Exercise-trained Rats Research Articles

The effect of reactive oxidant generation in acute exercise-induced proteinuria in trained and untrained rats.

Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. We investigated whether free radicals generated during exercise play a role in post-exercise proteinuria in sedentary and treadmill-running trained rats, separately. Sedentary and trained rats were randomly divided into four sub-groups: control, antioxidant treatment, exhaustive exercise and an exhaustive exercise plus antioxidant treatment group. Antioxidant therapy was applied by intragastric catheter for 4 weeks with vitamin C (ascorbic acid, 50 mg x kg(-1) x day(-1)) and vitamin E (alpha-tocopherol, 20 mg x kg(-1).day(-1)). Twenty-four-hour urine samples were used for measuring protein levels and protein electrophoresis. Thiobarbituric acid (TBARS) and glutathione (GSH) levels, superoxide dismutase (SOD) and catalase (CAT) activities were assayed in blood and tissues. Increased urinary protein levels and mixed type proteinuria in electrophoresis were identified after exhaustive exercise in sedentary rats. Erythrocyte, kidney and muscle TBARS levels were significantly elevated in this group. Antioxidant treatment prevented the increase in urinary protein levels, TBARS levels and the occurrence of mixed type proteinuria after exhaustive exercise in sedentary rats. Exhaustive exercise in trained rats resulted in elevation of urine protein levels and mixed type proteinuria although kidney TBARS levels were not changed compared to those of the trained controls. Antioxidant therapy in trained and exhausted-trained animals resulted in decreased TBARS levels in the kidney but it did not affect urinary-increased protein levels or electrophoresis in exhausted animals. This findings suggest that the exercise-induced oxidant stress may contribute to post-exercise proteinuria in sedentary rats. However, this mechanism may not be responsible for proteinuria in trained rats.

Attenuation of homocysteine-induced endothelial dysfunction by exercise training

Hyperhomocysteinemia is an independent risk factor for the development of cardiovascular disease. Exposure of endothelial cells to elevated levels of homocysteine (HCY) results in decreased availability of nitric oxide (NO) and impaired vascular function, both of which are early events in atherogenesis. Exercise training improves vascular function by increasing endothelial NO production secondary to an increase in the enzyme responsible for its synthesis, endothelial nitric oxide synthase (eNOS). We hypothesized that exercise training would increase endothelial NO production, which would attenuate the endothelial dysfunction associated with HCY exposure. Rats were randomly assigned to either sedentary (SED) or exercise (EX) groups. The exercise regimen consisted of treadmill running at 20–25 m/min, 15% grade, 30 min/day, 5 day/week for 6 weeks. Aortic rings obtained from SED and EX trained rats were incubated with 2 mM HCY for 120 min, then exposed to norepinephrine (NE 100 nM) to induce vasoconstriction. Once a stable contraction plateau was achieved, rings were exposed to increasing concentrations of the receptor-mediated endothelium-dependent vasodilator acetylcholine (ACh; 0.1, 1, 10, 100 nM). This procedure was repeated with the non-receptor-mediated endothelium-dependent vasodilator A-23187 (0.1, 1, 10, 100 nM), and the endothelium-independent vasodilator, NaNO 2 (0.1, 1, 10, 100 μM). In addition, eNOS protein content and eNOS enzyme activity were determined. Aortic rings obtained from exercise trained rats demonstrated significantly ( P<0.05) greater relaxation to both ACh and A-23187 in comparison to aortic rings obtained from SED rats following exposure to HCY. Additionally, exercise training increased aortic eNOS protein content and activity. Our data demonstrate that exercise training improves endothelium-dependent vasorelaxation following HCY exposure and this may be due, at least in part, to elevated levels of eNOS protein and an increase in eNOS activity. These results suggest the possible role exercise may play in attenuating the endothelial dysfunction associated with hyperhomocysteinemia.

84 Altered gene expression in the remodeled myocardium of prior exercise-trained rats

84 Altered gene expression in the remodeled myocardium of prior exercise-trained rats

SEARCHING FOR NEW PLAYERS IN CARDIOPROTECTION

Exercise training induces adaptations that improve pump performance and protect the heart from disease-related challenges. To understand the molecular signaling mechanisms of cardioprotection, it will be necessary to identify the proteins involved, as well as the transcriptional, translational, and posttranslational changes they undergo in response to exercise. PURPOSE Our long-term goal was to identify novel cardiac proteins that regulate exercise effects. The short-term goals were to evaluate the potential of a proteomic approach, and to optimize quantitation of protein abundance and peptide mass fingerprinting (PMF). METHODS Proteins were prepared from left ventricles of 8 sedentary and 8 exercise-trained rats. Two-dimensional electrophoresis (2-DE) consisted of isoelectric focusing with immobilized pH gradient strips (pH 5–8) and vertical polyacrylamide slab gels (8–12% gradient). A modified silver-staining (SS) technique was compared with ruthenium-based (RU) fluorescent dyes for quantitative linearity and for compatibility with PMF. Automated PMF (APMF) was compared to a manual procedure (MPMF) for identification of proteins extracted from the 2-DE gels. RESULTS The average coefficient of variation (CV) between gels was 49% for SS, and 32% for RU. Log transformation reduced the CV of spot ratios for SS gels from 49% to 14%, and for RU from 32% to 3%. Using MPMF, 6 of 34 reference spots (18%) were identified. APMF identified 36 of 45 reference spots (80%). Nineteen of 22 (86%) spots from SS gels were identified, and 26 of 36 (72%) spots from RU gels were identified. Among candidate spots that differed in abundance (p < 0.05) between exercise-trained and sedentary proteomes were 3α-hydroxysteroid dehydrogenase and a 20 kDa heat shock protein. CONCLUSION Reliability in protein abundance measurements was greatest with ruthenium-based dyes and was markedly improved by log transformation of the data. APMF is superior to MPMF and is equally compatible with SS and RU. Candidate proteins for the cardioprotective effects of exercise have been identified using a proteomic approach and require further study. Supported by the American Heart Association-Midwest Affiliate

Influence of regular exercise on age-related changes in arterial elasticity: mechanistic insights from wall compositions in rat aorta.

Arterial stiffness increases with age in healthy sedentary adults. We previously reported that the age-related increases in arterial stiffness are absent or attenuated in regularly exercising adults. However, the mechanism underlying this training effect is unknown. One possibility is that regular exercise minimizes age-related changes in the arterial wall composition of elastin and collagen. To gain insight into this issue, we studied four groups of rats (N = 23): young (42-46 wks) and old (80-84 wks), sedentary and exercise-trained. The exercise group swam 1 hr.d-1, 6 d.wk-1 for 17-21 weeks. There was no significant difference in the incremental elastic modulus between young sedentary and exercise-trained rats. The elastic moduli of the old exercise-trained rats were 31% lower than in the old sedentary controls. As such, the magnitude of age-related increase in the elastic modulus was smaller in the exercise-trained (110%) vs. the sedentary group (151%) (p < 0.05). In both activity groups, elastin content was lower and collagen content was higher in old vs. young rats (p < 0.05). However, there were no significant differences between the two activity groups. These results are not consistent with the hypothesis that regular physical exercise minimizes age-related compositional changes in the arterial wall and attenuates the age-related increase in arterial stiffness.

Heavy load exercise induced dysfunction of immunity and neuroendocrine responses in rats

To determine whether immunity and neuroendocrine system is altered by different loads of exercise training in rats, eight-week-old male Sprague–Dawley rats were randomly assigned to one of the three groups: 1) cage control group (CCG); 2) moderate load training (MLT) (swimming at the intensity of 1.4 m/sec water flowing for 60 min per day); 3) heavy load training (HLT) (swimming at the intensity of 1.8 m/sec water flowing for 120 min per day). MLT and HLT rats were assigned to swim for 6 days per week for total of 6 weeks. All rats were sacrificed 36 h after their last training session. Splenocytes were pooled for assay of cell proliferation and neuropeptide contents in the hypothalamus, hypophysis and plasma were determined by radioimmunoassay while glucocorticoid specific binding in intact thymus was measured by radioligand binding assay. All rats were weighed weekly. The results showed that after 6-week training, rat splenocyte proliferation in response to Con A and LPS decreased in HLT rats compared with MLT and CCG rats. In addition, the contents of beta-endorphin, dynorphin A, arginine vasopressin and oxytocin in the hypothalamus, hypophysis and plasma were altered by HLT, as shown by increased plasma concentration of glucocorticoids and decreased glucocorticoids specific binding in intact thymus compared with MLT and CCG. Furthermore, a decreased body mass in HLT rats has been observed. The body mass of HLT rats was significantly lower than that in CCG and MLT rats at the end of the swimming training period. These data suggest that 6-week heavy load training induces the dysfunction of immunity and neuroendocrine responses, which might be one of the underlying mechanisms of immune dysfunction in overtraining.

Angiogenic growth factor expression in rat skeletal muscle in response to exercise training.

Angiogenesis occurs in skeletal muscle in response to exercise training. To gain insight into the regulation of this process, we evaluated the mRNA expression of factors implicated in angiogenesis over the course of a training program. We studied sedentary control (n = 17) rats and both sedentary (n = 18) and exercise-trained (n = 48) rats with bilateral femoral artery ligation. Training consisted of treadmill exercise (4 times/day, 1-24 days). Basal mRNA expression in sedentary control muscle was inversely related to muscle vascularity. Angiogenesis was histologically evident in trained white gastrocnemius muscle by day 12. Training produced initial three- to sixfold increases in VEGF, VEGF receptors (KDR and Flt), the angiopoietin receptor (Tie-2), and endothelial nitric oxide synthase mRNA, which dissipated before the increase in capillarity, and a substantial (30- to 50-fold) but transient upregulation of monocyte chemoattractant protein 1 mRNA. These results emphasize the importance of early events in regulating angiogenesis. However, we observed a sustained elevation of the angiopoietin 2-to-angiopoietin 1 ratio, suggesting continued vascular destabilization. The response to exercise was (in general) tempered in high-oxidative muscles. These findings place importance on cellular events coupled to the onset of angiogenesis.

Altered single cell force-velocity and power properties in exercise-trained rat myocardium.

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. The ability of the myocardium to perform external work is a critical aspect of ventricular function, but previous studies of myocardial adaptation to exercise training have been limited to measurements of isometric tension or unloaded shortening velocity, conditions in which work output is zero. We measured force-velocity properties in single permeabilized myocyte preparations to determine the effect of exercise training on loaded shortening and power output. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise trained (T) groups. T rats underwent 11 wk of progressive treadmill exercise. Myocytes were isolated from T and C hearts, chemically skinned, and attached to a force transducer. Shortening velocity was determined during loaded contractions at 15 degrees C by using a force-clamp technique. Power output was calculated by multiplying force times velocity values. We found that unloaded shortening velocity was not significantly different in T vs. C myocytes (T = 1.43 muscle lengths/s, n = 46 myocytes; C = 1.12 muscle lengths/s, n = 43 myocytes). Training increased the velocity of loaded shortening and increased peak power output (peak power = 0.16 P/P(o) x muscle length/s for T myocytes; peak power = 0.10 P/P(o) x muscle length/s for C myocytes, where P/P(o) is relative tension). We found no effect of training on myosin heavy chain isoform content. These results suggest that training alters power output properties of single cardiac myocytes and that this adaptation may improve the work capacity of the myocardium.

Decreased blood levels of lactic acid and urinary excretion of 3-methylhistidine after exercise by chronic taurine treatment in rats.

Taurine is reported to increase contractility of skeletal muscle and cardiac myocyte, which can increase exercise performance. The present study aimed to clarify taurine's effect on chronic endurance exercise, especially accumulation of lactic acid (LA), a marker of fatigue and ability of aerobic exercise, and urinary secretion of 3-methylhistidine (3-MH), a marker of muscle breakdown in rats. After exercise blood levels of LA and urinary excretion of 3-MH were significantly increased and this increase was significantly less in those with chronic treatment of taurine. Taurine treatment also significantly decreased fat accumulation and blood levels of cholesterol and triglyceride, which might improve insulin resistance and utilization of fat and glucose. These results indicate taurine treatment is useful for reducing physical fatigue and muscle damage during exercise training in rats, presumably due to antioxidant property and improvement of muscle and cardiac functions by taurine.

Decreased chaos after exercise in cardiac output time series of rats: a preliminary report

1. Background: The post-exercise period is associated with a profound decrease in sympathetic activity and arterial pressure. We have recently shown that endurance exercise training in rats is associated with highly significant decreases of low frequency (LF: 0.19– 0.61 Hz ) power of blood pressure (BP). In this study, we measured cardiac output (CO) and systolic blood pressure (SBP) continuously for at least 5 min in rats before ( n=5) and after ( n=4) exercise. The purpose of this study was to determine if acute exercise produces post-exercise changes in the low frequency power (LF: 0.19– 0.61 Hz ) of CO as the decrease in this band of BP appears to be mediated by the sympathetic nervous system. 2. Methods: The data were sampled at 200 Hz and the HR time series were derived from the SBP signal. The signals were sampled at 16 Hz and the spectral powers were obtained in the following bands; total power (TP: 0– 2.5 Hz ), very low frequency power (VLF: 0– 0.19 Hz ), low frequency power (LF: 0.19– 0.61 Hz ) and high frequency power (HF: 1.2– 2.5 Hz ). We also obtained the transfer magnitude and coherence between HR and CO. Finally, largest Lyapunov exponent (LLE) was obtained as a measure of chaos for HR and CO before and after exercise. 3. Results: There was a significant decrease in LLE of CO ( p<0.05) after exercise. 4. Conclusions: These results suggest that the CO time series appear to be chaotic in nature and the decrease in LLE after exercise, especially in relation to HR appears to be due to a decrease in sympathetic activity. These new nonlinear techniques may prove to be of additional value to the linear measures such as spectral analysis.

Regulation of nitric oxide production in limb and ventilatory muscles during chronic exercise training.

In this study, we evaluated the differential influence of chronic treadmill training (30 m/min, 15% incline, 1 h/day, 5 days/wk) on nitric oxide (NO) production and NO synthase (NOS) isoform expression as well as 3-nitrotyrosine formation (footprint of peroxynitrite) both in limb (gastrocnemius) and ventilatory (diaphragm) muscles. A group of exercise-trained rats and a control group (no training) were examined after a 4-wk experimental period. Exercise training elicited an approximate fourfold rise in gastrocnemius NOS activity and augmented protein expression of the endothelial (eNOS) and neuronal (nNOS) isoforms of NOS to approximately 480% and 240%, respectively. Qualitatively similar but quantitatively smaller elevations in NOS activity and eNOS and nNOS expression were observed in the diaphragm. No detectable inducible NOS (iNOS) protein expression was found in any of the muscle samples. Training increased the intensity of 3-nitrotyrosine only in the gastrocnemius muscle. We conclude that whole body exercise training enhances both limb and ventilatory muscle NO production and that constitutive and not iNOS isoforms are responsible for increased protein tyrosine nitration in trained limb muscles.

Possible mechanisms by which adipocyte lipolysis is enhanced in exercise-trained rats

A possible mechanism(s) behind exercise training-enhanced lipolysis was investigated in rat adipocytes. Exercise training (9 weeks; running) enhanced the activity of cAMP-dependent protein kinase (PKA) and the protein expressions of PKA subunits (catalytic, RIIα, and RIIβ) in P 40 fraction (sedimenting at 40,000 g), but not in I 40 fraction (infranatant of 40,000 g) of adipocyte homogenate. The expression of PKA-anchoring protein 150 (AKAP150) in P 40 fraction was greater in exercise-trained (TR) than in control (C) rats. Hormone-sensitive lipase (HSL) activities in both fractions were also greater in TR. On the other hand, stimulated lipolysis was accompanied by increased activities of HSL in P 40 but not in I 40 fraction. The decreases in stimulated lipolysis due to St-Ht31 were greater in TR rats. Thus, the mechanisms behind exercise training-enhanced adipocyte lipolysis could involve the increased activities of PKA and HSL with enhanced expressions of AKAP150 and some subunits of PKA, all of which may be compartmentalized within adipocytes.

Exercise training increases membrane bound form of tumor necrosis factor-α receptors with decreases in the secretion of soluble forms of receptors in rat adipocytes

We examined the effects of exercise training (treadmill running over 9 weeks) on the ability of isolated adipocytes to secrete tumor necrosis factor-α (TNF–α) and type 1 soluble TNF receptor (sTNFR1) in vitro in Wistar rats. We also examined the effects of exercise training on the expression of membrane bound forms of type 1 TNF receptor (mTNFR1) in adipocyte crude membranes of the same rat subjects. Exercise training significantly increased the secretions of TNF–α from isolated adipocytes. Treatment with a cyclooxygenase inhibitor, either indomethacin (100 μM) or eicosatetraynoic acid (100 μM), significantly blocked the release of TNF–α from adipocytes in both exercise-trained rat group and sedentary control rat group, suggesting that some cyclooxygenase metabolite(s) acts as a ligand in TNF–α synthesis. Decreased amounts of TNF–α were found to be significantly greater in both exercise-trained rat group than in sedentary control rat group after incubation with inhibitors. Thus, the inhibitory effect of both indomethacin and eicosatetraynoic acid was significantly greater in adipocytes from exercise-trained rats. Both plasma sTNFR1 levels and adipocytes-derived sTNFR1 were found to be significantly less in the exercise-trained rat group. Western blot analysis revealed that exercise training remarkably increased the expressions of mTNFR1 in adipocyte crude membrane. Thus, exercise training enhanced the ability of isolated adipocytes to secrete TNF–α with reduced secretion of sTNFR1, and provoked the greater expressions of mTNFR1 in adipocyte crude membrane. These alterations may induce enhanced the autocrine effects of TNF–α within adipocytes in exercise-trained rats.

ATTENUATION OF CHEMOTHERAPY-INDUCED VASCULAR DYSFUNCTION BY EXERCISE TRAINING

We have previously shown that exercise training enhances endothelium-dependent vasodilation in a rat mammary tumor model, and that these changes resulted in an attenuation of vasoconstriction caused by the chemotherapeutic agent 5-fluororuacil (5-FU). We hypothesized that this was the result of increased nitric oxide (NO) production by the vasculature. In order to investigate possible mechanisms involved with the exercise-induced attenuation of vascular dysfunction, we determined endothelial nitric oxide synthase (eNOS) protein content in the aorta of N-methyl-N-nitrosourea (MNU)-treated rats following eight weeks of moderate exercise training. Virgin female Sprague Dawley rats were injected with MNU (25 mg/kg, i.p.) at 21 days of age, and at 28 days assigned to either sedentary or exercise groups. The exercise regimen consisted of treadmill running at 20–25 m/min, +15% grade, 30 min/d, 5 d/wk for 8 weeks. Our results show no significant differences in aortic eNOS protein content between sedentary and exercise groups following 2 or 4 weeks of exercise training. However, after 6 weeks of exercise training, significant (p < 0.05) increases in aortic eNOS protein content were observed in exercise trained rats when compared to sedentary animals. Following 8 weeks of exercise training, increases in eNOS protein content were sustained, however differences between sedentary and exercise trained animals were not statistically significant. These data demonstrate that moderate exercise training increases aortic eNOS protein content in a rat mammary tumor model. This suggests that the attenuation of 5-FU-induced vasoconstriction may be due, at least in part, to an increase in aortic eNOS protein content.

Exercise training improves acetylcholine-induced endothelium-dependent hyperpolarization in type 2 diabetic rats, Otsuka Long-Evans Tokushima fatty rats

We investigated whether endothelium-derived relaxing (EDRF) and hyperpolarizing factor (EDHF) is impaired in type 2 diabetic rats (Otsuka Long-Evans Tokushima Fatty (OLETF) rat) and whether the exercise training improves impaired EDRF and EDHF. Diabetic rats were divided into the sedentary and exercise-trained groups at the age of 16 weeks. Long-Evans Tokushima Otsuka (LETO) rats were used as age-matched non-diabetic controls. EDRF as well as EDHF induced by acetylcholine in the presence of indomethacine and l-nitro N -arginine was significantly attenuated in the diabetic rats, and was further impaired with age. Exercise training significantly improved it. Both insulin resistance and abdominal fat accumulation were significantly greater in the diabetic rats, compared with the non-diabetic rats, but were decreased in exercise-trained rats. Urinary NO 2 secretion was decrease in the diabetic rats at each age, and it was improved by exercise training. The results of the study indicated that exercise training prevented impairment of EDHF, as well as EDRF in type 2 diabetic rats, presumably due to improvement of hyperglycemia and insulin resistance and increase in the production of nitric oxide by exercise training.

Differential integrin expression by cardiac fibroblasts from hypertensive and exercise-trained rat hearts

The cardiac fibroblast is the principal cell type responsible for extracellular matrix (ECM) synthesis in the heart during growth and pathophysiological conditions. A dynamic interaction exists between the cardiac ECM and fibroblasts that is sensitive to the local mechanical and chemical tissue environment. We propose here that cardiac fibroblasts structurally and functionally adapt to changing local environments by altering their expression of receptor integrins. Changes in the extracellular environment are communicated in part by integrins, which link the ECM to the cell and regulate phenotype and function. In this report, we analyze integrin protein expression, migration and gel contraction by cardiac fibroblasts from rats subjected to 10 weeks of treadmill exercise (XTR), experimental hypertension (HYP) or controls (CONT). Immunoprecipitation shows that β1 protein increases in XTR and HYP. Also, α1 and α2 integrins are lower in XTR and HYP, and α5 integrin is higher in XTR and lower in HYP. Functional assays show that XTR and HYP migrate slower on collagen, while XTR migrate faster and HYP slower on fibronectin. Cell isolation procedure, population expansion number or a general adaptation to culture conditions does not explain the differences observed. No significant differences in collagen gel contraction are detected. These results indicate that cardiac fibroblasts retain their in vivo patterns in vitro for a limited number of population expansions. This tissue-specific phenotype is exhibited in early passage (≤6). However, by late passage (>8), cells begin to show adaptation to the in vitro conditions. These results show that cardiac fibroblasts respond to changing environments in pathophysiological conditions by modulating integrin expression, which is associated with changes in cell migration. They also suggest a pragmatic use for primary cardiac fibroblasts as a model to study the cardiac matrix remodeled by physiological (exercise) and pathological (hypertension) stressors.

Possible role of nitric oxide on adipocyte lipolysis in exercise-trained rats.

A possible role of nitric oxide (NO) on adipocyte lipolysis was studied in exercise-trained (9 weeks of running) rats. Lipolysis in adipose tissue tended to be greater in trained rats than in control rats. A treatment of adipose tissue with 5 mM N(G)-nitro-L-arginine methyl ester (L-NAME) showed that basal and isoproterenol-stimulated lipolysis were both significantly greater in trained rats than in control rats. In contrast, in isolated adipocytes L-NAME had no effect on lipolysis in either group of rats, though the lipolysis of isolated adipocytes was significantly greater in trained rats than in control rats. Training significantly reduced nitrite/nitrate production in adipocytes, but not in tissue. On the other hand, training increased the protein expression of endothelial nitric oxide synthase (eNOS), but not that of inducible NOS (iNOS) in the extracts of tissue homogenates. In tissue homogenates, eNOS activity but not iNOS activity was significantly greater in trained rats than in control rats. In cellular extracts, training significantly reduced the activities of both NOS's, but the mRNA expressions of both NOS's were not different between groups. The NO donors, S-nitroso-N-acetyl-penicillamine (SNAP) and 1-propamine, 3-(2-hydroxy-2-nitroso-1-propyl-hydrazine) (PAPA-NONOate), significantly inhibited adipocyte lipolysis in response to isoproterenol in both groups. This inhibitory effect of SNAP, but not that of PAPA-NONOate, was greater in the adipocytes of trained rats than in those of the control rats. Thus it is possible that NO is involved in the regulation of lipolysis and that exercise training enhances the responsiveness of adipocytes to extracellular NO with the reduced production of nitrite/nitrate in adipocytes because of decreased activities of NOS's. On the other hand, it is also possible that exercise increases either the activity or the protein expression of eNOS in adipose tissue.

Exercise-induced oxidative stress affects erythrocytes in sedentary rats but not exercise-trained rats.

Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically significant increments in the levels of thiobarbituric acid-reactive substance (TBARS) and H2O2-induced TBARS in Sed rats and resulted in functional and structural alterations in erythrocytes (plasma hemoglobin concentrations, methemoglobin levels, and rise in osmotic fragility of erythrocytes with decrease in erythrocyte deformability). Administration of antioxidant vitamin for 1 mo before exhaustive exercises prevented lipid peroxidation (TBARS, H2O2-induced TBARS) in Sed rats without any functional or structural alterations in erythrocytes. Parameters indicating erythrocyte lipid peroxidation and deterioration after exhaustive exercise in rats trained regularly with treadmill running for 1 mo were not different from those in Sed controls. Erythrocyte lipid peroxidation (TBARS) increased in exhausted-ET rats compared with ET controls; however, the plasma hemoglobin, methemoglobin levels, and erythrocyte osmotic fragility and deformability did not differ. Exhaustive exercise-induced lipid peroxidation in ET rats on antioxidant vitamin treatment was prevented, whereas functional and structural parameters of erythrocytes were not different from those of the ET controls. We conclude that exertional oxidant stress contributed to erythrocyte deterioration due to exercise in Sed but not in ET rats.

Cardiac adaptation to endurance exercise training in rats

Cardiac adaptation to endurance exercise training in rats

Effects of chronic food restriction and exercise training on the recovery of cardiac function following ischemia.

Clinical and experimental data suggest that exercise training (ET) and food restriction (FR) improve cardiovascular function. However, the effects of long-term FR or FR in combination with ET on the recovery of cardiac function following ischemia have not been determined. Male Wistar rats were assigned to ad libitum-fed, FR, ad libitum-exercise, and FR-exercise groups. Mechanical function of isolated working hearts was assessed in response to increases in afterload resistance and following global no-flow ischemia. At low workload, there was a significant FR effect on aortic flow as well as an interaction between FR and ET on systolic pressure. These effects remained when hearts were subjected to increases in aortic afterload resistance. During reperfusion of ischemic hearts, there was a significant FR effect on aortic flow and systolic pressure and a significant ET effect on diastolic pressure. An interaction between FR and ET on heart rate was also seen during reperfusion. In terms of percent recovery of heart function following ischemia, FR continued to affect aortic flow, and we observed an interaction between FR and ET on aortic flow. Our results clearly indicate that the myocardium from the FR animal or the FR, exercise-trained rat is more resistant to ischemia.