scholarly journals Effect of a High Fat and High Protein Diet on Exercise-Induced Skeletal Muscle Hypertrophy in Rats

2019 ◽  
Vol 4 (3) ◽  
pp. 29-40
Author(s):  
Takako Fujii ◽  
Tomohiro Sonou ◽  
Naoya Nakai ◽  
Koji Okamura

The skeletal muscle mass varies by race. Dietary habits over generations are a factor that influences the skeletal muscle mass, as well as genetic factors. Therefore, we investigated the effects of diets with different macronutrient contents on exercise-induced muscle hypertrophy in rats. Male 4-week-old Sprague–Dawley rats were randomly divided into three groups: a normal-diet (N), high-protein diet (HP) and high-fat diet (HF) group. The food intake was manipulated to gain comparable body weight across the three groups. All rats were performed a climbing training exercise for 8 weeks. The final body weight and weight of the liver, kidneys and adipose tissues did not significantly differ among the groups. The flexor hullucis lingus was significantly higher in the HF group than in the HP group. The total lipid content in the muscle was significantly higher in the HF group than in the N group, while it did not differ significant between the HF and HP groups. There were no marked differences in the water or protein content in the muscle among the groups. The plasma amino acid concentration was significantly or tended to be lower in the HP group than in the HF or N group, except for the branched-chain amino acid concentration, which tended to be higher after ingesting the HP diet than other diets. These findings suggest that consuming an HP diet is not likely to facilitate exercise-induced muscle hypertrophy, partly due to the plasma amino acid imbalance induced by habitual HP diet consumption.

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 141 ◽  
Author(s):  
Sophie Joanisse ◽  
Changhyun Lim ◽  
James McKendry ◽  
Jonathan C. Mcleod ◽  
Tanner Stokes ◽  
...  

Skeletal muscle plays a pivotal role in the maintenance of physical and metabolic health and, critically, mobility. Accordingly, strategies focused on increasing the quality and quantity of skeletal muscle are relevant, and resistance exercise is foundational to the process of functional hypertrophy. Much of our current understanding of skeletal muscle hypertrophy can be attributed to the development and utilization of stable isotopically labeled tracers. We know that resistance exercise and sufficient protein intake act synergistically and provide the most effective stimuli to enhance skeletal muscle mass; however, the molecular intricacies that underpin the tremendous response variability to resistance exercise-induced hypertrophy are complex. The purpose of this review is to discuss recent studies with the aim of shedding light on key regulatory mechanisms that dictate hypertrophic gains in skeletal muscle mass. We also aim to provide a brief up-to-date summary of the recent advances in our understanding of skeletal muscle hypertrophy in response to resistance training in humans.


Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2023
Author(s):  
Louise Deldicque

Skeletal muscle mass is critical for sport performance and in many pathological conditions. The combination of protein intake and resistance exercise is the most efficient strategy to promote skeletal muscle hypertrophy and remodeling. However, to be really efficient, certain conditions need to be considered. The amount, type and source of proteins do all matter as well as the timing of ingestion and spreading over the whole day. Optimizing those conditions favor a positive net protein balance, which in the long term, may result in muscle mass accretion. Last but not least, it is also essential to take the nutritional status and the exercise training load into consideration when looking for maintenance or gain of skeletal muscle mass.


2019 ◽  
Vol 1 (10) ◽  
pp. 456-461
Author(s):  
Shuhei Tsuji ◽  
Satoshi Koyama ◽  
Ryoji Taniguchi ◽  
Takako Fujiwara ◽  
Hisayoshi Fujiwara ◽  
...  

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Tomoaki Takata ◽  
Yukari Mae ◽  
Kentaro Yamada ◽  
Sosuke Taniguchi ◽  
Shintaro Hamada ◽  
...  

Abstract Background Hyporesponsiveness to erythropoietin stimulating agent (ESA) is associated with poor outcomes in patients with chronic kidney disease. Although ESA hyporesponsiveness and sarcopenia have a common pathophysiological background, clinical evidence linking them is scarce. The purpose of the study was to investigate the relationship between ESA responsiveness and skeletal muscle mass in hemodialysis patients. Methods This cross-sectional study analyzed 70 patients on maintenance hemodialysis who were treated with ESA. ESA responsiveness was evaluated by erythropoietin resistance index (ERI), calculated as a weekly dose of ESA divided by body weight and hemoglobin (IU/kg/week/dL), and a weekly dose of ESA/hemoglobin (IU/week/dL). A dose of ESA is equivalated to epoetin β. Correlations between ESA responsiveness and clinical parameters including skeletal muscle mass were analyzed. Results Among the 70 patients, ERI was positively correlated to age (p < 0.002) and negatively correlated to height (p < 0.001), body weight (p < 0.001), BMI (p < 0.001), skeletal muscle mass (p < 0.001), transferrin saturation (TSAT) (p = 0.049), and zinc (p = 0.006). In the multiple linear regression analysis, TSAT, zinc, and skeletal muscle mass were associated with ERI and weekly ESA dose/hemoglobin. Conclusions Skeletal muscle mass was the independent predictor for ESA responsiveness as well as TSAT and zinc. Sarcopenia is another target for the management of anemia in patients with hemodialysis.


2016 ◽  
Vol 41 (6) ◽  
pp. 611-617 ◽  
Author(s):  
Jameason D. Cameron ◽  
Ronald J. Sigal ◽  
Glen P. Kenny ◽  
Angela S. Alberga ◽  
Denis Prud’homme ◽  
...  

There has been renewed interest in examining the relationship between specific components of energy expenditure and the overall influence on energy intake (EI). The purpose of this cross-sectional analysis was to determine the strongest metabolic and anthropometric predictors of EI. It was hypothesized that resting metabolic rate (RMR) and skeletal muscle mass would be the strongest predictors of EI in a sample of overweight and obese adolescents. 304 post-pubertal adolescents (91 boys, 213 girls) aged 16.1 (±1.4) years with body mass index at or above the 95th percentile for age and sex OR at or above the 85th percentile plus an additional diabetes risk factor were measured for body weight, RMR (kcal/day) by indirect calorimetry, body composition by magnetic resonance imaging (fat free mass (FFM), skeletal muscle mass, fat mass (FM), and percentage body fat), and EI (kcal/day) using 3 day food records. Body weight, RMR, FFM, skeletal muscle mass, and FM were all significantly correlated with EI (p < 0.005). After adjusting the model for age, sex, height, and physical activity, only FFM (β = 21.9, p = 0.007) and skeletal muscle mass (β = 25.8, p = 0.02) remained as significant predictors of EI. FFM and skeletal muscle mass also predicted dietary protein and fat intake (p < 0.05), but not carbohydrate intake. In conclusion, with skeletal muscle mass being the best predictor of EI, our results support the hypothesis that the magnitude of the body’s lean tissue is related to absolute levels of EI in a sample of inactive adolescents with obesity.


2017 ◽  
Vol 10 (2) ◽  
pp. 28
Author(s):  
Ha Cao Thi Thu ◽  
Satoshi Kurose ◽  
Yaeko Fukushima ◽  
Nana Takao ◽  
Natsuko Nakamura ◽  
...  

This study evaluated the impact of exercise training with amino acid and vitamin D supplementation on muscle and bone mass in participants with low muscle volume. Twenty-nine Japanese participants (56-84 years old) were enrolled and assigned into the supplement (n=15) and non-supplement (n=14) groups. All participants underwent a 6-month exercise program. Supplements and nutrition support were provided to the participants in the supplement group for 12 weeks. Body composition and whole bone mineral density (BMD) were measured using dual energy x-ray absorptiometry. The outcomes, including body composition, whole BMD, and skeletal muscle mass index (SMI), were evaluated twice: pre- and post-intervention. The SMI was 6.51(6.28; 7.14) and 5.58 (5.24; 6.05) (kg/m2) in men and women, respectively. The average SMI change was 0.13% (-0.05%; 0.31%) and 2.33% (-0.88%; 5.48%); [mean (lower; upper quartile)]. The average BMD loss in the non-supplement group was -2.78%, and the BMD increased in the supplement group by 4.34%; there was an absolute difference between the two groups (p<0.05). After the intervention, serum myostatin was changed (p=0.001, non-supplement>supplement), serum vitamin D was increased (p=0.03; supplement>non-supplement), and BMD was maintained (p=0.03, supplement>non-supplement). There was a significant difference in the serum myostatin level at baseline and at 6-month in the non-supplement group, with a mean difference of 483.78 ng/ml (p=0.01). There was no significant improvement in the total lean mass, and handgrip strength. Resistance exercise combined with an amino acid supplement affects muscle and bone mass in the short-term intervention.


2020 ◽  
Vol 67 (7) ◽  
pp. 733-740 ◽  
Author(s):  
Kensuke Nishida ◽  
Yoshitaka Hashimoto ◽  
Ayumi Kaji ◽  
Takuro Okamura ◽  
Ryousuke Sakai ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Naoki Kuramoto ◽  
Kazuhiro Nomura ◽  
Daisuke Kohno ◽  
Tadahiro Kitamura ◽  
Gerard Karsenty ◽  
...  

AbstractPhosphatidylinositol 3-kinase (PI3K) plays an important role in protein metabolism and cell growth. We here show that mice (M-PDK1KO mice) with skeletal muscle–specific deficiency of 3′-phosphoinositide–dependent kinase 1 (PDK1), a key component of PI3K signaling pathway, manifest a reduced skeletal muscle mass under the static condition as well as impairment of mechanical load–induced muscle hypertrophy. Whereas mechanical load-induced changes in gene expression were not affected, the phosphorylation of ribosomal protein S6 kinase (S6K) and S6 induced by mechanical load was attenuated in skeletal muscle of M-PDK1KO mice, suggesting that PDK1 regulates muscle hypertrophy not through changes in gene expression but through stimulation of kinase cascades such as the S6K-S6 axis, which plays a key role in protein synthesis. Administration of the β2-adrenergic receptor (AR) agonist clenbuterol activated the S6K-S6 axis in skeletal muscle and induced muscle hypertrophy in mice. These effects of clenbuterol were attenuated in M-PDK1KO mice, and mechanical load–induced activation of the S6K-S6 axis and muscle hypertrophy were inhibited in mice with skeletal muscle–specific deficiency of β2-AR. Our results suggest that PDK1 regulates skeletal muscle mass under the static condition and that it contributes to mechanical load–induced muscle hypertrophy, at least in part by mediating signaling from β2-AR.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15633-e15633
Author(s):  
Matthew Peloquin ◽  
Brianna LaCarubba ◽  
Stephanie Joaqium ◽  
Gregory Weber ◽  
John Stansfield ◽  
...  

e15633 Background: Almost half of cancer deaths are attributed to cancers most frequently associated with cachexia. Cachexia is a complex metabolic disease characterized by anorexia and unintentional weight loss. Skeletal muscle depletion has been recognized as a key feature of the disease, however muscle anabolic therapies have not been successful, suggesting that treatments that target multiple aspects of the disease will be most effective. Growth differentiation factor 15 (GDF-15) is a cytokine that induces anorexia and weight loss and is associated with cachexia in cancer patients. In preclinical cancer cachexia models, GDF-15 inhibition is sufficient to normalize food intake and body weight, including skeletal muscle mass. However, it remains to be determined whether the increased skeletal muscle mass also results in restoration of muscle function. Therefore, we examined the effect of GDF-15 inhibition on muscle mass and function in mouse models of cancer cachexia in comparison with myostatin inhibition, an established muscle anabolic pathway. Methods: Cachectic mouse tumor models were established with subcutaneous implantation of tumor cell lines reported to be GDF-15-dependent; mouse renal cell carcinoma (RENCA) and human ovarian cancer (TOV-21G) cell lines. Mice were treated with anti-GDF-15 (mAB2) or anti-myostatin (RK35) monoclonal antibodies and skeletal muscle function was assessed in vivo via maximum force, maximum rate of contraction and half relax time. In the RENCA tumor model, GDF-15 inhibition fully restored body weight and skeletal muscle mass whereas myostatin inhibition showed only a modest effect. Results: Consistent with the muscle mass improvement, GDF-15 inhibition dramatically increased functional muscle endpoints compared to the partial effect of myostatin inhibition. Interestingly, in the TOV-21G tumor model GDF-15 inhibition only partially restored body weight, however skeletal muscle mass and muscle function were completely normalized. Consistent with the functional assessment, GDF-15 inhibition in the RENCA tumor model decreased the expression of several catabolic genes (i.e. Trim63, Fbxo32, Myh7 and Myh2). The GDF-15 effect is likely to be secondary to the reversal of anorexia since wildtype mice pair-fed to Fc-GDF-15-treated mice demonstrated equivalent muscle mass loss. Conclusions: Taken together these data suggest that GDF-15 inhibition holds potential as an effective therapeutic approach to alleviate multiple aspects of cachexia.


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