Effects of lower leg compression sleeves on muscle strength, elasticity, and architecture following eccentric contraction.

To measure the morphology of the pelvic floor muscle and levator ani hiatus (LAH) using 3D MRI segmentation in females with (SUI) and to assess correlations with age, body mass index (BMI), and parity. This study includes 80 patients with SUI who underwent 3.0 T pelvic MRI. Patients were grouped based on age, BMI, and parity. Manual segmentation and 3D modeling of the pelvic floor muscle and LAH were performed to get volumetric and dimensional measurements. Statistical analysis included Kruskal-Wallis, Mann-Witney, and post hoc testing to evaluate group variations. The cohort included patients from 20 to 90 years old (mean 53.9 ± 11.7), with a mean BMI of 25.3 ± 3.4 and a mean parity of 1.85 ± 1.03. Significant variations in LAM surface (H(2) = 6.650, p = 0.036), flatness (H(2) = 6.471, p = 0.039), median intensity (H(2) = 8.218, p = 0.016), and curvature mean (H(2) = 7.382, p = 0.025) among age groups. The greatest LAM surface rankings were found in the 50-65 age range, whereas the highest LAM flatness ranks were found in those over 65 years old. BMI demonstrated a limited association, with overweight/obese participants exhibiting 11.3% larger LAM surface area compared to normal/underweight individuals (p = 0.044, r = 0.225). No significant associations were found between parity and any pelvic floor morphometric parameters (all p > 0.05). This study identifies age-dependent morphological changes in levator ani muscle architecture as the primary determinant of pelvic floor structural adaptation in women with stress urinary incontinence. These quantitative shape-based parameters offer novel diagnostic and therapeutic insights, advancing precision medicine approaches in urogynecological assessment and management.

Skeletal muscle loss is a common consequence of critical illness, yet its determinants and prognostic significance remain unclear. This study investigated muscle trajectory during hospitalization in critically ill patients, factors predicting these changes, and the associations between early muscle changes with clinical and functional outcomes. Adults (≥18 years) with severe pneumonia requiring supplemental oxygen were enrolled within 72 h of ICU admission. Two groups were recruited: RT-PCR-confirmed COVID-19 and non-COVID pneumonia, individually matched by age (±10 years), sex, and ventilatory support. Ultrasound assessments of quadriceps muscles (quadriceps muscle layer thickness, rectus femoris cross-sectional area, pennation angle, fascicle length) and forearm muscle thickness were performed in the ICU on study Days 1, 7, and 14, at ICU discharge (if later), and at hospital discharge. Muscle trajectories were evaluated using linear mixed-effects models. Regression analyses examined associations of relative muscle changes with (1) potential predictors, (2) 60-day time-to-discharge alive, and (3) hospital discharge handgrip and knee extension strength. Fifty-nine patients (29 COVID-19, 30 non-COVID) were analyzed. Quadriceps muscles changed significantly over time, while forearm muscle thickness did not; trajectories were comparable between groups. No patient characteristics, laboratory, or clinical factors were associated with muscle changes on Day 7 or hospital discharge. Day 7 muscle changes were not associated with time-to-discharge-alive at 60 days or muscle strength after baseline adjustment (all p > 0.05). In critically ill patients, significant muscle changes occurred during hospitalization irrespective of COVID-19 status, but no predictors were identified. Early muscle change alone was not predictive of clinical or functional outcomes. This study demonstrates that skeletal muscle changes significantly over the course of hospitalization with similar trajectories in COVID-19 and non-COVID patients, independent of patient characteristics or routine clinical and laboratory factors. Early muscle loss alone was not predictive of clinical and functional outcomes, highlighting the need for combined or alternative markers to better identify high-risk patients and guide targeted interventions in critical care.

The aims of this study were to investigate gastrocnemius medialis (GM) muscle properties in male academy soccer players (ASP) and age- and sex-matched control participants (CON); and to explore the relationships between GM characteristics and jump performance. Thirty-four participants (ASP, n = 22, age 18.8 ± 1.4years, height 1.82 ± 0.08m, mass 75.1 ± 5.9kg; and CON, n = 12, 22.2 ± 2.9years, 1.75 ± 0.05m, 71.6 ± 7.4kg) completed the following assessments: ultrasound measurements of GM anatomical cross-sectional area (ACSA), volume, muscle thickness (MT), fascicle pennation angle (θp) and fascicle length (Lf); isokinetic dynamometry measurements of isometric plantar flexion and dorsiflexion maximum voluntary torque; and unilateral and bilateral, vertical and horizontal, countermovement jumps (CMJ), and bilateral drop jumps on a force platform. θp (17.4° ± 2.5° vs. 14.3° ± 1.2°, P < 0.001); unilateral horizontal CMJ peak power (30.14 ± 3.53 vs. 23.18 ± 3.72W kg- 1); and projectile range during unilateral (104 ± 16 vs. 89 ± 12cm, P = 0.006) and bilateral (140 ± 14 vs. 129 ± 14cm, P = 0.041) horizontal CMJ were greater in ASP vs. CON. In ASP alone, Lf correlated inversely with vertical CMJ performance but positively with horizontal CMJ performance (R2 ≥ 0.200, P ≤ 0.042). Conversely, θp correlated positively with vertical CMJ performance but inversely with horizontal CMJ performance (R2 ≥ 0.194, P ≤ 0.044). In CON only, ACSA, MT, volume and Lf all correlated inversely with vertical CMJ performance (R2 ≥ 0.366, P ≤ 0.037). The opposing θp and Lf correlations with vertical and horizontal CMJ jump performance in ASP suggest GM architecture influences CMJ performance in a direction-specific manner in this population, while the different correlation patterns between ASP and CON suggest that GM architecture contributes to CMJ performance differently in these two populations.

Although fibroblast growth factor 8 (FGF8) is a critical regulator of skeletal morphogenesis in vertebrates, its specific role in the formation and development of intermuscular bones (IBs) in teleost fish remains insufficiently characterized. In this study, we generated double mutants (fgf8a+/- + fgf8b+/-) in diploid Chongming crucian carp (Carassius auratus) using CRISPR/Cas9-mediated gene editing. Compared to wild-type fish, the double mutants exhibited significantly reduced IB number (p < 0.01), demonstrating a synergistic role of fgf8a and fgf8b in IB formation. Notably, reduced number of IBs did not compromise overall growth, muscle architecture, or reproductive performance. Integrated transcriptomic and metabolomic analyses revealed that the reduced IB phenotype was linked to modifications in relevant signaling pathways and a concomitant upregulation of metabolites beneficial for muscle quality and health. Our findings highlight the crucial role of fgf8 in regulating IB formation and development in crucian carp, providing insights into the genetic mechanisms underlying this process in teleosts.

Skeletal muscle fibrosis is a hallmark of muscular dystrophies, aging or severe muscle injuries. It is characterized by the extensive accumulation of extracellular matrix (ECM), primarily composed of type I collagen, which disrupts muscle architecture, impairs contractile function, and compromises muscle regenerative abilities. Despite its clinical relevance, to date, no animal or in vitro models recapitulate the main features of muscle fibrosis. In this study, we designed both healthy and fibrotic 3D matrices to investigate the impact of fibrotic environment on myoblast behavior. Fibrotic matrices were engineered by 3D printing of dense collagen solutions in air, followed by slow gelation to yield non-porous, isotropic hydrogels. Subsequent cross-linking using EDC/NHS chemistry yielded matrices with a Young's modulus of approximately 50 kPa. These fibrotic matrices successfully recapitulated the main characteristics of muscle fibrosis, including compact structure of collagen bundles and increased stiffness, consequently limiting oxygen and nutrient diffusion. C2C12 myoblasts cultured within the fibrotic matrices exhibited altered behavior compared to those grown in healthy matrices. In the fibrotic environment, myoblasts failed to differentiate into mature myotubes, lacked proper alignment, and showed signs of hypoxia. Additionally, they secreted pro-inflammatory cytokines and were unable to remodel their surrounding ECM. Together, these findings underscore the detrimental effects of a fibrotic environment on skeletal muscle cell behavior. The development of these two distinct 3D in vitro muscle models, one representing healthy muscle and the other fibrotic, offers a valuable platform for investigating the pathophysiology of skeletal muscle fibrosis for testing potential therapeutic strategies.

Mechanics of aponeurosis and its role in muscle contraction: current insights and future directions.

The sarcomere is the basic contractile unit of muscle fibers, bordered by Z-discs. In Drosophila, Z-disc structure and maintenance rely on actinin and the Z band alternatively spliced PDZ-motif protein 52 (Zasp52), a member of the Alp/Enigma family. Zasp52 has been shown to bind actin, actinin, and itself, but its full range of functions remains unclear, as a null mutant has not been previously analyzed. To address this, we generated a CRISPR-based null mutant of Zasp52, deleting most of the ∼50 kb locus. Null mutants are viable but flightless and display severe defects in indirect flight muscle architecture. To test redundancy, we also analyzed a double null of Zasp52 and Zasp67, the latter one being a Zasp member restricted to flight muscles. Both single and double mutants exhibit damaged myofibrils, with the double mutant showing a more severe collapse of sarcomere organization. Given the clinical importance of LIM domain-binding 3 (LDB3) mutations, the human ortholog of Zasp52, we next modeled a pathogenic variant. In humans, the P615L mutation in LDB3 has been linked to cardiomyopathy and skeletal myopathy. We engineered the orthologous substitution, Zasp52-P607L, and expressed it in Drosophila indirect flight muscles. The variant produced enlarged sarcomeres and enhanced binding, consistent with a gain-of-function disease phenotype. Together, these findings indicate that Drosophila indirect flight muscles can be used as a system to dissect Zasp function, reveal redundancy in Z-disc assembly, and provide mechanistic insight into how conserved mutations contribute to human myopathies.

A comprehensive understanding of the underlying molecular mechanisms of prostate cancer is essential for the development of precise diagnostic biomarkers. In this study, we applied the unsupervised multi-omics factor analysis framework (MOFA) to integrate DNA methylation, gene expression, and metabolic profiles derived from the same individuals, aiming to characterize the biological landscape of normal, malignant, and aggressive prostate tissue. Our analysis identified distinct molecular pathways associated with aggressive disease, specifically those involved in zinc metabolism, cell cycle regulation, smooth muscle architecture, immune activation, and tissue morphology. Key metabolites within the TCA cycle, amino acid metabolism, and lipid pathways were central to these signatures. Furthermore, we observed a consistent co-enrichment of SP1 and CTCFL binding regions among factor-associated CpGs, suggesting a model of global epigenetic reprogramming. These findings indicate a novel interplay between Polycomb deregulation, CTCFL-mediated chromatin remodeling, and SP1-driven transcriptional activation in shaping the prostate cancer epigenome. Apart from immune activation, the identified molecular signatures were validated in the TCGA cohort and demonstrated significant predictive value for disease recurrence. Overall, these results underscore the power of multi-omics integration in providing a holistic understanding of prostate cancer biology and its potential for clinical translation into prognostic biomarkers.

Human atrial chambers derive from distinct embryonic anlagens, the original embryonic atria gradually transforming into the so-called auricles, or atrial appendages. This study quantifies macroscopic variations in pectinate muscle architecture in human atrial appendages and evaluates their visualization using clinical imaging modalities. We examined 153 cadaveric donor hearts (103 specified sex: 61 female, 42 male; plus 50 unspecified), employing gross dissection, exvivo micro-CT, histology, and invivo clinical imaging (CT angiography, MRI, and transthoracic/transesophageal echocardiography). Left atrial appendage (LAA) morphologies (Wang classification) comprised chicken-wing (41%), cactus (23%), cauliflower (22%), and windsock (14%) types, with 11 ± 4 (mean ± SD) main pectinate muscles (length: 47 ± 16 mm). Right atrial appendage (RAA) pectinate muscle arrangements (Loukas classification) were dominated by type IV (41%), followed by types I/II (22%/20%), with 17 ± 4 muscles (length: 75 ± 17 mm); the RAAs were larger (p < 0.001) but showed lower muscle density (p = 0.007) than the LAAs. All modalities resolved main pectinate bundles, with angio-CT providing superior LAA detail; transesophageal echocardiography excelled for both sides. Precise atrial appendage morphology informs catheter ablation, pacing, and stroke risk stratification, bridging anatomical and clinical perspectives.

ABSTRACTWe aimed to identify the physiological and muscle characteristics associated with mean power output in the final stage of a rowing incremental test in elite rowers. Twenty‐two national level rowers (n = 9 female) completed the following assessments (i) a 7‐stage incremental rowing ergometer test to determine V̇O2peak, maximal muscle deoxygenation and final incremental stage mean power output, (ii) strength and power, (iii) lean body mass (LBM) by dual‐energy X‐ray absorptiometry, (iv) lower extremity muscle volumes using MR imaging, (v) muscle architecture using diffusion tensor imaging; and (vi) estimated muscle typology via proton MR spectroscopy. Hierarchical multiple linear regression was used to identify the characteristics associated with final incremental stage mean power output with sex and LBM as covariates. Sex explained a substantial proportion of the variance in final incremental stage mean power output (R2 = 0.74; adjusted ΔR2 = 0.72; p < 0.001), while inclusion of LBM further improved model fit (R2 = 0.87; ΔR2 = 0.13; adjusted ΔR2 = 0.13; p = 0.006). After accounting for sex and LBM, V̇O2peak demonstrated the largest independent association with final incremental stage mean power output (ΔR2 = 0.047; adjusted ΔR2 = 0.047; partial r = 0.60; p = 0.0048), followed by the estimated proportion of type II fibers (ΔR2 = 0.035; adjusted ΔR2 = 0.033; partial r = 0.52; p = 0.0188). Most other muscle characteristics explained minimal additional variance. Sex and muscle characteristic interaction terms indicated no detectable sex‐specific differences in this small cohort. These findings highlight the diversity in the underpinning muscle characteristics and may inform personalized interventions targeted at improving rowing performance.

Primate tongue morphology and function are critical to understanding the evolution of feeding, swallowing, and vocalization. In this paper, we examine the primate tongue as a muscular hydrostat with regionally specialized neuromuscular compartments. We integrate anatomical, kinematic, and biomechanical modeling approaches to analyze how muscle architecture and fiber orientation drive complex tongue deformations during functional behaviors. We evaluate the hydraulic mechanisms underlying tongue-base retraction, highlight species-specific adaptations in macaques and humans, and review primate tongue kinematics across distinct feeding stages. Finally, we synthesize recent advances in biomechanical modeling and experimental studies of tongue kinematics and their contributions to advancing three-dimensional analyses of tongue movement during feeding and speech.

The poultry industry faces increasing demand for sustainable production aligned with meat quality and animal welfare. This study examined effects of space allowance (39 vs. 21kg/m2) and dietary fibre (DF) supplementation (control vs. DF) on broiler pectoralis major muscle using mass spectrometry-based proteomics under higher-welfare conditions. While yield characteristics were unaffected, reduced space allowance significantly increased intramuscular fat and altered the proteome, with enrichment of proteins in oxidative phosphorylation, transcriptional stress and shifts in carbohydrate metabolism. Broilers receiving DF exhibited lower physical activity and feeding behaviours, with proteomic profiles linked to glycolysis, glycogen turnover and muscle architecture, as well as with reduced drip loss regardless of space allowance. Under higher space, DF induced broader proteomic adaptations, including cytoskeletal remodelling, lipid biosynthesis regulation and vascular homeostasis. These findings highlight how husbandry factors interact to shape meat phenotypes, offering a molecular framework to support quality-focused, welfare-aligned and environmentally conscious meat production.

Stimuli-responsive 4D-bioprinted constructs for musculoskeletal tissue regeneration: Shape-morphing mechanisms, cell-laden bioink engineering, and preclinical outcomes.

Cellular aquaculture offers a sustainable solution to global seafood demand, yet the production of high-value, whole-cut fillets is hindered by the "texture gap," the inability to replicate the complex, anisotropic architecture of native fish muscle and its collagenous myosepta. This critical review addresses this challenge by evaluating the necessary paradigm shift from reductionist mammalian-centric tissue engineering to marine-biomimetic scaffolding strategies. We systematically analyze the efficacy of marine-derived biomaterials, such as cold-water fish skin collagen, sponge chitin, and algal polysaccharides, demonstrating their superior capacity to meet the distinct metabolic and thermal requirements of piscine cells. Our analysis reveals that advanced fabrication technologies, including electrospinning, cryo-templating, and 3D bioprinting, successfully achieve the micro-scale alignment necessary for myotome mimicry, though macroscopic scalability remains a current industrial bottleneck. Furthermore, we establish that structural fidelity must be coupled with sensoric integration; incorporating marine protein hydrolysates and lipid co-cultures significantly enhances umami intensity and authentic mouthfeel, as validated by electronic sensory analytics. To translate these advancements into commercial viability, the cellular seafood industry must transition from chemical crosslinking to food-grade enzymatic alternatives. By integrating circular bioeconomy principles specifically, valorizing seafood processing waste to secure affordable scaffold materials this review provides a strategic roadmap for scaling structurally accurate, sensorically authentic, and economically competitive cell-cultured seafood products.

Aging reshapes the architecture of human skeletal muscle, yet objective tissue-level markers that capture this process remain limited. We combined large-scale histology with deep learning to identify reproducible features of muscle aging and to test their biological relevance. We analyzed 974 hematoxylin-eosin whole-slide images from a population resource using a dual-attention convolutional neural network and an independent Mask R-CNN model to quantify nuclear size and density, verified by manual review. The classifier distinguished young from aged muscle with high accuracy (AUC 0.91; accuracy 86.2%), and attention maps consistently highlighted nuclear enlargement and spatial disorganization as salient features. Nuclear diameter increased with age (Spearman's ρ = 0.71, p < 0.0001) across automated and manual measurements. Transcriptomes matched to the same donors showed that samples with larger nuclei were enriched for pathways related to chromatin remodeling, proteostasis, cellular senescence, mitochondrial activity, and telomere regulation, whereas smaller nuclei aligned with anti-inflammatory and DNA repair programs. External pediatric inflammatory myopathies exhibited nuclear enlargement comparable to aged muscle, suggesting inflammation-related premature histologic aging. These findings identify nuclear enlargement as a robust, quantifiable feature that integrates structural and molecular signatures of muscle aging. The proposed deep learning-based nuclear morphometry provides a scalable framework for tissue-level aging biomarkers and suggests a potential "muscle aging clock" applicable to both physiological aging and disease states.

A 91-yr-old female set the W90+ world record in the 200 m sprint in 2024. We characterized her neuromuscular function, fatigability, denervation markers, and single-fiber contractile properties, and, where possible, compared these outcomes with published reference data. Knee extensor muscle architecture, force, power, fatigability, and motor unit (MU) behavior were assessed in vivo, and a vastus lateralis biopsy was analyzed for single-fiber contractile properties and markers of denervation. Quadriceps cross-sectional area was 36.5 cm2, with fascicle length, pennation angle, and muscle thickness of 6.7 cm, 11.6°, and 1.4 cm, respectively. Knee extensor maximal voluntary isometric contraction (MVIC) torque was 79 Nm, power was 28 W, and power declined by 43% during a 4-min fatiguing task. MU recruitment threshold was 12 ± 11% of MVIC. Single-fiber absolute and specific force were 0.88 ± 0.19 mN and 114 ± 10 kN/m2 for myosin heavy chain (MyHC) I and 0.74 ± 0.23 mN and 171 ± 23 kN/m2 for MyHC IIa fibers. Less than 1% of fibers were positive for the denervation marker neural cell adhesion molecule (NCAM), no fibers expressed embryonic MyHC, and ∼1% of MyHC II fibers expressed neonatal MyHC. In vivo muscle size, force, power, and fatigability were largely within the range for individuals one decade younger. MU behavior was comparable with individuals 20 yr younger. MyHC I fibersproduced greater absolute force than reported in untrained young females and females in their eighth decade, whereas MyHC II fiber force was lower because of smaller fiber size. Denervation markers were less prevalent than typically reported at this age. Collectively, these findings illustrate the heterogeneous effects of aging on different features of neuromuscular function, even in an elite older female sprint athlete.NEW & NOTEWORTHY We report in vivo neuromuscular function, single-fiber mechanics, and denervation markers in a 91-yr-old female who holds the W90+ 200 m world record. Despite reduced muscle size, force, and power, as well as pronounced fast-fiber atrophy, markers of denervation were similar to those in young females and single-fiber force in slow fibers was preserved. Together, these data highlight the differential effects of lifelong sprint training and aging on neural versus muscular components of the neuromuscular system.

Ischemia-reperfusion (I/R) injury remains a major complication in peripheral arterial disease, characterized by oxidative stress, inflammation, and apoptosis. Body Protection Compound-157 (BPC 157), a stable gastric pentadecapeptide, has demonstrated cytoprotective properties in multiple tissues. This study aimed to evaluate the protective effects of BPC 157 in a rat model of lower limb I/R injury. Twenty-four male Wistar albino rats were randomized into four groups (n = 6): SHAM, B (BPC 157 only), IR (I/R), and IRB (I/R + BPC 157). I/R was induced by abdominal aortic clamping for 45min followed by 2h of reperfusion. BPC 157 (20µg/kg, intraperitoneal) was administered at the 45th minute of ischemia in B and IRB groups. Biochemical markers (MDA, SOD, TAS, TOS) were measured in serum. Gene expression of Il-6, Hif-1α, p53, Bcl-2, Bax, and Casp3 was assessed by qRT-PCR, while immunohistochemistry evaluated VEGF, eNOS, IL-6, and Caspase-3 expression. Histopathological changes were scored with hematoxylin-eosin and Masson's trichrome staining. I/R significantly increased MDA, TOS, p53, Bax, Casp3, Hif-1α, Il-6, and histopathological injury scores, while reducing SOD, TAS, and VEGF expression. Bcl-2 mRNA was not significantly reduced by I/R compared with SHAM; however, BPC 157 significantly increased Bcl-2 expression compared with IR. In the IRB group, BPC 157 reduced MDA and TOS, restored SOD and TAS, downregulated p53, Bax, and Casp3, reduced IL-6 and Caspase-3 immunoreactivity, and partially restored VEGF expression. Histological analysis confirmed improved muscle architecture and reduced collagen deposition in IRB compared with IR. BPC 157 appears to exert protective effects against skeletal muscle I/R injury by attenuating oxidative stress, modulating apoptosis, reducing inflammation, and supporting angiogenic activity. These findings suggest that BPC 157 may represent a potential therapeutic candidate for mitigating reperfusion injury; however, further studies with larger cohorts and dose-response evaluations are required to confirm these effects and establish clinical relevance.

Research on mule and donkey muscle composition remains limited despite their global importance as working equids. The objective of this study is to identify Mammoth donkey jacks with higher percentage of fast twitch fibers for racing mule production. A total of 33 animals were biopsied; however, only 12 samples were suitable for analysis, including racing mules (n = 7) and male Mammoth donkeys (n = 5). Animals were sedated with detomidine (10 µg/kg body weight) and butorphanol (20 µg/kg body weight). Middle gluteal muscle biopsies were collected using a 6 mm Bergström biopsy needle at a site located 20 cm dorsocaudal to the tuber coxae at a 45° angle to the base of the tail. Collection depth was 7.5 cm in adult mules and 5 cm in donkeys. Samples were prepared aseptically, anesthetized subcutaneously with lidocaine hydrochloride, and frozen in liquid nitrogen. Histochemical analysis included myosin adenosine triphosphatase (ATPase) staining at pH 9.5, 4.6, and 4.3. Fibers were classified as Type I, Type IIA, or Type IIB, and CSA measurements were obtained using NIH ImageJ software. Statistical analysis included group contrasts, summarized as mean ± SD with 95% confidence intervals, while Bayesian ANOVA outputs were presented as exploratory evidence summaries. Type IIA fibers were greater in mules (47.84 ± 7.30%) than donkeys (38.47 ± 4.48%). Results suggest that differences in equid muscle architecture may be associated with variation in Type IIA fiber composition related to work or use.

There has been an increasing prevalence of prostate cancer worldwide, and therefore a growing clinical need to understand and maintain whole body health in this cohort. There is currently limited evidence of the underlying physiology which leads to certain patients developing cancer cachexia. Based on pre-clinical evidence, skeletal muscle (SKM) mitochondria are suspected to play an integral role, however to date, there is little human data to support this. This study compares SKM mitochondrial oxidative phosphorylation (OXPHOS) in prostate cancer patients due to undergo treatment with curative intent to healthy volunteers, with a hypothesis that this would be lower in the cancer cohort. Twelve prostate cancer patients and 8 disease-free males matched for age and body mass index (BMI) were recruited to this study. All participants completed assessments of physical function using clinically recognised tools (handgrip strength, timed up-and-go, and short physical performace battery) and muscle architecture via ultrasound. All participants also had a SKM (vastus lateralis) biopsy collected. Using a high-resolution respirometer (OROBOROS) and standardised substrate uncoupled inhibitor titration (SUIT) protocol, SKM OXPHOS was assessed, with the biopsy also analysed for citrate synthase activity and gene expression via RT-PCR. Despite our groups being well-matched in terms of age and BMI, and there being no differences in SKM physical function or architecture, extrinsic OXPHOS was significantly lower in the prostate cancer cohort compared to healthy controls (maximal complex I activity: 47.1 ± 19.7 vs. 27.1 ± 12.1, p = 0.01; maximal complex I + II activity: 74.8 ± 26.7 vs. 50.7 ± 13.4, p = 0.01; maximal activity: healthy: 95.9 ± 37.4 vs. 62.1 ± 16.3, p = 0.02). The same was true for Respiratory Control Ratio (2.7 ± 0.9 vs. 1.8 ± 0.9, p = 0.04). There was no difference in intrinsic OXPHOS between the groups. This study found lower SKM extrinsic OXPHOS in those with prostate cancer, in the absence of muscle mass or functional loss, when compared to age-matched disease-free volunteers. This appears to be due to changes in mitochondrial content or remodelling, with preservation of intrinsic function.