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Sep 2025 DOI 10.14302/issn.2643-2811.jmbr-25-5688
Dahlmann NicolausCorresponding author
Obesity is associated with functional limitations in muscle performance. The true effect of obesity on skeletal muscle mass, including any interactions with aging effects, remains to be elucidated. The present study investigated the impact of obesity on the stimulation of muscle growth, based on a new model of body composition. A dataset of 44 men and 64 women was analysed. Body weight (Wt), body height (Ht), hand circumference (HdC) and waist circumference (WC) were measured. Processed by the Dahlmann-Body-Analysis (DBA) system, a new model of body composition, the increase of skeletal muscle mass (ΔSMM) compared to the individual reference weight was calculated. Muscle mass data derived by the DBA model are compared with DXA-derived predictive equations of studies representing different countries and ethnicities estimating the appendicular skeletal muscle mass. Means of these groups are tested by ANOVA. Age ranged from 18 to 72 years. All subjects had a BMI ≥ 29.7 (kg/m²). The mean values of ΔSMM as an estimate of muscle mass gain calculated by the DBA-system were 11.8 ±3.6 kg for men and 8.9 ±2.6 kg for women, respectively, demonstrating a linear, significantly rising relationship with BMI (ß > 0, p<0.001). The study population did not show a decrease in muscle mass with age in either men or women up to an age of 65 years. The results suggest that the present model has satisfactory prediction qualities to detect an increase in skeletal muscle mass associated with a growing burden of body fat.
Jul 2021 DOI 10.14302/issn.2576-6694.jbbs-21-3819
Jana SnehasisCorresponding author
Trivedi Science Research Laboratory Pvt. Ltd., Thane (W), Maharashtra, India.
The present study aimed to evaluate the effect of the Trivedi Effect®- Biofield Energy Treated/Blessed Test formulation/item (TI) composed of minerals (magnesium, zinc, copper, calcium, selenium, and iron), vitamins (ascorbic acid, pyridoxine HCl, alpha tocopherol, cyanocobalamin, and cholecalciferol), Panax ginseng extract, CBD isolates, and β-carotene on elasticity of skin, heart, muscle, and neuronal cells in the H9C2 (rat cardiomyocytes), C2C12 (mouse myoblast cells), HaCaT (human keratinocytes), and SH-SY5Y (human neuroblastoma cells) cell line in DMEM medium. The test formulation constituents were divided into two parts; one section was defined as untreated test formulation (UT), while the other portion of test formulation received Biofield Energy Healing/Blessing Treatment (BT) by a renowned Biofield Energy Healer, Mr. Mahendra Kumar Trivedi. The test items were treated with Biofield Energy Healing/Blessing Treatment and divided as Biofield Energy Treated/Blessed (BT) and untreated (UT) test items. MTT data showed that the test formulation in various concentrations was found as safe and nontoxic in the tested concentrations with viability range from 73% to 307%. Young’s modulus (YM) is a measure of cell stiffness, a decrease in YM value indicates increase elasticity of the cells and vice-versa. YM in H9C2 cells were decreased by 9.6% and 66.1% in the BT-DMEM + UT-TI group at 0.1 and 1 µg/mL respectively, as compared with untreated test group. However, C2C21 cells showed increased YM by 443.9% at 1 µg/mL in the UT-DMEM + BT-TI group, while 869.6% increased YM in the BT-DMEM + UT-TI group at 1 µg/mL as compared with untreated test group. However, 314% increased YM was reported in the BT-DMEM + BT-TI group at 1 µg/mL as compared with the untreated test group. However, the value of YM was significantly decreased in the HaCaT cell line by 247.7% (at 1 µg/mL), 225.8% (at 0.1 µg/mL), and 97.9% (at 1 µg/mL) in the UT-DMEM + BT-TI, BT-DMEM + UT-TI, and BT-DMEM + BT-TI group respectively, as compared with the untreated group. In addition, YM was significantly decreased in the SH-SY5Y cell line by 92.6%, 18.1%, and 26.6% at 1 µg/mL in the UT-DMEM + BT-TI, BT-DMEM + UT-TI, and BT-DMEM + BT-TI group respectively, as compared with the untreated group. Overall, the results showed the significant decreased YM among the SH-SY5Y, HaCaT, and H9C2 cells, while it was increased in the C2C21 cell line. Thus, the mechanical properties of cells such as cellular function, including shape, motility, differentiation, division, and adhesion to its surrounding extracellular matrix were improved. Overall, it can be useful in many disease progressions with improved cellular elasticity and its associated complications/symptoms.
Apr 2020 DOI 10.14302/issn.2832-4048.jsm-20-3211
Papaconstantinou JohnCorresponding author
The Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch, Galveston Texas 77555-0643
Aging mammalian skeletal muscle satellite cells (MuSCs) undergo a decline of stem cell/progenitor cell proliferative and regenerative capacity, and the development of a physiological milieu characteristic of a state of chronic sterile inflammation. p38αMAPK and ERK1/2 are two major signaling pathways that regulate the age-associated decline of MuSC proliferative capacity. In this review we propose the following mechanism that links the p38αMAPK pathway to the decline of self-renewal and regenerative capacity of aged MuSCs: a) the HS-FGF-2-FGFR1-p38αMAPK-Axis, a tightly linked homeostatic signaling complex, is in synchrony with the autoinhibition of FGFR1; b) autoinhibition contributes to the Axis’ regulation of the homeostasis of P-p38αMAPK activity in juvenile MuSC; c) this combination of protein-protein interactions is characteristic of a juvenile cytoplasmic milieu of beneficial P-p38αMAPK activity and d) includes Sprouty1 inhibition that supports the stimulation of FGF-2 --> miR-29a; e) the miR29a dismantles the basement membrane in preparation for the initiation of replication; f) an age-associated impaired, dysregulated, over-sulfated heparan sulfate ligand (HS)-FGF-2 fails to activate FGFR1 in aged MuSCs; g) this uncouples its regulation of p38αMAPK and ERK1/2 pathways and results in desensitization of FGFR1; h) desensitization of FGFR1 and Sprouty1 interaction in aged MuSC uncouples their regulation of P-p38αMAPK in the aged MuSCs; i) this enables a state of chronic sterile inflammation to promote and sustain an increased level of P-p38αMAPK activity; and, j) the increased activity of P-p38αMAPK in aged MuSC stimulates the production of cell cycle inhibitors, miR-1 and miR-133, thereby attenuating the expression of the cell cycle regulators, SP1 and cyclin D1, resulting in a G1/S arrest; j) the increased level of p38αMAPK activity promotes the apoptosis of the aged activated MuSCs. This mechanism involves the synergistic interactions of HS-FGF2-FGFR-1, Sprouty (spry1), miR-1, miR-133 and miR-29a that unify the extracellular niche and intracellular milieu for the juvenile vs age-associated regulation of proliferative capacity of the MuSC. Our hypothesis unifies these interactions with the role of the extracellular niche and intracellular milieu in the stimulation of juvenile proliferation vs age-associated decline of skeletal muscle satellite cell self-renewal and regenerative proliferation. Word Count = 344
Oct 2019 DOI 10.14302/issn.2379-7835.ijn-19-3011
Fujii TakakoCorresponding author
Exercise Nutrition Laboratory, Graduate School of Sport and Exercise Sciences, Osaka University of Health and Sport Sciences, Osaka, Japan
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 exercise training 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 hallucis longus 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 significantly 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.
Jan 2018 DOI 10.14302/issn.2832-4048.jsm-18-1941
Gomes Ferreira Padilha FelipeCorresponding author
Federal Fluminense University
A review of transcriptomic tools for skeletal muscle research, covering experimental design, data analysis, and applications in physiology and disease.
Jun 2016 DOI 10.14302/issn.2470-5020.jnrt-16-993
Jurkat-Rott KarinCorresponding author
Division of Neurophysiology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany
Autosomal dominant inherited hypokalemic periodic paralysis (HypoPP) is caused by S4 voltage sensor mutations in skeletal muscle CaV1.1 calcium or NaV1.4 sodium channels. In the present study, a small German family with the known CaV1.1-R528G is described. The phenotype consists of short and infrequent episodes of limb weakness with ictal respiratory and cardiac involvement. There is incomplete penetrance in women, and acetazolamide is beneficial in two patients also taking daily potassium. Expression of the mutation in the GLT mouse muscle cell line revealed accelerated kinetics of inactivation by twofold, a left-shift of the steady-state inactivation curve by 13mV and a reduced recovery from fast inactivation by up to 39%. These changes suggest a stabilization of the inactivated state. Additional significant slowing of activation may support a second open state with differing ion selectivity or decreased activation of calcium-activated potassium channels and thereby contribute to weakness similar to other CaV1.1 mutations. Also, as documented for other HypoPP mutants, we found a hyperpolarization-induced inward guanidinium current of 22nS/nF which can be interpreted as an omega current along the voltage sensor gating pore that leads to a gain- of- function at potentials near the resting membrane potential. This finding can explain the long-lasting depolarizations that are known to lead to paralysis. The omega current is large enough so that a relatively mild hypokalemic trigger of 2.4mM already produces episodes of weakness in vivo.
Apr 2026 DOI 10.14302/issn.2574-450X.jom-26-6138
Dahlmann NicolausCorresponding author
Indices, based on data such as height and weight in general and in particularly the body mass index (BMI), are often used to assess overweight. However, there is limited capacity to differentiate the amount of fat mass between individuals. This review refers to an anthropometric model called Dahlmann-Body-Analysis (DBA), which uses simple anthropometric parameters to define a Reference Weight (Ref-Wt). It is based on hand circumference as a proxy for the skeletal frame and, in addition, the circumference of the abdomen as a proxy for central obesity. Processed through a network of algorithms, the DBA model enabled to differentiate the Difference Weight – that means the difference between the Actual Weight and the Reference Weight – into fat mass and skeletal muscle mass. The DBA-model resembles the 2-component model of Albert R. Behnke, which he considered as a living functional construct including essential fat. The DBA-model matches with Behnke`s 2-component model insofar, as the essential fat is replaced by a physiological amount of fat tissue. The review summarizes studies to compare DBA-derived data with Metropolitan Life Insurance tables, evaluates DBA-derived fat tissue mass with bioelectrical impedance analysis (BIA) derived results and analyses the meaning of the DBA model in clinical settings to uncover the underlying mechanisms of metabolic syndrome (MetS) pathogenesis with increasing amounts of fat mass. The model offers the opportunity to calculate changes in fat or muscle tissue in an absolute (kg) or relative (%) amount on individuals. The data suggest that the DBA-model has satisfactory prediction qualities for use as a practical tool in public health care.
Jun 2021 DOI 10.14302/issn.2474-7785.jarh-21-3867
Marks RayCorresponding author
Department of Health and Behavior Studies, Teachers College, Columbia University, New York, NY 10027, USA.
Background Aging is said to represent a declining state that is possibly especially compromised by sleep issues, and declining melatonin levels. Aim This review examined the idea that aging can be favorably influenced in numerous ways by the addition or maintenance of adequate melatonin levels. Specifically, the impact of melatonin on skeletal muscle was the key topic of interest. Method Reviewed were peer reviewed research and review articles specifically pertaining to healthy aging, melatonin, and muscle associated observations. Results Declining melatonin levels greatly impact multiple essential body systems and tissues. Supplements or interventions that heighten melatonin presence appear to have beneficial impacts on aging in general, and muscle function and structure, in particular. Conclusion The use of melatonin early on in the aging process is likely to produce more favorable long-term outcomes than not in cases of deficiency, and should be further investigated.
Jan 2019 DOI 10.14302/issn.2641-9181.ijnr-18-2530
Ozcelik FatihCorresponding author
University of Health Sciences, Faculty of Medicine, Department of Medical Biochemistry, Istanbul, Turkey
Nowadays, obesity is seriously threatening healthy life in all societies, especially in developed societies. Obesity is showing its likely effects through biologically active substances called adipokines. The most familiar of these is leptin. Leptin is synthesized in directly proportional to the amount of adipose tissue and reduced appetite by stimulating the satiety center. This status is like a protective mechanism that tries to reverse severe pathological process. Similar to this behavior of leptin, thyroid hormones are increasing in the advanced stages of obesity, increasing the resting energy expenditure (REE). The accelerating oxidative phosphorylation causes the use of energy as heat, the energy that has not transformed into ATP, together with ATP synthesis. This situation, the significant portion of energy provides to consumed instead of storing as fat. In addition, finding that T3 accelerates glucose transport and the TCA cycle without changing the rate of ATP synthesis in skeletal muscles suggests that thyroid hormones may be an effective tool in standing against obesity. In addition of that, the presence of studies indicating that thyroid hormones have an increasing tendency in the advanced stages of obesity is likely thought to be a rescuer mechanism to increase the effectiveness of suppressed thyroid hormones. On the contrary of these ideas, having been reported suppressing 5’-deiodinease enzyme activity in chronic diseases causes anxiety about the effectiveness of thyroid hormones in obesity. Based on available information, we aimed to prepare a review evaluating of this adaptive condition of thyroid hormones.
Dec 2016 DOI 10.14302/issn.2379-7835.ijn-16-1360
Kaneko MichiyoCorresponding author
Department of Home Economics, Kobe Women’s University 2-1 Aoyama, Higashisuma, Suma-ku, Kobe, Hyogo Prefecture 654-8585, Japan
Energy intake has been decreasing these ten years in Japan, and low energy intake is remarkable especially among young women. We attempted to show the dietary habits and physiological function including glucose tolerance and stamina for endurance-running in contemporary young Japanese women who take insufficient energy. 85 healthy women aged 20.5±1.1 years were enrolled in the present study. Subjects were categorized in two groups; Group I (n=70) with higher energy intake, and Group II (n=15) with lower energy intake than the basal metabolic rate (BMR). Actual energy intake in Group I was 1598.8±282.1 kcal/day, and it was 1019.9±127.1 kcal/day in Group II (p<0.01). Standard 75-g oral glucose-tolerance test was performed, and the capillary glucose value was measured at the fingertip. In Group I, glucose values at fasting, 30, 60 and 120 min were 75.0±9.1, 132.1±25.2, 120.5±27.4, 105.3±19.5 mg/dl, and those in Group II were 78.9±7.7, 155.8±26.6, 142.2±26.6, 112.3±16.0 mg/dl, respectively. The values of Group II at 30 and 60 min showed significantly high (p< 0.01). Stamina and the intake of protein in Group II were significantly lower than those in Group I (p<0.05), and muscle mass and grip strength were less in Group II than in Group I, though there was no significant difference. We indicated with these results that low skeletal muscle was considered to be responsible for the impairment of glucose regulation in Group II. This study showed that young women with low energy intake should take sufficient energy and build skeletal muscle to prevent the impairment of glucose regulation.