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An increase in oxidative stress and decrease in antioxidant enzymes have been suggested to be involved in the pathophysiology of myocardial infarction (MI). In this study in rats, treadmill exercise training and losartan treatment began 1 week post-myocardial infarction (MI) and lasted 8 weeks. We evaluated the changes in the mRNA and protein expressions for the enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase after exercise and losartan treatment post-MI. Our results demonstrated that GPx and catalase mRNA levels were comparable among all the groups, while the mRNA level for manganese SOD (MnSOD) was significantly increased in exercise training with/without losartan treatment compared with the sedentary post-MI group. Moreover, the mRNA level for gp91(phox) was dramatically decreased by a combination of exercise and losartan treatment. The protein levels for MnSOD were significantly elevated by exercise training in combination with losartan treatment. The protein levels for catalase were significantly increased in response to exercise, and further augmented by exercise together with losartan treatment. Thiobarbituric acid-reactive substances in plasma were significantly increased in the post-MI rats, but were decreased by exercise or losartan treatment, indicating that both exercise and losartan may reduce lipid oxidative damage. In addition, catalase and SOD enzymatic activities were significantly enhanced by exercise combined with losartan treatment. Our results suggest that exercise training improves catalase and MnSOD expression and attenuates oxidative stress. These effects are potentiated when combining exercise with angiotensin II receptor blockade.

We examined the effect of exercise on postprandial hypertriglyceridemia (PHTG) and insulin resistance in individuals with metabolic syndrome. Subjects were 10 hypertriglyceridemic men with insulin resistance [age = 35.0 ± 1.8 yr, body weight = 90.7 ± 3.3 kg, fasting triglyceride (TG) = 2.6 ± 0.4 mmol/l, peak oxygen consumption (V̇o2peak) = 36.0 ± 1.3 ml−1·kg−1·min−1, and homeostatic model assessment of insulin resistance (HOMA-IR)= 3.1 ± 0.3]. Each participant performed a control trial (Ctr; no exercise) and three exercise trials at 60% of their V̇o2peakfor 30 min (30 min-Ex), 45 min (45 min-Ex) and 60 min (60 min-Ex). All subjects had a fat meal in each trial. In the exercise trials, the subject jogged on a treadmill for a designated duration of 12 h before ingestion of a fat meal. Blood samples were taken at 0 h (before the meal) and at 2, 4, 6, and 8 h after the meal. The plasma TG, area score under TG concentration curve over an 8-h period (TG AUC) after the meal, and HOMA-IR were analyzed. The TG AUC scores in both the 45 min-Ex and 60 min-Ex were 31 and 33% lower, respectively, than Ctr ( P < 0.02). There were no significant differences in TG AUC scores between the 30 min-Ex and the Ctr ( P > 0.05). There were no trial differences in the fasting plasma glucose concentration ( P > 0.05). HOMA-IR values in the 30 min-Ex, 45 min-Ex, and 60 min-Ex trials were lower than the Ctr ( P < 0.03), but no significant differences were found in HOMA-IR among the exercise trials. The results suggest that for physically inactive individuals with metabolic syndrome, exercising at moderate intensity for 45 min effectively attenuates PHTG while exercise for 30 min is sufficient to improve insulin action.

We examined the effect of exercise on postprandial lipemia (PPL) and insulin resistance in individuals with metabolic syndrome. Subjects were 10 hypertriglyceridemia (HTG) males with insulin resistance [age = 40.1 +/- 2.2 years, body weight = 96.3 +/- 3.3 kg, fasting triglyceride (TG) = 263 +/- 25 mg/dl, VO(2)max = 37 +/- 1.1 ml/kg/min, and Homeostatic Model Assessment (HOMA-IR, an index of insulin resistance) = 3.05 +/- 0.40]. Each subject performed a control trial (Ctr, no exercise), and three exercise trials at 40% (40%T), 60% (60%T), and 70% (70%T) of their VO(2)max. The order of trials was randomized and there were 1-2 weeks wash-out period between the trials. All subjects had a fat-meal in each trial. In the exercise trials, subjects jogged on a treadmill for 1 h at a designated intensity 12 h prior to a fat-meal ingestion. Blood samples were taken at 0 h (before the meal), and 2, 4, 6, and 8 h after the meal. The plasma TG, area score under TG concentration curve for over an 8 h-period (TG AUC) after the meal, and HOMA-IR were analyzed. The TG AUC score in 40%T was 30% lower (P = 0.003), 60%T was 31% lower (P = 0.02), and 70%T was 39% lower (P = 0.02) than Ctr. There were no significant differences in the TG AUC scores among the exercise trials (P > 0.05). The insulin concentrations in both 60 and 70%T were lower than Ctr (P < 0.01) which did not differ from 40%T. HOMA-IR in both 60%T (P = 0.041) and 70%T (P = 0.002) were lower than Ctr, but not different from 40%T (HOMA-IR: Ctr = 3.05 +/- 0.40, 40%T = 2.67 +/- 0.35, 60%T = 2.49 +/- 0.31, 70%T = 2.21 +/- 0.27). The results suggest that for physically inactive individuals with metabolic syndrome, exercising at low to moderate intensity may be sufficient to attenuate PPL and increase insulin sensitivity, whereas higher intensity exercise may be needed to normalize blood glucose.

We studied c-Fos staining in adult male rats after 48 h of water deprivation and after 46 h of water deprivation with 2 h of access to water or physiological saline. Controls were allowed ad libitum access to water and physiological saline. For immunocytochemistry, anesthetized rats were perfused with a commercially available antibody for c-Fos. Dehydration significantly increased plasma vasopressin (AVP), osmolality, plasma renin activity (PRA), hematocrit, and sodium concentration and decreased urinary volume. Fos staining was significantly increased in the median preoptic nucleus, organum vasculosum of the lamina terminalis, supraoptic nucleus (SON), and magnocellular and parvocellular paraventricular nucleus (PVN), as well as the area postrema, nucleus of the solitary tract (NTS), and rostral ventrolateral medulla (RVL). Rehydration with water significantly decreased AVP levels and Fos staining in the SON, PVN, and RVL and significantly increased Fos expression in the perinuclear zone of the SON, NTS, and parabrachial nucleus. Rehydration with water was associated with decreased urinary sodium concentration and hypotonicity, and hematocrit and PRA were comparable to levels seen after dehydration. After rehydration with saline, plasma osmolality, hematocrit, and PRA were not different from control, but plasma AVP and urinary sodium concentration were increased. In the SON, Fos staining was significantly increased, with a great percentage of the Fos cells also stained for oxytocin compared with water deprivation. Changes in Fos staining were also observed in the NTS, RVL, parabrachial nucleus, and PVN. Rehydration with water or saline produces differential effects on plasma AVP, Fos staining, and sodium concentration.

We investigated the effect of exercise timing on attenuation of postprandial hyper-triglyceridemia (PHTG) in individuals with hypertriglyceridemia (HTG). Subjects were 10 males (TG = 290.1 ± 28.5 mg/dl). Each subject performed a control trial (Ctr), 12-hr premeal exercise trial (12-hr Pre), and 24-hr premeal exercise trial (24-hr Pre). In each trial, subjects had a fat-rich meal. In the exercise trials they jogged on a treadmill at 60% of their [Formula: see text] for 1 hr at a designated time. Blood samples were taken at 0 (immediately before the fat meal), and at 2, 4, 6, 8, and 24 hrs after the meal. The results indicated that plasma TG concentrations in 12-hr Pre were lower than in Ctr and 24-hr Pre (p 2-Ch. These results suggest that exercising 12 hrs prior to a fat-meal intake significantly reduces PHTG response whereas exercising 24 hrs prior to the meal does not attenuate PHTG in hypertriglyceridemic men. The effect of an acute exercise bout on PHTG lowering may be short-lived and diminished by 24 hrs. Key words: high-density lipoprotein cholesterol, triglyceride, lipoprotein lipase, insulin