Sarcopenia a progressive and multifactorial musculoskeletal syndrome characterized by loss of muscle mass and function, poses a significant global health challenge, particularly in aging populations. Epidemiological studies reveal that sarcopenia affects approximately 5-10% of the general population, with prevalence rates escalating dramatically after age 60 to reach 10-27% in older adults. This age-associated increase contributes significantly to healthcare burdens by elevating risks of disability, frailty, and mortality. Despite its profound impact, current clinical approaches to sarcopenia remain limited. While resistance exercise and protein supplementation form the cornerstone of management, their efficacy is often constrained by poor long-term adherence and variable individual responses, highlighting the urgent need for more comprehensive and personalized treatment strategies. The pathogenesis of sarcopenia is complex and influenced by various factors, including aging, inflammation, nutritional deficits, physical inactivity, and mitochondrial dysfunction. However, the precise molecular mechanisms underlying this condition are still not fully understood. Recent research has made significant strides in elucidating the intricate mechanisms contributing to sarcopenia, revealing novel insights into its molecular and cellular underpinnings. Notably, emerging evidence points to the pivotal role of mitochondrial dysfunction, altered myokine profiles, and neuromuscular junction degeneration in sarcopenia progression. Additionally, breakthroughs in stem cell therapy, exosome-based treatments, and precision nutrition offer promising avenues for clinical intervention. This review aims to synthesize the latest advancements in sarcopenia research, focusing on the novel contributions to its pathogenesis and treatment strategies. We explore emerging trends such as the role of cellular senescence, epigenetic regulation, and targeted therapeutic interventions that could reshape future approaches to managing sarcopenia. By highlighting recent breakthroughs and cutting-edge research, we hope to advance the understanding of sarcopenia and foster the translation of these findings into effective clinical therapies.

Aging is associated with a reduction in skeletal muscle fiber size and number, leading to a decline in physical function and structural integrity-a condition known as sarcopenia. This syndrome is further characterized by elevated levels of inflammatory mediators that promote skeletal muscle catabolism and reduce anabolic signaling.Androgens are involved in various biological processes, including the maintenance, homeostasis and trophism of skeletal muscle mass. The decline in androgen levels contributes, indeed, to androgen deficiency in aging people. Such clinical syndrome exacerbates the muscle loss and fosters sarcopenia progression. Nevertheless, the mechanism(s) by which the reduction in androgen levels influences sarcopenia risk and progression remains debated and the therapeutic benefits of androgen-based interventions are still unclear. Given the significant societal and economic impacts of sarcopenia, investigating the androgen/androgen receptor axis in skeletal muscle function is essential to enhance treatment efficacy and reduce healthcare costs.This review summarizes current knowledge on the role of male hormones and their-dependent signaling pathways in sarcopenia. We also highlight the cellular and molecular features of this condition and discuss the mechanisms by which androgens preserve the muscle homeostasis. The pros and cons of clinical strategies and emerging therapies aimed at mitigating muscle degeneration and aging-related decline are also presented.

The European Working Group on Sarcopenia in Older People (EWGSOP2) defines sarcopenia as a muscle disease (muscle failure) rooted in adverse muscle changes that accrue across a lifetime; sarcopenia is common among adults of older age. New findings on the hormonal and metabolic characteristics of patients with sarcopenia have aided in developing more targeted therapeutic strategies. However, treating older patients with sarcopenia still poses a number of challenges. Despite numerous studies on sarcopenia, no comprehensive phenotyping of older sarcopenic patients has yet to be offered. Cluster analysis has been successfully used to study various diseases. It may be extremely advantageous for collecting data on specific sarcopenia progressions based on a simultaneous assessment of a whole range of factors.

To identify disease progression specific to older patients based on cluster analysis of blood biomarkers and lifestyle.

 This study included 1709 participants aged 90 and older. The median age was 92. Seventy-one percent of participants were female. Participants underwent a comprehensive geriatric assessment and had their metabolic, hormonal, and inflammatory blood biomarkers measured. The data were analyzed and clustered using the R programming language.

 Seven sarcopenia clusters were identified. The most significant variables, in descending order, were malnutrition, physical activity, body mass index, handgrip strength, testosterone, albumin, sex, adiponectin, total protein, vitamin D, hemoglobin, estradiol, C-reactive protein, glucose, monocytes, and insulin. Handgrip strength measurements and free T3 levels increased linearly between the cluster with the lowest measurements and the cluster with the highest measurements.

The findings of this study may greatly aid in understanding the relationship between blood biomarkers, lifestyle and sarcopenia progression in older adults, and may help in developing better prevention and diagnostic strategies as well as more personalized therapeutic interventions.

The prolyl hydroxylase domain-containing (PHD or EGL9-homologs) enzyme family is mainly known for its role in the cellular response to hypoxia. HIF-PH inhibitors can stabilize hypoxia-inducible factors (HIFs), activating transcriptional programs that promote processes such as angiogenesis and erythropoiesis to adapt to changes in oxygen levels. HIF-PH inhibitors have been clinically approved for treating several types of anaemia. While most discussions of the HIF-PH signalling axis focus on hypoxia, there is a growing recognition of its importance under normoxic conditions. Recent advances in PHD biology have highlighted the potential of targeting this pathway therapeutically for a range of aging-related diseases. In this article, we review these recent discoveries, situate them within the broader context of aging and disease, and explore current therapeutic strategies that target PHD enzymes for these indications.

Sarcopenia is characterized by the progressive loss of skeletal muscle mass, strength, and function, significantly impacting overall health and quality of life in older adults. This narrative review explores emerging targets and potential treatments for sarcopenia, aiming to provide a comprehensive overview of current and prospective interventions.

The review synthesizes current literature on sarcopenia treatment, focusing on recent advancements in muscle regeneration, mitochondrial function, nutritional strategies, and the muscle-microbiome axis. Additionally, pharmacological and lifestyle interventions targeting anabolic resistance and neuromuscular junction integrity are discussed.

Resistance training and adequate protein intake remain the cornerstone of sarcopenia management. Emerging strategies include targeting muscle regeneration through myosatellite cell activation, signaling pathways, and chronic inflammation control. Gene editing, stem cell therapy, and microRNA modulation show promise in enhancing muscle repair. Addressing mitochondrial dysfunction through interventions aimed at improving biogenesis, ATP production, and reducing oxidative stress is also highlighted. Nutritional strategies such as leucine supplementation and anti-inflammatory nutrients, along with dietary modifications and probiotics targeting the muscle-microbiome interplay, are discussed as potential treatment options. Hydration and muscle-water balance are emphasized as critical in maintaining muscle health in older adults.

A combination of resistance training, nutrition, and emerging therapeutic interventions holds potential to significantly improve muscle function and overall health in the aging population. This review provides a detailed exploration of both established and novel approaches for the prevention and management of sarcopenia, highlighting the need for further research to optimize these strategies.

Depression and multiple musculoskeletal disorders are overrepresented in women compared with men. Given that depression is a modifiable risk factor and improvement of depressive symptoms increases positive outcomes following orthopedic intervention, efforts to improve clinical recognition of depressive symptoms and increased action toward ameliorating depressive symptoms among orthopedic patients are positioned to reduce complications and positively affect patient-reported outcomes. Although psychosocial factors play a role in the manifestation and remittance of depression, it is also well appreciated that primary biochemical changes are capable of causing and perpetuating depression. Unique insight for novel treatments of depression may be facilitated by query of the bidirectional relationship between musculoskeletal health and depression. This Review aims to synthesize the diverse literature on sex, depression, and orthopedics and emphasize the potential for common underlying biological substrates. Given the overrepresentation of depression and musculoskeletal disorders among women, increased emphasis on the biological drivers of the co-occurrence of these disorders is positioned to improve women's health.

The triad of vascular impairment, muscle atrophy, and cognitive decline represents critical age-related conditions that significantly impact health. Vascular impairment disrupts blood flow, precipitating the muscle mass reduction seen in sarcopenia and the decline in neuronal function characteristic of neurodegeneration. Our limited understanding of the intricate relationships within this triad hinders accurate diagnosis and effective treatment strategies. This review analyzes the interrelated mechanisms that contribute to these conditions, with a specific focus on oxidative stress, chronic inflammation, and impaired nutrient delivery. The aim is to understand the common pathways involved and to suggest comprehensive therapeutic approaches. Vascular dysfunctions hinder the circulation of blood and the transportation of nutrients, resulting in sarcopenia characterized by muscle atrophy and weakness. Vascular dysfunction and sarcopenia have a negative impact on physical function and quality of life. Neurodegenerative diseases exhibit comparable pathophysiological mechanisms that affect cognitive and motor functions. Preventive and therapeutic approaches encompass lifestyle adjustments, addressing oxidative stress, inflammation, and integrated therapies that focus on improving vascular and muscular well-being. Better understanding of these links can refine therapeutic strategies and yield better patient outcomes. This study emphasizes the complex interplay between vascular dysfunction, muscle degeneration, and cognitive decline, highlighting the necessity for multidisciplinary treatment approaches. Advances in this domain promise improved diagnostic accuracy, more effective therapeutic options, and enhanced preventive measures, all contributing to a higher quality of life for the elderly population.

Chronic pancreatitis (CP) in young individuals may lead to disease-related secondary sarcopenia (SSARC), characterized by muscle loss and systemic inflammation. In this study, CP was induced in young pigs, and serum levels of key hormones, muscle fiber diameters in various muscles, and the mRNA expression of genes related to oxidative stress and programmed cell death were assessed. A decrease in muscle fiber diameters was observed in SSARC pigs, particularly in the longissimus and diaphragm muscles. Hormonal analysis revealed alterations in dehydroepiandrosterone, testosterone, oxytocin, myostatin, and cortisol levels, indicating a distinct hormonal response in SSARC pigs compared to controls. Oxytocin levels in SSARC pigs were significantly lower and myostatin levels higher. Additionally, changes in the expression of catalase (CAT), caspase 8 (CASP8), B-cell lymphoma 2 (BCL2), and BCL2-associated X protein (BAX) mRNA suggested a downregulation of oxidative stress response and apoptosis regulation. A reduced BAX/BCL2 ratio in SSARC pigs implied potential caspase-independent cell death pathways. The findings highlight the complex interplay between hormonal changes and muscle degradation in SSARC, underscoring the need for further research into the apoptotic and inflammatory pathways involved in muscle changes due to chronic organ inflammation in young individuals.

Sarcopenia and pelvic floor disorders (PFDs) are prevalent and often cooccurring conditions in the aging population. However, their bidirectional relationship and underlying mechanisms remain underexplored. This narrative review aims to elucidate this relationship by exploring potential causative interplays, shared pathophysiological mechanisms, and common risk factors. A comprehensive literature search was conducted to identify relevant studies focusing on epidemiological associations, interaction mechanisms, and implications for patient care. While epidemiological studies demonstrate associations between sarcopenia and PFDs, our findings reveal a cyclical relationship where sarcopenia may exacerbate PFDs through mechanisms such as decreased muscle strength and mobility. Conversely, the presence of PFDs often leads to reduced physical activity due to discomfort and mobility issues, which in turn exacerbate the muscle atrophy associated with sarcopenia. Additionally, shared risk factors such as physical inactivity, nutritional deficiencies, metabolic syndrome, and menopausal hormonal changes likely contribute to the onset and progression of both conditions. These interactions underscore the importance of concurrently integrated care approaches that address both conditions. Effective management requires comprehensive screening, the recognition of contributing factors, and tailored exercise regimens supported by a multidisciplinary approach. Future research should focus on longitudinal studies tracking disease progression and evaluating the efficacy of multidisciplinary care models in optimizing patient outcomes.

Sarcopenia is a prevalent and clinically significant condition, particularly among older age groups and those with chronic disease. Patients with cancer frequently suffer from sarcopenia and progressive loss of muscle mass, strength, and function. The complex interplay between cancer and its treatment, including medical therapy, radiotherapy, and surgery, significantly contributes to the onset and worsening of sarcopenia. Cancer induces muscle wasting through inflammatory processes, metabolic alterations, and hormonal imbalance. Moreover, medical and radiation therapies exert direct toxic effects on muscles, contributing to the impairment of physical function. Loss of appetite, malnutrition, and physical inactivity further exacerbate muscle wasting in cancer patients. Imaging techniques are the cornerstones for sarcopenia diagnosis. Magnetic resonance imaging, computed tomography, and dual-energy X-ray absorptiometry provide valuable insights into muscle structure and quality. Although each modality has advantages and limitations, magnetic resonance imaging produces high-resolution images and provides dynamic information about muscle function. Despite these challenges, addressing sarcopenia is essential for optimizing treatment outcomes and improving survival rates in patients with cancer. This review explored the factors contributing to sarcopenia in oncologic patients, emphasizing the importance of early detection and comprehensive management strategies.

Selective androgen (ostarine, OST) and estrogen (raloxifene, RAL) receptor modulators with improved tissue selectivity have been developed as alternatives to hormone replacement therapy. We investigated the combined effects of OST and RAL on muscle tissue in an estrogen-deficient rat model of postmenopausal conditions.

Three-month-old Sprague Dawley rats were divided into groups: (1) untreated non-ovariectomized rats (Non-OVX), (2) untreated ovariectomized rats (OVX), (3) OVX rats treated with OST, (4) OVX rats treated with RAL, (5) OVX rats treated with OST and RAL. Both compounds were administered in the diet. The average dose received was 0.6 ± 0.1 mg for OST and 11.1 ± 1.2 mg for RAL per kg body weight/day. After thirteen weeks, rat activity, muscle weight, structure, gene expression, and serum markers were analyzed.

OST increased muscle weight, capillary ratio, insulin-like growth factor 1 (Igf-1) expression, serum phosphorus, uterine weight. RAL decreased muscle weight, capillary ratio, food intake, serum calcium and increased Igf-1 and Myostatin expression, serum follicle stimulating hormone (FSH). OST + RAL increased muscle nucleus ratio, uterine weight, serum phosphorus, FSH and luteinizing hormone and decreased body and muscle weight, serum calcium. Neither treatment changed muscle fiber size. OVX increased body and muscle weight, decreased uterine weight, serum calcium and magnesium.

OST had beneficial effects on muscle in OVX rats. Side effects of OST on the uterus and serum electrolytes should be considered before using it for therapeutic purposes. RAL and RAL + OST had less effect on muscle and showed endocrinological side effects on pituitary-gonadal axis.

Sarcopenia is a skeletal muscle disorder characterized by progressive and generalized decline in muscle mass and function. Although it is mostly known as an age-related disorder, it can also occur secondary to systemic diseases such as malignancy or organ failure. It has demonstrated a significant relationship with adverse outcomes, e.g., falls, disabilities, and even mortality. Several breakthroughs have been made to find a pharmaceutical therapy for sarcopenia over the years, and some have come up with promising findings. Yet still no drug has been approved for its treatment. The key factor that makes finding an effective pharmacotherapy so challenging is the general paradigm of standalone/single diseases, traditionally adopted in medicine. Today, it is well known that sarcopenia is a complex disorder caused by multiple factors, e.g., imbalance in protein turnover, satellite cell and mitochondrial dysfunction, hormonal changes, low-grade inflammation, senescence, anorexia of aging, and behavioral factors such as low physical activity. Therefore, pharmaceuticals, either alone or combined, that exhibit multiple actions on these factors simultaneously will likely be the drug of choice to manage sarcopenia. Among various drug options explored throughout the years, testosterone still has the most cumulated evidence regarding its effects on muscle health and its safety. A mas receptor agonist, BIO101, stands out as a recent promising pharmaceutical. In addition to the conventional strategies (i.e., nutritional support and physical exercise), therapeutics with multiple targets of action or combination of multiple therapeutics with different targets/modes of action appear to promise greater benefit for the prevention and treatment of sarcopenia.

We aimed to evaluate the effects of postpartum progesterone on obstetric anal sphincter injury (OASI) healing in female rats using an experimental OASI model. Twenty-eight female rats were divided into four groups after birth: sham-30, sham-90, progesterone (P4)-30, and P4-90. Moreover, OASI model was established in all groups. Subsequently, except for the sham groups, medroxyprogesterone acetate (0.15 mg) was intramuscularly injected into the P4 groups. After 30 and 90 days, the rats were euthanized under general anesthesia after recording the data. The anal sphincter region was collected for histopathological examination. Progesterone and thiol/disulfide homeostasis studies were performed on blood samples. No significant differences were observed between the groups regarding the external anal sphincter (EAS), internal anal sphincter (IAS), or connective tissue thickness (p = 0.714, p = 0.135, and p = 0.314, respectively). No statistically significant differences in the total thiol, native thiol, disulfide, and progesterone levels were found between the groups (p = 0.917, p = 0.503, p = 0.361, and p = 0.294, respectively). The endometrial thickness was lower in the P4 groups than in the sham groups (p = 0.031). Postpartum progesterone administration did not affect IAS and EAS or connective tissue thickness or disrupt the thiol-disulfide balance. However, this administration led to endometrial thinning.

Sarcopenia generally refers to the age-related reduction in muscle strength, functional ability, and muscle mass. Sarcopenia is a multifactorial condition associated with poor glucose disposal, insulin resistance, and subsequently type 2 diabetes (T2D). The pathophysiological connection between sarcopenia and T2D is complex but likely involves glycemic control, inflammation, oxidative stress, and adiposity.

Resistance exercise and aerobic training are two lifestyle interventions that may improve glycemic control in older adults with T2D and counteract sarcopenia. Further, there is evidence that dietary protein, Omega-3 fatty acids, creatine monohydrate, and Vitamin D hold potential to augment some of these benefits from exercise.

The purpose of this narrative review is: (1) discuss the pathophysiological link between age-related sarcopenia and T2D, and (2) discuss lifestyle interventions involving physical activity and nutrition that may counteract sarcopenia and T2D.

Increasing evidence suggests that skeletal muscles may play a role in the pathogenesis of obesity and associated conditions due to their impact on insulin resistance and systemic inflammation. Skeletal muscles, as well as adipose tissue, are largely recognized as endocrine organs, producing biologically active substances, such as myokines and adipokines. They may have either beneficial or harmful effects on the organism and its functions, acting through the endocrine, paracrine, and autocrine pathways. Moreover, the collocation of adipose tissue and skeletal muscles, i.e., the amount of intramuscular, intermuscular, and visceral adipose depots, may be of major importance for metabolic health. Traditionally, the generalized and progressive loss of skeletal muscle mass and strength or physical function, named sarcopenia, has been thought to be associated with age. That is why most recently published papers are focused on the investigation of the effect of obesity on skeletal muscle function in older adults. However, accumulated data indicate that sarcopenia may arise in individuals with obesity at any age, so it seems important to clarify the possible mechanisms linking obesity and skeletal muscle dysfunction regardless of age. Since steroids, namely, glucocorticoids (GCs) and sex steroids, have a major impact on the amount and function of both adipose tissue and skeletal muscles, and are involved in the pathogenesis of obesity, in this review, we will also discuss the role of steroids in the interaction of these two metabolically active tissues in the course of obesity.

Sarcopenia is prevalent among the older population and severely affects human health. Tea catechins may benefit for skeletal muscle performance and protect against secondary sarcopenia. However, the mechanisms underlying their antisarcopenic effect are still not fully understood. Despite initial successes in animal and early clinical trials regarding the safety and efficacy of (-)-epigallocatechin-3-gallate (EGCG), a major catechin of green tea, many challenges, problems, and unanswered questions remain. In this comprehensive review, we discuss the potential role and underlying mechanisms of EGCG in sarcopenia prevention and management. We thoroughly review the general biological activities and general effects of EGCG on skeletal muscle performance, EGCG's antisarcopenic mechanisms, and recent clinical evidence of the aforesaid effects and mechanisms. We also address safety issues and provide directions for future studies. The possible concerted actions of EGCG indicate the need for further studies on sarcopenia prevention and management in humans.

Sarcopenia is a syndrome of age-related loss of muscle mass and strength that seriously affects human health, and there are currently no effective drugs to treat the disease. Linolenic acid as a common n-3 polyunsaturated fatty acid (n-3 PUFA) is known to have many beneficial functions. Some studies have found that n-3 PUFA might have the potential to improve sarcopenia. In this study, Caenorhabditis elegans (C. elegans) was used as a model animal to investigate the effects of linolenic acid on C. elegans muscles. The results showed that 50 μg mL-1 linolenic acid significantly improved sarcopenia by repairing mitochondrial function by promoting mitophagy and fighting oxidative stress (p < 0.05). This included the increase of the expression of the mitophagy gene pink-1 and DAF-16/FOXO transcription factors, respectively, by linolenic acid. This study could provide some evidence for the application of n-3 PUFA in improving sarcopenia.

To investigate the association between body fat (BF%) and sarcopenia in older adults with type 2 diabetes mellitus (T2DM) and potential link with increased levels of inflammatory indicators and insulin resistance.

A total of 543 older adults with T2DM were included in this cross-sectional study. Appendicular skeletal muscle (ASM), handgrip strength and gait speed were measured to diagnose sarcopenia according to the updated Asian Working Group for Sarcopenia (AWGS) 2019 criteria. Body composition data were tested using dual-energy X-ray absorptiometry (DEXA). Levels of serum high-sensitive C-reactive protein (hs-CRP), interleukin-6, fasting blood insulin (FINS), hemoglobin A1c (HbA1c), 25-hydroxyvitamin D₃ [25(OH) D₃] were also determined.

The prevalence of sarcopenia in all participants was 8.84%, of which 11.90% were male and 5.84% females. The Pearson's correlation analysis revealed that BF% was negatively correlated with gait speed in men and women (R =-0.195, P=0.001; R = -0.136, P =0.025, respectively). After adjusting for all potential confounders, sarcopenia was positive associated with BF% (male, OR: 1.38, 95% CI: 1.15-1.65, P< 0.001; female, OR: 1.30, 95% CI: 1.07-1.56, P=0.007), and negatively associated with body mass index (BMI) (male, OR: 0.57, 95% CI: 0.44-0.73, P<0.001; female, OR: 0.48, 95% CI: 0.33-0.70, P<0.001). No significant differences were found in hs-CRP, interleukin-6, and insulin resistance between older T2DM adults with and without sarcopenia.

Higher BF% was linked to an increased risk of sarcopenia in older adults with T2DM, suggesting the importance of assessing BF% rather than BMI alone to manage sarcopenia.

Animal and human studies suggest that low concentrations of circulating sex steroid hormones play a critical role in the accelerated loss of muscle mass and strength after menopause. The skeletal muscle can produce sex steroid hormones locally, however, their presence and regulation remain mostly elusive. The purpose of this study was to examine sex steroid hormone concentrations in skeletal muscle biopsies from postmenopausal women before and after 12-weeks of resistance training with (n = 15) or without (n = 16) estrogen therapy, and after acute exercise. Furthermore, associations between circulating sex hormones, intramuscular sex steroid hormones and muscle parameters related to muscle strength, mass and quality were elucidated. Blood and muscle samples, body composition (DXA-scan), muscle size (MR), and muscle strength measures were determined before and after the intervention. An additional blood and muscle sample was collected after the last resistance exercise bout. The results demonstrated reduced intramuscular estradiol, testosterone and dehydroepiandrosterone (DHEA) concentrations after resistance training irrespective of estrogen therapy. Acute exercise had no effect on intramuscular sex hormone levels. Low circulating levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) associated with high muscle mass at baseline, and a decline in circulating FSH after the intervention associated with a greater gain in muscle cross-sectional area in response to the resistance training. In conclusion, intramuscular estradiol, testosterone and DHEA were reduced by resistance training and unaffected by changes in circulating estrogen levels induced by estrogen therapy. Serum FSH and LH were superior predictors of muscle mass compared to other circulating and intramuscular sex steroid hormones.

Sarcopenia is a phenomenon in which skeletal muscle mass decreases with age, causing many health problems. Many studies have been conducted to improve sarcopenia nutritionally. Ishige okamura (IO) is a genus of brown algae and plays a role in anti-diabetes, anti-obesity, and myogenesis. However, the effect of IO extract (IOE) on human muscle strength and mass is unclear. Therefore, we will examine the impact and safety of consumption of IOE for 12 weeks on muscle strength and mass in middle-aged and old-aged adults with relatively low skeletal muscle mass.

A randomized controlled trial is conducted on 80 adults aged 50-80. A total of 80 participants will be enrolled in this study. Participants assign IOE-taking group (n = 40) and placebo taking group (n = 40). At a baseline and 12 weeks after treatment, the following parameters of the participants are checked: knee extension strength, handgrip strength, body composition, laboratory tests, dietary recall, physical activity, and EQ-5D-5L.

The present study will be the first randomized, double-blind placebo-controlled trial to examine the efficacy and tolerability of IOE supplementation in adults with relatively low muscle mass. The nutritional intake and physical activity that might influence muscle strength and mass will be considered as covariates for transparency of results. The results of this study will provide clinical evidence for sarcopenia patients with nutrient treatment.

www.clinicaltrials.gov/, Identifier: NCT04617951.

Selective androgen and estrogen receptor modulators, ostarine (OST) and raloxifen (RAL), reportedly improve muscle tissue and offer therapeutic approaches to muscle maintenance in the elderly. The present study evaluated the effects of OST and RAL and their combination on musculoskeletal tissue in orchiectomized rats.

Eight-month-old Sprague Dawley rats were analyzed. Experiment I: (1) Untreated non-orchiectomized rats (Non-ORX), (2) untreated orchiectomized rats (ORX), (3) ORX rats treated with OST during weeks 0-18 (OST-P), (4) ORX rats treated with OST during weeks 12-18 (OST-T). Experiment II: 1) Non-ORX, (2) ORX, 3) OST-P, (4) ORX rats treated with RAL, during weeks 0-18 (RAL-P), 5) ORX rats treated with OST + RAL, weeks 0-18 (OST + RAL-P). The average daily doses of OST and RAL were 0.4 and 7 mg/kg body weight (BW). Weight, fiber size, and capillarization of muscles, gene expression, serum markers and the lumbar vertebral body were analyzed.

OST-P exerted favorable effects on muscle weight, expression of myostatin and insulin growth factor-1, but increased prostate weight. OST-T partially improved muscle parameters, showing less effect on the prostate. RAL-P did not show anabolic effects on muscles but improved body constitution by reducing abdominal area, food intake, and BW. OST + RAL-P had an anabolic impact on muscle, reduced androgenic effect on the prostate, and normalized food intake. OST and RAL improved osteoporotic bone.

The OST + RAL treatment appeared to be a promising option in the treatment of androgen-deficient conditions and showed fewer side effects than the respective single treatments.

The diagnosis of functional hypogonadism should prompt a thorough assessment and optimization of general health, including lifestyle changes, weight reduction, care of comorbidities and cessation of offending medications, some of which can lead to meaningful gains in endogenous testosterone (T) concentrations. Having excluded or addressed reversible causes and contra-indications, patients with functional hypogonadism can be offered a trial of testosterone replacement therapy (TRT) after full discussion on the anticipated benefits and potential risks. T treatment improves libido but may be less effective for erectile dysfunction (ED). T treatment can also have modest positive effects on insulin resistance, bone strength, some measures of physical strength, and mild depressive symptoms but the clinical significance of these relatively short-term improvements remain uncertain in terms of longer-term patient-important outcomes. Initiation of TRT is a joint decision between patient and clinician since longer-term benefits and risks have not been adequately defined.