scholarly journals Factors determining stress-reactivity of hemodynamics in the adolescents

2008 ◽  
Vol 14 (2) ◽  
pp. 165-171 ◽  
Author(s):  
A. Sumin ◽  
L. Sumina ◽  
N. Vasilyeva

Resume In order to assess factors contributing to stress reactivity of blood pressure 66 adolescents (25 boys and 41 girles) form 14 to 17 yrs (15,2+0,1 yrs) were examined. Test with oral calculation, psychological (questionnaires of Bass-Darky, Kettle, Spielberg) as well as force of skeletal muscles and were assessed. Hyperreaction of blood pressure (BP) was observed in 27% of adolescents, normal reaction - in 47% cases, low reactivity - in 26%. In hyperreactive subjects lower parameters of skeletal muscle force were documented. Psychological discrepancies were insignificant between the groups. The BP raise during mental stress correlated with muscle force, body weight, baseline BP level and mental development. The data obtained can indicate that reducing stress reactivity can be important instrument in primary prevention of cardiovascular diseases in psychogenic rest groups.

1959 ◽  
Vol 196 (3) ◽  
pp. 512-516 ◽  
Author(s):  
Adam Anthony ◽  
Eugene Ackerman ◽  
G. K. Strother

Analyses were made of myoglobin content of rat skeletal and cardiac muscle following continuous exposure to simulated altitudes of 18,000 feet for a 2–10-week period. About five dozen rats were used. Acclimatization was associated with an increase in the myoglobin concentration of thigh, diaphragm, gastrocnemius and heart muscles. Total myoglobin content, however, increased during acclimatization in cardiac muscle but not in the three skeletal muscles. This finding together with the body weight changes and muscle weight changes suggested that the increases in myoglobin concentration of skeletal muscle may be merely a reflection of a decreased water content of muscles.


2019 ◽  
Vol 286 (1903) ◽  
pp. 20190719 ◽  
Author(s):  
André Tomalka ◽  
Oliver Röhrle ◽  
June-Chiew Han ◽  
Toan Pham ◽  
Andrew J. Taberner ◽  
...  

Force enhancement (FE) is a phenomenon that is present in skeletal muscle. It is characterized by progressive forces upon active stretching—distinguished by a linear rise in force—and enhanced isometric force following stretching (residual FE (RFE)). In skeletal muscle, non-cross-bridge (XB) structures may account for this behaviour. So far, it is unknown whether differences between non-XB structures within the heart and skeletal muscle result in deviating contractile behaviour during and after eccentric contractions. Thus, we investigated the force response of intact cardiac trabeculae during and after isokinetic eccentric muscle contractions (10% of maximum shortening velocity) with extensive magnitudes of stretch (25% of optimum muscle length). The different contributions of XB and non-XB structures to the total muscle force were revealed by using an actomyosin inhibitor. For cardiac trabeculae, we found that the force–length dynamics during long stretch were similar to the total isometric force–length relation. This indicates that no (R)FE is present in cardiac muscle while stretching the muscle from 0.75 to 1.0 optimum muscle length. This finding is in contrast with the results obtained for skeletal muscle, in which (R)FE is present. Our data support the hypothesis that titin stiffness does not increase with activation in cardiac muscle.


1956 ◽  
Vol 185 (2) ◽  
pp. 348-350 ◽  
Author(s):  
George R. Hearn ◽  
W. W. Wainio

Male albino rats of the Wistar Institute strain with an average beginning weight of 250 gm were exercised from 5–8 weeks on a training regimen consisting of swimming for 1/2 hour daily. Pair-fed, nonswimming animals served as controls. All exercised animals gained less body weight than did their controls. The adrenals and heart ventricles of the exercised animals hypertrophied significantly ( P < 0.01), while the skeletal muscles (gastrocnemii) did not. Succinic dehydrogenase activities (reduction of ferricytochrome c) were determined in the heart ventricles and the gastrocnemii. The results were expressed in terms of unit activities, actual total activities and relative total activities. The exercise, whether for 5, 6, 7 or 8 weeks, did not significantly alter the unit and actual total activities of either tissue, or the relative total activities of skeletal muscles, but did significantly increase the relative total activities of the heart ventricle ( P < 0.02).


2010 ◽  
Vol 298 (1) ◽  
pp. R2-R8 ◽  
Author(s):  
M. C. Gomez-Cabrera ◽  
G. L. Close ◽  
A. Kayani ◽  
A. McArdle ◽  
J. Viña ◽  
...  

Skeletal muscle contractions increase superoxide anion in skeletal muscle extracellular space. We tested the hypotheses that 1) after an isometric contraction protocol, xanthine oxidase (XO) activity is a source of superoxide anion in the extracellular space of skeletal muscle and 2) the increase in XO-derived extracellular superoxide anion during contractions affects skeletal muscle contractile function. Superoxide anion was monitored in the extracellular space of mouse gastrocnemius muscles by following the reduction of cytochrome c in muscle microdialysates. A 15-min protocol of nondamaging isometric contractions increased the reduction of cytochrome c in microdialysates, indicating an increase in superoxide anion. Mice treated with the XO inhibitor oxypurinol showed a smaller increase in superoxide anions in muscle microdialysates following contractions than in microdialysates from muscles of vehicle-treated mice. Intact extensor digitorum longus (EDL) and soleus muscles from mice were also incubated in vitro with oxypurinol or polyethylene glycol-tagged Cu,Zn-SOD. Oxypurinol decreased the maximum tetanic force produced by EDL and soleus muscles, and polyethylene glycol-tagged Cu,Zn-SOD decreased the maximum force production by the EDL muscles. Neither agent influenced the rate of decline in force production when EDL or soleus muscles were repeatedly electrically stimulated using a 5-min fatiguing protocol (stimulation at 40 Hz for 0.1 s every 5 s). Thus these studies indicate that XO activity contributes to the increased superoxide anion detected within the extracellular space of skeletal muscles during nondamaging contractile activity and that XO-derived superoxide anion or derivatives of this radical have a positive effect on muscle force generation during isometric contractions of mouse skeletal muscles.


1990 ◽  
Vol 78 (5) ◽  
pp. 515-519 ◽  
Author(s):  
Pierre-Yves Marie ◽  
Jean-Marie Escanye ◽  
François Brunotte ◽  
Brigitte Robin ◽  
Paul Walker ◽  
...  

1. Using 31P nuclear magnetic resonance, it has previously been demonstrated that patients with congestive heart failure exhibit a greater than normal phosphocreatine (PCr) depletion in the working skeletal muscles of the arm. We have studied the importance of the work necessary to reach a similar PCr depletion {[PCr]/([PCr] + [Pi]) = 0.5} in calf muscle. Our results show significantly lower values for patients with congestive heart failure in both aerobic and ischaemic conditions (respectively: 0.009 ± 0.007 vs 0.026 ± 0.013 W/kg body weight, P <0.01; 0.29 ± 0.16 vs 0.90 ± 0.25 J/kg body weight, P <0.01). 2. This original model of skeletal muscle exercise facilitates a comparison of PCr recovery rate due to a similarity in the PCr depletion and intracellular pH in the two series at the start of recovery. However, the PCr recovery rate is similar after both normoxic and ischaemic exercise, i.e. respective percentages of PCr increase in the first 25 s recovery spectrum were: (a) aerobic exercise, congestive heart failure 133 ± 18%, control series 138 ± 18%; (b) ischaemic exercise, congestive heart failure 114 ± 13%, control series 118 ± 12%. The absence of a difference in PCr recovery rate and the greater PCr depletion by ischaemic work in patients with congestive heart failure suggest modifications that cannot be explained by a reduced blood flow to the muscle. 3. When comparing the two series, intracellular pH evolved similarly in normoxia and ischaemia during both work and recovery. Thus, no increase in anaerobic glycolytic activity appears when equivalent PCr depletion has occurred.


2021 ◽  
Author(s):  
Amira Ahmed ◽  
Huda Farah ◽  
Omnia Ahmed ◽  
Dina Elsayegh ◽  
Abdelrahman Elgamal ◽  
...  

Background: Oxidative stress (OS) is an imbalance between free radical production and the antioxidants defense in the body. Previous studies demonstrated the correlation of OS to the increased risk of developing metabolic disorders such as obesity. Sulforaphane (SFN), a bioactive compound, can protect against inflammation and OS, thus an effective anti-obesity supplement. Aim: This study explores the impact of SNF on OS in diet induced obese (DIO) mice via profiling of OS genes and pathways in skeletal muscles related to the anti-obesity effect. Methods: Wild-type CD1 male mice and the knockout of nuclear factor (erythroid-derived 2) like 2 (NrF2) mice were fed a high-fat diet (HFD) for 16 weeks; to induce obesity. Subsequently, each group was subdivided into two subgroups and received either Vehicle (25μl) or SFN (5 mg/kg BW) for four weeks. Body weight was measured daily, and a glucose tolerance test (GTT) was performed after 21 days of treatment. Afterward, mice were decapitated, blood and tissue samples were collected and snap-frozen immediately. Total RNA was extracted from Skeletal muscle and epididymal white adipose tissue (eWAT), leptin expression was measured in (eWAT), and 84 OS genes in skeletal muscle were examined using RT-PCR. Results: Significant reduction in body weight in SFN treated WT mice, while no change in KO mice. Plasma glucose, leptin, and leptin gene expression (eWAT) were significantly reduced in the WT-DIO SFN treated group, while no changes were detected in KO mice. SFN decreases OS damage in skeletal muscles, such as lipid peroxidation and production of reactive oxygen species (ROS). Conclusion: This study demonstrated that SFN had lowered body weight in WT-DIO mice by decreasing OS damage in skeletal muscles through the NrF2 pathway and can be a potential anti-obesity drug.


Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Iva Miljkovic ◽  
Allison Kuipers ◽  
Clareann Bunker ◽  
Alan Patrick ◽  
Joseph Zmuda

Background: Intramuscular fat is greater in African compared with European ancestry men and is now recognized as a major risk factor for cardio-metabolic diseases, independent of general obesity. However, prospective studies examining health consequences of this important ectopic fat depot are lacking, particularly in high-risk African ancestry populations. Therefore, we sought to determine if change in skeletal muscle density, a measure of intramuscular fat, predicts subsequent development of hypertension in African ancestry men. Methods: We measured at two time points calf skeletal muscle density (MD; mg/cm 3 ) using computed tomography in 1504 Afro-Caribbean men aged 40-92 years (mean, 59 years), who were recruited without regard to their health status. Hypertension was defined as having a systolic blood pressure of 140 mm Hg or greater, having a diastolic blood pressure of 90 mm Hg or greater, or taking antihypertensive medications. Logistic regression was used to estimate the association between change in MD and incident hypertension adjusting for follow-up time, baseline age and muscle density, and covariates known to be associated with hypertension and intramuscular fat (baseline body weight, body weight change, waist circumference, waist circumference change, current smoking, alcohol intake, physical activity, and baseline type 2 diabetes status). Results were expressed as the odds (95% CI) of hypertension per one standard deviation decrease in muscle density. Results: During the 6.2 years follow-up (range of follow-up years: 4.9-9.1 years), we observed a significant annualized percent decrease in muscle density (-0.43 %/yr; P<0.0001). Among the 777 men who were normotensive at the baseline visit, 224 (28.8%) developed hypertension during follow-up. Decreased MD during follow-up was associated with an increased risk of hypertension (odds ratio [95% CI] per SD decrease in MD: 1.31 [1.03, 1.67]). This association remained significant after additional adjustment for baseline waist circumference and change in waist circumference in a separate model (odds ratio [95% CI] per SD decrease in MD: 1.27 [1.02, 1.59]). Conclusions: Our novel findings show that ectopic intramuscular fat increases with advancing age, and support a causal role of intramuscular fat in hypertension risk among middle-aged and elderly African ancestry men. Additional studies are needed to elucidate the mechanisms behind this association, and to confirm our findings in other populations.


1999 ◽  
Vol 77 (4) ◽  
pp. 300-304 ◽  
Author(s):  
A Ramamani ◽  
M M Aruldhas ◽  
P Govindarajulu

Although reports on sex steroids have implicated them as promoting protein synthesis and also providing extra strength to the skeletal muscle, it remains unclear whether sex steroids affect glycogen metabolism to provide energy for skeletal muscle functions, since glycogen metabolism is one of the pathways that provides energy for the skeletal muscle contraction and relaxation cycle. The purpose of the current study was to show that testosterone and estradiol act differentially on skeletal muscles from different regions, differentially with reference to glycogen metabolism. To study this hypothesis, healthy mature male Wistar rats (90-120 days of age, weighing about 180-200 g) were castrated (a bilateral orchidectomy was performed to test the significance of skeletal muscle glycogen metabolism in the absence of testosterone). One group of castrated rats was supplemented with testosterone (100 µg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards). To test whether estradiol has any effect on male skeletal muscle glycogen metabolism 17beta-estradiol (5 µg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards) was administered to orchidectomized rats. To test whether these sex steroids have any differential effect on skeletal muscles from different regions, skeletal muscles from the temporal region (temporalis), muscle of mastication (masseter), forearm muscle (triceps and biceps), thigh muscle (vastus lateralis and gracilis), and calf muscle (gastrocnemius and soleus) were considered. Castration enhanced blood glucose levels and decreased glycogen stores in skeletal muscle from head, jaw, forearm, thigh, and leg regions. This was accompanied by diminished activity of glycogen synthetase and enhanced activity of muscle phosphorylase. Following testosterone supplementation to castrated rats, a normal pattern of all these parameters was maintained. Estradiol administration to castrated rats did not bring about any significant alteration in any of the parameters. The data obtained suggest a stimulatory effect of testosterone on skeletal muscle glycogenesis and an inhibitory effect on glycogenolysis. Estradiol did not play any significant role in the skeletal muscle glycogen metabolism of male rats.Key words: testosterone, estradiol, skeletal muscle, glycogen metabolism.


2017 ◽  
Vol 86 (3) ◽  
pp. 219-222 ◽  
Author(s):  
Katarína Holovská ◽  
Viera Almášiová ◽  
Lucia Tarabová ◽  
Eva Petrovová ◽  
Viera Cigánková

Bendiocarb belongs to the group of carbamate insecticides that inhibit acetylcholinesterase. In agriculture, it is used to control a variety of insects, therefore it is important to examine every potential aspect of its toxicology. The aim of this study was to observe the effect of bendiocarb on the ultrastructure of the skeletal muscle in rabbits. Rabbits in all experimental groups received capsules of bendiocarb (96% Bendiocarb, Bayer, Germany) per os daily at a dose of 5 mg/kg body weight. Samples of skeletal muscles were collected on days 10 and 20. On day 10 of the experiment, muscle fibres were not affected consistently. The observed changes were moderate and focal. Electron microscopy revealed dilatation of sarcoplasmic reticulum, and myofilament disorganization. On day 20 of the experiment, the ultrastructural changes in muscle fibres were more intense and more frequent. The most important alteration was the disruption of the sarcomeres due to the lysis of both thick and thin myofilaments. However, in the unchanged regions of muscle fibres a prominent mitochondrial swelling was observed. Many mitochondria lacked cristae and thus appeared as large membrane-bound cytoplasmic vesicles. The results presented in this study indicate that bendiocarb affects the ultrastructure of skeletal muscles. The intensity of damage (dissolution of myofilaments and disruption of sarcomeres) was related to the duration of administration of bendiocarb.


Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Ian M Williams ◽  
David H Wasserman ◽  
Italo Biaggioni ◽  
Amy C Arnold

Angiotensin (Ang)-(1-7) is a vasodilatory peptide implicated in the pathophysiology of hypertension, in part by opposing deleterious Ang II cardiovascular actions. Recent studies show that Ang-(1-7) restoration lowers blood pressure and improves glycemic control in animal models of cardiometabolic syndrome. The tissue-specific sites of action and blood pressure dependence for these metabolic effects, however, remain unclear. We hypothesized that Ang-(1-7) improves insulin sensitivity by enhancing peripheral glucose delivery. To test this hypothesis, adult male C57BL/6 mice were placed on standard chow or 60% high-fat diet for 11 weeks, with Ang-(1-7) [400 ng/kg/min] or saline given during the last 3 weeks of diet by subcutaneous osmotic mini-pump. Hyperinsulinemic (4 mU/kg/min) euglycemic clamps were performed in conscious, unrestrained mice at the end of the treatment period. High-fat fed mice exhibited modest hypertension (systolic blood pressure: 137±3 high-fat vs. 123±5 mmHg chow; p=0.043), which was not altered by Ang-(1-7) infusion (141±4 mmHg; p=0.516). Body weight, body composition, and fasting plasma glucose and insulin levels were not significantly different following Ang-(1-7) treatment in chow or high-fat fed mice. Ang-(1-7) increased the glucose infusion rate (GIR) needed to maintain euglycemia in high-fat fed mice (steady-state GIR: 31±5 Ang-(1-7) vs. 16±1 mg/kg/min vehicle; p=0.017) indicating enhanced whole-body insulin sensitivity, with no significant effect in chow fed mice. The improvement in insulin sensitivity in high-fat fed mice was due to an enhanced rate of whole-body glucose disappearance (R d : 34±5 Ang-(1-7) vs. 20±2 mg/kg/min vehicle; p=0.049), with increased rates of glucose uptake in gastrocnemius, vastus, and soleus muscle. There was no effect of Ang-(1-7) on insulin-mediated suppression of hepatic glucose production. Our data shows that Ang-(1-7) has direct insulin-sensitizing effects on skeletal muscle, which are independent of changes in body weight or systemic blood pressure. These overall findings provide new insight into mechanisms by which Ang-(1-7) improves insulin action, and provide further support to targeting this peptide for treatment of cardiometabolic disease.


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