skeletal muscle and lung. NAC protected against oxidative injury caused by sprinting in the heart, aorta and muscle but not the lung, and it induced aortic inflammation. Full article

Cell death and inflammation are key innate immune responses, but excessive activation can cause tissue damage. The NLRP3 inflammasome is a promising target for reducing inflammation and promoting recovery. Immunometabolism regulates NLRP3 responses in neurological and inflammatory diseases through cyclic nucleotide signaling. Targeting phosphodiesterases (PDEs), which hydrolyze cAMP and cGMP, offer a novel approach to mitigate inflammation. While 14 PDE inhibitors are FDA-approved, PDE10A’s role in NLRP3 inflammasome activation remains unclear. This study investigates the effects of PDE10A inhibition on inflammasome-driven inflammation using two PDE10A inhibitors, MP-10 and TP-10, in macrophage and animal models of sepsis and traumatic nerve injury. Our results show that PDE10A inhibition reduces inflammasome activation by preventing ASC speck formation and by lowering levels of cleaved caspase-1, gasdermin D, and IL-1β, which are key mediators of pyroptosis. In the sepsis model, MP-10 significantly reduced inflammation, decreased plasma IL-1β, alleviated thrombocytopenia, and improved organ damage markers. In the nerve injury model, PDE10A inhibition enhanced motor function recovery and reduced muscle atrophy-related gene expression. These findings suggest that PDE10A inhibition could be a promising therapeutic approach for inflammatory and neuromuscular injuries. Given MP-10’s established safety in human trials, Phase 2 clinical studies for sepsis and nerve injury are highly promising. Full article

Background/Objectives: The aim of this study was to assess the effects of cold-water immersion (CWI) post-eccentric muscle contraction exercise on skin temperature, pain score, maximum voluntary isometric contraction (MVIC), muscle damage, and muscle mechanical properties. Methods: Twenty-seven male participants (age 20.6 ± 0.6; body mass 69.4 ± 8.1; body fat % 13.7 ± 4.3) were divided into three treatments: whole-body CWI treatment group (n = 9), lower-body CWI treatment group (n = 9), and control treatment group (n = 9). Results: MVIC did not show a significant interaction effect between group and time but demonstrated a significant main effect for time (p = 0.001). The pain scale demonstrated a significant interaction effect between group and treatment (p = 0.049), in addition to significant main effects for both time and treatment (both p = 0.001). While blood creatine kinase (CK) concentration revealed no significant interaction effect between group and time, a significant main effect was observed for time (p = 0.001). Blood lactate dehydrogenase (LDH) concentration showed both a significant interaction effect between group and time (p = 0.02) and a significant main effect for time (p = 0.001). The tensiomyography (TMG) results for Dm showed a significant interaction effect between group and treatment (p = 0.047), as well as a significant main effect for time (p = 0.001). Conclusions: Lower-body CWI is effective in reducing pain indices and blood LDH levels, a marker of muscle damage. It may serve as an effective method for preventing and minimizing pain and muscle damage, comparable to whole-body CWI. Full article

In older adults with reduced physical performance, an increase in the labile iron pool within skeletal muscle is observed. This accumulation is associated with an altered expression of mitochondrial quality control (MQC) markers and increased mitochondrial DNA damage, supporting the hypothesis that impaired MQC contributes to muscle dysfunction during aging. The autophagy–lysosome system plays a critical role in MQC by tagging and engulfing proteins and organelles for degradation in lysosomes. The endolysosomal system is also instrumental in transferrin recycling, which, in turn, regulates cellular iron uptake. In the neuromuscular system, the autophagy–lysosome system supports the structural integrity of neuromuscular junctions, and its dysfunction contributes to muscle atrophy. While MQC was thought to protect against iron-induced cell death, the discovery of ferroptosis, a form of iron-dependent cell death, has highlighted a complex interplay between MQC and iron-inflicted damage. Ferritinophagy, the autophagic degradation of ferritin, if overactivated, can induce ferroptosis. Alternatively, aging may impair ferritinophagy, leading to ferritin accumulation and the release of toxic labile iron under stress, exacerbating oxidative damage and cellular senescence. Physical activity supports muscle health also by preserving mitochondrial quantity and quality and enhancing bioenergetics. However, therapeutic strategies for preventing or reversing physical function decline in aging are still lacking due to the insufficient understanding of the underlying mechanisms. Unveiling how disruptions in iron homeostasis impact muscle quality in older adults may allow for the development of therapeutic strategies targeting iron handling to alleviate age-associated muscle decline. Full article

Background/Objectives: Recent studies have highlighted the role of the gut–muscle axis, suggesting that modulation of the gut microbiota may indirectly benefit skeletal muscle. This study aimed to evaluate the effects of Lactobacillus fermentum (L. fermentum) supplementation in a model of muscle atrophy induced by chronic ethanol (EtOH) intake, focusing on inflammatory and antioxidant mechanisms. Methods: Sixty 12-month-old female Balb/c mice were divided randomly into three groups (n = 20/group): (1) Ethanol (EtOH) group, receiving ethanol daily for 8 and 12 weeks to induce systemic oxidative stress and inflammation; (2) Ethanol + Probiotic (EtOH + P) group, receiving both ethanol and L. fermentum supplementation for the same durations; and (3) Control (Ctrl) group, receiving only water. Muscle samples were analyzed for the fiber morphology, inflammatory markers, oxidative stress indicators, and satellite cell (SC) activity. All data were tested for normality using the Shapiro–Wilk test before applying a parametric analysis. A statistical analysis was performed using one-way ANOVA followed by a Bonferroni post-hoc test. The level of significance was set at p < 0.05. Results: EtOH exposure caused significant atrophy in all muscle fiber types (type I, IIa, and IIb), with the most pronounced effects on oxidative fibers. L. fermentum supplementation significantly reversed atrophy in type I and IIa fibers, accompanied by a significant reduction in IL-6, TNF-α, and Hsp60 expression levels, indicating the protective effect of L. fermentum against oxidative stress and inflammation. Moreover, the probiotic treatment increased MyoD expression in SCs, suggesting enhanced regenerative activity, without histological evidence of fibrosis. Conclusions: These findings suggest that L. fermentum supplementation could counteract EtOH-induced skeletal muscle damage by reducing inflammation and oxidative stress and promoting muscle repair, indicating its potential as an adjuvant, in the therapeutic strategy of models of muscle degeneration. Full article

Objectives: This study examined physiological, biochemical, and performance adaptations in 18 semi-professional male soccer players across three seasonal phases: pre-season initiation (PS), pre-competition (PC), and mid-season (MS). Methods: Assessments included physical/performance/hormonal/biochemical markers. Results: From PS to PC, body fat (Cohen’s d = −0.88; p ≤ 0.01) and speed drop rate (Cohen’s d = −1.52; p ≤ 0.01) significantly decreased, while V̇O₂max (Cohen’s d = 0.80; p ≤ 0.01), velocity at V̇O₂max (Cohen’s d = 1.86; p ≤ 0.01), and velocity at the second ventilatory threshold (Cohen’s d = 1.54; p ≤ 0.01) significantly increased. Significant fluctuations were observed in creatine kinase (Cohen’s d = 4.34; p ≤ 0.01), myoglobin (Cohen’s d = 0.66; p ≤ 0.01), and cortisol (Cohen’s d = −1.14; p ≤ 0.01) levels. From PS to MS, further reductions in body fat (Cohen’s d = −0.81; p ≤ 0.01) and speed drop rate (Cohen’s d = −1.12; p ≤ 0.01) were observed, along with significant improvements in countermovement jump performance (Cohen’s d = 1.08; p ≤ 0.01) and cardiorespiratory fitness (Cohen’s d ≥ 0.83; p ≤ 0.01). Creatine kinase (Cohen’s d = 3.82; p ≤ 0.01), myoglobin (Cohen’s d = 1.50; p ≤ 0.01), interleukin-6 (Cohen’s d = 1.24; p ≤ 0.01), and testosterone (Cohen’s d = 0.92; p ≤ 0.01) significantly increased. Stability in lower limb strength, flexibility, triglycerides, C-reactive protein, ferritin, liver enzymes, and most hematological parameters suggest resilience to seasonal demands. Conclusions: Seasonal training enhanced fitness and hormonal balance while maintaining physiological stability. These findings underscore the importance of periodized training to manage muscle damage and sustain an anabolic hormonal profile for peak performance. Consistent diet and training support metabolic health, while tailored recovery strategies and season-specific interventions are essential for optimizing performance and minimizing injury risk. Full article

The chicken infectious anemia virus (CIAV) and fowl adenovirus serotype E8b (FAdV E8b) are pathogens that cause aplastic anemia and inclusion body hepatitis (IBH) in chickens, respectively. The co-infection of CIAV and FAdV E8b poses a significant threat to poultry health, potentially worsening clinical symptoms and increasing mortality rates. This study aimed to explore the combined pathogenic effects of FAdV E8b and CIAV co-infection on one-day-old specific pathogen-free (SPF) chickens. The results showed that co-infection led to significantly higher clinical scores and mortality rates compared to FAdV E8b infection alone. Additionally, there were different tissue distribution patterns for FAdV E8b between the single infection and co-infection groups, indicating potential changes in viral tropism. Biochemical analysis revealed elevated markers of liver and/or muscle damage in both the FAdV E8b infection group and the co-infection group, consistent with the viral infection process. These findings suggest that co-infection with FAdV E8b and CIAV can intensify clinical signs and mortality, and may potentially alter viral replication and tissue tropism in chickens. This study establishes a foundation for future investigations into the underlying mechanisms governing the interaction between CIAV and FAdV E8b during co-infection. Full article