The sympathetic nervous system (SNS) is recognized for its role in the physiological regulation of organs, such as heart, vasculature and lungs, and has emerged as a potential player in skeletal muscle metabolic and neuromuscular junction (NMJ) health. However, the mechanism through which SNS signaling influences skeletal muscle function and adaptation to exercise remains unclear. Using molecular, electrophysiological, immunohistochemical, and high-resolution respirometry techniques, we tested the role of sympathetic innervation to skeletal muscle in response to exercise. Our findings reveal that sympathetic denervation disrupts the NMJ, reducing motor and sympathetic receptor expression, with concomitant deficits in skeletal muscle function. Mechanistically, these deficits are linked to diminished CPT1 enzyme activity, which impairs long-chain fatty acid-mediated oxidation in skeletal muscle mitochondria. These findings reveal a key role for sympathetic innervation in maintaining mitochondrial metabolic function and by extension, skeletal muscle performance, offering novel insight into the interplay between the SNS, exercise, and muscle mitochondria.

ABSTRACTMitochondrial function is essential for skeletal muscle health, and its disruption leads to atrophy and functional decline. This study examines the impact of denervation on skeletal muscle mitochondria in polymerase gamma (PolG)(+/mut) mice, which accumulate mitochondrial DNA (mtDNA) mutations due to a partial deficiency in polymerase gamma proofreading. Using a 14‐day denervation protocol, we assessed muscle mass, mtDNA copy number, oxidative stress and mitochondrial dynamics in wild‐type (WT) and PolG(+/mut) mice. Our findings reveal that while denervation significantly reduced muscle wet weight and mitochondrial enzyme activity, no genotype‐specific differences in muscle atrophy were observed. However, PolG(+/mut) mice displayed more disorganized mitochondrial cristae and elevated oxidative stress markers, indicating greater mitochondrial vulnerability. Despite these changes, the lack of significant differences in mitochondrial proteins and gene expression between genotypes may reflect an adaptive antioxidant response, including increased catalase expression, although the compensatory nature of this response cannot be conclusively determined. These results suggest that oxidative stress–related responses are involved in mitochondrial adaptations during denervation‐induced muscle atrophy. The increased expression of antioxidant enzymes, such as catalase, in PolG(+/mut) mice suggests that antioxidant mechanisms are activated in response to increased oxidative stress. These findings underscore the importance of controlling oxidative stress for maintaining muscle health.

Age-related skeletal muscle deterioration is a commonly reported disability among older adults, attributed to several factors including mitochondrial dysfunction, a major hallmark of aging. Therapies to attenuate or reverse mitochondrial decline are limited. Despite identified positive relationships between vitamin B12 (B12) and mitochondrial biology, the impact of B12 supplementation on skeletal muscle mitochondria, in advanced aged, has not been examined. Thus, the impact of B12 supplementation on skeletal muscle mitochondrial biology was examined in (i) aged female mice, given 12 weeks of B12 supplementation (SUPP) or vehicle control, and (ii) in human primary myotubes. In the mouse model, mitochondrial DNA and content were measured with PCR and citrate synthase activity, respectively; mitochondrial morphology was examined using transmission electron microscopy; mitochondrial function was examined using extracellular metabolic flux analysis; and proteins and pathway enrichment was identified with proteomics. In the cell model, ROS and glutathione was measured using luminescent assays. The results demonstrated that SUPP in aged mice increased muscle mitochondrial content and improved morphology. Further, differentially expressed proteins were enriched in TCA cycle, OXPHOS, and oxidative stress pathways. In the cell model, B12 supplementation reduced ROS levels. This is the first study, to our knowledge, examining the impact of B12 supplementation on skeletal muscle mitochondrial biology in aged female mice. Results suggest that B12 supplementation improves mitochondrial biology in aged female mice.

Body mass shapes mitochondrial NADH and NADPH sources in mammalian skeletal muscle.

ABSTRACTSkeletal muscle mitochondria adaptation to exercise training is mediated by molecular factors that are not fully understood. Mitochondria import over 1000 proteins encoded by the nuclear genome, but the RNA population resident within the organelle is generally thought to be exclusively encoded by the mitochondrial genome. However, recent in vitro evidence suggests that specific nuclear‐encoded miRNAs and other noncoding RNAs (ncRNAs) can reside within the mitochondrial matrix. Whether these are present in mitochondria of skeletal muscle tissue, and whether this is affected by endurance training—a potent metabolic stimulus for mitochondrial adaptation—remains unknown. Rats underwent 4 weeks of moderate‐intensity treadmill exercise training, then were humanely killed and tissues were collected for molecular profiling. Mitochondria from gastrocnemius skeletal muscle were isolated by immunoprecipitation, further purified, and then the resident RNA was sequenced to assess the mitochondrial transcriptome. Exercise training elicited typical transcriptomic responses and functional adaptations in skeletal muscle, including increased mitochondrial respiratory capacity. We identified 24 nuclear‐encoded coding or noncoding RNAs in purified mitochondria, in addition to 50 nuclear‐encoded miRNAs that met a specified abundance threshold. Although none were differentially expressed in the exercise vs. control group at FDR < 0.05, exploratory analyses suggested that the abundance of 3 miRNAs was altered (p < 0.05) in mitochondria isolated from trained compared with sedentary skeletal muscle. We report the presence of a specific population of nuclear‐encoded RNAs in the mitochondria isolated from rat skeletal muscle tissue, which could play a role in regulating exercise adaptations and mitochondrial biology.

Skeletal and cardiac muscle mitochondria exist in a dynamic reticulum that is maintained by a balance of mitochondrial biogenesis, fusion, fission, and mitophagy. This balance is crucial for adequate ATP production, and alterations in skeletal muscle mitochondria have been implicated in aging-associated declines in mitochondrial function. We sought to determine whether age and biological sex affect mitochondrial content [Complex IV (CIV)], biogenesis (PGC-1ɑ), fusion (MFN2, OPA1), fission (DRP1, FIS1), and mitophagy (Parkin, Pink1) markers in skeletal and cardiac muscle by assessing protein expression in tibialis anterior (TA) and ventricular tissue from 16 young (≤6 months) and 16 old (≥20 months) male and female Sprague-Dawley rats. In the TA, CIV expression was 40% lower in old vs. young rats (p < 0.001), indicating lower mitochondrial content, and coincided with higher expression of Parkin (+4-fold, p < 0.001). Further, MFN2 expression was higher (+2-fold, p < 0.005) and DRP1 expression was lower (-40%, p = 0.014) in older rats. In cardiac muscle, mitochondrial content was maintained in old vs. young rats, and this occurred concomitantly with higher expression of both PGC-1ɑ and Parkin. MFN2 and OPA1 expression were also 1.2-5-fold higher in older rats (p < 0.05 for all). Largely, protein expression did not differ between male and female rats, with the exception of Pink1 and FIS1 expression in the TA. Collectively, older skeletal and cardiac muscle demonstrated higher expression of fusion and mitophagy proteins, which indicates age alters the balance of biogenesis, fission, fusion, and mitophagy. This may, in turn, affect the ability to provide ATP to these metabolically active tissues.

IntroductionDyslipidaemia, affecting approximately 39% of adults worldwide, is a major risk factor for cardiovascular disease. Individuals with dyslipidaemia are often prescribed statins, which effectively lower plasma low-density lipoprotein cholesterol (LDL-C), thereby reducing the risk of cardiovascular events and mortality. Although statins lower LDL-C, emerging evidence suggests that they may counteract the beneficial adaptations to exercise in skeletal muscle mitochondria and whole-body aerobic capacity. The underlying mechanisms remain unclear, and there is a need for studies investigating how statins influence molecular adaptations to exercise. The primary objective of this study is to investigate the combined effects of statin therapy and focused exercise training on mitochondrial function and whole-body aerobic capacity in people with dyslipidaemia. The untargeted proteomic analysis will be incorporated to provide detailed insights into how statins may affect mitochondrial proteins and other muscle metabolic traits, offering molecular explanations for altered functional readouts at both the muscle and whole-body levels.Methods and analysisA total of 100 women and men (aged 40–65 years) diagnosed with dyslipidaemia without atherosclerotic cardiovascular disease will be enrolled in this 12-week, double-blinded, randomised, placebo-controlled trial. Participants will be randomised into one of four groups using a block randomisation approach to ensure an allocation ratio of 60:40 for exercise and non-exercise conditions, respectively. The four groups will be: (1) exercise+placebo, (2) exercise+atorvastatin (80 mg/day), (3) atorvastatin (80 mg/day) and (4) placebo. The primary outcome is mitochondrial function, measured by changes in skeletal muscle citrate synthase activity from baseline to post-intervention. Secondary outcomes include whole-body aerobic capacity (VO2peak) and proteomic analyses. Genetic analysis will be conducted to assess the role of genetic polymorphisms in individual responses to statins and exercise.Ethics and disseminationThe trial has received ethical approval from the Faroe Islands Ethical Committee (2024-10) and adheres to the Declaration of Helsinki and General Data Protection Regulation (GDPR). Results will be published in peer-reviewed international journals.Trial registration numberNCT06841536.

Effects of X-ray irradiation and housing conditions on mitochondria in Peromyscus maniculatus.

Sarcopenia, a condition associated with aging, involves progressive loss of muscle mass, strength, and function, leading to impaired mobility, health, and increased mortality. The underlying mechanisms remain unclear, which limits the development of effective therapeutic interventions. Emerging evidence implicates chronodisruption as a key contributor to sarcopenia, emphasizing the role of Bmal1, a circadian clock gene critical for muscle integrity and mitochondrial function. In a skeletal muscle-specific and inducible Bmal1 knockout model (iMS-Bmal1-/-), we observed hallmark features of sarcopenia, including disrupted rhythms, impaired muscle function, and mitochondrial dysfunction. Exercise and melatonin treatment reversed these deficits independently of Bmal1. Building on these findings, the present study elucidates several mechanisms underlying these changes and the pathways by which melatonin and exercise exert their beneficial effects. Our findings indicate that iMS-Bmal1-/- mice exhibit reduced expression of satellite cell and muscle regulatory factors, indicating impaired muscle regeneration. While mitochondrial respiration remained unchanged, notable alterations in mitochondrial dynamics disrupted mitochondria in skeletal muscle. In addition, these mice showed alterations in muscle energy metabolism, compromised antioxidant defense, and inflammatory response. Remarkably, exercise and/or melatonin successfully mitigated these deficits, restoring muscle health in Bmal1-deficient mice. These findings position exercise and melatonin as promising therapeutic candidates for combating sarcopenia and emphasize the need to elucidate the molecular pathways underlying their protective effects.

Apolipoprotein E4 (APOE4) is the greatest genetic risk factor for Alzheimer's (AD) and is linked to whole-body metabolic dysfunction. However, it is unclear how APOE4 interacts with modifiable factors like diet to impact tissues central to regulating whole-body metabolism. We examined APOE4- and Western diet-driven effects in skeletal muscle using APOE3 (control) and APOE4 targeted replacement mice on a C57BL/6NTac background fed a high-fat diet (HFD, 45%kcal fat) or low-fat diet (LFD, 10%kcal fat) for 4 months (n=7-8 per genotype/diet/sex combination). We assessed body composition and whole-body outcomes linked to skeletal muscle function including respiratory exchange ratio (RER) and resting energy expenditure (REE). In skeletal muscle, we evaluated the proteome and mitochondrial respiration. In males only, APOE4 drove greater gains in fat mass and lower gains in lean mass on both diets. APOE4 did not affect daily RER but was associated with elevated REE in males and lower REE in HFD females after covarying for body composition. Skeletal muscle proteomics showed APOE4 exerts several diet- and sex-specific effects on mitochondrial pathways, including elevations in branched-chain amino catabolism in HFD males and reductions in oxidative phosphorylation in LFD females. This did not translate to differences in skeletal muscle mitochondrial respiration, suggesting that compensatory mechanisms may sustain mitochondrial function at this age. Our work indicates that genetic risk may mediate early life effects on skeletal muscle mitochondria and energy expenditure that are partially dependent on diet. This has important implications for mitigating ad risk in APOE4 carriers.

Endurance athletes exhibit higher skeletal muscle mitochondrial and lipid droplet (LD) content compared with recreationally active individuals, along with greater whole body oxygen uptake and maximal fat oxidation rates. In this study, we investigated whether these differences manifest in a greater LD-mitochondria contact and how this may relate to the organelles' size, shape, and numerical densities. We obtained skeletal muscle biopsies from 17 male elite triathletes and road cyclists and seven recreationally active men. Using quantitative transmission electron microscopy, we found that the endurance athletes had two- to threefold greater LD-mitochondria total contact length than the recreationally active individuals. This was related to higher numerical densities of both mitochondria (+30%) and LDs (+100%) in the intermyofibrillar space. Adding data from untrained individuals with equally high intermyofibrillar LD density as the endurance athletes revealed a 24% greater total LD-mitochondria contact length in the endurance athletes. We observed small trivial differences in the shape of both organelles between populations. However, large mitochondrial profiles were more elongated and irregular in shape than small mitochondrial profiles, whereas large LD profiles were more circular and less irregular than small LD profiles. Within athletes, large intermyofibrillar LD profiles correlated (r = 0.72) with a high fraction of PLIN5-positive LDs and their maximal fat oxidation rate was positively associated with an interaction between the profile size of both intermyofibrillar LDs and mitochondria. In conclusion, male endurance athletes have a greater LD-mitochondria contact than recreationally active and untrained individuals. This muscular phenotype is restricted to the intermyofibrillar space and to fibers rich in mitochondria.NEW & NOTEWORTHY Lipid droplets and mitochondria form membrane contacts in skeletal muscle fibers, but the quantitative magnitude of these contacts remains unknown. Our study reveals that endurance athletes exhibit greater contact length between lipid droplets and mitochondria compared with recreationally active and untrained individuals. This difference is influenced by the content and spatial distribution of mitochondria and lipid droplets. The results provide quantitative insights into lipid droplet and mitochondria morphology across various human populations, including endurance athletes.

Amyotrophic lateral sclerosis (ALS) is a progressive multisystem disease characterized by limb and trunk muscle weakness that is attributed, in part, to abnormalities in mitochondrial ultrastructure and impaired mitochondrial functions. This study investigated the time course of structural and functional rearrangements in skeletal muscle mitochondria in combination with motor impairments in Tg (copper-zinc superoxide dismutase enzyme (SOD1) G93A) dl1/GurJ (referred to as SOD1-G93A/low) male mice, a familial ALS model, as compared with non-transgenic littermates. The neurological status and motor functions were assessed weekly using the paw grip endurance method and the grid suspension test with two-limb and four-limb suspension tasks. Transmission electron microscopy followed by quantitative analysis was performed to study ultrastructural alterations in the quadriceps femoris. Functional analysis of skeletal muscle mitochondria was performed using high-resolution Oxygraph-2k (O2K) respirometry and methods for assessing the calcium retention capacity index and the content of lipid peroxidation products in freshly isolated preparations. Based on the behavioral phenotyping data, specific age groups were identified: postnatal day 56 (P56) (n = 10-11), 84 (P84) (n = 10-11), and 156 (P154) (n = 10-12), representing the pre-symptomatic, early-symptomatic and late-symptomatic stages of ALS progression in SOD1-G93A/low mice, respectively. Electron microscopy showed mosaic destructive changes in subsarcolemmal mitochondria in fibers of the quadriceps femoris from 84-day-old SOD1-G93A/low mice. Morphometric analysis revealed an elevation in the mean size of the mitochondria in SOD1-G93A mice at P84 and P154. In addition, the P154 transgenic group demonstrated a decrease in sarcomere width and the number of mitochondria per unit area. At the symptomatic stage, SOD1-G93A mice exhibited a decreased respiratory control ratio, ADP-stimulated, and uncoupled respiration rates of mitochondria isolated from the quadriceps femoris muscle, as measured by high-resolution respirometry. In parallel, the mitochondria showed lower calcium retention capacity and increased levels of lipid peroxidation products compared with the control. Taken together, these results indicate stage-dependent changes in skeletal muscle mitochondrial ultrastructure and functions associated with defective oxidative phosphorylation, impaired calcium homeostasis, and oxidative damage in the SOD1-G93A/low mouse model, which appears to be a promising direction for the development of combination therapies for ALS.

Introduction: Mitochondria play a vital role in skeletal muscle function, and their adaptations to exercise are regulated by key proteins like PGC-1α (mitochondrial biogenesis) and mTOR (muscle hypertrophy). Varying training modalities, including endurance, HIIT, resistance, and concurrent training, induce distinct mitochondrial changes. Methods: A literature review was conducted using PubMed to identify human studies published after 2014 on exercise-induced mitochondrial adaptations. The accepted articles focussed on different training intensities and their effects on the skeletal muscle mitochondria. Results: Endurance and HIIT training enhance mitochondrial biogenesis and efficiency, increasing oxidative capacity and mitochondrial density. Resistance training improves mitochondrial function to support muscle growth, though its effects on mitochondrial biogenesis are less pronounced. Concurrent training, combining endurance and resistance training, optimizes both mitochondrial adaptations and muscle hypertrophy by activating both PGC-1α and mTOR pathways. Discussion: Exercise intensity and modality-specific adaptations are regulated by the interaction of PGC-1α and mTOR pathways, with mitochondrial fusion and fission enzymes playing a crucial role in maintaining mitochondrial function. Endurance and HIIT training focus on mitochondrial function, while resistance training primarily addresses muscle hypertrophy. Concurrent training optimally stimulates both PGC-1α and mTOR pathways, offering synergistic benefits for mitochondrial and muscle adaptations. Due to individual variability in response to exercise stimuli, personalized training approaches are crucial for maximal athletic performance. Conclusion: Mitochondrial adaptations depend on exercise type and intensity. Concurrent training provides a promising strategy to maximize both mitochondrial function and muscle growth. Future research should explore optimal training sequencing and molecular mechanisms to refine personalized exercise programs.

The target of rapamycin(TOR)gene is closely related to metabolism and cellular aging, but it is unclear whether the TOR pathways mediate endurance exercise against the accelerated aging of skeletal muscle induced by high salt intake. In this study, muscular TOR gene overexpression and RNAi were constructed by constructing MhcGAL4/TOR-overexpression and MhcGAL4/TORUAS-RNAi systems in Drosophila. The results showed that muscle TOR knockdown and endurance exercise significantly increased the climbing speed, climbing endurance, the expression of autophagy related gene 2(ATG2), silent information regulator 2(SIR2), and pparγ coactivator 1(PGC-1α) genes, and superoxide dismutases(SOD) activity, but it decreased the expression of the TOR gene and reactive oxygen species(ROS) level, and it protected the myofibrillar fibers and mitochondria of skeletal muscle in Drosophila on a high-salt diet. TOR overexpression yielded similar results to the high salt diet(HSD) alone, with the opposite effect of TOR knockout found in regard to endurance exercise and HSD-induced age-related skeletal muscle degradation. Therefore, the current findings confirm that the muscle TOR gene plays an important role in endurance exercise against HSD-induced age-related skeletal muscle degeneration, as it determines the activity of the mammalian target of rapamycin(MTOR)/SIR2/PGC-1α and MTOR/ATG2/PGC-1α pathways in skeletal muscle.

Mitochondria, the power plants of cells, are essential for various cellular functions. In skeletal muscle, mitochondria form a network, called mitochondrial reticulum, which fuels muscle contractile and metabolic functions. The high degree of structure-to-function specialization of mitochondria in skeletal muscle implies that it is closely gauged and regulated to maintain energy production capacity to match the functional demands. The processes that regulate the overall structure and function of mitochondrial reticulum are collectively referred to as mitochondrial quality control. Mitochondrial quality control consists of mitochondrial biogenesis, dynamics (i.e., fission and fusion), and selective degradation via proteolysis and mitophagy. In this chapter, we will discuss different aspects of contemporary understanding of mitochondrial quality control, their respective mechanisms, and their adaptability to exercise training.

Skeletal muscle abnormalities, including mitochondrial dysfunction, play a crucial role in decreasing exercise capacity in patients with heart failure (HF). Although enhanced reactive oxygen species (ROS) production in skeletal muscle mitochondria has been implicated in skeletal muscle abnormalities, the underlying mechanisms have not been fully elucidated to date. Superoxide dismutase 2 (SOD2), an antioxidant enzyme present in mitochondria, is modified by acetylation, which reduces its activity. The aim of this study was to clarify whether reducing SOD2 acetylation by sirtuins 3 (SIRT3) activation improves skeletal muscle mitochondrial function and exercise capacity in HF model mice. Myocardial infarction (MI) by ligation of the coronary artery or sham surgery was performed in male C57BL/6 J mice. Two weeks after surgery, these mice were treated with either the SIRT3 activator Honokiol (5 mg/kg body weight/day, i.p.) or vehicle. After 2 weeks of treatment, exercise capacity was evaluated by the treadmill test. Gastrocnemius muscle samples collected from the mice were used to measure mitochondrial function, as well as the levels of SIRT3, acetylated SOD2, and ROS production. Finally, the effect of adeno-associated virus serotype 9 (AAV9)-mediated overexpression of SIRT3 in the skeletal muscle on the exercise capacity of MI mice was investigated. MI mice showed decreased cardiac function and skeletal muscle weight, but Honokiol did not affect these. Exercise capacity was significantly decreased in MI mice compared with sham mice by 24.9%, and Honokiol treatment improved the exercise capacity of MI mice by 40.4% (p < 0.05). The mitochondrial oxygen consumption rate was impaired in MI mice, but was improved by Honokiol treatment. SIRT3 expression was decreased by 26.8%, and SOD2 acetylation was increased by 36.9% in the skeletal muscle of MI mice compared with sham (p < 0.05), and Honokiol treatment resulted in complete recovery of these levels (p < 0.05). Consistent with SOD2 acetylation, ROS production in the skeletal muscle was increased in MI mice and was ameliorated by Honokiol (p < 0.05). SIRT3 expression was increased in MI + AAV9-SIRT3 mice compared with MI + AAV9-Control mice. The overexpression of SIRT3 improved exercise capacity without altering cardiac function. The SIRT3 activator Honokiol improved exercise capacity in MI model mice with HF, by improving mitochondrial function in skeletal muscle through the reduction of SOD2 acetylation. SIRT3 activation may thus be a novel therapeutic target for improving exercise capacity in patients with HF.

Background: Mitochondria are considered the powerhouse of cells, and skeletal muscle cells are no exception. However, information regarding muscle mitochondria from different species is limited. Methods: Different muscles from cattle, pigs and chickens were analyzed for mitochondrial DNA (mtDNA), protein and oxygen consumption. Results: Bovine oxidative muscle mitochondria contain greater mtDNA (p < 0.05), protein (succinate dehydrogenase, SDHA, p < 0.01; citrate synthase, CS, p < 0.01; complex I, CI, p < 0.05), and oxygen consumption (p < 0.01) than their glycolytic counterpart. Likewise, porcine oxidative muscle contains greater mtDNA (p < 0.01), mitochondrial proteins (SDHA, p < 0.05; CS, p < 0.001; CI, p < 0.01) and oxidative phosphorylation capacity (OXPHOS, p < 0.05) in comparison to glycolytic muscle. However, avian oxidative skeletal muscle showed no differences in absolute mtDNA, SDHA, CI, complex II, lactate dehydrogenase, or glyceraldehyde 3 phosphate dehydrogenase compared to their glycolytic counterpart. Even so, avian mitochondria isolated from oxidative muscles had greater OXPHOS capacity (p < 0.05) than glycolytic muscle. Conclusions: These data show avian mitochondria function is independent of absolute mtDNA content and protein abundance, and argue that multiple levels of inquiry are warranted to determine the wholistic role of mitochondria in skeletal muscle.

Physical activity is human body movement of any type, while physical education programs use physical activity to teach children how to improve and sustain an active lifestyle. One of the most crucial factors to think about when evaluating a subject&amp;apos;s cardiorespiratory efficiency is their Physical Fitness Index (PFI). The risks involved in implementing BMI for adults also affect kids and teenagers. The term &amp;quot;maximal oxygen consumption capacity&amp;quot; (VO&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;max) refers to the body&amp;apos;s capacity to consume oxygen in the skeletal muscle mitochondria at a maximum rate during vigorous full-body exercise. To investigate correlation body mass index, physical fitness index and maximal oxygen capacity (VO&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;max) among physical education students. The investigator was selected 36 BPED students (Male: 20 &amp; Female: 16) from University of Kalyani, Kalyani, Nadia. The age range of subject from 19 to 25 years. To conduct this study measured body mass index though Quetelet index, physical fitness index through Harvard step test and maximal oxygen capacity (VO&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;max) through Queens College Step test were considered. Conclusion of this present study were no significant relationship between physical fitness index and body mass index of male, female students and students as a whole. Significantly relationship between VO&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; max and body mass index for female students but in case of male and student as a whole found no relationship. Positive relationship between physical fitness index and VO&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; max for male students and student as a whole but in case of female found no relationship.

Illusory movements for immobile patients with extensive burns (IMMOBILE): A randomized, controlled, cross-over trial

Tcap deficiency impedes striated muscle function and heart regeneration with elevated ROS and autophagy