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Muscle Temperature (muscle + temperature)
Selected AbstractsElevated core and muscle temperature to levels comparable to exercise do not increase heat shock protein content of skeletal muscle of physically active menACTA PHYSIOLOGICA, Issue 4 2007Yasuharu Oishi No abstract is available for this article. [source] The role of peripheral Na+ channels in triggering the central excitatory effects of intravenous cocaineEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2006P. Leon Brown Abstract While alterations in dopamine (DA) uptake appear to be a critical mechanism underlying locomotor and reinforcing effects of cocaine (COC), many centrally mediated physiological and affective effects of this drug are resistant to DA receptor blockade and are expressed more quickly following an intravenous (i.v.) injection than expected based on the dynamics of drug concentration in the brain. Because COC is also a potent local anesthetic, its rapid action on Na+ channels may be responsible for triggering these effects. We monitored temperatures in the nucleus accumbens, temporal muscle and skin together with conventional locomotion during a single i.v. injection of COC (1 mg/kg), procaine (PRO, 5 mg/kg; equipotential anesthetic dose), a short-acting local anesthetic drug that, like COC, interacts with Na+ channels, and cocaine methiodide (COC-MET, 1.31 mg/kg, equimolar dose), a quaternary COC derivative that is unable to cross the blood,brain barrier. In this way, we explored not only the importance of Na+ channels in general, but also the importance of central vs. peripheral Na+ channels specifically. COC induced locomotor activation, temperature increase in the brain and muscle, and a biphasic temperature fluctuation in skin. Though PRO did not induce locomotor activation, it mimicked, to a greater degree, the temperature effects of COC. Therefore, Na+ channels appear to be a key substrate for COC-induced temperature fluctuations in the brain and periphery. Similar to PRO, COC-MET had minimal effects on locomotion, but mimicked COC in its ability to increase brain and muscle temperature, and induce transient skin hypothermia. It appears therefore that COC's interaction with peripherally located Na+ channels triggers its central excitatory effects manifested by brain temperature increase, thereby playing a major role in drug sensing and possibly contributing to COC reinforcement. [source] Allometric scaling of maximum metabolic rate: the influence of temperatureFUNCTIONAL ECOLOGY, Issue 4 2008C. R. White Summary 1Maximum aerobic metabolic rate, measured in terms of rate of oxygen consumption during exercise (), is well known to scale to body mass (M) with an exponent greater than the value of 0·75 predicted by models based on the geometry of systems that supply nutrients. 2Recently, the observed scaling for (,M0·872) has been hypothesized to arise because of the temperature dependence of biological processes, and because large species show a greater increase in muscle temperature when exercising than do small species. 3Based on this hypothesis, we predicted that will be positively related to ambient temperature, because heat loss is restricted at high temperatures and body temperature is likely to be elevated to a greater extent than during exercise in the cold. 4This prediction was tested using a comparative phylogenetic generalized least-squares (PGLS) approach, and 34 measurements of six species of rodent (20·5,939 g) maximally exercising at temperatures from ,16 to 30 °C. 5 is unrelated to testing temperature, but is negatively related to acclimation temperature. We conclude that prolonged cold exposure increases exercise-induced by acting as a form of aerobic training in mammals, and that elevated muscle temperatures of large species do not explain the scaling of across taxa. [source] Neuroprotective effects of a combination of dexmedetomidine and hypothermia after incomplete cerebral ischemia in ratsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2010K. SATO Background: Dexmedetomidine and hypothermia are known to reduce neuronal injury following cerebral ischemia. We examined whether a combination of dexmedetomidine and hypothermia reduces brain injury after transient forebrain ischemia in rats to a greater extent than either treatment alone. Methods: Thirty-eight male Sprague,Dawley rats were anesthetized with fentanyl and nitrous oxide in oxygen. Four groups were tested: group C (saline 1 ml/kg, temporal muscle temperature 37.5 °C); group H (saline 1 ml/kg, 35.0 °C); group D (dexmedetomidine 100 ,g/kg, 37.5 °C); and group DH (dexmedetomidine 100 ,g/kg, 35.0 °C). Dexmedetomidine or saline was administered intraperitoneally 30 min before ischemia. Cerebral ischemia was produced by right carotid artery ligation with hemorrhagic hypotension (mean arterial pressure 40 mmHg) for 20 min. Neurologic outcome was evaluated at 24, 48, and 72 h after ischemia. Histopathology was evaluated in the caudate and hippocampus at 72 h after ischemia. Results: Neurologic outcome was significantly better in the group DH than the group C (P<0.05), whereas it was similar between the group DH and the groups D or H. Survival rate of the hippocampal CA1 neurons was significantly greater in groups D, H, and DH than group C (P<0.05). Histopathologic injury in the caudate section was significantly less in groups H and DH than group C (P<0.05). Conclusion: The combination of dexmedetomidine and hypothermia improved short-term neurologic outcome compared with the control group, whereas the combination therapy provided comparable neuroprotection with either of the two therapies alone. [source] Drip loss in pork: influencing factors and relation to further meat quality traitsJOURNAL OF ANIMAL BREEDING AND GENETICS, Issue 2007K. Fischer Summary The paper deals with some general features of drip loss and the most important factors influencing it. Moreover, it shows some exemplary results of an own investigation. Up to now there is no generally valid definition of drip loss available. Therefore measurement procedures have to be strongly standardized, otherwise they provide no comparable results. Drip loss depends on the shortening of sarcomeres which is regulated by the interaction of muscle temperature and rigour development. Hence, the chilling conditions are highly important. However, the main point is the velocity and the extent of the pH fall after slaughter. All factors influencing the occurrence of quality deviations like PSE, DFD, Acid meat, RSE, PFN will inevitably affect the degree of drip loss too. Under the conditions of an own study, investigating material of a progeny testing station, untypically, one third of the loins with higher-than-average wateriness were red rather than pale, and one third of the loins with higher-than-average brightness were only slightly exudative, which is untypical too. Pork with higher-than-average brightness and low wateriness exhibited, apart from the colour deviation, no crucial disadvantages. It showed only a marginally higher loss during storage, thawing and heating. Pork with higher-than-average drip loss , regardless of dark or pale colour , was predominantly combined with a pH1 less than 6.2, an electrical conductivity 24 h p.m. higher than 5.0 and a loin area higher than 56 cm2. [source] Effect of mivazerol, a ,2 -agonist, on striatal norepinephrine concentration during transient forebrain ischemia in rats,ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2008T. KIMURA Background: We have previously reported that mivazerol, a ,2 -agonist, possibly provides neuroprotection against transient forebrain ischemia in rats. This study was designed to investigate the ability of mivazerol to attenuate ischemia-induced increase in striatal norepinephrine concentration after transient forebrain ischemia in rats. Methods: Male Sprague,Dawley rats, anesthetized with halothane, were assigned to one of three groups (n=10 each); control (C, normal saline 1 ml/kg), mivazerol 20 ,g/kg (M20), and 40 ,g/kg (M40) groups. Monitored variables included temporal muscle temperature (maintained at 37.5±0.1 °C), electroencephalogram, systolic/diastolic blood pressure, heart rate, arterial blood gases, and blood glucose concentrations. Thirty minutes after subcutaneous drug administration, forebrain ischemia was induced with hemorrhagic hypotension (systolic arterial pressure: 40,50 mmHg) and bilateral carotid artery occlusion for 10 min, and then the brain was reperfused. Norepinephrine concentration in the interstitial fluids in the striatum was analyzed using in vivo microdialysis in combination with high-performance liquid chromatography. Results: Ischemia resulted in a prompt increase in norepinephrine concentrations in the striatum in all groups. However, there were no significant differences in norepinephrine concentrations in the striatum between the three groups at any period. Conclusions: Our results indicate that mivazerol did not attenuate ischemia-induced increase in striatal norepinephrine concentration. This suggests that the possible neuroprotective property of mivazerol is not related to inhibition of norepinephrine release in the brain. [source] High temperature does not alter fatigability in intact mouse skeletal muscle fibresTHE JOURNAL OF PHYSIOLOGY, Issue 19 2009Nicolas Place Intense activation of skeletal muscle results in fatigue development, which involves impaired function of the muscle cells resulting in weaker and slower contractions. Intense muscle activity also results in increased heat production and muscle temperature may rise by up to ,6°C. Hyperthermia is associated with impaired exercise performance in vivo and recent studies have shown contractile dysfunction and premature fatigue development in easily fatigued muscle fibres stimulated at high temperatures and these defects were attributed to oxidative stress. Here we studied whether fatigue-resistant soleus fibres stimulated at increased temperature show premature fatigue development and whether increasing the level of oxidative stress accelerates fatigue development. Intact single fibres or small bundles of soleus fibres were fatigued by 600 ms tetani given at 2 s intervals at 37°C and 43°C, which is the highest temperature the muscle would experience in vivo. Tetanic force in the unfatigued state was not significantly different at the two temperatures. With 100 fatiguing tetani, force decreased by ,15% at both temperatures; the free cytosolic [Ca2+] (assessed with indo-1) showed a similar ,10% decrease at both temperatures. The oxidative stress during fatigue at 43°C was increased by application of 10 ,m hydrogen peroxide or tert-butyl hydroperoxide and this did not cause premature fatigue development. In summary, fatigue-resistant muscle fibres do not display impaired contractility and fatigue resistance at the highest temperature that mammals, including humans, would experience in vivo. Thus, intrinsic defects in fatigue-resistant muscle fibres cannot explain the decreased physical performance at high temperatures. [source] Allometric scaling of maximum metabolic rate: the influence of temperatureFUNCTIONAL ECOLOGY, Issue 4 2008C. R. White Summary 1Maximum aerobic metabolic rate, measured in terms of rate of oxygen consumption during exercise (), is well known to scale to body mass (M) with an exponent greater than the value of 0·75 predicted by models based on the geometry of systems that supply nutrients. 2Recently, the observed scaling for (,M0·872) has been hypothesized to arise because of the temperature dependence of biological processes, and because large species show a greater increase in muscle temperature when exercising than do small species. 3Based on this hypothesis, we predicted that will be positively related to ambient temperature, because heat loss is restricted at high temperatures and body temperature is likely to be elevated to a greater extent than during exercise in the cold. 4This prediction was tested using a comparative phylogenetic generalized least-squares (PGLS) approach, and 34 measurements of six species of rodent (20·5,939 g) maximally exercising at temperatures from ,16 to 30 °C. 5 is unrelated to testing temperature, but is negatively related to acclimation temperature. We conclude that prolonged cold exposure increases exercise-induced by acting as a form of aerobic training in mammals, and that elevated muscle temperatures of large species do not explain the scaling of across taxa. [source] | |||||||||||||