Characterization of Age-Dependent Changes in Skeletal Muscle Repair and Regeneration Using a Mouse Model of Acute Muscle Injury.

Acute skeletal muscle injury initiates a process of necrosis, debris clearance, and ultimately tissue regeneration via myogenesis. While skeletal muscle stem cells (MuSCs) are responsible for populating the proliferative myogenic progenitor pool to fuel muscle repair, recruited and resident immune cells have a central role in the regulation of muscle regeneration via the execution of phagocytosis and release of soluble factors that act directly on MuSCs to regulate myogenic differentiation. Therefore, the timing of MuSC proliferation and differentiation is closely linked to the populations and behaviors of immune cells present within skeletal muscle. This has important implications for aging and muscle repair, as systemic changes in immune system function contribute to a decline in muscle regenerative capacity. Here, we present adapted protocols for the isolation of mononuclear cells from skeletal muscles for the quantification of immune cell populations using flow cytometry. We also describe a cardiotoxin skeletal muscle injury protocol and detail the expected outcomes including immune cell infiltration to the injured sites and formation of new myocytes. As immune cell function is substantially influenced by aging, we extend these approaches and outcomes to aged mice.

Comprehensive Proteomic Analysis of Dysferlinopathy Unveiling Molecular Mechanisms and Biomarkers Linked to Pathological Progression.

AIMS: Previous proteomics studies in dysferlinopathy muscle have been limited in scope, often utilizing 2D-electrophoresis and yielding only a small number of differential expression calls. To address this gap, this study aimed to employ high-resolution proteomics to explore the proteomic landscapes of dysferlinopathy and analyze the correlation between muscle pathological changes and alterations in protein expression in muscle biopsies. METHODS: We conducted a comprehensive approach to investigate the proteomic profile and disease-associated changes in the muscle tissue proteome from 15 patients with dysferlinopathy, exhibiting varying degrees of dystrophic pathology, alongside age-matched controls. Our methodology encompasses tandem mass tag (TMT)-labeled liquid chromatography-mass spectrometry (LC-MS/MS)-based proteomics, protein-protein interaction (PPI) network analysis, weighted gene co-expression network analysis, and differential expression analysis. Subsequently, we examined the correlation between the expression of key proteins and the clinical characteristics of the patients to identify pathogenic targets associated with DYSF mutations in dysferlinopathy. RESULTS: A total of 1600 differentially expressed proteins were identified, with 1321 showing high expression levels and 279 expressed at lower levels. Our investigation yields a molecular profile delineating the altered protein networks in dysferlinopathy-afflicted skeletal muscle, uncovering dysregulation across numerous cellular pathways and molecular processes, including mRNA metabolic processes, regulated exocytosis, immune response, muscle system processes, energy metabolic processes, and calcium transmembrane transport. Moreover, we observe significant associations between the protein expression of ANXA1, ANXA2, ANXA4, ANXA5, LMNA, PYGM, and the extent of histopathologic changes in muscle biopsies from patients with dysferlinopathy, validated through immunoblotting and immunofluorescence assays. CONCLUSIONS: Through the aggregation of expression data from dysferlinopathy-impacted muscles exhibiting a range of pathological alterations, we identified multiple key proteins associated with the dystrophic pathology of patients with dysferlinopathy. These findings provide novel insights into the pathogenesis of dysferlinopathy and propose promising targets for future therapeutic endeavors.

Effects of coffee intake on skeletal muscle microvascular reactivity at rest and oxygen extraction during exercise: a randomized cross-over trial.

PURPOSE: The effects of coffee ingestion on skeletal muscle microvascular function are not well understood. This study aimed to investigate the acute effects of coffee intake with varying levels of caffeine on skeletal muscle microvascular reactivity at rest and oxygen extraction during maximal incremental exercise in physically active individuals. METHODS: Twenty healthy young male participants were administered coffee with low caffeine (3 mg/kg body weight; LC), high caffeine (6 mg/kg body weight; HC), and placebo (decaf) in different sessions. Skeletal muscle reactivity indexes, including tissue saturation index 10s slope (TSI10) and TSI half time recovery (TSI ½) following 5-minute ischemia were measured at rest and were measured at baseline and post-coffee consumption using near-infrared spectroscopy (NIRS). Post-coffee intake, NIRS was also used to measure microvascular oxygen extraction during exercise via maximal incremental exercise. Peak oxygen consumption and peak power output (Wpeak) were simultaneously evaluated. RESULTS: Post-coffee consumption, TSI10 was significantly higher in the LC condition compared to placebo (p = 0.001) and significantly higher in the HC condition compared to placebo (p < 0.001). However, no difference was detected between LC and HC conditions (p = 0.527). HC condition also showed significant less TSI ½ compared to placebo (p = 0.005). However, no difference was detected for microvascular oxygen extraction during exercise, despite the greater Wpeak found for HC condition (p < 0.001) compared to placebo. CONCLUSION: Coffee ingestion with high caffeine level (6 mg/kg body weight) significantly enhanced skeletal muscle reactivity at rest. However, the improvement of exercise performance with coffee intake is not accompanied by alterations in muscle oxygen extraction.

A Cross-Sectional Study of the Normative Data of the Side-To-Side Soleus Hoffmann Reflex from the Calf Muscle in Healthy Individuals in the Lying Down Position.

The goal of this study was to find out from the calf muscle, the normal H-reflex is in a group of healthy adults. This study is conducted for the period of one year in 2020-2021, in the department of Physiology AIIMS Bhopal, 119 adult male healthy volunteers who were asymptomatic from peripheral neuropathy and had a mean age of 30.40±6.78 were evaluated, to compare the normative tibial H reflex to their stature, body mass index, core body temperature, and limb length. The parameters considered were M- Latency, H-Latency, M-Amplitude, H- Amplitude and H/M Ratio in their left and right legs, respectively. A total of 111 participants (93.3%) were in the age group of 40 years or younger, with the mean age (in years) being 30.40±6.78. Only eight (8) participants (6.7%) belonged to the over-40 age group. The average weight (Kg), height (cm), and limb length (cm) were 173.11 cm, 10.48 cm, and 94.28 cm respectively. The mean ±SD latencies of the H reflex were 30.93±4.42 and 31.01±5.21 milliseconds in the right and left legs, respectively. Leg length and H reflex latency had a significant correlation (r = 0.55, p=0.05). There was no discernible correlation between age and the H reflex latency. The right and left H reflex latencies should vary by no more than 1.8 ms to be deemed normal. This research examined tibia H-reflex side-to-side latency variability and amplitude. Neurologic function may be assessed using the H-reflex. Due of its sensitivity to external circumstances, the H-reflex must be elicited carefully. The H-reflex may reveal neuronal function following damage if assessed appropriately.

The Rate of Leg Fat Oxidation Is Not Attenuated During Incremental Intensity One-Leg Knee Extensor Exercise.

It is not clear if fat oxidation is attenuated at higher exercise intensities, when exercising with a small muscle mass, and therefore, we studied leg fat oxidation during graded one-leg exercise. Ten males (age: 27 ± 2 years, body mass: 82 ± 3 kg, BMI: 24 ± 1 kg m-2, V̇O2max: 49 ± 2 mL min-1 kg-1) performed one-leg exercise at 25% of maximal workload (Wmax) for 30 min, followed by 120-min exercise at 55% Wmax with the contralateral leg, and finally 30-min exercise at 85% Wmax with the first leg. Blood was sampled from an artery and both femoral veins, and blood flow was determined using Doppler ultrasound. Muscle biopsies were obtained before and after 30 min at each workload. One-way RM ANOVA was applied to determine the impact of exercise intensity. Data are expressed as mean ± SEM. From rest through exercise average blood flow (0.4 ± 0.1, 2.1 ± 0.1, 2.6 ± 0.2, 3.7 ± 0.2 L min-1) and oxygen uptake across the leg (0.03 ± 0.01, 0.23 ± 0.02, 0.35 ± 0.03, 0.53 ± 0.04 L min-1) increased with exercise intensity (p < 0.001). Leg RQ (0.76 ± 0.04, 0.86 ± 0.02,0.87 ± 0.01, 0.92 ± 0.01, p < 0.001), leg plasma FA uptake (2 ± 2, 46 ± 8,83 ± 9, 114 ± 16 µmol min-1; p < 0.001) and rate of leg fat oxidation (0.016 ± 0.005, 0.062 ± 0.012, 0.075 ± 0.011, 0.084 ± 0.018 g min-1, p < 0.007) increased with exercise intensity. Muscle-free carnitine content was unchanged from rest at 25% Wmax and decreased after 30 min exercise at 55% and 85% Wmax (17.4 ± 1.6, 16.6 ± 0.7, 14.5 ± 1.2, 10.5 ± 1.0 mmol/kg dry muscle, respectively; p < 0.006). During incremental one-leg exercise, the rate of leg fat oxidation was not attenuated with increasing exercise intensity, probably due to an insufficient muscle metabolic stress response.

Loss of SELENOW aggravates muscle loss with regulation of protein synthesis and the ubiquitin-proteasome system.

Sarcopenia is characterized by accelerated muscle mass and function loss, which burdens and challenges public health worldwide. Several studies indicated that selenium deficiency is associated with sarcopenia; however, the specific mechanism remains unclear. Here, we demonstrated that selenoprotein W (SELENOW) containing selenium in the form of selenocysteine functioned in sarcopenia. SELENOW expression is up-regulated in dexamethasone (DEX)-induced muscle atrophy and age-related sarcopenia mouse models. Knockout (KO) of SELENOW profoundly aggravated the process of muscle mass loss in the two mouse models. Mechanistically, SELENOW KO suppressed the RAC1-mTOR cascade by the interaction between SELENOW and RAC1 and induced the imbalance of protein synthesis and degradation. Consistently, overexpression of SELENOW in vivo and in vitro alleviated the muscle and myotube atrophy induced by DEX. SELENOW played a role in age-related sarcopenia and regulated the genes associated with aging. Together, our study uncovered the function of SELENOW in age-related sarcopenia and provides promising evidence for the prevention and treatment of sarcopenia.

The Effects of the StartReact on Reaction Time, Rate of Force Development, and Muscle Activity in Biceps Brachii.

The StartReact test, increasingly popular for assessing cortico-reticular functioning, is a valid method to influence the firing of reticulospinal tract neurons noninvasively. However, there remains limited evidence on how different stimuli employed in the StartReact test impact motor output in humans. The present study tested elbow flexor responses of 33 adults (aged 26-48 years) to visual stimuli only (LED light), audio-visual (80 dB) stimuli, and startle-inducing audio-visual (120 dB) stimuli sitting with the arm supinated in an electromechanical dynamometer. Surface electromyogram (EMG) recorded muscle activity from the right biceps brachii muscle. Participants were presented with 20 stimuli for each of the three conditions in pseudorandom order with interstimulus intervals of ~8 s. Reaction times were calculated from the stimulus trigger to the initial rise in the EMG signal above 7 × SD from baseline. Rate of torque development (RTD) and EMG signals were recorded throughout and analyzed over their initial 50 ms and 100 ms time-windows. Reaction times were reduced from visual (169 ± 23) to audio-visual (140 ± 23) and further reduced to startle-inducing audio-visual stimuli (108 ± 19, p < 0.001). While RTD and EMG were consistently greatest following startle-inducing stimuli (p < 0.001), they were also enhanced following all audio-visual stimuli over 100 ms (p < 0.05). It appears that startle-inducing audio-visual stimuli result in shorter reaction times, increased RTD, and enhanced muscle activity within the initial 50 ms, likely from subcortical upregulation. However, the 100 ms time-window suggests cortical upregulation following all audio-visual stimuli considering the longer transmission times.

No Effects of Carbohydrate Ingestion on Muscle Metabolism or Performance During Short-Duration High-Intensity Intermittent Exercise.

Carbohydrates are critical for high-intensity exercise performance. However, the effects of carbohydrate supplementation on muscle metabolism and performance during short-duration high-intensity intermittent exercise remain inadequately explored. Our aim was to address this aspect in a randomized, counterbalanced, double-blinded crossover design. Eleven moderately-to-well-trained males performed high-intensity intermittent cycling receiving carbohydrate (CHO, ~55 g/h) or placebo (PLA) fluid supplementation. Three exercise periods (EX1-EX3) were completed comprising 10 × 45 s at ~105% Wmax interspersed with 135 s rest between bouts and ~20 min between periods. Repeated sprint ability (5 × 6 s sprints with 24 s recovery) was assessed at baseline and after each period. Thigh muscle biopsies were obtained at baseline and before and after EX3 to determine whole-muscle and fiber-type-specific glycogen depletion. No differences were found in muscle glycogen degradation at the whole-muscle (p = 0.683) or fiber-type-specific level (p = 0.763-0.854) with similar post-exercise whole-muscle glycogen concentrations (146 ± 20 and 122 ± 15 mmol·kg-1 dw in CHO and PLA, respectively). Repeated sprint ability declined by ~9% after EX3 with no between-condition differences (p = 0.971) and no overall differences in ratings of perceived exertion (p = 0.550). This was despite distinctions in blood glucose concentrations throughout exercise, reaching post-exercise levels of 5.3 ± 0.2 and 4.1 ± 0.2 mmol·L-1 (p < 0.001) in CHO and PLA, respectively, accompanied by fivefold higher plasma insulin levels in CHO (p < 0.001). In conclusion, we observed no effects of carbohydrate ingestion on net muscle glycogen breakdown or sprint performance during short-duration high-intensity intermittent exercise despite elevated blood glucose and insulin levels. These results therefore question the efficacy of carbohydrate supplementation strategies in high-intensity intermittent sports.

Amyotrophic lateral sclerosis as a disease model of sarcopenia.

Sarcopenia, the progressive decline of muscle mass and function, has traditionally been viewed as an age-related process leading to a broad range of adverse outcomes. However, it has been widely reported that sarcopenia can occur earlier in life in association with various conditions (i.e. disease-related sarcopenia), including neuromuscular disorders. As early as 2010, the European Working Group on Sarcopenia in Older People included neurodegenerative diseases characterised by motor neuron loss among the mechanisms underlying sarcopenia. Despite some differences in pathogenetic mechanisms, both amyotrophic lateral sclerosis (ALS) and age-related sarcopenia share common characteristics, such as the loss of motor units and muscle fibre atrophy, oxidative stress, mitochondrial dysfunction and inflammation. The histology of older muscle shows fibre size heterogeneity, fibre grouping and a loss of satellite cells, similar to what is observed in ALS patients. Regrettably, the sarcopenic process in ALS patients has been largely overlooked, and literature on the condition in this patient group is very scarce. Some instruments used for the assessment of sarcopenia in older people could also be applied to ALS patients. At this time, there is no approved specific pharmacological treatment to reverse damage to motor neurons or cure ALS, just as there is none for sarcopenia. However, some agents targeting the muscle, like myostatin and mammalian target of rapamycin inhibitors, are under investigation both in the sarcopenia and ALS context. The development of new therapeutic agents targeting the skeletal muscle may indeed be beneficial to both ALS patients and older people with sarcopenia.

Adults born preterm have lower peripheral skeletal muscle area and strength.

Prematurity is associated with lower exercise capacity, which relies on the integrity of the cardiovascular, pulmonary, and skeletal muscle systems. Our animal model mimicking prematurity-associated conditions showed altered muscle composition and atrophy in adulthood. This study aimed to compare muscle composition and strength in adults born preterm versus full-term controls. This observational cohort study recruited 55 adults born preterm, ≤ 29 weeks' of gestation and 53 full-term controls who underwent musculoskeletal ultrasound imaging to assess morphology of the rectus femoris at rest and during a maximal voluntary contraction. Maximal voluntary contraction of the hands and legs were measured by manual dynamometry. In adults born preterm, there was lower muscle strength (handgrip: - 4.8 kg, 95% CI - 9.1, - 0.6; knee extensor: - 44.6 N/m, 95% CI - 63.4, - 25.8) and smaller muscle area (- 130 mm2, 95% CI - 207, - 53), which was more pronounced with a history of bronchopulmonary dysplasia. Muscle stiffness was increased in the preterm versus term group (0.4 m/s, 95% CI 0.04, 0.7). Prematurity is associated with alterations in skeletal muscle composition, area, and function in adulthood. These findings highlight the necessity to implement preventive and/or curative approaches to improve muscle development and function following preterm birth to enhance overall health in this population.

Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in Mice.

Chronic kidney disease (CKD) is associated with various pathologic changes, including elevations in serum phosphate levels (hyperphosphatemia), vascular calcification, and skeletal muscle atrophy. Elevated phosphate can damage vascular smooth muscle cells and cause vascular calcification. Here, we determined whether high phosphate can also affect skeletal muscle cells and whether hyperphosphatemia, in the context of CKD or by itself, is associated with skeletal muscle atrophy. As models of hyperphosphatemia with CKD, we studied mice receiving an adenine-rich diet for 14 weeks and mice with deletion of Collagen 4a3 (Col4a3-/-). As models of hyperphosphatemia without CKD, we analyzed mice receiving a high-phosphate diet for three and six months as well as a genetic model for klotho deficiency (kl/kl). We found that adenine, Col4a3-/-, and kl/kl mice have reduced skeletal muscle mass and function and develop atrophy. Mice on a high-phosphate diet for six months also had lower skeletal muscle mass and function but no significant signs of atrophy, indicating less severe damage compared with the other three models. To determine the potential direct actions of phosphate on skeletal muscle, we cultured primary mouse myotubes in high phosphate concentrations, and we detected the induction of atrophy. We conclude that in experimental mouse models, hyperphosphatemia is sufficient to induce skeletal muscle atrophy and that, among various other factors, elevated phosphate levels might contribute to skeletal muscle injury in CKD.

Photobiomodulation therapy as an adjunct to resistance exercises on muscle metrics, functional balance, functional capacity, and physical performance among older adults: A systematic scoping review.

This scoping review aims to summarize the literature on photobiomodulation (PBM) therapy as an adjunct to resistance exercise among older adults, focusing on its effects on muscle metrics, functional balance, capacity, and physical performance. The participants included were older adults aged ≥ 60 years and either gender. The concept was the application of PBM and resistance exercises with no limits on the context parameters. The databases Medline, Embase, Scopus and Web of Science were searched from inception till February 2024. Methodological quality was assessed using the Cochrane risk of bias 2.0. A total of 10 studies were included in the review. PBM, along with resistance training, was reported in six studies, whereas four reported PBM with isometric fatigue protocol. PBM with a wavelength of 808 nm was given on the belly of the rectus femoris muscle in most of the studies. The common dosimetry parameters used were- power density 35.7 W/cm2, energy density 250 J/cm2, 8 sites, energy per site 7 J, duration of 70 s per site, spot size per diode of 0.028 cm2, and stationary contact of application. The application of PBM therapy alongside resistance exercise has been found to improve muscle metrics, functional capacity, and functional performance and reduce fatigability when compared with the control group in most of the studies. When incorporating PBM therapy as an adjunct to resistance training, it is crucial to consider the dosimetry parameters involved-to achieve the intended therapeutic effect. Adjusting treatment parameters with this information can optimize the effectiveness of PBM therapy and improve treatment outcomes for patients.

Clinical effect of anti-resistance exercise combined with nutritional intervention in the treatment of elderly patients with sarcopenia.

This study aims to evaluate the efficacy of a combined intervention involving resistance exercise and nutritional support in improving grip strength, walking speed, and skeletal muscle density among elderly individuals suffering from sarcopenia. Data from a cohort of 500 elderly sarcopenic patients were segregated into observation and control cohorts based on distinct treatment modalities. Baseline evaluations included weight, grip strength, walking speed, and skeletal muscle density. Changes in these parameters and oxidative stress markers were monitored and compared at 1-, 3-, and 6-month intervals. Baseline grip strength for the observation and control groups stood at (20.25 ±â€…2.34) and (21.06 ±â€…2.97) kg, respectively. Walking speed was measured at (0.99 ±â€…0.12) and (0.98 ±â€…0.20) m/s, respectively. Skeletal muscle density registered (42.98 ±â€…4.17) and (42.77 ±â€…5.02) Hu for the observation and control groups, respectively, while muscle mass index was recorded as (6.19 ±â€…1.46) and (6.20 ±â€…1.68) kg/m2, respectively. Limb skeletal muscle mass for both cohorts was (16.83 ±â€…3.57) and (16.77 ±â€…3.89) kg. No significant disparities were discerned in baseline characteristics between the groups. Following 1, 3, and 6 months, the observation group exhibited marked enhancements in grip strength and walking speed (P < .05), with substantially superior grip strength compared to the control cohort (P < .05). Notably, skeletal muscle density, muscle mass index, and limb skeletal muscle mass exhibited significant augmentation in the observation group (P < .05), while no significant alterations were observed in the control cohort. Oxidative stress-related parameters displayed no notable differences between groups pretreatment (P > .05). Post-treatment, levels of Hcy, IFN-γ, and MDA markedly decreased in both groups, with considerably lower levels evident in the observation cohort (P < .05). Moreover, SOD levels exhibited significant post-treatment increments in both groups, with markedly higher levels observed in the observation group (P < .05). An integrated approach of resistance exercise and nutritional support significantly enhances grip strength, walking speed, and skeletal muscle density in elderly patients with sarcopenia, contributing to better prognoses and improved quality of life.

Relative muscle indices and healthy reference values for sarcopenia assessment using T10 through L5 computed tomography skeletal muscle area.

Sarcopenia is the age-related loss of skeletal muscle mass and function. Computed tomography (CT) assessments of sarcopenia utilize measurements of skeletal muscle cross-sectional area (SMA), radiation attenuation (SMRA), and intramuscular adipose tissue (IMAT). Unadjusted SMA is strongly correlated with both height and body mass index (BMI); therefore, SMA must be adjusted for body size to assess sarcopenic low muscle mass fairly in individuals of different heights and BMI. SMA/height (rather than S M A / h e i g h t 2 ) provides optimal height adjustment, and vertebra-specific relative muscle index (RMI) equations optimally adjust for both height and BMI. Since L3 measurement is not available in all CT scans, sarcopenic low muscle mass may be assessed using other levels. Both a mid-vertebral slice and an inferior slice have been used to define 'L3 SMA', but the effect of vertebral slice location on SMA measurements is unexplored. Healthy reference values for skeletal muscle measures at mid- and inferior vertebra slices between T10 and L5, have not yet been reported. We extracted T10 through L5 SMA, SMRA, and IMAT at a mid-vertebral and inferior slice using non-contrast-enhanced CT scans from healthy, adult kidney donor candidates between age 18 and 73. We compared paired differences in SMA between the mid-vertebral slice versus the inferior slice. We calculated the skeletal muscle gauge as S M G HT = S M R A ∗ S M I HT . We used allometric analysis to find the optimal height scaling power for SMA. To enable comparisons with other published reference cohorts, we computed two height-adjusted measures; S M I HT = S M A / h e i g h t (optimal) and S M I H T 2 = S M A / h e i g h t 2 (traditional). Using the young, healthy reference cohort, we utilized multiple linear regression to calculate relative muscle index z-scores ( R M I HT , R M I H T 2 ), which adjust for both height and BMI, at each vertebra level. We assessed Pearson correlations of each muscle area measure versus age, height, weight, and BMI separately by sex and vertebra number. We assessed the differences in means between age 18-40 versus 20-40 as the healthy, young adult reference group. We reported means, standard deviations, and sarcopenia cutpoints (mean-2SD and 5th percentile) by sex and age group for all measures. Sex-specific allometric analysis showed that height to the power of one was the optimal adjustment for SMA in both men and women at all vertebra levels. Differences between mid-vertebra and inferior slice SMA were statistically significant at each vertebra level, except for T10 in men. S M I HT was uncorrelated with height, whereas S M I H T 2 was negatively correlated with height at all vertebra levels. Both S M I HT and S M I H T 2 were positively correlated with BMI at all vertebra levels. R M I HT was uncorrelated with BMI, weight, and height (minimal positive correlation in women at L3 inf , L4 mid , and L5 inf ) whereas R M I H T 2 was uncorrelated with BMI, but negatively correlated with height and weight at all levels. There were no significant differences in SMA between 18-40 versus 20-40 age groups. Healthy reference values and sarcopenic cutpoints are reported stratified by sex, vertebra level, and age group for each measure. Height to the power of one (SMA/height) is the optimal height adjustment factor for SMA at all levels between T10 mid through L5 inf . The use of S M A / h e i g h t 2 should be discontinued as it retains a significant negative correlation with height and is therefore biased towards identifying sarcopenia in taller individuals. Measurement of SMA at a mid-vertebral slice is significantly different from measurement of SMA at an inferior aspect slice. Reference values should be used for the appropriate slice. We report sarcopenic healthy reference values for skeletal muscle measures at the mid-vertebral and inferior aspect slice for T10 through L5 vertebra levels. Relative muscle index (RMI) equations developed here minimize correlation with both height and BMI, producing unbiased assessments of relative muscle mass across the full range of body sizes. We recommend the use of these RMI equations in other cohorts.

The effects of hydrotherapy and cryotherapy on recovery from acute post-exercise induced muscle damage-a network meta-analysis.

BACKGROUND: This systematic review and network meta-analysis assessed via direct and indirect comparisons the recovery effects of hydrotherapy and cold therapy at different temperatures on exercise induced muscle damage. METHODS: Five databases were searched in English and Chinese. The included studies included exercise interventions such as resistance training, high-intensity interval training, and ball games, which the authors were able to define as activities that induce the appearance of EIMD. The included RCTs were analyzed using the Cochrane Risk of Bias tool. Eligible studies were included and and two independent review authors extracted data. Frequentist network meta-analytical approaches were calculated based on standardized mean difference (SMD) using random effects models. The effectiveness of each intervention was ranked and the optimal intervention was determined using the surface under the cumulative ranking curve (SUCRA) indicator. RESULTS: 57 studies with 1220 healthy participants were included, and four interventions were examined: Cold Water Immersion (CWI), Contrast Water Therapy (CWT), Thermoneutral or Hot Water Immersion (TWI/HWI), and Cryotherapy(CRYO). According to network meta-analysis, Contrast Water Immersion (SUCRA: 79.9% )is most effective in recovering the biochemical marker Creatine Kinase. Cryotherapy (SUCRA: 88.3%) works best to relieve Delayed Onset Muscle Soreness. In the recovery of Jump Ability, cryotherapy (SUCRA: 83.7%) still ranks the highest. CONCLUSION: We found that CWT was the best for recovering biochemical markers CK, and CRYO was best for muscle soreness and neuromuscular recovery. In clinical practice, we recommend the use of CWI and CRYO for reducing EIMD. SYSTEMATIC REVIEW REGISTRATION: [PROSPERO], identifier [CRD42023396067].

Elbow Flexion Reconstruction after Traumatic Amputation Using Hinged External Fixator and Muscle Transfer: A Case Report.

CASE: A 40-year-old man sustained a traumatic elbow disarticulation without any fracture, accompanied by severe damage of the biceps and brachialis. After replantation, passive elbow motion was used with a hinged external fixator to facilitate elbow joint reduction and mobility. Eight months after the injury, a functional latissimus dorsi transfer for elbow flexion restoration was performed. Ten years postoperatively, he achieved antigravity elbow flexion and 120° of flexion and -15° extension of the elbow. CONCLUSION: This reconstruction technique was useful for reconstructing elbow flexion after traumatic elbow disarticulation.

Effects of Trimethylamine N-Oxide in Improving Exercise Performance in Mice: A 1H-NMR-Based Metabolomic Analysis Approach.

To improve exercise performance, the supplement of nutrients has become a common practice before prolonged exercise. Trimethylamine N-oxide (TMAO) has been shown to ameliorate oxidative stress damage, which may be beneficial in improving exercise capacity. Here, we assessed the effects of TMAO on mice with exhaustive swimming, analyzed the metabolic changes, and identified significantly altered metabolic pathways of skeletal muscle using a nuclear magnetic resonance-based (NMR-based) metabolomics approach to uncover the effects of TMAO improving exercise performance of mice. We found that TMAO pre-administration markedly prolonged the exhaustive time in mice. Further investigation showed that TMAO pre-administration increased levels of 3-hydroxybutyrate, isocitrate, anserine, TMA, taurine, glycine, and glutathione and disturbed the three metabolic pathways related to oxidative stress and protein synthesis in skeletal muscle. Our results provide a metabolic mechanistic understanding of the effects of TMAO supplements on the exercise performance of skeletal muscle in mice. This work may be beneficial in exploring the potential of TMAO to be applied in nutritional supplementation to improve exercise performance. This work will lay a scientific foundation and be beneficial to exploring the potential of TMAO to apply in nutritional supplementation.

Exogenous Lactate Treatment Immediately after Exercise Promotes Glycogen Recovery in Type-II Muscle in Mice.

Recent studies suggest that lactate intake has a positive effect on glycogen recovery after exercise. However, it is important to verify the effect of lactate supplementation alone and the timing of glycogen recovery. Therefore, in this study, we aimed to examine the effect of lactate supplementation immediately after exercise on glycogen recovery in mice liver and skeletal muscle at 1, 3, and 5 h after exercise. Mice were randomly divided into the sedentary, exercise-only, lactate, and saline-treated groups. mRNA expression and activation of glycogen synthesis and lactate transport-related factors in the liver and skeletal muscle were assessed using real-time polymerase chain reaction. Skeletal muscle glycogen concentration showed an increasing trend in the lactate group compared with that in the control group at 3 and 5 h after post-supplementation. Additionally, exogenous lactate supplementation significantly increased the expression of core glycogen synthesis enzymes, lactate transporters, and pyruvate dehydrogenase E1 alpha 1 in the skeletal muscles. Conversely, glycogen synthesis, lactate transport, and glycogen oxidation to acetyl-CoA were not significantly affected in the liver by exogenous lactate supplementation. Overall, these results suggest that post-exercise lactate supplement enables glycogen synthesis and recovery in skeletal muscles.

IA-Body Composition CT at T12 in Idiopathic Pulmonary Fibrosis: Diagnosing Sarcopenia and Correlating with Other Morphofunctional Assessment Techniques.

BACKGROUND: Body composition (BC) techniques, including bioelectrical impedance analysis (BIVA), nutritional ultrasound® (NU), and computed tomography (CT), can detect nutritional diagnoses such as sarcopenia (Sc). Sc in idiopathic pulmonary fibrosis (IPF) is associated with greater severity and lower survival. Our aim was to explore the correlation of BIVA, NU and functional parameters with BC at T12 level CT scans in patients with IPF but also its relationship with degree of Sc, malnutrition and mortality. METHODS: This bicentric cross-sectional study included 60 IPF patients (85.2% male, 70.9 ± 7.8 years). Morphofunctional assessment (MFA) techniques included BIVA, NU, CT at T12 level (T12-CT), handgrip strength, and timed up and go. CT data were obtained using FocusedON®. Statistical analysis was conducted using JAMOVI version 2.3.22 to determine the cutoff points for Sc in T12-CT and to analyze correlations with other MFA techniques. RESULTS: the cutoff for muscle area in T12-CT was ≤77.44 cm2 (area under the curve (AUC) = 0.734, sensitivity = 41.7%, specificity = 100%). The skeletal muscle index (SMI_T12CT) cutoff was ≤24.5 cm2/m2 (AUC = 0.689, sensitivity = 66.7%, specificity = 66.7%). Low SMI_T12CT exhibited significantly reduced median survival and higher risk of mortality compared to those with normal muscle mass (SMI cut off ≥ 28.8 cm/m2). SMI_T12CT was highly correlated with body cell mass from BIVA (r = 0.681) and rectus femoris cross-sectional area (RF-CSA) from NU (r = 0.599). Cronbach's α for muscle parameters across different MFA techniques and CT was 0.735, confirming their validity for evaluating muscle composition. CONCLUSIONS: T12-CT scan is a reliable technique for measuring low muscle mass in patients with IPF, specifically when the L3 vertebrae are not captured. An SMI value of <28.8 is a good predictor of low lean mass and 12-month mortality in IPF patients.

Effect of Lactational Low-Protein Diet on Skeletal Muscle during Adulthood and Ageing in Male and Female Mouse Offspring.

Sarcopenia is characterised by the loss of skeletal muscle mass and function, which leads to a high risk of increased morbidity and mortality. Maternal malnutrition has been linked to impaired development of skeletal muscle of the offspring; however, there are limited studies that report the long-term effect of a maternal low-protein diet during lactation on the ageing of skeletal muscles. This study aimed to examine how a maternal low-protein diet (LPD) during lactation affects skeletal muscle ageing in the offspring. Pups born from control mothers were lactated by mothers fed with an LPD. Post-weaning, mice were either maintained on an LPD or switched to a control, normal-protein diet (NPD). In males, an LPD mainly affected the size of the myofibres without a major effect on fibre number and led to reduced grip strength in ageing mice (24 months). Female mice from mothers on an LPD had a lower body and muscle weight at weaning but caught up with control mice at 3 months. During ageing, the muscle weight, myofibre number and survival rate of female pups were significantly affected. These findings highlight the effect of an LPD during lactation on skeletal muscle ageing, the lifespan of offspring and the importance of sexual dimorphism in response to dietary challenges.