Search Results (117)

Background/Objectives: The global prevalence and incidence of inflammatory bowel diseases have risen in the past two decades. Among them, Crohn’s disease and ulcerative colitis are still challenging to treat due to vascular and proliferative alterations. Studies in rats suggest that blocking histamine receptors (H1–H4) can improve colitis progression. However, the specific histamine receptor responsible for this effect remains debated. The experiment aimed to assess the role of specific histamine receptor subtypes in colitis development, focusing on oxidative stress markers in the liver and skeletal muscle. Methods: The study involved 60 adult male Wistar rats, divided into control and colitis experimental groups. Colitis was induced through intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid. Animals in both experimental groups received intramuscular injections of NaCl (non-treated, NT) or H1, H2, H3, and H4 receptor antagonists (10 study subgroups in total). On day eight, the animals were re-anesthetized and euthanized via exsanguination. Then, liver and skeletal muscle (m. soleus) samples were collected for analysis of oxidative stress markers. Results: The analyses of skeletal muscle samples showed that using the H1 and H2 receptor antagonists increased superoxide dismutase (SOD) and catalase (CAT) activities, as well as parameters related to glutathione metabolism (reduced glutathione (GSH), glutathione S-transferase (GST)) in rats from the control groups, indicating enhanced antioxidant defense. In rats with chemically induced colitis, we observed that H1 receptor antagonists elevated CAT activity, whereas β-esterase (β-EST) activity remained elevated across all colitis subgroups. In the liver, histamine receptor antagonists produced receptor-specific redox effects: the H2 receptor antagonist reduced oxidative damage (malondialdehyde (MDA)); the H1 receptor antagonist attenuated SOD hyperactivity, but depleted GSH; and the H4 receptor antagonist increased GSH while elevating MDA. Chemically induced colitis increased α- and β-EST activities, whereas administration of the H1 or H3 antagonist reduced β-EST levels. Conclusions: Histamine receptor antagonists modulated oxidative stress responses in both liver and skeletal muscle tissues in a receptor-dependent manner. Among them, the H2 receptor antagonist most effectively mitigated hepatic oxidative injury, highlighting its potential as a therapeutic target in colitis-associated systemic oxidative stress. Full article

Background/Objectives: In all types of diabetes, elevated blood glucose levels cause pathological changes in skeletal muscle, primarily due to oxidative stress, mitochondrial dysfunction, and excessive production of reactive oxygen species (ROS). Regular exercise can help mitigate these effects; however, the underlying mechanisms, particularly those involving the mitochondrial permeability transition pore (mPTP), remain incompletely understood. This study aimed to explore the effects of aerobic exercise training (AET) on oxidative stress and the expression of mPTP components in the skeletal muscle of streptozotocin-induced diabetic rats. Methods: Male Wistar rats were randomly divided into three groups: Healthy Sedentary (H-SED), Diabetic Sedentary (D-SED), and Diabetic Exercise-trained (D-EXER); n = 6 per group. The D-EXER group performed AET (0° slope) 5 days/week for 8 weeks. After the intervention period, body weight and fasting blood glucose (FBG) levels were measured, and soleus muscles were collected and analyzed for oxidative stress biomarkers, Western blotting, and gene expression using qRT-PCR. Results: Following an 8-week intervention, AET reduced FBG concentrations. Accordingly, in the soleus muscles of the D-EXER group, ROS levels decreased, and redox balance was improved compared to the D-SED group. Exercise training reduced CypD and Casp9 mRNA expression and increased Bcl-2 mRNA expression, whereas Ant1 mRNA expression was only slightly altered. CypD protein expression was decreased in exercised diabetic rats, while VDAC1 protein and mRNA levels remained unchanged. In the D-EXER group, there were significant inverse correlations between CypD and Casp9 mRNA expression levels and glutathione redox state. Conclusions: The current study suggests that 8 weeks of AET, in addition to reducing hyperglycemia, may favorably influence oxidative balance and the expression of mPTP-related molecular components in diabetic skeletal muscle. Full article

Background/Objectives: Running is associated with increased Achilles Tendon (AT) loading and cross-sectional area (CSA). Achilles tendinopathy is a common unilateral injury. Differences in AT loading variables between dominant and non-dominant lower extremities while running have not been characterized. This study examined the AT loading variables between dominant and non-dominant lower extremities in healthy recreational runners. Methods: Twenty-four females ran at 3.3 m/s (11.88 km/hr) on an instrumented treadmill. Achilles Tendon CSA (AT-CSA) was measured from ultrasound images. Kinematic and kinetic data were used as input into a musculoskeletal model. Paired t-tests examined inter-limb differences in peak vertical ground reaction force, Achilles Tendon-related loading variables (AT force, AT-CSA, AT stress), total gastrocnemius force, soleus force, foot strike angle, and stance time. Results: No differences were shown between dominant and non-dominant lower extremities in stance time, vertical ground reaction force, gastrocnemius and soleus force, AT force, AT-CSA, or AT stress. Foot strike angle was different between limbs (p = 0.015); however, the absolute difference was about 2°. Conclusions: These data indicated that AT loading was similar between dominant and non-dominant lower extremities in healthy female recreational runners. While some asymmetry can be expected during a bilateral task such as running, runners displayed differences in AT force and stress less than 18%. These data may assist clinicians in the assessment and management of runners recovering from AT tendinopathy. Full article

Purpose: This study investigated how variations in approach speed and distance influence lower-limb muscle activation, joint co-contraction ratios (CCRs), and mechanical joint stiffness during single-leg approach run jump landings (ARJSL), to clarify adaptive neuromuscular strategies for joint stiffness regulation. Methods: Twenty-five physically active male university students performed ARJSLs under six randomized conditions combining two approach speeds (fast > 4.0 m/s; slow < 4.0 m/s) and three approach distances (3, 6, and 9 m). Surface electromyography (sEMG) from five dominant-limb muscles—rectus femoris, biceps femoris, tibialis anterior, gastrocnemius, and soleus—was analyzed across three movement phases: pre-activation, downward (braking), and push-off. Knee and ankle CCRs were computed, while kinematic and kinetic data were used to calculate mechanical joint stiffness via inverse dynamics. A two-way repeated-measures ANOVA evaluated the main and interaction effects of approach speed and distance. Results: Significant speed × distance interactions were observed for tibialis anterior activation, several CCRs, and eccentric ankle stiffness (p < 0.05). Pre-activation knee CCR increased with longer, faster approaches, indicating anticipatory joint pre-stiffening. During braking, greater ankle co-contraction under fast–9 m conditions coincided with reduced mechanical ankle stiffness, suggesting a compensatory yielding strategy under high kinetic loads. In the push-off phase, faster approaches elicited higher concentric stiffness at the hip and ankle, supporting efficient energy transfer. Rectus femoris and gastrocnemius activation scaled with both approach speed and distance. Conclusions: Athletes adapt neuromuscular co-contraction and mechanical stiffness in a coordinated, phase-dependent manner to balance protection and performance. These insights may inform targeted training strategies for enhancing jump efficiency and mitigating ACL injury risk. Full article

Background: Wireless surface electromyography (sEMG) enables the investigation of neuromuscular control in realistic sports settings; however, ensuring reliable signal acquisition during sprinting remains challenging. This study examined the feasibility of continuous wireless EMG recording in sprinting athletes and evaluated their agonist–antagonist coordination patterns. Methods: Ten trained sprinters performed four maximal 50-m sprints on a force plate–equipped track. sEMG was recorded from the biceps femoris (BF), rectus femoris (RF), soleus (Sol), and tibialis anterior (TA) under two receiver configurations: fixed-receiver condition (FRC) and mobile-receiver condition (MRC). Integrated EMG, kinematics, and cross-correlation analyses were performed on a stride-by-stride basis. Results: Continuous high-quality EMG was feasible under MRC, highlighting the practical importance of maintaining receiver proximity in sprint experiments. BF activity during the late swing phase correlated positively with sprint velocity, supporting the performance relevance of pawing. BF/RF interactions varied substantially across individuals, whereas Sol/TA were consistently coactivated, indicating ankle stabilization. Conclusions: Wireless EMG enables reliable in-field monitoring of sprinting athletes, revealing both individualized and shared coordination strategies relevant to performance and injury prevention in athletes. Full article

Background/Objectives: Swing leg resistance may stimulate propulsive force, required for forward progression and leg swing, in post-stroke patients. To assess the potential of swing leg resistance in rehabilitation, more knowledge is needed on how this unilateral manipulation affects gait. Therefore, we explored the bilateral effects of a unilateral swing leg resistance on muscle activity, kinematics, and kinetics of gait in able-bodied individuals. Methods: Fourteen able-bodied participants (8 female, aged 20.7 ± 0.8 years, BMI 23.5 ± 1.9) walked on an instrumented treadmill at 0.28 m/s, 0.56 m/s, and 0.83 m/s with and without unilateral swing leg resistance provided by a weight (0 kg, 0.5 kg, 1.25 kg, and 2 kg) attached to the leg through a pulley system. Propulsion and braking forces, swing time, step length, transverse ground reaction torques, and muscle activity in the gluteus medius (GM), biceps femoris (BF), rectus femoris (RF), vastus medialis (VM), medial gastrocnemius (MG), and soleus (SOL) were compared between conditions. Statistical analyses were performed using repeated measures ANOVAs, with a significance level of 5%. Results: Peak propulsive force and propulsive duration increased bilaterally, while peak braking force decreased bilaterally with unilateral swing leg resistance. In addition, the swing time of the perturbed leg increased with swing leg resistance. Muscle activity in the perturbed leg (GM, BF, RF, VM, MG) and the unperturbed leg (GM, BF, VM, MG, SOL) increased. Only in the BF (perturbed leg, late swing) and MG (unperturbed leg, early stance) did the muscle activity decrease with swing leg resistance. No adaptations in step length and transverse ground reaction torques were observed. Specific effects were enhanced by gait speed. Conclusions: Unilateral swing leg resistance can evoke effects that might stimulate the training of propulsion. A study in post-stroke patients should be conducted to test whether prolonged exposure to unilateral swing leg resistance leads to functional training effects. Full article

Sarcopenia, the progressive loss of skeletal muscle mass and function with age, significantly contributes to frailty and mortality in older adults. Notably, muscles do not age uniformly—some retain structure and strength well into old age. This review explores the mechanisms underlying differential resistance to muscle aging, with a focus on sarcopenia-resistant muscles. We analyzed current literature across molecular biology, genetics, and physiology to identify key regulators of muscle preservation during aging. Special attention was given to muscle fiber types, mitochondrial function, neuromuscular junctions, and satellite cell activity. Muscles dominated by slow-twitch (type I) fibers—such as the soleus, diaphragm, and extraocular muscles—demonstrate enhanced resistance to sarcopenia. This resilience is linked to sustained oxidative metabolism, high mitochondrial density, robust antioxidant defenses, and preserved regenerative capacity. Key molecular pathways include mTOR, PGC-1α, and SIRT1/6, while genetic variants in ACTN3, MSTN, and FOXO3 contribute to interindividual differences. In contrast, fast-twitch muscles are more vulnerable due to lower oxidative capacity and satellite cell depletion. Unique innervation patterns and neurotrophic support further protect muscles like extraocular muscles from age-related atrophy. Resistance to sarcopenia is driven by a complex interplay of intrinsic and extrinsic factors. Understanding why specific muscles age more slowly provides insights into muscle resilience and suggests novel strategies for targeted prevention and therapy. Expanding research beyond traditionally studied muscles is essential to develop comprehensive interventions to preserve mobility and independence in aging populations. Full article

Diabetic muscular atrophy is a complication of diabetes mellitus that can decrease quality of life. Its complex mechanisms include alterations in proteolytic pathways, oxidative stress, and intracellular lipid accumulation. NADPH oxidase enzymes (NOX) play a key role in the production of ROS, contributing to oxidative damage and insulin resistance. Apocynin, a NOX inhibitor, has antioxidant and anti-inflammatory effects, suggesting its therapeutic potential in various diabetic complications. This study evaluated the impact of apocynin on the mechanisms of muscle atrophy in slow- and fast-twitch muscles of diabetic rats. Diabetes was induced in male Wistar rats by intraperitoneal injection of a single dose of streptozotocin (60 mg/kg). Apocynin treatment (3 mg/kg/day) was administered for 8 weeks. Fasting blood glucose levels, lipid profile, and weight gain were measured. Both slow-twitch (soleus) and fast-twitch (extensor digitorum longus, EDL) skeletal muscles were weighed and used to assess triglycerides (TG) content, histological analysis, lipid peroxidation levels, and gene expression evaluated by qRT-PCR. Apocynin reduced blood glucose levels, improved body weight, and exhibited hypolipidemic effects. It significantly increased muscle weight in EDL and soleus, especially in EDL muscle, lowering triglycerides, lipid peroxidation, and increasing fiber size. Additionally, it decreased mRNA expression levels of MuRF-1, atrogin-1, myostatin and p47phox mRNA and upregulated PGC-1α and follistatin mRNA. Apocynin exerted a myoprotective effect by mitigating muscle atrophy in diabetic rats. Its effects were differentially mediated on TG accumulation and muscle fiber size, reducing oxidative stress, atrogene expression, and positively regulating PGC-1α. Full article

Background/Objectives: After spinal cord injury (SCI), poor dorsiflexor control and involuntary plantar-flexor contraction impair walking. As whole-body vibration (WBV) improves voluntary muscle activation and modulates reflex excitability, it may improve ankle control. In this study, the dosage effects of WBV on walking speed, dorsiflexion, and spinal reflex excitability were examined. Methods: Sixteen people with chronic motor-incomplete SCI participated in this randomized sham-control wash-in study. Two weeks of sham stimulation (wash-in phase) were followed by either 2 weeks of eight repetitions (short bout) or sixteen repetitions of WBV (long bout; intervention phase) per session. Walking speed, ankle angle at mid-swing, and low-frequency depression of the soleus H-reflex were measured before and after the wash-in phase and before and after the intervention phase. Results: A significant dosage effect of WBV was not observed on any of the measures of interest. There were no between-phase or within-phase differences in ankle angle during the swing phase or in low-frequency depression. When dosage groups were pooled together, there was a significant change in walking speed during the intervention phase (mean = 0.04 m/s, standard deviation = 0.06, p = 0.02). There was not a significant correlation between overall change in walking speed and dorsiflexion angle or low-frequency depression during the study. Conclusions: Whole-body vibration did not have a dosage-dependent effect on dorsiflexion during the swing phase or on spinal reflex excitability. Future studies assessing the role of corticospinal tract (CST) descending drive on increased dorsiflexor ability and walking speed are warranted. Full article

Adequate exercise prescription requires a deep understanding of the body’s response to exercise. This study explored the responses of heart rate (HR), muscle oxygen saturation (SmO₂), and perceived exertion (RPE) during six body-weight squat exercise variations. A total of 15 recreationally active participants (age: 28.2 ± 8.0 years; body mass: 71.1 ± 11.2 kg; height: 1.73 ± 0.08 m) were recruited. Six body-weight squat variations (deep, jumping, single-leg, uneven, unstable, and wall-sit) were randomly performed for 90 s. Results revealed that the jumping squat promoted a higher average and peak HR (165.3 ± 14.5 and 146.1 ± 14.8 bpm, respectively), and a lower average SmO₂ and higher deoxygenation SmO₂ in the soleus muscle (40.3 ± 15.4 and 46.0 ± 11.4%, accordingly). No differences were observed in recovery time or in the same SmO₂ derived-parameters in the vastus lateralis muscle. The jumping variation promoted a greater response at a physiological level, both centrally, related to cardiovascular response, and peripherally, related to soleus SmO₂. It was also the more demanding variation at both the overall and lower limb muscular level of RPE. This holistic view allows a precise identification of the response patterns in body-weight squat exercise variations to an acute session, with a training intervention providing additional information. Full article

Background/Objectives: Our previous study demonstrated that 3-(4-hydroxy-3-methoxyphenyl)propionic acid (HMPA) administration improved grip strength and reduced blood urea nitrogen levels, but its underlying mechanisms remain unclear. This study aimed to investigate the effects of HMPA on oxidative stress and muscle fiber composition, emphasizing its potential role in modulating redox signaling pathways and influencing muscle development. Methods: Eight-week-old male C57BL/6 mice were orally administered HMPA solution (50 or 500 mg/kg/day) or distilled water (10 mL/kg) for 14 days, and then divided into sedentary and exhaustive exercise groups to evaluate oxidative stress status, myosin heavy chain (MHC) isoform expression, and underlying mechanisms. Results: Both low and high doses of HMPA reduced oxidative stress by decreasing plasma reactive oxygen metabolites. High-dose HMPA reduced plasma nitrite/nitrate levels and enhanced antioxidant capacity post-exercise, accompanied by changes in the mRNA abundance of antioxidant enzymes (e.g., Sod1 and Nqo1) and reductions in the mRNA abundance of nitric oxide synthases (e.g., Nos2 and Nos3) in the soleus. Additionally, high-dose HMPA administration increased the protein expression of MYH4 in the soleus, while low-dose HMPA enhanced the gene expression of Myh4 and Igf1, suggesting that HMPA may promote fast-twitch fiber hypertrophy through the activation of the IGF-1 pathway. Furthermore, low-dose HMPA significantly increased the gene expression of Sirt1 and Nrf1, as well as AMPK phosphorylation post-exercise, suggesting low-dose HMPA may improve mitochondrial biogenesis and exercise adaptation. Conclusions: These findings suggest that HMPA may serve as a dietary supplement to regulate redox balance, enhance antioxidant defenses, and promote the formation of fast-twitch fibers. Full article

Background: Reciprocal inhibition (RI) is a spinal reflex that controls posture and movement. The modulation of spinal RI represented by the H-reflex has been studied, before and after voluntary contraction and electrical nerve stimulation but not during voluntary, electrically induced muscle contraction or a combination of voluntary and electrically induced muscle contractions. This study investigates the effects of the ongoing voluntary isometric contraction, the electrically induced isometric contraction, and the combination of voluntary with electrically induced isometric contraction of the Tibialis Anterior (TA) muscle on spinal RI represented by Soleus H-reflex. Methods: Eighteen healthy adults participated. Soleus H-reflex and M-response were measured during four different conditions as follows: (1) at rest, (2) electrically induced isometric contraction of the TA, (3) voluntary isometric contraction of the TA with a 1 kg force, and (4) combined voluntary and electrically induced isometric contraction of the TA with a 1 kg force. Results: The ANOVA clearly demonstrated significant differences in Soleus H-reflex amplitude across the four recording conditions (F3,16, 17.28, p < 0.001). The amplitude at rest was significantly higher than during electrically induced isometric contraction, voluntary isometric contraction, and the combined contraction conditions (p < 0.05). Furthermore, the amplitude recorded during the electrically induced isometric contraction condition significantly surpassed that of voluntary isometric contraction and the combined contraction conditions (p < 0.05). Moreover, there was no significant difference between Soleus H-reflex amplitude recorded during voluntary isometric contraction and the combined voluntary isometric contraction and electrically induced isometric contraction (p < 0.87). The combined voluntary isometric contraction and electrically induced isometric contraction condition had a higher inhibitory effect on the Soleus H-reflex with no significant differences from voluntary isometric contraction. Moreover, both were significantly better than electrically induced isometric contraction (p = 0.05). In terms of Soleus H-reflex latency, there was no significant difference among all four conditions (p > 0.05), meaning Soleus H-reflex latency was not influenced by the conditions. Conclusions: RI can be best modulated by combining voluntary with electrically induced isometric muscle contractions. Full article

Background: Achilles tendon rupture rehabilitation protocols often emphasize two key factors, namely plantar flexion and load restriction during the early recovery stages. However, we hypothesize that variations in walking speed also play a significant role in affecting the load on the Achilles tendon. This study aims to explore the combined impact of plantar flexion angle and walking speed on the surface electromyography (EMG) activity of the calf muscles. Methods: Surface EMG measurements on 24 healthy volunteers assessed the activity of the calf muscles (gastrocnemius lateralis, gastrocnemius medialis, and soleus). Participants walked on a treadmill using two designs of ankle foot orthoses set at three different angles of the ankle joint (mainly 0°, 15°, or 30° plantar flexion), as well as barefoot and in sports shoes. The tests were performed at full loads of 1, 2 and 4 km/h or with additional measurements at 1 and 2 km/h with a partial load of 20 kg. The walking speed of 4 km/h in sports shoes was used as reference, corresponding to the maximum load on the calf muscles during walking. Results: Both orthoses demonstrated a significant reduction in EMG activity by more than half even at a 0° setting and 1 km/h compared to walking barefoot or in sports shoes. However, as walking speed increased to 2 km/h and especially to 4 km/h, EMG activity significantly increased, approaching the level of walking with sports shoes at 1 km/h. The results indicated that even minor changes in walking speed had a significant impact on muscle activity, underscoring the importance of this parameter. Conclusions: This study suggests that walking speed should be considered a crucial factor in rehabilitation protocols for Achilles tendon ruptures, alongside plantar flexion and load restrictions, to optimize recovery outcomes. Full article

The chemotherapeutic agent doxorubicin (DOX) leads to the loss of skeletal muscle and adipose tissue mass, contributing to cancer cachexia. Experimental research on the molecular mechanisms of long-term DOX treatment is modest, and its effect on both skeletal muscle and adipose tissue has not been studied in an integrative manner. Dexrazoxane (DEXRA) is used to prevent DOX-induced cancer-therapy-related cardiovascular dysfunction (CTRCD), but its impact on skeletal muscle and adipose tissue remains elusive. Therefore, this study aimed to investigate the long-term effects of DOX on adipose tissue and skeletal muscle metabolism, and evaluate whether DEXRA can mitigate these effects. To this end, 10-week-old male C57BL6/J mice (n = 32) were divided into four groups: (1) DOX, (2) DOX-DEXRA combined, (3) DEXRA and (4) control. DOX (4 mg/kg weekly) and DEXRA (40 mg/kg weekly) were administered intraperitoneally over 6 weeks. Indirect calorimetry was used to assess metabolic parameters, followed by a molecular analysis and histological evaluation of skeletal muscle and adipose tissue. DOX treatment led to significant white adipose tissue (WAT) loss (74%) and moderate skeletal muscle loss (Gastrocnemius (GAS): 10%), along with decreased basal activity (53%) and energy expenditure (27%). A trend toward a reduced type IIa fiber cross-sectional area and a fast-to-slow fiber type switch in the Soleus muscle was observed. The WAT of DOX-treated mice displayed reduced Pparg (p < 0.0001), Cd36 (p < 0.0001) and Glut4 (p < 0.05) mRNA expression—markers of fat and glucose metabolism—compared to controls. In contrast, the GAS of DOX-treated mice showed increased Cd36 (p < 0.05) and Glut4 (p < 0.01), together with elevated Pdk4 (p < 0.001) mRNA expression—suggesting reduced carbohydrate oxidation—compared to controls. Additionally, DOX increased Murf1 (p < 0.05) and Atrogin1 (p < 0.05) mRNA expression—markers of protein degradation—compared to controls. In both the WAT and GAS of DOX-treated mice, Ppard mRNA expression remained unchanged. Overall, DEXRA failed to prevent these DOX-induced changes. Collectively, our results suggest that DOX induced varying degrees of wasting in adipose tissue and skeletal muscle, driven by distinct mechanisms. While DEXRA protected against DOX-induced CTRCD, it did not counteract its adverse effects on skeletal muscle and adipose tissue. Full article

During skeletal muscle unloading, phosphoinositide 3-kinase (PI3K), and especially PI3K gamma (PI3Kγ), can be activated by changes in membrane potential. Activated IP3 can increase the ability of Ca²⁺ to enter the nucleus through IP3 receptors. This may contribute to the activation of transcription factors that initiate muscle atrophy processes. LY294002 inhibitor was used to study the role of PI3K in the ATP-dependent regulation of skeletal muscle signaling during three days of unloading. Inhibition of PI3K during soleus muscle unloading slows down the atrophic processes and prevents the accumulation of ATP and the expression of the E3 ubiquitin ligase MuRF1 and ubiquitin. It also prevents the increase in the expression of IP3 receptors and regulates the activity of Ca²⁺-dependent signaling pathways by reducing the mRNA expression of the Ca²⁺-dependent marker calcineurin (CaN) and decreasing the phosphorylation of CaMKII. It also affects the regulation of markers of anabolic signaling in unloaded muscles: IRS1 and 4E-BP. PI3K is an important mediator of skeletal muscle atrophy during unloading. Developing strategies for the localized skeletal muscle release of PI3K inhibitors might be one of the future treatments for inactivity and disease-induced muscle atrophy. Full article