Recovery from exercise refers to the period between the end of a bout of exercise and the subsequent return to a resting or recovered state. It is a dynamic period in which many physiological changes occur. A large amount of research has evaluated the effect of training on intramuscular lipid metabolism. However, data are limited regarding intramuscular lipid metabolism during the recovery period. In this study, lipid metabolism-related proteins were examined after a single bout of exercise in a time-dependent way to explore the mechanism of how exercise induces intramuscular lipid metabolism adaptation. Firstly, all rats in the exercise group underwent a five-week training protocol (HIIT, five times/week), and then performed a more intense HIIT session after 72 h of the last-time five-week training. After that, rats were sampled in a time-dependent way, including 0 h, 6 h, 12 h, 24 h, 48 h, 72 h, and 96 h following the acute training session. Our results discovered that five weeks of HIIT increased the content of intramuscular triglyceride (IMTG) and enhanced the lipolytic and lipogenesis-related proteins in skeletal muscle. Furthermore, IMTG content decreased immediately post HIIT and gradually increased to baseline levels 48 h postexercise, continuing to over-recover up to 96 h postexercise. Following acute exercise, lipolytic-related proteins showed an initial increase (6-12 h) before decreasing during recovery. Conversely, lipogenesis-related proteins decreased following exercise (6-12 h), then increased in the recovery period. Based on the changes, we speculate that skeletal muscle is predominated by lipid oxidative at the first 12 h postexercise. After this period, lipid synthesis-related proteins increased, which may be the result of body recovery. Together, these results may provide insight into how the lipid metabolism-related signaling changes after chronic and acute HIIT and how protein levels lipid metabolism correlates to IMTG recovery., Min Chen, Lei Zhou, Siyu Chen, Ruonan Shangguan, Yaqian Qu, Jingquan Sun., and Obsahuje bibliografii
The biosynthesis and metabolism of testosterone and cortisol are altered by the high levels of adipose tissue and the constant state of low-grade inflammation of obesity. Resistance exercise (REx) has become one of the main lifestyle interventions prescribed to obese individuals due to its ability to positively influence body composition and some biomarkers, such as cholesterol and insulin resistance. Yet, little research has been done in obese examining the effects of REx on the testosterone and blood cortisol responses, two integral hormones in both exercise and obesity. The obese testosterone response to REx and whether or not it is blunted compared to lean individuals remains elusive. Conflicting findings concerning the blood cortisol response have also been reported, likely due to variance in REx protocol and the level of obesity in the participants in studies. Comparatively, both of these hormones have been extremely well studied in untrained lean males, which could be used as a basis for future research in obese males. However, without this endocrinological information, it is unknown if the current acute REx prescriptions are appropriate for eliciting a favorable acute endocrinological response, and ultimately, a positive chronic adaptation in obese males., C. B. O'Leary, A: C. Hackney., and Obsahuje bibliografii
Principal vasoactive systems - renin-angiotensin system (RAS), sympathetic nervous system (SNS), nitric oxide (NO) and prostanoids - exert their vascular effects through the changes in calcium levels and/or calcium sensitization. To estimate a possible modulation of calcium sensitization by the above vasoactive systems, we studied the influence of acute and chronic blockade of particular vasoactive systems on blood pressure (BP) changes elicited in conscious normotensive rats by acute dose-dependent administration of Rho-kinase inhibitor fasudil. Adult male chronically cannulated Wistar rats were used throughout this study. The acute inhibition of NO synthase (NOS) by L-NAME enhanced BP response to fasudil, the effect being considerably augmented in rats deprived of endogenous SNS. The acute inhibition of prostanoid synthesis by indomethacin modified BP response to fasudil less than the acute NOS inhibition. The chronic NOS inhibition caused moderate BP elevation and a more pronounced augmentation of fasudilinduced BP changes compared to the effect of acute NOS inhibition. This indicates both short-term and long-term NOdependent attenuation of calcium sensitization. Long-term inhibition of RAS by captopril caused a significant attenuation of BP changes elicited by fasudil. In contrast, a long-term attenuation of SNS by chronic guanethidine treatment (in youth or adulthood) had no effect on BP response to fasudil, suggesting the absence of SNS does not affect calcium sensitization in vascular smooth muscle of normotensive rats. In conclusion, renin-angiotensin system contributes to the long-term increase of calcium sensitization and its effect is counterbalanced by nitric oxide which decreases calcium sensitization in Wistar rats., A. Brunová, M. Bencze, M. Behuliak, J. Zicha., and Obsahuje bibliografii
Natural glucocorticoid hydrocortisone was suggested as a potent substitution for dexamethasone in the treatment of bronchopulmonary dysplasia in neonates. The aim of this study was to investigate whether hydrocortisone is able to affect the expression of apoptotic genes and the intensity of naturally occurring cell death in the developing rat hippocampus. Hormone treatment decreased procaspase-3 and active caspase-3 levels as well as DNA fragmentation intensity in the hippocampal formation of one-week-old rats in 6 h after injection. These changes were accompanied by an upregulation of antiapoptotic protein Bcl-XL, while expression of proapoptotic protein Bax remained unchanged. The action of hydrocortisone was glucocorticoid receptor-independent, as the selective glucocorticoid receptor agonist dexamethasone did not affect either apoptotic protein levels or DNA fragmentation intensity in the hippocampal region. The data are the first evidences for in vivo antiapoptotic effects of hydrocortisone in the developing hippocampus., P. N. Menshanov, ... [et al.]., and Obsahuje seznam literatury
The effect of the chronic and acute antioxidant tempol (superoxide dismutase mimetic) treatment on cardiac ischemic tolerance was investigated in adult male Wistar rats. The first experimental group was given tempol (1 mM) in drinking water for three weeks, the second group received tempol (100 mg/kg, i.v.) 10 min before test ischemia, and control rats received the same volume of solvent. Anesthetized open-chest animals (pentobarbitone 60 mg/kg, i.p.) were subjected to 20-min coronary artery occlusion and 3-h reperfusion for infarct size determination. Ventricular arrhythmias were monitored during ischemia and at the beginning (5 min) of reperfusion. Acute tempol administration shifted the time profile of ischemic arrhythmias to the later phase and significantly increased the number of ischemic and reperfusion premature ventricular complexes, respectively (504±127 and 84±21) as compared with the chronically treated group (218±36 and 47±7) or controls (197±26 and 31±7). Acute tempol-treated rats exhibited a tendency to decrease infarct size (P = 0.087). The mechanism of proarrhythmic tempol action during ischemia and reperfusion remains to be elucidated., J. Neckář, B. Ošťádal, F. Kolář., and Obsahuje bibliografii a bibliografické odkazy
Cadmium (Cd), an environmental and industrial pollutant, poses a potential threat and affects many systems in human and animals. Although several reports on Cd toxicity were presented, the acute effect of Cd on systemic and thrombotic events was not reported so far. Cd (2.284 mg/kg) or saline (control) was injected intraperitoneally (ip), and the systemic parameters were assessed in mice. Compared to control group, acute intraperitoneal injection of Cd, in mice showed significant quickening of platelet aggregation (P<0.001) leading to pial cerebral thrombosis. Likewise, Cd exposure caused a significant increase in white blood cell numbers (P<0.05) indicating the occurrence of systemic inflammation. Also, alanine aminotransferase (ALT) (P<0.05) and creatinine (P<0.01) levels were both significantly increased. Interestingly, the superoxide dismutase activity was significantly decreased in Cd treated group compared to control group (P<0.001), suggesting the occurrence of oxidative stress. We conclude that the Cd exposure in mice causes acute thromboembolic events, oxidative stress and alter liver and kidney functions., M.A. Fahim ... [et al.]., and Obsahuje seznam literatury
The diabetogenic effect of prolactin observed in patients with pathological hyperprolactinaemia was verified in healthy subjects. Plasma prolactin elevation was induced by administration of a dopamine antagonist drug domperidone (Motilium 10 mg orally, 9 subjects) and 2 h later the oral glucose tolerance test was performed. The influence of dopamine receptor stimulation on glucose homeostasis was tested by dopamine infusion (0.3 mg in saline or 20 % glucose, 1 g/min for 60 min, 11 subjects). After the blockade of dopamine receptors, a significant and prolonged increase of prolactin concentration was found. However, the levels of glucose, insulin, and C- peptide either before or after the glucose load were not different from control ones. The decreased number of insulin receptors (1.97±0.41 vs 0.51 ±0.14 pmol per 2.109 red blood cells) was compensated by increased affinity (0.51 ±0.17 vs 1.00±0.22 K* 108 mol.-1 per 1]) of insulin receptors. The stimulation of dopamine receptors showed a negligible effect on glucose regulation. It may be suggested that an endogenous increase of prolactin concentration in the physiological range does not participate in the regulation of glucose homeostasis in healthy subjects.
One explanation of the mechanism of hypoxic pulmonary vasoconstriction (HPV) suggests that hypoxia shifts the redox status of the pulmonary artery smooth muscle cell towards a more reduced state, through changes in the redox couples and the activated oxygen species generation. The outward K+ current is then reduced and the membrane depolarized, leading to Ca++ influx through the voltage dependent Ca++ channels and vasoconstriction. The response of both pulmonary and systemic vessels to hypoxia may depend on the expression of different K+ channels in the two sites. While the oxygen sensor in pulmonary artery smooth muscle cells may be the delayed rectifier K+ channel, in the systemic arteries, hyperpolarization of the smooth muscle cell membrane, leading to vasodilatation, probably represents the effect of hypoxia in opening ATP-sensitive and Ca++-dependent K+ channels. The similarities between oxygen sensing mechanisms in several oxygen sensing cells (pulmonary artery smooth muscle cell, carotid body type 1 cell, neuroepithelial body) are striking. It is very likely that the mechanisms by which hypoxia is sensed at the molecular level are highly conserved and tightly regulated.
Hypoxic vasoconstriction (HPV) has been shown to consist of a biphasic contraction change. The first phase of the hypoxic response peaks at approximately five minutes. The second phase is at about 30 minutes. The force of contraction of both phases of HPV were found to be significantly greater in pulmonary resistance vessels (PRV) than in pulmonary artery (PA) (P<0.01). The endothelium modulates the hypoxic response, especially of the second phase of HPV (68 % reduction in PRV) (P<0.05). In Ca2+-free solution, the first peak and the second peak of HPV were reduced to 11 and 32 % contraction in PRV and to 26 and 21 % contraction in PA. A calcium channel antagonist (amlodipine) caused significant dose-dependent inhibition of the first phase of HPV (P=0.001), with a significantly greater effect on PRV compared to PA (P<0.01). Levcromakalim caused a dose- dependent inhibition of HPV in PRV (58 % at 10 /utA). In contrast, HPV in PA was not significantly inhibited by levcromakalim. In conclusion, this study has confirmed that hypoxia induces a biphasic contractile response in isolated pulmonary arteries requiring extracellular calcium. Both amlodipine and levcromakalim inhibit hypoxic pulmonary vasoconstriction and these agents may be of value in the treatment of pulmonary hypertension.