Hypertension alters phosphorylation of VASP in brain endothelial cells.

Hypertension impairs cerebral vascular function. Vasodilator-stimulated phosphoprotein (VASP) mediates active reorganization of the cytoskeleton via membrane ruffling, aggregation and tethering of actin filaments. VASP regulation of endothelial barrier function has been demonstrated by studies using VASP(-/-) animals under conditions associated with tissue hypoxia. We hypothesize that hypertension regulates VASP expression and/or phosphorylation in endothelial cells, thereby contributing to dysfunction in the cerebral vasculature. Because exercise has direct and indirect salutary effects on vascular systems that have been damaged by hypertension, we also investigated the effect of exercise on maintenance of VASP expression and/or phosphorylation. We used immunohistochemistry, Western blotting and immunocytochemistry to examine the effect of hypertension on VASP expression and phosphorylation in brain endothelial cells in normotensive [Wistar-Kyoto (WKY)] and spontaneously hypertensive (SH) rats under normal and exercise conditions. In addition, we analyzed VASP regulation in normoxia- and hypoxia-induced endothelial cells. Brain endothelial cells exhibited significantly lower VASP immunoreactivity and phosphorylation at the Ser157 residue in SHR versus WKY rats. Exercise reversed hypertension-induced alterations in VASP phosphorylation. Western blotting and immunocytochemistry indicated reduction in VASP phosphorylation in hypoxic versus normoxic endothelial cells. These results suggest that diminished VASP expression and/or Ser157 phosphorylation mediates endothelial changes associated with hypertension and exercise may normalize these changes, at least in part, by restoring VASP phosphorylation.

Nitric oxide generated by red blood cells following exposure to shear stress dilates isolated small mesenteric arteries under hypoxic conditions.

Red blood cells (RBC) possess a functional nitric oxide synthase (NOS) enzyme located in the cell membrane and cytoplasm. It has previously been observed that shear stress acting on RBC activates NOS and causes enhanced NO export. The aim of the present study was to investigate the physiological importance (e.g., in local blood flow regulation) of RBC-derived NO stimulated by application of shear stress. Blood samples and arterial vessel segments were obtained from Wistar rats; RBC suspensions were adjusted to a hematocrit of 0.1 l/l using Krebs solution. In order to apply shear stress to the RBC suspensions they were continuously flowed through a small-bore glass tube for 20 minutes at a wall shear stress of 2 Pa. The RBC suspensions were then perfused through endothelium denuded small mesenteric arteries having a diameter of ~300 µm under both high oxygen (PO2 ~130 mmHg) and hypoxic conditions. Perfusion of vessel segments with sheared RBC suspensions caused a significant dilation response under hypoxic conditions but not at high oxygen levels. Incubation of RBC suspensions with the non-specific NOS inhibitor L-NAME (10-3 M) prior to shear stress application abolished this dilation response. Our results indicate that NO released from RBC due to shear stress activation of NOS results in vasodilation of vessel segments under hypoxic conditions, and strongly suggest that NO originating from RBC may have a functional role in local blood flow regulation.

The effect of exercise training on the responsiveness of renal resistance arteries in rats.

Blood flow to several tissues changes during an acute bout of exercise. The kidney is one of the organs that are most affected by exercise-induced blood redistribution. The aim of the present study was to investigate possible exercise-induced vascular reactivity changes in renal resistance arteries in rats. Renal resistance arteries were isolated from rats that underwent 8 weeks of swimming and sedentary control rats, and the arteries were evaluated using wire myography. Similar dilation responses to acetylcholine, bradykinin, adenosine, isoproterenol, and sodium nitroprusside were observed in both groups. The vasoconstrictive agents vasopressin, endothelin-1, potassium chloride, and thromboxane A(2) also induced similar responses in both groups; however, the trained group had an increased constrictive response to norepinephrine compared to the control rats. The results of our study show that renal resistance arteries of trained rats behave differently than conduit-type renal arteries and exhibit an increased contractile response to sympathetic agonists. This finding provides supporting evidence that renal blood flow markedly decreases during exercise in trained individuals.

Gastric perforation after corrosive ingestion.

PURPOSE: To describe a series of children with gastric perforation (GP) after corrosive ingestion. METHODS: Case notes of children treated for GP complicating corrosive ingestion between May 2001 and April 2010 were retrospectively reviewed. RESULTS: Seventy-six children with corrosive ingestion were treated during the study period of which 5 (6.6%) developed GP. This complication was evident on admission in one case and developed within 48 h in the others. The major clinical findings were abdominal pain, tenderness, and distension with radiologic evidence of pneumoperitoneum. Associated pathology included necrosis of the abdominal esophagus in one case and duodenal perforation in another. Two cases have died during surgery while three survived with free of complications related to GP repair. Two patients developed gastric outlet obstruction (one with an esophageal stricture) on follow-up. CONCLUSIONS: GP is a rare but major complication of corrosive ingestion. Children who swallow corrosives should be closely monitored and pediatric surgeons should be aware of this potential early complication. The possibility of associated pathology should be considered when undertaking surgical repair.

Vascular dilation responses of rat small mesenteric arteries at high intravascular pressure in spontaneously hypertensive rats.

BACKGROUND: Hypertension is associated with remodeling and mechanical alterations of resistance arteries. Numerous studies have investigated the mechanical and morphometric properties of small arteries obtained from hypertensive animals and humans. However, the functional properties of resistance arteries from normotensive and hypertensive subjects have only been examined under normotensive conditions. The objective of the present study was to evaluate the dilation responses of small mesenteric arteries (SMA) from spontaneously hypertensive rats (SHR) at various levels of intraluminal pressure. METHODS AND RESULTS: SMA segments from Wistar Kyoto (WKY) rats and SHR were pressurized using pressure myography. Endothelium-dependent and -independent dilation responses of the SMA were examined under 3 different intravascular pressures (50, 80 and 120 mmHg). Endothelium-dependent dilation was evaluated by measuring vasodilator responses to increasing doses of acetylcholine or increases in intraluminal flow rate. Endothelium-independent vasodilator function was examined by using sodium nitroprusside. The results indicate that both endothelium-dependent and -independent dilation responses of SMA from WKY progressively decrease with increased intravascular pressure. In contrast, all dilatation responses of the SMA from SHR were enhanced at higher intraluminal pressures. CONCLUSIONS: These findings of differential sensitivity to luminal pressure should be considered during in vitro examination of vessels from normotensive and hypertensive subjects.

Effect of exercise training on resistance arteries in rats with chronic NOS inhibition.

Regular exercise has blood pressure-lowering effects, as shown in different types of experimental hypertension models in rats, including the nitric oxide synthase (NOS) inhibition model. We aimed to investigate possible mechanisms implicated in the exercise effect by evaluating the vasoreactivity of resistance arteries. Exercise effects on agonist-induced vasodilatory responses and flow-mediated dilation were evaluated in vessel segments of the rat chronic NOS inhibition model. Normotensive and hypertensive rats were subjected to swimming exercise (1 h/day, 5 days/wk, 6 wk), while rats in other sedentary and hypertensive groups did not. Hypertension was induced by oral administration of the nonselective NOS inhibitor l-NAME (25 mg/kg day) for 6 wk. Systolic blood pressure, as measured by the tail-cuff method, was significantly decreased by the training protocol in exercising hypertensive rats. The vasoreactivity of resistance arteries was evaluated by both wire and pressure myography studies. An impaired nitric oxide-mediated relaxation pathway in untrained hypertensive rats led to decreased relaxation responses in vessels with intact endothelium. Exercise training significantly improved the responses to acetylcholine and flow-mediated dilation in exercise-trained hypertensive rats in parallel with a decrease in blood pressure. On the other hand contraction (norepinephrine and KCl) and relaxation (sodium nitroprusside) responses of vascular smooth muscle were not different between the groups. Vascular endothelial NOS protein expression was found to be increased in both exercising groups. In conclusion, these results revealed evidence of an increased role of the nitric oxide-dependent relaxation pathway in exercising hypertensive rats.

[E-learning and problem based learning integration in cardiology education]. / Kardiyoloji egitiminde e-ögrenme ve probleme dayali ögrenme entegrasyonu.

OBJECTIVE: The aim of this study was to determine students' satisfaction with an e-learning environment which is developed to support classical problem-based learning (PBL) in medical education and its effect on academic achievement. METHODS: In this cross-sectional study, students were provided with a web-based learning environment including learning materials related to objectives of the subject of PBL module, which could be used during independent study period. The study group comprised of all of the second year students (164 students) of Akdeniz University, Medical Faculty, during 2007-2008 education period. In order to gather data about students' satisfaction with learning environment, a questionnaire was administered to the students. Comparison of students' academic achievement was based on their performance score in PBL exam. Statistical analyses were performed using unpaired t test and Mann Whitney U test. RESULTS: Findings indicated that 72.6% of the students used e-learning practice. There is no statistically significant difference between mean PBL performance scores of users and non-users of e-learning practice (103.58 vs. 100.88) (t=-0.998, p=0.320). It is found that frequent users of e-learning application had statistically significant higher scores than non-frequent users (106.28 vs. 100.59) (t=-2.373, p=0.01). In addition, 72.6% of the students declared they were satisfied with the application. CONCLUSION: Our study demonstrated that the most of the students use e-learning application and are satisfied with it. In addition, it is observed that e-learning application positively affects the academic achievement of the students. This study gains special importance by providing contribution to limited literature in the area of instructional technology in PBL and Cardiology teaching.

Exercise training reverses age-related decrements in endothelium-dependent dilation in skeletal muscle feed arteries.

We tested two hypotheses, first that exercise training reverses age-related decrements in endothelium-dependent dilation in soleus muscle feed arteries and second that this improved endothelium-dependent dilation is the result of increased nitric oxide (NO) bioavailability due to increased content and phosphorylation of endothelial NO synthase (eNOS) and/or increased antioxidant enzyme content. Young (2 mo) and old (22 mo) male Fischer 344 rats were exercise trained (Ex) or remained sedentary (Sed) for 10-12 wk, yielding four groups of rats: 1) young Sed (4-5 mo), 2) young Ex (4-5 mo), 3) old Sed (24-25 mo), and 4) old Ex (24-25 mo). Soleus muscle feed arteries (SFA) were isolated and cannulated with two glass micropipettes for examination of endothelium-dependent (ACh) and endothelium-independent [sodium nitroprusside (SNP)] vasodilator function. To determine the mechanism(s) by which exercise affected dilator responses, ACh-induced dilation was assessed in the presence of N(omega)-nitro-l-arginine (l-NNA; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), and l-NNA + Indo. Results indicated that ACh-induced dilation was blunted in old Sed SFA relative to young Sed SFA. Exercise training improved ACh-induced dilation in old SFA such that vasodilator responses in old Ex SFA were similar to young Sed and young Ex SFA. Addition of l-NNA, or l-NNA + Indo, abolished the exercise effect. Immunoblot analysis revealed that extracellular superoxide dismutase (SOD) protein content was increased by training in old SFA, whereas eNOS and SOD-1 protein content were not altered. Addition of exogenous SOD, or SOD + catalase, improved ACh-induced dilation in old Sed SFA such that vasodilator responses were similar to young Sed SFA. Addition of l-NNA abolished the effect of exogenous SOD in old Sed arteries. Collectively, these results indicate that exercise training reverses age-induced endothelial dysfunction in SFA by increasing NO bioavailability and that increases in vascular antioxidant capacity may play an integral role in the improvement in endothelial function.

Potential sources of oxidative stress that induce postexercise proteinuria in rats.

Exercise-induced proteinuria is a common consequence of physical activity and is caused predominantly by alterations in renal hemodynamics. Although it has been shown that exercise-induced oxidative stress can also contribute to the occurrence of postexercise proteinuria, the sources of reactive oxygen species that promote it are unknown. We investigated the enzymes nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase (XO) as possible sources of oxidative stress in postexercise proteinuria. First, we evaluated the effect of blocking the NADPH oxidase enzyme on postexercise proteinuria. We found a significant increase in urinary protein level, kidney thiobarbituric acid-reactive substances (TBARS), and protein carbonyl content after exhaustive exercise, and NADPH oxidase activity was induced by exercise. Rats that were treated with an NADPH oxidase inhibitor for 4 days before exhaustive exercise showed no increase in kidney TBARS or protein carbonyl derivative level and no proteinuria or NADPH oxidase activation. In the next set of experiments, we investigated the effect of XO blockage on postexercise proteinuria. Oxypurinol, an XO inhibitor was administered to rats for 3 days before exercise. Although XO inhibition significantly decreased kidney TBARS levels and protein carbonyl content in exercised rats, the inhibition did not prevent exercise-induced proteinuria. However, plasma and kidney XO activity was not induced by exercise, but rather it was suppressed under oxypurinol treatment. These results suggest that increased NADPH oxidase activity induced by exhaustive exercise is an important source of elevated oxidative, stress during exercise, which contributes to the occurrence of postexercise proteinuria.

High intravascular pressure attenuates vascular dilation responses of small mesenteric arteries in the rat.

BACKGROUND: Alterations in intravascular pressure can affect vascular function and the morphological properties of arteries. Although it has been shown that a transient elevation of blood pressure impairs endothelium-dependent dilation in small arteries, the vascular dilation responses during high intravascular pressure have not yet been investigated. METHODS AND RESULTS: Using pressure myography, the endothelium-dependent and -independent dilation responses of small mesenteric arteries of rats were examined under 3 different intravascular pressure conditions (50, 80 and 120 mmHg). Endothelium-dependent dilation was evaluated by measuring vasodilator responses to increasing doses of acetylcholine (ACh, 10(-9) to 10(-4) mol/L) or increases in intraluminal flow (7-36 microl/min). Endothelium-independent vasodilator function was examined by using sodium nitroprusside (SNP, 10(-9) to 10(-4) mol/L). Flow-mediated dilation was significantly attenuated at 120 mmHg whereas ACh-induced dilation was progressively decreased with increases in intravascular pressure (at 80 and 120 mmHg). Significant attenuation in the vasodilator response to SNP was also observed at 80 and 120 mmHg. CONCLUSION: Endothelium-dependent and-independent dilation responses are progressively attenuated with acute increases in intravascular pressure.

Biphasic pattern of exercise-induced proteinuria in sedentary and trained men.

BACKGROUND/AIMS: Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. Oxidant stress has been proposed as one of different factors involved in postexercise proteinuria in rats. In this study we investigated whether reactive oxygen radicals generated during exercise play a role in exercise-induced proteinuria in sedentary and trained men. METHODS: The validity of oxidant stress following stepwise maximal exercise on proteinuria was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 months. While protein carbonyl content in serum and thiobarbituric acid reactive substances (TBARS) in erythrocytes and urine were used as oxidant stress markers, total protein, albumin, beta(2)-microglobulin in urine were assayed for proteinuria in five consecutive specimens after exercise. Urines were collected before exercise, then 30 min, 2, 8 and 24 h postexercise. RESULTS: Increased urinary protein levels and mixed type proteinuria were determined after 30 min of exercise in sedentary and trained subjects. Proteinuria was normalized at 2 and 8 h specimens. However, glomerular type proteinuria was identified at 24 h specimen in both groups. Oxidant stress markers were significantly elevated in sedentary and trained subjects. Antioxidant treatment prevented the increase in oxidant stress markers, urinary protein levels and the occurrence of glomerular type proteinuria after exhaustive exercise at 24 h in both groups. CONCLUSIONS: These findings suggest that the exercise-induced oxidant stress may contribute to exercise-induced proteinuria in sedentary and trained men.

Physical training increases renal injury in rats with chronic NOS inhibition.

Nitric oxide (NO) is involved in regulation of vascular tone and renal hemodynamics. Inhibition of NO synthase (NOS) by Nomega-nitro-L-arginine methyl ester (L-NAME) promotes systemic hypertension and glomerular damage. Exercise is effective in reducing elevated blood pressure in hypertensive individuals and rats treated with L-NAME. We investigated the effects of regular aerobic exercise on renal injury in hypertensive rats with NOS inhibition. Adult Wistar rats were divided into four groups: sedentary or exercising, nonhypertensive (two groups) and hypertensive, sedentary or exercising (two groups). Treadmill running exercise was prolonged for 4 weeks (60 min.day(-1), 5 days/week, 20 m.min(-1), no incline), and hypertension was induced by L-NAME given orally to rats for 4 weeks (25 mg.kg(-1).day(-1) in drinking water). Blood pressure was monitored at baseline and then once a week throughout L-NAME administration. Kidney sections were examined for renal histopathology. Hypertensive animals exhibited elevated blood pressure, and exercise partly prevented this elevation. Renal injury observed as arteriolar wall thickening, focal tubular atrophy, and interstitial inflammatory infiltration was apparent in hypertensive animals, and exercise induced further renal damage in hypertensive animals. The present training protocol exacerbates renal insufficiency in NOS-blockage hypertension in rats.

Exercise-induced oxidative stress leads hemolysis in sedentary but not trained humans.

Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans.

Effect of antioxidant vitamin treatment on the time course of hematological and hemorheological alterations after an exhausting exercise episode in human subjects.

This study examined the effects of a 2-mo antioxidant vitamin treatment on acute hematological and hemorheological alterations induced by exhausting exercise; both sedentary and trained individuals were employed. Eighteen young male, human subjects (9 sedentary, 9 trained by regular exercise) participated in the study and performed an initial maximal aerobic cycle ergometer exercise with frequent blood sampling over a 24-h period and analysis of hematological and hemorheological parameters. All subjects were treated with an antioxidant vitamin A, C, and E regimen, supplemented orally for 2 mo, and then subjected to a second exercise test and blood sampling at the end of this period. In the sedentary group during the first testing period (before vitamin treatment), white blood cell counts and granulocyte percentages were increased at 2 h after the exercise test and remained elevated for 4-12 h. Red blood cell (RBC) deformability and aggregation were also altered by exercise in the sedentary group before vitamin treatment. However, none of these parameters in the sedentary group were altered by exercise after the 2-mo period of antioxidant vitamin treatment. With the exception of a transient rise in granulocyte percentage, these parameters were also not affected in the trained subjects before the vitamin treatment. Significant increases of RBC lipid peroxidation observed 12 h after the exercise test in both sedentary and trained subjects were also totally prevented by vitamin treatment. Our results indicate that antioxidant vitamin treatment is effective in preventing the inflammation-like response and coincident adverse hemorheological changes after an episode of exhausting exercise, and suggest that such changes may be related to exercise-induced death events.

Levels of zinc and magnesium in senile and diabetic senile cataractous lenses.

Zinc and magnesium in serum, hair, and lens were determined in diabetic and nondiabetic patients who have been operated because of senile cataract. Both trace elements were measured by atomic absorption spectrometry, after acidic digestion of the lens and hair samples. Although there was no difference in serum, lens, and hair levels of magnesium between the two groups, the lens levels of zinc in diabetic patients (0.56+/-0.05 micromol/g dry weight) were significantly higher as compared with nondiabetic group (0.42+/-0.03 micromol/g dry weight). There was no statistically significant difference in serum and hair levels of zinc between the groups. The increased concentration of zinc in the lens of diabetic patients suggests that zinc might play a role in developmental mechanism of the diabetic senile cataract.

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.

Effect of nitric oxide on exercise-induced proteinuria in rats.

Temporary proteinuria occurring after exercise is a common finding, and it is explained predominantly by alterations in renal hemodynamics. In this study, we investigated whether nitric oxide (NO), which is known to have an effect on renal hemodynamics and to increase during exercise, has a role in postexercise proteinuria. In the first step of this study, the effect of acute NO synthase blockage on exercise proteinuria was evaluated. The urinary protein levels in animals that performed acute exhaustive treadmill running exercise were considerably elevated compared with the control animals. Significantly elevated urinary protein levels were also detected in animals that received Nomega-nitro-L-arginine methyl ester before exhaustion, compared with both control and exhausted groups, and mixed-type proteinuria was detected in electrophoresis, as in all exhausted animals. In the second step of the study, a NO donor (isosorbide mononitrate) was given to rats 1 h before exhaustive exercise. Mixed-type proteinuria and the elevation in urinary protein levels that occur as a consequence of exhaustive exercise were prevented by NO donor treatment. Finally, in the third step of our study, a calcium channel blocker (diltiazem), another vasodilator, was applied to the rats 1 h before exhaustive exercise. Urinary protein levels were not different in exhausted rats with or without calcium channel blocker treatment. On the other hand, in both groups, urinary protein levels were higher than in the control group. The tail-cuff blood pressure alterations caused by vasodilator drug applications before exercise were not different for NO donor and calcium channel blocker groups. These results suggest that endogenous NO might prevent the postexercise proteinuria from becoming more severe by affecting hemodynamic changes that occur during exercise.

Effect of long-term swimming exercise on zinc, magnesium, and copper distribution in aged rats.

Trace element content of different tissues might be altered by both age and exercise training. We aimed to determine the effects of a 1-yr swimming protocol (60 min/d, 5 day/wk) on tissue levels and the distribution of zinc (Zn), magnesium (Mg), and copper (Cu) in aging rats. Three groups were formed: sedentary and trained old groups and a young control group. Tissue Zn, Mg, and Cu concentrations were measured in the kidney, heart, liver, lungs, and gastrocnemius and soleus muscles. Kidney zinc concentration significantly decreased in the sedentary old group compared to the young control group (p<0.01) and was significantly higher in the trained old group compared to the sedentary old group (p<0.01), whereas Zn levels in the soleus muscle significantly increased in the sedentary old group in comparison to young controls (p<0.05). Tissue Mg concentrations remained unchanged. The sedentary old group exhibited a significant decrease in kidney Cu concentration compared to the young control group (p<0.01). Although kidney Cu levels also decreased in trained old rats in comparison to young controls (p<0.05), they were significantly higher than in sedentary old rats (p<0.01). The decrease in kidney Zn and Cu content as a result of aging was partly prevented by long-term swimming exercise.