Nutrition and muscle potassium: differential effect in rat slow and fast muscles

1987 ◽  
Vol 65 (11) ◽  
pp. 2188-2190 ◽  
Author(s):  
C. N. Fong ◽  
H. L. Atwood ◽  
K. N. Jeejeebhoy ◽  
M. P. Charlton

The effects of malnutrition on intracellular K+ activity, (aK)i, and membrane potential, Em, were measured by means of double-barrelled K+ -selective microlectrodes in the soleus and gastrocnemius muscles of the rat. (aK)i and Em were measured in vivo in normal anaesthetized animals and in rats subjected to one of two diet restrictions: a 2-day fast or a long-term hypocaloric diet. In the soleus muscle, (aK)i fell by similar amounts in both 2-day fasted and long-term hypocalorically fed rats, while Em depolarized significantly only in hypocalorically fed rats. In the gastrocnemius muscle, neither the 2-day fast nor the hypocaloric diet affected (aK)i or Em. It is suggested that the selective loss of K+ from the soleus muscle may be related to its activity pattern.

1999 ◽  
Vol 46 (3) ◽  
pp. 823-835 ◽  
Author(s):  
A Jakubiec-Puka ◽  
I Ciechomska ◽  
U Mackiewicz ◽  
J Langford ◽  
H Chomontowska

The myosin heavy chain (MHC) was studied by biochemical methods in the slow-twitch (soleus) and two fast-twitch leg muscles of the triiodothyronine treated (hyperthyroid), thyroidectomized (hypothyroid) and euthyroid (control) rats. The changes in the contents of individual MHC isoforms(MHC-1, MHC-2A, MHC-2B and MHC-2X) were evaluated in relation to the muscle mass and the total MHC content. The MHC-1 content decreased in hyperthyreosis, while it increased in hypothyreosis in the soleus and in the fast muscles. The MHC-2A content increased in hyperthyreosis and it decreased in hypothyreosis in the soleus muscle. In the fast muscles hyperthyreosis did not affect the MHC-2A content, whereas hypothyreosis caused an increase in this MHC isoform content. The MHC-2X, present only in traces or undetected in the control soleus muscle, was synthesised in considerable amount in hyperthyreosis; in hypothyreosis the MHC-2X was not detected in the soleus. In the fast muscles the content of MHC-2X was not affected by any changes in the thyroid hormone level. The MHC-2B seemed to be not influenced by hyperthyreosis in the fast muscles, whereas the hypothyreosis caused a decrease of its content. In the soleus muscle the MHC-2B was not detected in any groups of rats. The results suggest that the amount of each of the four MHC isoforms expressed in the mature rat leg muscles is influenced by the thyroid hormone in a different way. The MHC-2A and the MHC-2X are differently regulated in the soleus and in the fast muscles; thyroid hormone seems to be necessary for expression of those isoforms in the soleus muscle.


2020 ◽  
Author(s):  
kun wang ◽  
Xiujie Gao ◽  
Kefeng Ma ◽  
Xiaojun She ◽  
Honglian Yang ◽  
...  

Abstract Background A reduction of energy used during walking could present a significant advantage for both healthy individuals and those with reduced mobility. Current unpowered exoskeletons have shown a net reduction in energy consumption for walking, but commonly with a clutch and assist on the heel. This paper presents the development of a lightweight energy recycling exoskeleton without a clutch and assists on the forefoot. Methods Eight healthy participants were tested during walking at 1.25 m/s on a treadmill wearing exoskeletons of four kinds of conditions. Electromyography (EMG) of the soleus muscle and gastrocnemius muscle were collected. Results Our results showed that the novel exoskeleton could make the peak and average EMG-values of soleus muscles drop about 13% and 8% respectively, and that of gastrocnemius muscles drop about 12% and 13% respectively. Conclusions The results of the present work demonstrate for the first time that the novel energy recycling exoskeleton can improve the walking economy, and this device could be feasibly worn for a broad range of individuals.


Molecules ◽  
2021 ◽  
Vol 26 (24) ◽  
pp. 7689
Author(s):  
Abilasha Deenadayalan ◽  
Vijayalakshmi Subramanian ◽  
Vijayalakshmi Paramasivan ◽  
Vishnu Priya Veeraraghavan ◽  
Gayathri Rengasamy ◽  
...  

Type-2 diabetes mellitus (T2DM), the leading global health burden of this century majorly develops due to obesity and hyperglycemia-induced oxidative stress in skeletal muscles. Hence, developing novel drugs that ameliorate these pathological events is an immediate priority. The study was designed to analyze the possible role of Stevioside, a characteristic sugar from leaves of Stevia rebaudiana (Bertoni) on insulin signaling molecules in gastrocnemius muscle of obesity and hyperglycemia-induced T2DM rats. Adult male Wistar rats rendered diabetic by administration of high fat diet (HFD) and sucrose for 60 days were orally administered with SIT (20 mg/kg/day) for 45 days. Various parameters were estimated including fasting blood glucose (FBG), serum lipid profile, oxidative stress markers, antioxidant enzymes and expression of insulin signaling molecules in diabetic gastrocnemius muscle. Stevioside treatment improved glucose and insulin tolerances in diabetic rats and restored their elevated levels of FBG, serum insulin and lipid profile to normalcy. In diabetic gastrocnemius muscles, Setvioside normalized the altered levels of lipid peroxidase (LPO), hydrogen peroxide (H2O2) and hydroxyl radical (OH*), antioxidant enzymes (CAT, SOD, GPx and GSH) and molecules of insulin signaling including insulin receptor (IR), insulin receptor substrate-1 (IRS-1) and Akt mRNA levels. Furthermore, Stevioside enhanced glucose uptake (GU) and oxidation in diabetic muscles by augmenting glucose transporter 4 (GLUT 4) synthesis very effectively in a similar way to metformin. Results of molecular docking analysis evidenced the higher binding affinity with IRS-1 and GLUT 4. Stevioside effectively inhibits oxidative stress and promotes glucose uptake in diabetic gastrocnemius muscles by activating IR/IRS-1/Akt/GLUT 4 pathway. The results of the in silico investigation matched those of the in vivo study. Hence, Stevioside could be considered as a promising phytomedicine to treat T2DM.


2007 ◽  
Vol 292 (5) ◽  
pp. C1681-C1689 ◽  
Author(s):  
H. Shi ◽  
C. Zeng ◽  
A. Ricome ◽  
K. M. Hannon ◽  
A. L. Grant ◽  
...  

The molecular mechanisms controlling β-adrenergic receptor agonist (BA)-induced skeletal muscle hypertrophy are not well known. We presently report that BA exerts a distinct muscle- and muscle fiber type-specific hypertrophy. Moreover, we have shown that pharmacologically or genetically attenuating extracellular signal-regulated kinase (ERK) signaling in muscle fibers resulted in decreases ( P < 0.05) in fast but not slow fiber type-specific reporter gene expressions in response to BA exposure in vitro and in vivo. Consistent with these data, forced expression of MAPK phosphatase 1, a nuclear protein that dephosphorylates ERK1/2, in fast-twitch skeletal muscle ablated ( P < 0.05) the hypertrophic effects of BA feeding (clenbuterol, 20 parts per million in water) in vivo. Further analysis has shown that BA-induced phosphorylation and activation of ERK occurred to a greater ( P < 0.05) extent in fast myofibers than in slow myofibers. Analysis of the basal level of ERK activity in slow and fast muscles revealed that ERK1/2 is activated to a greater extent in fast- than in slow-twitch muscles. These data indicate that ERK signaling is differentially involved in BA-induced hypertrophy in slow and fast skeletal muscles, suggesting that the increased abundance of phospho-ERK1/2 and ERK activity found in fast-twitch myofibers, compared with their slow-twitch counterparts, may account, at least in part, for the fiber type-specific hypertrophy induced by BA stimulation. These data suggest that fast myofibers are pivotal in the adaptation of muscle to environmental cues and that the mechanism underlying this change is partially mediated by the MAPK signaling cascade.


2021 ◽  
Author(s):  
Ruo-nan Zhang ◽  
Xin Bao ◽  
Yan Wang ◽  
Xin-Yuan Li ◽  
MagdaleenaNaemi Mbadhi ◽  
...  

Abstract Background: Muscular dystrophy is a destructive neuromuscular disease characterized by progressive muscle weakness and muscle atrophy. The role of Ezrin in myoblast differentiation/fusion and muscle atrophy is still unknown.Method: Gastrocnemius muscle atrophy model were prepared by mechanical clamp of peroneal nerve. Differentiating C2C12 cells treated with Ad-Ezrin or Ad-shEzrin were detected by gene chip, Q-PCR, immunofluorescence staining and Western blot.Results: Ezrin was expressed in MyHC I/II myofibers in vivo, and time-dependently increased during myoblast differentiation/fusion characterized by MyoG+/MEF2c nuclei and MyHC+ myotubes in vitro. Overexpression of Ezrin promoted myoblast differentiation/fusion in time-dependent manner, inducing the increased MyHC-I+ and MyHC-II+ muscle fiber specialization, the specific effects could be abolished by addition of Ad-Periaxin. Ad-Ezrin did not alter PKA and PKAreg II α levels, but PKAreg I α/β. The PKA inhibitor, H-89, remarkably abolished the over-expression effects by Ezrin on an increased myoblast differentiation/fusion. By contrast, Knockdown of Ezrin by shRNA significantly delayed myoblast differentiation/fusion accompanied by the decreased PKA reg I/II ratio, the inhibitory effects could be eliminated by PKAreg I activator N6-Bz-cAMP. Meanwhile, Ad-Ezrin enhanced type I muscle fiber specialization, accompanied by the increased levels of NFATc1/c2.Furthermore, Ad-NFATc2 or Ad-NFATc4 reversed the inhibitory effects of Ad-shEzrin on myoblast differentiation/fusion. Importantly, in vivo transfection of Ad-Ezrin into gastrocnemius muscles in peroneal nerve injury model increased the numbers of MyHC-I+ and MyHC-II+ myofibers, reducing muscle atrophy and fibrosis.Conclusions: Ezrin activated PKA-NFAT-MyoD/MyoG/MEF2C signaling pathway, triggering myoblast differentiation/fusion and muscle fiber specialization in periaxin-depentdent manner, contributing to gastrocnemius muscles repair.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Paweł Szaro ◽  
Walter Cifuentes Ramirez ◽  
Simon Borkmann ◽  
Alexander Bengtsson ◽  
Mateusz Polaczek ◽  
...  

Abstract The aim of the study was to check if the subtendons of the Achilles tendon can be identified in vivo on MRI in the midportion of the tendon. The relation of the plantaris tendon to the Achilles tendon was also examined. A retrospective study of 200 MRI of ankle joints including the Achilles tendon was conducted. Statistical analysis of the correlation between the possibility of identifying the subtendons and the side, gender, presence of the central soleus tendon and plantaris tendon variation was performed. The inter-observer agreement between two reviewers in their evaluation of the subtendons was assessed using kappa statistics. The subtendon from the lateral head of the gastrocnemius muscle was identified in 65% (k = 0.63) and was located in the anterior part of the Achilles tendon. The subtendon from the soleus muscle was recognized in 12% (k = 0.75) comprising anterior part of the tendon. In 6% the subtendon from the medial head of the gastrocnemius muscle was identified (k = 0.58). The central soleus tendon was identified in 85% of cases. Statistical analysis shows the weak correlation of the presence of the central soleus tendon and the possibility of identifying the subtendon from the soleus muscle. The plantaris tendon was directly related to the insertion of the Achilles tendon in 42.5%. Identification of the subtendons of the Achilles tendon on MRI is challenging, and most often it is only possible to find the subtendon of the lateral head of the gastrocnemius muscle.


1988 ◽  
Vol 60 (3) ◽  
pp. 517-523 ◽  
Author(s):  
Y. Pinchasov ◽  
I. Nir ◽  
Zafrira Nitsan

1. Protein synthesis was estimated in vivo in breast (superficial pectoral) and tibia (gastrocnemius) muscles, liver, kidney, pancreas, crop, duodenum, jejunum and ileum, using L-[U-14C]lysine injection. The effect on incorporation of [14C]lysine 1 and 2 h after injection was examined in five chickens adapted or not adapted to intermittent feeding.2. Incorporation of [14C]lysine into tissue decreased in magnitude in the following descending order: pancreas > jejunum, duodenum > ileum, crop, liver > kidney > tibia, breast muscle and blood plasma.3. The incorporation of [14C]lysine into muscle protein was higher in chicks after 24 h of refeeding than after 24 h of food deprivation. These differences were higher in adapted than in non-adapted birds. On days of refeeding the rate of incorporation exceeded that found in chickens fed ad lib.4. Bound 14C from lysine in the intestinal segments was less than in control birds after food deprivation and greater after refeeding in non-adapted chicks only.5. A negative relation was observed between bound and free 14C in muscles and in other tissues.6. Short- and long-term adaptations to feeding regimens are discussed.


1998 ◽  
Vol 275 (1) ◽  
pp. E118-E123 ◽  
Author(s):  
Tor H. Bark ◽  
Margaret A. McNurlan ◽  
Charles H. Lang ◽  
Peter J. Garlick

The purpose of the present study was to determine the effect of acute administration of insulin-like growth factor I (IGF-I) or insulin on in vivo protein synthesis in muscle and other organs in fasted mice and to compare this response with that produced by feeding. Recombinant IGF-I (3.3 nmol prime, 3.33 nmol/h) or insulin (0.056 nmol/h) was infused intravenously for 60 min along with glucose to prevent hypoglycemia. Fractional rates of tissue protein synthesis (FSR) were determined by injection of [2H5]phenylalanine (25 mg/100 g body wt, 40% enriched). Both IGF-I and insulin caused a 25% increase in FSR of heart ( P < 0.001) and soleus muscle ( P < 0.05) and a 65% increase in gastrocnemius and plantaris muscle (both P < 0.001), thus restoring rates to those seen in fed animals. A fivefold lower dose of IGF-I also stimulated protein synthesis in gastrocnemius muscle and heart (both P < 0.05) but not in soleus muscle. No significant effects of IGF-I on FSR were detected in liver, kidney, spleen, proximal small intestine, colon, lung, or brain. The results indicate that the ability of an overnight fast to decrease protein synthesis and the acute effects of insulin and IGF-I to stimulate protein synthesis are restricted to skeletal and cardiac muscles.


1998 ◽  
Vol 274 (2) ◽  
pp. R311-R317 ◽  
Author(s):  
Jiri Turinsky ◽  
Alice Damrau-Abney ◽  
Daniel J. Loegering

To investigate whether changes in blood flow contribute to the insulin resistance in denervated muscles, basal and insulin-stimulated 2-deoxy-d-glucose (2-DG) uptake in vivo and blood flow were measured in soleus (slow twitch), plantaris (fast twitch), and gastrocnemius (fast twitch) muscles at 1 and 3 days after a right hindlimb denervation in the rat. Muscles of the contralateral sham hindlimb served as an internal control. Sham plantaris and gastrocnemius muscles showed 32 and 60% lower basal 2-DG uptake, 46 and 66% lower insulin-stimulated 2-DG uptake, and 79 and 81% lower blood flow, respectively, compared with sham soleus muscle. At 1 day after denervation, soleus, plantaris, and gastrocnemius muscles exhibited an 80, 64, and 42% decrease in insulin-stimulated 2-DG uptake, respectively, in the presence of 63, 323, and 304% higher blood flow, respectively. At 3 days after denervation, soleus muscle showed a 60% decrease in basal 2-DG uptake, complete unresponsiveness to insulin, and an 86% decrease in blood flow. In contrast, the denervated plantaris and gastrocnemius muscles exhibited a 262 and 105% increase in basal 2-DG uptake, respectively, no change in insulin-stimulated 2-DG uptake, and no change in blood flow compared with corresponding contralateral sham muscles. The results demonstrate that muscle blood flow is influenced by muscle fiber population and time after denervation and that changes in blood flow do not contribute to the insulin resistance in the denervated muscles.


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