scholarly journals Differential expression of stress proteins in rat myocardium after free wheel or treadmill run training

1999 ◽  
Vol 86 (5) ◽  
pp. 1696-1701 ◽  
Author(s):  
Earl G. Noble ◽  
Albert Moraska ◽  
Robert S. Mazzeo ◽  
David A. Roth ◽  
M. Charlotte Olsson ◽  
...  
Keyword(s):  
Exercise Training ◽  
Stress Proteins ◽  
Citrate Synthase ◽  
Treadmill Exercise ◽  
Stress Protein ◽  
Critical Factor ◽  
Voluntary Exercise ◽  
Similar Response ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

High-intensity treadmill exercise increases the expression of a cardioprotective, inducible 72-kDa stress protein (SP72) in cardiac muscle. This investigation examined whether voluntary free wheel exercise training would be sufficient to confer a similar response. Male Sprague-Dawley rats were randomly assigned to either treadmill (TM-Tr) or free wheel (FW-Tr) training groups. By the end of the 8-wk training period, TM-Tr animals ran 1 h/day, 5 days/wk up a 10% grade, covering a distance of 8,282 m/wk. FW-Tr rats ran, on average, 5,300 m/wk, with one-third of the animals covering distances similar to those for the TM-Tr group. At the time of death, hearts of trained and caged sedentary control (Sed) animals were divided into left (LV) and right (RV) ventricles. Citrate synthase activity and the relative immunoblot contents of SP72, SP73 (the constitutive isoform of the SP70 family), and a 75-kDa mitochondrial chaperone (SP75) were subsequently determined. LV and RV did not differ on any measure, and SP73, SP75, and citrate synthase were not affected by training. Cardiac SP72 levels were elevated over fourfold in both ventricles of TM-Tr compared with RV of FW-Sed rats. Despite the animals having run a similar total distance, cardiac SP72 content in FW-Tr rats was not different from that in Sed animals. These data indicate that voluntary exercise training is insufficient to elicit an elevation of SP72 in rat heart and suggest that exercise intensity may be a critical factor in evoking the cardioprotective SP72 response.

Changes in insulin response to glucose after exercise training in partially pancreatectomized rats

1991 ◽  
Vol 70 (4) ◽  
pp. 1563-1568 ◽  
Author(s):  
P. A. Farrell ◽  
A. L. Caston ◽  
D. Rodd
Keyword(s):  
Exercise Training ◽  
Acute Exercise ◽  
Citrate Synthase ◽  
Blood Glucose Concentration ◽  
Insulin Response ◽  
Similar Response ◽  
Sprague Dawley ◽  
Partial Pancreatectomy ◽  
Fed State ◽  
Arterial Blood

The effects of exercise training on glucose-stimulated insulin secretion (GSIS) were studied in male Sprague-Dawley rats made mildly to severely diabetic by partial pancreatectomy. Exercise trained (10 wk treadmill; T) and untrained (Unt) rats were grouped according to posttraining fed-state hyperglycemia as follows: T less than 200 and Unt less than 200 (glucose concn less than 200 mg/dl), T 200-300 and Unt 200-300 (glucose concn 200-300 mg/dl), and T greater than 300 and Unt greater than 300 (glucose concn greater than 300 mg/dl). After exercise training, hyperglycemic glucose clamps were performed in awake rats by elevation of arterial blood glucose concentration 126 mg/dl above fasting basal levels for 90 min. Exercise training significantly increased muscle citrate synthase activity. Prevailing hyperglycemia was reduced during the 10-wk exercise training period in all T rats with fed-state glucose concentrations less than 300, and only 53% of Unt rats in these groups had reduced glycemia. GSIS was significantly higher in T less than 200 [2.4 +/- 0.7 (SD) ng/ml at 90 min] than in Unt less than 200 (1.5 +/- 0.3). A similar response was found for T 200-300 (1.1 +/- 0.3 ng/dl) vs. Unt 200-300 (0.7 +/- 0.1) but not T greater than 300 (0.36 +/- 0.2) vs Unt greater than 300 (0.44 +/- 0.05). Sham-operated control rats had insulin concentrations of 6.6 +/- 1.6 ng/ml at the 90th min of the clamp. Acute exercise reduced fed-state glycemia in rats with mild-to-moderate (less than 300 mg/dl) diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular responses to voluntary and treadmill exercise in rats

1993 ◽  
Vol 75 (3) ◽  
pp. 1334-1340 ◽  
Author(s):  
S. L. Yancey ◽  
J. M. Overton
Keyword(s):  
Blood Flow ◽  
Treadmill Exercise ◽  
Exercise Bout ◽  
Cardiovascular Responses ◽  
Voluntary Exercise ◽  
Treadmill Running ◽  
Sprague Dawley ◽  
Mesenteric Blood Flow ◽  
Doppler Flow ◽  
Sprague Dawley Rats

Male Sprague-Dawley rats (n = 12) were housed in activity wheels and familiarized with treadmill running 2 wk before they were instrumented with Doppler flow probes and a carotid catheter. Mean arterial pressure (MAP), heart rate (HR), mesenteric blood flow (BFmes), and iliac blood flow were determined during bouts of voluntary and treadmill exercise. One voluntary exercise bout (speed = 33 +/- 2 m/min, duration = 26 +/- 5 s) from each rat was selected to compare with 30 s of treadmill exercise at 30 m/min. Voluntary exercise produced increases in MAP (7 +/- 3 mmHg) and HR (63 +/- 7 beats/min) that were significantly less than the increases of 21 +/- 5 mmHg and 95 +/- 9 beats/min, respectively, with treadmill exercise. Voluntary exercise caused an immediate reduction in BFmes of 32 +/- 6%, whereas treadmill exercise produced a significantly greater reduction of 57 +/- 4%. Voluntary and treadmill exercise caused similar increases in iliac blood flow of 112 +/- 15 and 169 +/- 31%, respectively. The patterns of cardiovascular adjustments to the initiation of voluntary exercise are similar to those observed at the initiation of treadmill exercise; however, MAP, HR, and BFmes responses were significantly greater with treadmill exercise.

Voluntary exercise protects against acute doxorubicin cardiotoxicity in the isolated perfused rat heart

2005 ◽  
Vol 289 (2) ◽  
pp. R424-R431 ◽  
Author(s):  
Adam J. Chicco ◽  
Carole M. Schneider ◽  
Reid Hayward
Keyword(s):  
Exercise Training ◽  
Rat Heart ◽  
Left Ventricular ◽  
Voluntary Exercise ◽  
Sprague Dawley ◽  
Perfused Rat Heart ◽  
Isolated Perfused Rat Heart ◽  
Sprague Dawley Rats ◽  
Developed Pressure ◽  
Running Wheels

The clinical use of doxorubicin (DOX) is limited by a dose-dependent cardiotoxicity. The purpose of this study was to determine whether voluntary exercise training would confer protection against DOX cardiotoxicity in the isolated perfused rat heart. Female Sprague-Dawley rats were randomly assigned to standard holding cages or cages with running wheels for 8 wk. Twenty-four hours after the sedentary (SED) or voluntary exercise (VEX) running period, rats were anesthetized with pentobarbital sodium, and hearts were isolated and perfused with oxygenated Krebs-Henseleit (KH) buffer at a constant flow of 15 ml/min. After a 20-min stabilization period, hearts were paced at 300 beats per minute and perfused with KH buffer containing 10 μM DOX for 60 min. A set of control hearts from SED and VEX rats were perfused under identical conditions without DOX for the same period. DOX perfusion led to significant decreases in left ventricular developed pressure, +dP/d t, and −dP/d t, and significant increases in LV lipid peroxidation in sedentary rats compared with non-DOX controls ( P < 0.05). Prior voluntary exercise training attenuated these DOX-induced effects and was associated with a significant increase (78%, P < 0.05) in heat shock protein (HSP72), but not mitochondrial isoform of SOD (MnSOD) or CuZnSOD protein expression in the hearts of wheel-run animals. These data indicate that chronic physical activity may provide resistance against the cardiac dysfunction and oxidative damage associated with DOX exposure and provide novel evidence of HSP72 induction in the heart after voluntary exercise.

Fatty acid oxidation and triacylglycerol hydrolysis are enhanced after chronic leptin treatment in rats

2002 ◽  
Vol 282 (3) ◽  
pp. E593-E600 ◽  
Author(s):  
Gregory R. Steinberg ◽  
Arend Bonen ◽  
David J. Dyck
Keyword(s):  
Fatty Acid ◽  
Citrate Synthase ◽  
Uncoupling Protein ◽  
Oxidative Capacity ◽  
Hormone Sensitive Lipase ◽  
Acid Oxidation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Triacylglycerol Hydrolysis ◽  
Hormone Sensitive

Leptin acutely increases fatty acid (FA) oxidation and triacylglycerol (TG) hydrolysis and decreases TG esterification in oxidative rodent muscle. However, the effects of chronic leptin administration on FA metabolism in skeletal muscle have not been examined. We hypothesized that chronic leptin treatment would enhance TG hydrolysis as well as the capacity to oxidize FA in soleus (SOL) muscle. Female Sprague-Dawley rats were infused for 2 wk with leptin (LEPT; 0.5 mg · kg−1 · day−1) by use of subcutaneously implanted miniosmotic pumps. Control (AD-S) and pair-fed (PF-S) animals received saline-filled implants. Subsequently, FA metabolism was monitored for 45 min in isolated, resting, and contracting (20 tetani/min) SOL muscles by means of pulse-chase procedures. Food intake (−33 ± 2%, P < 0.01) and body mass (−12.5 ± 4%, P = 0.01) were reduced in both LEPT and PF-S animals. Leptin levels were elevated (+418 ± 7%, P < 0.001) in treated animals but reduced in PF-S animals (−73 ± 8%, P< 0.05) relative to controls. At rest, TG hydrolysis was increased in leptin-treated rats (1.8 ± 2.2, AD-S vs. 23.5 ± 8.1 nmol/g wet wt, LEPT; P < 0.001). In contracting SOL muscles, TG hydrolysis (1.5 ± 0.6, AD-S vs. 3.6 ± 1.0 μmol/g wet wt, LEPT; P = 0.02) and palmitate oxidation (18.3 ± 6.7, AD-S vs. 45.7 ± 9.9 nmol/g wet wt, LEPT; P < 0.05) were both significantly increased by leptin treatment. Chronic leptin treatment had no effect on TG esterification either at rest or during contraction. Markers of overall (citrate synthase) and FA (hydroxyacyl-CoA dehydrogenase) oxidative capacity were unchanged with leptin treatment. Protein expression of hormone-sensitive lipase (HSL) was also unaltered following leptin treatment. Thus leptin-induced increases in lipolysis are likely due to HSL activation (i.e., phosphorylation). Increased FA oxidation secondary to chronic leptin treatment is not due to an enhanced oxidative capacity and may be a result of enhanced flux into the mitochondrion (i.e., carnitine palmitoyltransferase I regulation) or electron transport uncoupling (i.e., uncoupling protein-3 expression).

Changes in total body calcium balance with exercise in the rat

1983 ◽  
Vol 55 (1) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. LeBlanc ◽  
H. J. Evans ◽  
P. C. Johnson ◽  
S. Jhingran
Keyword(s):  
Least Squares ◽  
Voluntary Exercise ◽  
Calcium Balance ◽  
Sprague Dawley ◽  
Total Body Calcium ◽  
Sprague Dawley Rats ◽  
Least Squares Fit ◽  
Significant Change ◽  
Total Body ◽  
And Control

The purpose of this study was to evaluate the effect of deconditioning on the total body calcium in rats. Two separate experiments were performed using female Sprague-Dawley rats, 187-266 days of age. Total body calcium was measured in experimental and control rats during and following several weeks of voluntary exercise. The slope from the least-squares fit of total body calcium with time was used to obtain an average calcium balance for each animal during each study period. In both groups the exercised rats had a significantly decreased calcium balance after cessation of exercise, whereas no significant change was seen in nonexercised controls. In both groups, the exercised animals gained calcium at a significantly greater rate than controls. Our findings indicate that while exercised rats may gain calcium at a faster rate compared with nonexercising controls, the rate of gain following cessation of exercise is less than the controls.

Exercise training and its effects with renal hypertensive rats

1985 ◽  
Vol 59 (5) ◽  
pp. 1410-1415 ◽  
Author(s):  
K. D. Marcus ◽  
C. M. Tipton
Keyword(s):  
Blood Pressure ◽  
Exercise Training ◽  
Capillary Density ◽  
Heart Weight ◽  
Sprague Dawley ◽  
Vo2 Max ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Resting Blood Pressure ◽  
Renal Hypertensive Rats

The influence of endurance training on functional capacity [maximal O2 consumption (VO2 max)], caudal arterial blood pressure, and myocardial capillary density were investigated in normotensive rats and rats made hypertensive using the two-kidney one-clip approach (Goldblatt's hypertension). Male Sprague-Dawley rats were assigned to sham (N: 120–140 mmHg), moderately hypertensive (MH = 0.30-mm clips, 150–170 mmHg), or severely hypertensive (SH = 0.25-mm clips, 190–230 mmHg) groups. Rats designated to be runners (T) were exercised on a motor-driven treadmill equal to 50–70% of their VO2 max values for 8–12 wk. Compared with their nontrained (NT) controls, training was associated with significantly higher VO2 max values (12–15%) and muscle cytochrome-c oxidase activities (33–78%). Resting systolic blood pressure was not significantly changed in the N-and MH-T subgroups; however, it was 20–30 mmHg higher in the SH-T subgroup. Mean absolute heart weight for only the N-T group was significantly heavier than their NT controls. However, the mean predicted heart weights (heart wt = 0.639 X body wt of N-NT + 0.001 g) of the two SH groups were significantly higher than expected. The SH-T group had a lower (11%) subepicardial capillary density mean than its NT control and significantly fewer capillaries in the subendocardial region than the other five subgroups. It was concluded that moderate exercise training appeared to be detrimental to rats with severe hypertension because it increased resting blood pressure and decreased myocardial capillary density, even though it improved their functioning capacity.

Exercise training attenuates diet-induced reduction in metabolic rate

1990 ◽  
Vol 68 (6) ◽  
pp. 2612-2617 ◽  
Author(s):  
D. L. Ballor ◽  
L. J. Tommerup ◽  
D. P. Thomas ◽  
D. B. Smith ◽  
R. E. Keesey
Keyword(s):  
Energy Expenditure ◽  
Exercise Training ◽  
Dietary Restriction ◽  
Food Restriction ◽  
Whole Body ◽  
Daily Energy Expenditure ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Daily Energy ◽  
Whole Body Metabolism

The combined influence of exercise training and dietary restriction on daily energy expenditure was evaluated by exposing 48 male Sprague-Dawley rats to one of three food intake conditions [ad libitum (AL), moderately restricted (MR), or severely restricted (SR)] and to one of two exercise conditions [treadmill exercised (E) or cage confined (CC)]. After 10 wk of exercise and dietary restriction, the MR-CC and MR-E rats weighed 84 and 86%, respectively, of AL-CC, whereas the SR-CC and SR-E rats weighed 66 and 68% of AL-CC. Dietary restriction and subsequent weight loss produced significant reductions in both total and resting daily energy expenditure. Exercise partially reversed this effect, but the extent of this reversal diminished as the severity of dietary restriction was increased. These results raise the distinct possibility that inconsistencies in the current literature concerning the effects of exercise on whole body metabolism during periods of dietary restriction might be reconciled by an appreciation and an understanding of the influence that duration of exercise training and severity of food restriction have on this measure.

Exercise training alters length dependence of contractile properties in rat myocardium

2003 ◽  
Vol 94 (3) ◽  
pp. 1137-1144 ◽  
Author(s):  
Gary M. Diffee ◽  
Daniel F. Nagle
Keyword(s):  
Exercise Training ◽  
Cardiac Myocytes ◽  
Sarcomere Length ◽  
Myocardial Function ◽  
Citrate Synthase ◽  
Heart Weight ◽  
Sprague Dawley ◽  
Cellular Mechanisms ◽  
Length Dependence ◽  
Maximal Tension

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. Exercise training increases the sensitivity of rat cardiac myocytes to activation by Ca2+, and this Ca2+ sensitivity has been shown to be highly dependent on sarcomere length. We tested the hypothesis that exercise training increases this length dependence in cardiac myocytes. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise-trained (T) groups. The T rats underwent 11 wk of progressive treadmill exercise. Heart weight increased by 14% in T compared with C rats, and plantaris muscle citrate synthase activity showed a 39% increase with training. Steady-state tension was determined in permeabilized myocytes by using solutions of various Ca2+concentration (pCa), and tension-pCa curves were generated at two different sarcomere lengths for each myocyte (1.9 and 2.3 μm). We found an increased sarcomere length dependence of both maximal tension and pCa50 (the Ca2+ concentration giving 50% of maximal tension) in T compared with C myocytes. The ΔpCa50 between the long and short sarcomere length was 0.084 ± 0.023 (mean ± SD) in myocytes from C hearts compared with 0.132 ± 0.014 in myocytes from T hearts ( n = 50 myocytes per group). The Δmaximal tension was 5.11 ± 1.42 kN/m2 in C myocytes and 9.01 ± 1.28 in T myocytes. We conclude that exercise training increases the length dependence of maximal and submaximal tension in cardiac myocytes, and this change may underlie, at least in part, training-induced enhancement of myocardial function.

Decreased vascular sensitivity to norepinephrine following exercise training

1981 ◽  
Vol 51 (2) ◽  
pp. 282-287 ◽  
Author(s):  
D. L. Wiegman ◽  
P. D. Harris ◽  
I. G. Joshua ◽  
F. N. Miller
Keyword(s):  
Blood Pressure ◽  
Exercise Training ◽  
Sprague Dawley ◽  
Maximal Increase ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Vascular Sensitivity ◽  
Series Of Experiments ◽  
High Concentrations ◽  
Alpha Chloralose

Twenty Sprague-Dawley rats (230 +/- 9 g; mean +/- SE) were exercised daily for 6 wk by swimming 1 h/day with weights (5% of body wt) attached to their tails. Nineteen additional rats (237 +/- 8 g) remained sedentary in their cages. All animals were anesthetized with urethan (800 mg/kg) and alpha-chloralose (60 mg/kg). In the first series of experiments, increasing doses of norepinephrine were injected into the jugular vein and the responses in mean arterial blood pressure was recorded from a cannulated femoral artery. Exercise training had no effect on the maximal increase in blood pressure, but significantly decreased blood pressure sensitivity to norepinephrine, expressed as a pD2 value (=-log ED 50), from 5.64 +/- 0.07 to 5.20 +/- 0.06. In the second series, the cremaster muscle with intact circulation and innervation was suspended in a tissue bath and norepinephrine in increasing concentrations was added to the cremaster bath. The responses of the main arteriole (approximately 110 micron) and venule (approximately 170 micron) were recorded by television microscopy. Exercise training had no effect on vessel diameters of resting muscle or on the maximal vessel constrictions obtained in response to high concentrations of norepinephrine. Arteriole sensitivity to norepinephrine was significantly decreased (pD2 of 6.69 +/- 0.24 vs. 5.96 +/- 0.18) and there was some tendency for reduced venule sensitivity. These data suggest that exercise training in rats produces a decrease in alpha- or an increase in beta-adrenergic receptor sensitivity.

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