Health and sociodemographic factors associated with low muscle strength, muscle mass, and physical performance among people living with HIV.

ABSTRACTThis study examined the factors associated with low muscle strength, muscle mass, and physical performance in 331 people living with HIV. Participants completed handgrip as a strength measure, appendicular skeletal muscle mass using bioimpedance analysis, and chair rise was a physical performance measure. Multivariate logistic regression was used to analyze the association between low values on these measures with sociodemographic, HIV-related factors, and comorbidities. Higher body mass index (BMI) (OR = 0.91; CI = 0.86-0.97) and higher CD4/CD8 ratio (OR = 0.38; 95% CI = 0.18-0.82) were associated with decreased likelihood of low handgrip strength. Being non-employed (OR = 2.08; 95% CI = 1.07-4.06), having hypertension (OR = 2.27; 95% CI = 1.13-4.54) and rheumatism (OR = 5.46; 95% CI = 1.68-17.74) increased the chance of low handgrip strength. Higher BMI (OR = 0.43; 95% CI = 0.34-0.56), CD4/CD8 ratio (OR = 0.29; 95% CI = 0.09-0.93), and bioimpedance phase angle (OR = 0.22; 95% CI = 0.12-0.40) were associated with decreased likelihood of low muscle mass. Lastly, having less than eight years of education (OR = 1.87; 95% CI = 1.02-3.41) and being non-employed (OR = 8.18; 95% CI = 3.09-21.61) increased the chance of low chair stand performance. In addition, higher CD4 + lymphocytes count (OR = 0.99; 95% CI = 0.99-0.99) was associated with a decreased likelihood of low chair stand performance. In conclusion, specific and non-specific HIV-related factors are associated with low handgrip strength, low muscle mass, and/or low chair stand performance.

Relationship Between Body Size and Skeletal Age with Muscle Damage in Young Soccer Players.

This study verified the relationship between body size and skeletal age (SA) with the behavior of blood markers of muscle damage and delayed onset muscle soreness (DOMS) after a soccer match in the U-13 and U-15 categories. The sample consisted of 28 soccer players in the U-13 and 16 in the U-15 categories. Creatine kinase (CK), lactate dehydrogenase (LDH), and DOMS were evaluated up to 72 h after the match. Muscle damage was elevated at 0 h in U-13, and from 0 h to 24 h in U-15. DOMS increased from 0 h to 72 h in U-13 and from 0 h to 48 h in U-15. Significant associations of SA and fat-free mass (FFM) with muscle damage markers and DOMS were observed only in U-13, specifically at time 0 h, when SA explained 56% of CK and 48% of DOMS and FFM explained 48% of DOMS. We concluded that in the U-13 category, higher SA is significantly associated with muscle damage markers, and increase in FFM is associated with muscle damage markers and DOMS. Furthermore, U-13 players need 24 h to recover pre-match muscle damage markers and more than 72 h to recover DOMS. In contrast, the U-15 category needs 48 h to recover muscle damage markers and 72 h to recover DOMS.

Sarcopenia Related to Human Immunodeficiency Virus: Protective Effects of Exercise.

We discuss recent evidence supporting the hypothesis that sarcopenia is an emerging health concern among people with human immunodeficiency virus (HIV) because of increasing life expectancy and HIV- and treatment-related comorbidities. We also hypothesize that combined exercise at higher intensity has a key role in managing sarcopenia in this population because it directly (increases muscle strength and stimulates hypertrophy) and indirectly (prevents mitochondrial dysfunction, oxidative stress, and persistent inflammation) counteracts sarcopenia hallmarks.

One-Carbon Metabolism in Fatty Liver Disease and Fibrosis: One-Carbon to Rule Them All.

Nonalcoholic fatty liver disease (NAFLD) is a term used to characterize a range of disease states that involve the accumulation of fat in the liver but are not associated with excessive alcohol consumption. NAFLD is a prevalent disease that can progress to organ damage like liver cirrhosis and hepatocellular carcinoma. Many animal models have demonstrated that one-carbon metabolism is strongly associated with NAFLD. Phosphatidylcholine is an important phospholipid that affects hepatic lipid homeostasis and de novo synthesis of this phospholipid is associated with NAFLD. However, one-carbon metabolism serves to support all cellular methylation reactions and catabolism of methionine, serine, glycine, choline, betaine, tryptophan, and histidine. Several different pathways within one-carbon metabolism that play important roles in regulating energy metabolism and immune function have received less attention in the study of fatty liver disease and fibrosis. This review examines what we have learned about hepatic lipid metabolism and liver damage from the study of one-carbon metabolism thus far and highlights unexplored opportunities for future research.

Effects of a Combined Exercise Training Program on Health Indicators and Quality of Life of People Living with HIV: A Randomized Clinical Trial.

The aim of this study was to evaluate the effects of 16 weeks of combined exercise training (CET) on muscle strength, body composition, depression, anxiety and quality of life of people living with HIV (PLHIV). Twenty-three participants completed the study, 14 in trained group (TG) and 9 in control group (CG). TG consisted of resistance and aerobic training three times a week, while the CG was exposed to recreational activities twice a week. CET promoted increased muscle strength (25% in overall strength) and aerobic capacity (+ 20% in training speed and + 23% in VO2 during aerobic training; p < 0.05). In addition, TG had better quality of life and reduced depression rates (from 7 subjects with mild, moderate or severe depression to 1 post-training). In conclusion, this pilot data demonstrated that 16 weeks of CET increased muscle strength, and improved depression and quality of life indexes in a small sample of PLHIV.

Creatine supplementation in Walker-256 tumor-bearing rats prevents skeletal muscle atrophy by attenuating systemic inflammation and protein degradation signaling.

PURPOSE: The aim of this study was to investigate the effects of creatine supplementation on muscle wasting in Walker-256 tumor-bearing rats. METHODS: Wistar rats were randomly assigned into three groups (n = 10/group): control (C), tumor bearing (T), and tumor bearing supplemented with creatine (TCr). Creatine was provided in drinking water for a total of 21 days. After 11 days of supplementation, tumor cells were implanted subcutaneously into T and TCr groups. The animals' weight, food and water intake were evaluated along the experimental protocol. After 10 days of tumor implantation (21 total), animals were euthanized for inflammatory state and skeletal muscle cross-sectional area measurements. Skeletal muscle components of ubiquitin-proteasome pathways were also evaluated using real-time PCR and immunoblotting. RESULTS: The results showed that creatine supplementation protected tumor-bearing rats against body weight loss and skeletal muscle atrophy. Creatine intake promoted lower levels of plasma TNF-α and IL-6 and smaller spleen morphology changes such as reduced size of white pulp and lymphoid follicle compared to tumor-bearing rats. In addition, creatine prevented increased levels of skeletal muscle Atrogin-1 and MuRF-1, key regulators of muscle atrophy. CONCLUSION: Creatine supplementation prevents skeletal muscle atrophy by attenuating tumor-induced pro-inflammatory environment, a condition that minimizes Atrogin-1 and MuRF-1-dependent proteolysis.

Mitochondrial dysfunction induces muscle atrophy during prolonged inactivity: A review of the causes and effects.

Prolonged skeletal muscle inactivity (e.g. limb immobilization, bed rest, mechanical ventilation, spinal cord injury, etc.) results in muscle atrophy that manifests into a decreased quality of life and in select patient populations, a higher risk of morbidity and mortality. Thus, understanding the processes that contribute to muscle atrophy during prolonged periods of muscle disuse is an important area of research. In this regard, mitochondrial dysfunction has been directly linked to the muscle wasting that occurs during extended periods of skeletal muscle inactivity. While the concept that mitochondrial dysfunction contributes to disuse muscle atrophy has been contemplated for nearly 50 years, the mechanisms connecting mitochondrial signaling events to skeletal muscle atrophy remained largely unexplained until recently. Indeed, emerging evidence reveals that mitochondrial dysfunction and the associated mitochondrial signaling events are a requirement for several forms of inactivity-induced skeletal muscle atrophy. Specifically, inactivity-induced alterations in skeletal muscle mitochondria phenotype and increased ROS emission, impaired Ca2+ handling, and release of mitochondria-specific proteolytic activators are established occurrences that promote fiber atrophy during prolonged periods of muscle inactivity. This review highlights the evidence that directly connects mitochondrial dysfunction and aberrant mitochondrial signaling with skeletal muscle atrophy and discusses the mechanisms linking these interconnected phenomena.

Effects of pre- or post-exercise whey protein supplementation on oxidative stress and antioxidant enzymes in older women.

BACKGROUND: Oxidative stress is an imbalance between antioxidant system and production of free radicals and has been associated with the age-related deleterious changes. The defense system can be modulated by exercise and nutrition. OBJECTIVE: The purpose of this investigation was to evaluate the effect of whey protein supplementation pre- or post-resistance training on oxidative stress and antioxidant enzyme activity in pre-conditioned older women. METHODS: In a randomized, double-blind, and placebo-controlled design, 70 older women (≥60 years) were randomly assigned to one of the following three groups: whey protein-placebo (WP-PLA, n = 24), placebo-whey protein (PLA-WP, n = 23), and placebo-placebo (PLA-PLA, n = 23). Each group received 35 g of whey product or placebo pre- and post-training. The RT program was carried out over 12 weeks (3x/week; 3x 8-12 repetitions maximal). Oxidative stress and blood markers were assessed before and after intervention period. ANOVA for repeated measures was used for data analysis. RESULTS: There was a significant time effect (P < 0.05), with all groups showing improvements in all oxidative stress markers and antioxidant enzyme activity. A significant (P < 0.001) interaction time vs group was observed for uric acid, with both WP-PLA and PLA-WP presenting greater reductions compared with the PLA-PLA, without differences between the timing of protein intake (WP-PLA: -8.3%; PLA-WP: -11.0%; PLA-PLA:-2.0%). CONCLUSION: In already pre-conditioned older women, whey protein supplementation reduces plasma uric acid concentration with no further effect on antioxidant enzyme activity and oxidative stress markers. ClinicalTrials.gov: NCT03247192.

Effect of combined training on body composition and metabolic variables in people living with HIV: A randomized clinical trial.

PURPOSE: The aim of this study was to conduct a randomized clinical trial to assess the effects of 16 weeks of combined training on body composition, lipid profile, adiponectin, C-reactive protein (CRP), and leptin levels in people living with HIV/AIDS (PLWHA). METHODS: Fifty-eight HIV-infected individuals were randomized into a training group (T) or a control group (C). Combined training consisted of aerobic and resistance exercises performed at the same training session, applied at a frequency of three times a week for a total of 16 weeks. Waist circumference, body mass, body fat percentage (%fat), fat mass, lipid profile, adiponectin, CRP, and leptin levels were measured pre- and post-training in both groups. RESULTS: Sixteen weeks of combined training decreased (P < 0.05) body fat in different body segments in PLWHA. Lipodystrophic PLWHA experienced greater reduction in body fat in the android region than non-lipodystrophic PLWHA after combined training. Lipid profile and circulating levels of adiponectin, leptin, and CRP remained unchanged. CONCLUSIONS: Sixteen weeks of combined training was effective to reduce body fat in different body segments, without altering plasma lipid and cytokine levels.

Effect of Resistance Training Systems on Oxidative Stress in Older Women.

The purpose of this study was to investigate the effect of two different resistance training (RT) systems on oxidative stress biomarkers in older women. Fifty-nine older women (67.9 ± 5.0 years) were randomly assigned to one of three groups. Two training groups performed an 8 week RT program either in traditional (TD, n = 20) or a pyramid (PR, n = 20) system 3 times per week, or a control group (CG, n = 19). The TD program consisted of 3 sets of 8-12 RM with constant load for the 3 sets, whereas the PR training consisted of 3 sets of 12/10/8 RM with incremental loads for each set. As compared with the CG, both TD and PR achieved upregulation of the antioxidant system as evidenced by higher (p < .05) values of total radical-trapping antioxidant parameter plasma concentration after intervention (TD= 930.4 ± 160.0 µmolTrolox, PR= 977.8 ± 145.2 µmolTrolox, CG= 794.4 ± 130.2 µmolTrolox). For the protein oxidation adducts, TD and PR presented lower (p < .05) scores compared with CG (TD= 91.2 ± 25.0 µmol/L, PR= 93.0 ± 30.3 µmol/L, CG= 111.0 ± 20.4 µmol/L). However, there were no differences (p < .05) between trained groups in the antioxidant capacity markers and in the protein oxidation adducts markers. The results suggest that 8 weeks of progressive RT promotes an improvement in markers of oxidative stress in older women independent of the load-management RT system.

Creatine supplementation as a possible new therapeutic approach for fatty liver disease: early findings.

Over the last few years, consistent data have demonstrated that creatine (Cr) supplementation prevents the accumulation of fat in rat liver as well as the progression of fatty liver disease in different situations. Studies have demonstrated that Cr is effective and prevents fatty liver in high-fat and choline-deficient diets and in hepatoma cells in vitro. Because Cr synthesis is responsible for a considerable consumption of hepatic methyl groups, studies have tested the idea that Cr supplementation could modulate phospholipid formation and VLDL secretion. Studies have also demonstrated Cr is able to modulate the expression of key genes related to fatty acid oxidation in hepatocyte cell culture and in rat liver. However, to date, the mechanism by which Cr exerts protective effects against fatty liver is poorly understood. Therefore, the present review aims to summarize the studies involving the therapeutic use of Cr supplementation on fatty liver disease and to explore the mechanisms involved in one-carbon and fatty acid metabolism for the preventive effects of Cr supplementation on fat liver accumulation. Although a small number of studies have been conducted to date, we consider Cr as a new and promising therapeutic strategy to control fat accumulation in the liver as well as the progression of fatty liver disease.

Creatine supplementation prevents hyperhomocysteinemia, oxidative stress and cancer-induced cachexia progression in Walker-256 tumor-bearing rats.

The purpose of this study was to investigate (1) the impact of tumor growth on homocysteine (Hcy) metabolism, liver oxidative stress and cancer cachexia and, (2) the potential benefits of creatine supplementation in Walker-256 tumor-bearing rats. Three experiments were conducted. First, rats were killed on days 5 (D5), 10 (D10) and 14 (D14) after tumor implantation. In experiment 2, rats were randomly assigned to three groups designated as control (C), tumor-bearing (T) and tumor-bearing supplemented with creatine (TCr). A life span experiment was conducted as the third experiment. Creatine was supplied in drinking water for 21 days (8 g/L) in all cases. Tumor implantation consisted of a suspension of Walker-256 cells (8.0 × 10(7) cells in 0.5 mL of PBS). The progressive increase (P < 0.05) in tumor mass coincided with a progressively lower body weight and higher hepatic oxidative stress; plasma Hcy concentration was 80 % higher (P < 0.05) by 10 days of tumor implantation. Impaired Hcy metabolism was evidenced by decreased hepatic betaine-homocysteine methyltransferase (Bhmt), glycine N-methyltransferase (Gnmt) and cystathionine beta synthase (CBS) gene expression. In contrast, creatine supplementation promoted a 28 % reduction of tumor weight (P < 0.05). Plasma Hcy (C 6.1 ± 0.6, T 10.3 ± 1.5, TCr 6.3 ± 0.9, µmol/L) and hepatic oxidative stress were lower in the TCr group compared to T. Creatine supplementation was unable to decrease Hcy concentration and to increase SAM/SAH ratio in tumor tissue. These data suggest that creatine effects on hepatic impaired Hcy metabolism promoted by tumor cell inoculation are responsible to decrease plasma Hcy in tumor-bearing rats. In conclusion, Walker-256 tumor growth is associated with progressive hyperhomocysteinemia, body weight loss and liver oxidative stress in rats. Creatine supplementation, however, prevented these tumor-associated perturbations.

Effects of 16 Weeks of Concurrent Training on Resting Heart Rate Variability and Cardiorespiratory Fitness in People Living With HIV/AIDS Using Antiretroviral Therapy: A Randomized Clinical Trial.

Pedro, RE, Guariglia, DA, Okuno, NM, Deminice, R, Peres, SB, and Moraes, SMF. Effects of 16 weeks of concurrent training on resting heart rate variability and cardiorespiratory fitness in people living with HIV/AIDS using antiretroviral therapy: a randomized clinical trial. J Strength Cond Res 30(12): 3494-3502, 2016-The study evaluated the effects of concurrent training on resting heart rate variability (HRVrest) and cardiorespiratory fitness in people living with HIV/AIDS undergoing antiretroviral therapy (ART). Fifty-eight participants were randomized into 2 groups (control and training group); however, only 33 were analyzed. The variables studied were HRVrest indices, submaximal values of oxygen uptake (V[Combining Dot Above]O2sub) and heart rate (HR5min), peak speed (Vpeak), and peak oxygen uptake (V[Combining Dot Above]O2peak). The training group performed concurrent training (15-20 minutes of aerobic exercise plus 40 minutes of resistance exercise), 3 times per week, for 16 weeks. Posttraining V[Combining Dot Above]O2peak and Vpeak increased, and HR5min decreased. Resting heart rate variability indices did not present statistical differences posttraining; however, the magnitude-based inferences demonstrated a "possibly positive effect" for high frequency (HF) and low frequency (LF) plus high frequency (LF + HF) and a "likely positive effect" for R-Rmean posttraining. In conclusion, concurrent training was effective at improving cardiorespiratory fitness and endurance performance. Moreover, it led to probably a positive effect on HF and a likely positive effect on R-Rmean in people living with HIV/AIDS undergoing ART.

Betaine supplementation prevents fatty liver induced by a high-fat diet: effects on one-carbon metabolism.

The purpose of this study was to examine the effects of betaine supplementation on the regulation of one-carbon metabolism and liver lipid accumulation induced by a high-fat diet in rats. Rats were fed one of three different liquid diets: control diet, high-fat diet and high-fat diet supplemented with betaine. The control and high-fat liquid diets contained, respectively, 35 and 71 % of energy derived from fat. Betaine supplementation involved the addition of 1 % (g/L) to the diet. After three weeks on the high-fat diet the rats had increased total liver fat concentration, liver triglycerides, liver TBARS and plasma TNF-α. The high-fat diet decreased the hepatic S-adenosylmethionine concentration and the S-adenosylmethionine/S-adenosylhomocysteine ratio compared to the control as well as altering the expression of genes involved in one-carbon metabolism. Betaine supplementation substantially increased the hepatic S-adenosylmethionine concentration (~fourfold) and prevented fatty liver and hepatic injury induced by the high-fat diet. It was accompanied by the normalization of the gene expression of BHMT, GNMT and MGAT, which code for key enzymes of one-carbon metabolism related to liver fat accumulation. In conclusion, the regulation of the expression of MGAT by betaine supplementation provides an additional and novel mechanism by which betaine supplementation regulates lipid metabolism and prevents accumulation of fat in the liver.

Dietary docosahexaenoic acid and eicosapentaenoic acid influence liver triacylglycerol and insulin resistance in rats fed a high-fructose diet.

This study aimed to examine the benefits of different amounts of omega-3 (n-3) polyunsaturated fatty acids from fish oil (FO) on lipid metabolism, insulin resistance and gene expression in rats fed a high-fructose diet. Male Wistar rats were separated into two groups: Control (C, n = 6) and Fructose (Fr, n = 32), the latter receiving a diet containing 63% by weight fructose for 60 days. After this period, 24 animals from Fr group were allocated to three groups: FrFO2 (n = 8) receiving 63% fructose and 2% FO plus 5% soybean oil; FrFO5 (n = 8) receiving 63% fructose and 5% FO plus 2% soybean oil; and FrFO7 (n = 8) receiving 63% fructose and 7% FO. Animals were fed these diets for 30 days. Fructose led to an increase in liver weight, hepatic and serum triacylglycerol, serum alanine aminotransferase and HOMA1-IR index. These alterations were reversed by 5% and 7% FO. FO had a dose-dependent effect on expression of genes related to hepatic ß-oxidation (increased) and hepatic lipogenesis (decreased). The group receiving the highest FO amount had increased markers of oxidative stress. It is concluded that n-3 fatty acids may be able to reverse the adverse metabolic effects induced by a high fructose diet.

Oxidative stress and inflammation in obesity after taurine supplementation: a double-blind, placebo-controlled study.

PURPOSE: Some researchers found decreased levels of plasma taurine in obese subjects and animals, and reduced expression of an important enzyme of taurine synthesis. These evidences, coupled with the metabolic imbalance of obesity and the possible anti-inflammatory and antioxidant effects of taurine, highlighted the use of taurine as a supplement in obesity treatment. The aim of the present study was to investigate whether taurine supplementation, associated with nutritional counseling, modulates oxidative stress, inflammatory response, and glucose homeostasis in obese women. METHODS: A randomized double-blind placebo-controlled study was conducted with 16 women with obesity diagnosis and 8 women in the normal weight range. The obese volunteers were matched by age and body mass index and randomly assigned to either the placebo (3 g/day starch flour) or taurine (3 g/day taurine) group. The study lasted 8 weeks, and the experimental protocol included nutritional assessment and determination of plasma sulfur amino acids, insulin, and adiponectin, serum glycemia, and markers of inflammatory response and oxidative stress. RESULTS: Plasma taurine levels were significantly decreased (41%) in the obese volunteers. Both the placebo and taurine groups showed significant reduction in weight (3%), with no differences between groups. Different from placebo, taurine-supplemented group showed significant increase in plasma taurine (97%) and adiponectin (12%) and significant reduction in the inflammatory marker hs-C-reactive protein (29%) and in the lipid peroxidation marker thiobarbituric acid reactive substances (TBARS) (20%). CONCLUSIONS: Eight weeks of taurine supplementation associated with nutritional counseling is able to increase adiponectin levels and to decrease markers of inflammation (high-sensitivity C-reactive protein) and lipid peroxidation (TBARS) in obese women.

Short-term creatine supplementation does not reduce increased homocysteine concentration induced by acute exercise in humans.

PURPOSE: The purpose of the study is to evaluate the effects of creatine supplementation on homocysteine (Hcy) plasma levels after acute exercise in humans. METHODS: Twenty-three young (under-20) soccer players were divided into 2 groups: creatine (Cr)- and placebo (Pla)-supplemented groups. The supplementation was performed in double-blind controlled manner using creatine or placebo tablets with 0.3 g/kg during 7 days. Before and after 7 days of supplementation, the athletes performed an acute high-intensity sprint exercise (two consecutive running-based anaerobic sprint test protocol consisted in 6 × 35 m sprint with 10 s between them). Blood samples were collected before and after 7 days of supplementation as well as 0 and 1 h after exercise protocol. RESULTS: Homocysteine concentration significant increased (P < 0.05) 1 h after acute exercise (18%). Acute exercise also decreased red blood cell S-adenosylmethionine (SAM) 30% with no changes in SAM/SAH ratio. Seven days of creatine supplementation were able to increase (P < 0.05) plasma creatine concentration (Pla 130.1 ± 21.7 vs Cr 1,557.2 ± 220.3 µmol/L) as well as decrease (P < 0.05) plasma guanidinoacetic acid (33%). Controversially, creatine supplementation did not change Hcy plasma level after 7-day supplementation (Pla 6.9 ± 0.2 vs Cr 7.2 ± 0.2 µmol/L) or after acute exercise (Pla 8.2 ± 0.3 vs Cr 8.4 ± 0.3 µmol/L). No changes in plasma vitamin B12 and folate as well as cysteine and methionine were found. CONCLUSIONS: Seven days of creatine supplementation does not avoid increased plasma Hcy induced by acute sprint exercise in humans.

Pre and Post-high-intensity Interval Training Delays Colon Tumor Onset in a Syngeneic Mouse Model.

BACKGROUND/AIM: High-intensity interval training (HIIT) can trigger transient anti-tumor cytotoxicity through the mobilization of natural killer cells (NK cells) and myokines. Yet, the effects of HIIT on tumor development and microenvironment are unclear. MATERIALS AND METHODS: Male C57/BL6 mice were administered either MC38 of syngeneic colon cancer cells or vehicle in a single subcutaneous injection. Before injection, the training group completed four weeks of the HIIT program (progressive swimming training, 3/week, 10-12 min, 4-6% of body weight for overload). Following injection, trained mice continued to exercise for two additional weeks. RESULTS: Pre and post-HIIT training was effective in preventing tumor onset (p=0.0065), maintaining body weight gain, and counteracting splenomegaly by 40% compared to the tumor group. However, HIIT had no impact on suppressing tumor growth, modifying final tumor volume, or significantly changing tumor proliferation (Ki-67), connective tissue content, or DNA double-strand damage detected by phospho-histone gamma-H2AX (γ-H2AX). CONCLUSION: Pre and post-HIIT program is feasible for mice carrying a subcutaneous syngeneic tumor and effective in delaying tumor burden; however, HIIT did not alter colon tumor endpoints.

Doxorubicin causes cachexia, sarcopenia, and frailty characteristics in mice.

While chemotherapy treatment can be lifesaving, it also has adverse effects that negatively impact the quality of life. To investigate the effects of doxorubicin chemotherapy on body weight loss, strength and muscle mass loss, and physical function impairments, all key markers of cachexia, sarcopenia, and frailty. Seventeen C57/BL/6 mice were allocated into groups. 1) Control (n = 7): mice were exposed to intraperitoneal (i.p.) injections of saline solution. 2) Dox (n = 10): mice were exposed to doxorubicin chemotherapy cycles (total dose of 18 mg/kg divided over 15 days). The body weight loss and decreased food intake were monitored to assess cachexia. To assess sarcopenia, we measured muscle strength loss using a traction method and evaluated muscle atrophy through histology of the gastrocnemius muscle. To evaluate physical function impairments and assess frailty, we employed the open field test to measure exploratory capacity. Doxorubicin administration led to the development of cachexia, as evidenced by a significant body weight loss (13%) and a substantial decrease in food intake (34%) over a 15-day period. Furthermore, 90% of the mice treated with doxorubicin exhibited sarcopenia, characterized by a 20% reduction in traction strength (p<0,05), a 10% decrease in muscle mass, and a 33% reduction in locomotor activity. Importantly, all mice subjected to doxorubicin treatment were considered frail based on the evaluation of their overall condition and functional impairments. The proposed model holds significant characteristics of human chemotherapy treatment and can be useful to understand the intricate relationship between chemotherapy, cachexia, sarcopenia, and frailty.