scholarly journals Effect of body temperature during exercise on skeletal muscle cytochrome c oxidase content

2002 ◽  
Vol 93 (2) ◽  
pp. 526-530 ◽  
Author(s):  
Christopher R. Mitchell ◽  
M. Brennan Harris ◽  
Anthony R. Cordaro ◽  
Joseph W. Starnes
Keyword(s):  
Body Temperature ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Sprague Dawley ◽  
Ambient Temperatures ◽  
Sprague Dawley Rats ◽  
Mitochondrial Heat Shock Protein

This study determined the role of body temperature during exercise on cytochrome- c oxidase (CytOx) activity, a marker of mitochondrial content, and mitochondrial heat shock protein 70 (mtHSP70), which is required for import of nuclear-coded preproteins. Male, 10-wk-old, Sprague-Dawley rats exercised identically for 9 wk in ambient temperatures of 23°C ( n = 10), 8°C with wetted fur ( n = 8), and 4°C with wetted fur and fan ( n = 7). These conditions maintained exercising core temperature (Tc) at 40.4, 39.2, or 38.0°C (resting temperature), respectively. During weeks 3–9, exercisers ran 5 days/wk up a 6% grade at 20 m/min for 60 min. Animals were housed at 23°C. Gastrocnemius CytOx activity in Tc=38.0°C (83.5 ± 5.5 μatoms O · min−1 · g wet wt−1) was greater than all other groups ( P< 0.05), exceeding sedentary ( n = 7) by 73.2%. Tc of 40.4 and 39.2°C also were higher than sedentary by 22.4 and 37.4%, respectively ( P < 0.05). Quantification of CytOx content verified that the increased activity was due to an increase in protein content. In extensor digitorum longus, a nonactive muscle, CytOx was not elevated in Tc = 38.0°C. mtHSP70 was significantly elevated in gastrocnemius of Tc = 38.0°C compared with sedentary ( P < 0.05) but was not elevated in extensor digitorum longus ( P > 0.05). The data indicate that decreasing exercise Tc may enhance mitochondrial biogenesis and that mtHSP70 expression is not dependent on temperature.

Spaceflight on STS-48 and earth-based unweighting produce similar effects on skeletal muscle of young rats

1993 ◽  
Vol 74 (5) ◽  
pp. 2161-2165 ◽  
Author(s):  
M. E. Tischler ◽  
E. J. Henriksen ◽  
K. A. Munoz ◽  
C. S. Stump ◽  
C. R. Woodman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Extensor Digitorum Longus ◽  
Space Shuttle ◽  
Weight Bearing ◽  
Similar Rate ◽  
Extensor Digitorum ◽  
Hindlimb Suspension ◽  
Albino Rats ◽  
Sprague Dawley ◽  
Ambient Temperatures

Our knowledge of the effects of unweighting on skeletal muscle of juvenile rapidly growing rats has been obtained entirely by using hindlimb-suspension models. No spaceflight data on juvenile animals are available to validate these models of simulated weightlessness. Therefore, eight 26-day-old female Sprague-Dawley albino rats were exposed to 5.4 days of weightlessness aboard the space shuttle Discovery (mission STS-48, September 1991). An asynchronous ground control experiment mimicked the flight cage condition, ambient shuttle temperatures, and mission duration for a second group of rats. A third group of animals underwent hindlimb suspension for 5.4 days at ambient temperatures. Although all groups consumed food at a similar rate, flight animals gained a greater percentage of body mass per day (P < 0.05). Mass and protein data showed weight-bearing hindlimb muscles were most affected, with atrophy of the soleus and reduced growth of the plantaris and gastrocnemius in both the flight and suspended animals. In contrast, the non-weight-bearing extensor digitorum longus and tibialis anterior muscles grew normally. Earlier suspension studies showed that the soleus develops an increased sensitivity to insulin during unweighting atrophy, particularly for the uptake of 2-[1,2–3H]deoxyglucose. Therefore, this characteristic was studied in isolated muscles within 2 h after cessation of spaceflight or suspension. Insulin increased uptake 2.5- and 2.7-fold in soleus of flight and suspended animals, respectively, whereas it increased only 1.6-fold in control animals. In contrast, the effect of insulin was similar among the three groups for the extensor digitorum longus, which provides a control for potential systemic differences in the animals.

Role of prostaglandins in exercise-induced core temperature elevation in female Sprague-Dawley rats

1993 ◽  
Vol 265 (5) ◽  
pp. R1121-R1125
Author(s):  
P. J. Rowsey ◽  
K. T. Borer ◽  
M. J. Kluger
Keyword(s):  
Body Temperature ◽  
Sodium Salicylate ◽  
Voluntary Exercise ◽  
Female Rats ◽  
Temperature Elevation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Exercise Induced ◽  
Running Wheels

Female Sprague-Dawley rats (12:12-h photoperiod; body temperature, BT, measured with biotelemetry) with access to running wheels for 6 wk have an elevated BT (compared with rats with no access to exercise wheels, i.e, sedentary) both during the period of voluntary exercise (nighttime) (0.5 degree C, P = 0.0001) and the nonexercise period (daytime) (0.3 degree C, P = 0.002). To determine whether prostaglandin (PG) E was responsible for any portion of this daytime rise in BT, we injected a dose of sodium salicylate (300 mg/kg), which was shown to produce complete antipyresis in rats injected with lipopolysaccharide (LPS), into exercised and sedentary rats 4 h after the onset of the lights-on period. The injections of sodium salicylate led to a fall in body temperature in both the exercised and sedentary rats of similar amounts (-0.88 degree C vs. -0.61 degree C at 2 h postinjection, P = 0.59). We conclude that the increase in daytime BT of exercised female rats is not mediated by prostaglandins.

Cytochrome C suppresses renal accumulation and nephrotoxicity of polymyxin B

2018 ◽  
Vol 38 (2) ◽  
pp. 193-200 ◽  
Author(s):  
Z-D Li ◽  
J Luo ◽  
L-H Jia ◽  
X-Y Wang ◽  
Z-K Xun ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Polymyxin B ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
C 30 ◽  
C 50

The receptor megalin plays an important role in the accumulation of polymyxin B (PMB) in renal cells in vitro. This study aimed to examine the effects of cytochrome c (cyto c), a typical megalin ligand, on renal accumulation and nephrotoxicity of PMB in vivo. Thirty Sprague-Dawley rats were randomly divided into the vehicle control group, PMB group, PMB + cyto c 50, 100, or 200 mg/kg group, respectively, and were treated with intravenous cyto c 30 min before the administration of PMB 4.0 mg/kg once a day for consecutive 5 days. On the 4th day after administration, 24 h urine was collected to determine N-acetyl-β-D-glucosaminidase excretion. Six hours after the last injection on the 5th day, kidneys were harvested to assay PMB concentration and observe pathological alterations, and blood samples were collected to assay serum creatinine (SCr), blood urea nitrogen (BUN), and blood β2-microglobulin (β2-MG) levels. Cyto c 50, 100, and 200 mg/kg decreased the accumulation of PMB in the kidney by 18.5%, 39.1% ( p < 0.01), and 36.8% ( p < 0.01), respectively, and reduced 24 h N-acetyl-β-D- glucosaminidase excretion by 22.5% ( p < 0.05), 40.4% ( p < 0.01), and 40.4% ( p < 0.01), respectively. Kidney pathological damage induced by PMB was markedly reduced by cyto c 100 mg/kg and 200 mg/kg. However, there were no significant differences in SCr, BUN, and blood β2-MG levels among the groups. These results indicated that cyto c may inhibit the renal accumulation and nephrotoxicity of PMB in a rat model, further proving the role of megalin in the accumulation of PMB.

Thermal dehydration-induced thirst in rats: role of body temperature

1995 ◽  
Vol 269 (3) ◽  
pp. R557-R564 ◽  
Author(s):  
C. C. Barney ◽  
M. M. Folkerts
Keyword(s):  
Body Temperature ◽  
Core Temperature ◽  
Water Intake ◽  
Thermal Dehydration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Access To Water

Male Sprague-Dawley rats were used to study the possible role of hyperthermia in the thirst associated with thermal dehydration. Rats were exposed to 40 degrees C for 4 h and then allowed access to water at different times after they were transferred to 25 degrees C. Delaying the time prior to allowing the rats to drink did not significantly alter either water intake or percent rehydration even though core temperature decreased during the first 1.5 h after removal from the heat. Exposing thermally dehydrated rats to 5 degrees C for 30 min prior to allowing them access to water also failed to significantly affect water intake or percent rehydration. Thermally dehydrated rats allowed to drink while remaining in the heat did not show a significant increase in water intake during the first hour or percent rehydration over rats drinking at 25 degrees C. Nondehydrated rats did show significant increases in water intake and percent rehydration when allowed to drink in the heat. Hyperthermia does not play a role in drinking in thermally dehydrated rats but can stimulate drinking in water-replete rats.

Glycogen and histological changes in muscle grafts of rats during fasting or exercise

1982 ◽  
Vol 60 (3) ◽  
pp. 387-391 ◽  
Author(s):  
Franz S. F. Mong ◽  
James L. Poland ◽  
Jerry W. Poland
Keyword(s):  
Skeletal Muscle ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Sprague Dawley ◽  
Normal Muscle ◽  
Histological Changes ◽  
Glycogen Concentration ◽  
Sprague Dawley Rats ◽  
Resting Muscle

The metabolic integrity of skeletal muscle grafts must be restored, along with histological regeneration, if muscle transplants are to be clinically acceptable. The purpose of the present study was to contrast glycogen changes in muscle grafts after exercise or fasting with those in normal muscles. The extensor digitorum longus (EDL) and soleus (SOL) muscles were switched to each other's muscle bed in one leg of male Sprague–Dawley rats. Fifty days later, some of the rats were fasted for 48 h and sacrificed either immediately or after 4 h of refeeding. Other rats were run on a treadmill for 30 min (1 mi/h (0.447 m/s)) and sacrificed either immediately or after 4 h of resting. Muscle grafts and contralateral normal muscles of these experimental, as well as control animals (neither exercised nor fasted), were removed for determination of glycogen concentration. The results show that glycogen in muscle grafts, as in normal muscles, decreases with exercise or fasting. After 4 h of rest or refeeding, glycogen is restored in both grafts and normal muscles. It is concluded, therefore, that muscle grafts are metabolically active and that their pattern of utilization and restoration of glycogen in response to physiological events, such as exercise or fasting, is similar to that of normal muscle.

Adrenalectomy eliminates both fiber-type differences and starvation effects on denervated muscle

1988 ◽  
Vol 255 (6) ◽  
pp. E850-E856 ◽  
Author(s):  
R. R. Almon ◽  
D. C. Dubois
Keyword(s):  
Muscle Mass ◽  
Extensor Digitorum Longus ◽  
Fiber Type ◽  
Sprague Dawley ◽  
Denervated Muscle ◽  
Adrenalectomized Animal ◽  
Sprague Dawley Rats ◽  
Starvation Effects ◽  
The Difference ◽  
Denervated Muscles

This report describes changes in muscle mass of innervated and denervated pairs of muscles taken from intact and adrenalectomized 250-g male Sprague-Dawley rats provided with different diets. Diets ranged from a nutritionally complete liquid diet to starvation (water only). In the intact animals, muscles with a more tonic character (soleus) are less sensitive to starvation than are muscles with a more phasic character (extensor digitorum longus), whereas the opposite is true of denervation. In the intact animals, starvation greatly increased the amount of atrophy following denervation. In the adrenalectomized animals, starvation had no effect on the amounts of atrophy following denervation. Furthermore, adrenalectomy virtually eliminated the fiber-type differences in the amount of atrophy following denervation. In addition, a comparison between denervated muscles from intact animals and adrenalectomized animals subjected to starvation demonstrates that all denervated muscles from the adrenalectomized animals atrophy less. Finally, it was observed that although an adrenalectomized animal can tolerate 6 days of starvation, an adrenalectomized-castrated animal cannot tolerate even short periods of starvation. The difference appears to be due to low amounts of corticosterone of testicular origin.

scholarly journals Mild DOCA-salt hypertension: sympathetic system and role of renal nerves

2011 ◽  
Vol 300 (5) ◽  
pp. H1781-H1787 ◽  
Author(s):  
Sachin S. Kandlikar ◽  
Gregory D. Fink
Keyword(s):  
Control Period ◽  
Whole Body ◽  
Renal Nerves ◽  
Experimental Hypertension ◽  
Sympathetic Activation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Salt Hypertension ◽  
Hypertension Development

Excess sympathetic nervous system activity (SNA) is linked to human essential and experimental hypertension. To test whether sympathetic activation is associated with a model of deoxycorticosterone acetate (DOCA)-salt hypertension featuring two kidneys and a moderate elevation of blood pressure, we measured whole body norepinephrine (NE) spillover as an index of global SNA. Studies were conducted in chronically catheterized male Sprague-Dawley rats drinking water containing 1% NaCl and 0.2% KCl. After a 7-day surgical recovery and a 3-day control period, a DOCA pellet (50 mg/kg) was implanted subcutaneously in one group of rats (DOCA), while the other group underwent sham implantation (Sham). NE spillover was measured on control day 2 and days 7 and 14 after DOCA administration or sham implantation. During the control period, mean arterial pressure (MAP) was similar in Sham and DOCA rats. MAP was significantly increased in the DOCA group compared with the Sham group after DOCA administration ( day 14: Sham = 109 ± 5.3, DOCA = 128 ± 3.6 mmHg). However, plasma NE concentration, clearance, and spillover were not different in the two groups at any time. To determine whether selective sympathetic activation to the kidneys contributes to hypertension development, additional studies were performed in renal denervated (RDX) and sham-denervated (Sham-DX) rats. MAP, measured by radiotelemetry, was similar in both groups during the control and DOCA treatment periods. In conclusion, global SNA is not increased during the development of mild DOCA-salt hypertension, and fully intact renal nerves are not essential for hypertension development in this model.

Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension

1994 ◽  
Vol 267 (2) ◽  
pp. H751-H756 ◽  
Author(s):  
A. W. Cowley ◽  
E. Szczepanska-Sadowska ◽  
K. Stepniakowski ◽  
D. Mattson
Keyword(s):  
Body Weight ◽  
Arginine Vasopressin ◽  
Plasma Catecholamines ◽  
Plasma Osmolality ◽  
Sprague Dawley ◽  
Prolonged Administration ◽  
Chronic Stimulation ◽  
Sustained Hypertension ◽  
Sprague Dawley Rats

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.

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