Erythrocytes (RBC) from untrained male Wistar rats and rat glomerular endothelial cells (EC) were used to investigate the effects of acute exercise (speed: 20 m/min, slope: 0, duration: 1 hour) on RBC membrane protein oxidation and adhesion to cultured EC. Experimental animals were divided into juvenile (age 10 weeks) and adult (age 30 weeks) groups for these studies. Immediately following exercise, juvenile rat RBC membrane protein oxidation was significantly enhanced. Adult rat RBC showed significantly higher basal protein oxidation than juvenile RBC; but the level of adult rat RBC membrane protein oxidation was unaffected by exercise. Prior to exercise, adult rat RBC showed significantly higher adhesion to EC than RBC of juvenile rat. There was no difference in plasma fibronectin or fibrinogen levels following exercise. Only juvenile rat RBC showed a significant decrease in sialic acid residue content following exercise. These experiments show that there are changes in RBC-EC interactions following exercise that are influenced by animal age.
a1_The effect of different muscle shortening velocity was studied during cycling at a pedalling rate of 60 and 120 rev.min-1 on the [K+]v in 21 healthy young men (aged 22.5±2.2 years, body mass 72.7±6.4 kg, VO2max 3.720±0.426 l . min-1) performing an incremental exercise test until exhaustion. The power output increased by 30 W every 3 min, using an electrically controlled ergometer Ergoline 800S (see Zoladz et al. J. Physiol. 488: 211-217, 1995). The test was performed twice: once at a cycling frequency of 60 rev.min-1 (test A) and a few days later at frequency of 120 rev.min-1 (test B). At rest and at the end of each step (i.e. the last 15 s) antecubital venous blood samples for [K+]v were taken. Gas exchange variables were measured continuously (breath-by-breath) using Oxycon Champion Jaeger. The pre-exercise [K+]v in both tests was not significantly different amounting to 4.24±0.36 mmol.l-1 in test A, and 4.37±0.45 mmol.l-1 in test B. However, the [K+]v during cycling at 120 rev.min-1 was significantly higher (p<0.001, ANOVA for repeated measurements) at each power output when compared to cycling at 60 rev.min-1. The maximal power output reached 293±31 W in test A which was significantly higher (p<0.001) than in test B, which amounted to 223±40 W. The VO2max values in both tests reached 3.720±0.426 l.min-1 vs 3.777±0.514 l.min-1. These values were not significantly different. When the [K+]v was measured during incremental cycling exercise, a linear increase in [K+]v was observed in both tests. However, a significant (p<0.05) upward shift in the [K+]v and a % VO2max relationship was detected during cycling at 120 rev.min-1. The [K+]v measured at the VO2max level in tests A and B amounted to 6.00±0.47 mmol.l-1 vs 6.04±0.41 mmol.l-1, respectively., a2_This difference was not significant. It can thus be concluded that a) generation of the same external mechanical power output during cycling at a pedaling rate of 120 rev.min-1 causes significantly higher [K+]v changes than when cycling at 60 rev.min-1, b) the increase of venous plasma potassium concentration during dynamic incremental exercise is linearly related to the metabolic cost of work expressed by the percentage of VO2max (increase as reported previously by Vollestad et al. J. Physiol. Lond. 475: 359-368, 1994), c) there is a tendency towards upward shift in the [K+]v and % VO2max relation during cycling at 120 rev.min-1 when compared to cycling at 60 rev.min-1., J. A. Zoladz, K. Duda, J. Majerczak, P. Thor., and Obsahuje bibliografii
The purpose of this study was to investigate the validity of non-invasive lactate threshold estimation using ventilatory and pulmonary gas exchange indices under condition of acute hypoxia. Seven untrained males (21.41.2 years) performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and other breathing 12 % O2. The lactate threshold was estimated using the following parameters: increase of ventilatory equivalent for O2 (VE/VO2) without increase of ventilatory equivalent for CO2 (VE/VCO2). It was also determined from the increase in blood lactate and decrease in standard bicarbonate. The VE/VO2 and lactate increase methods yielded the respective values for lactate threshold: 1.910.10 l/min (for the VE/VO2) vs. 1.890.1 l/min (for the lactate). However, in hypoxic condition, VE/VO2 started to increase prior to the actual threshold as determined from blood lactate response: 1.670.1 l/min (for the lactate) vs. 1.370.09 l/min (for the VE/VO2) (P=0.0001), i.e. resulted in pseudo-threshold behavior. In conclusion, the ventilatory and gas exchange indices provide an accurate lactate threshold. Although the potential for pseudo-threshold behavior of the standard ventilatory and gas exchange indices of the lactate threshold must be concerned if an incremental test is performed under hypoxic conditions in which carotid body chemosensitivity is increased.
We investigated the effects of different weight loss protocols on leptin levels in obese females with the aim of addressing the leptin resistance which has been found to be an aggravating factor in obesity. Twenty-four obese females enrolled to one of three 12-week weight loss protocols: orlistat-induced weight loss (OWL, n=8), exercise-induced weight loss (EWL, n=8) and orlistat plus exercise-induced weight loss (OEWL, n=8). Serum leptin levels were measured in duplicate by radioimmunoassay. There were significant reductions (P<0.01) in body weight and fat mass after the 12 week period in all groups: -11.4±0.5 kg and -9.8
±0.5 kg (OEWL), -8.3±0.8 kg and -5.7±0.9 kg (OWL), -8.9±1.2 kg and -7.4±1.2 kg (EWL), respectively. Serum leptin levels were also decreased markedly in all groups: -59.2 %(OEWL1), -37.8 % (OWL) and -48.6 % (EWL) (P<0.01 all). In addition, there were marked decreases in leptin levels for each kilogram of fat mass after the 12 week period: -48.2
±7.2 % (OEWL), -27.8±4.8 % (OWL) and -39.3±4.3% (EWL) (P<0.01 all). Decreases in serum leptin levels expressed per kilogram of fat mass were significantly higher in the OEWL group compared to the OWL group (P=0.03). Consequently, an exercise training program in adjunct to
pharmacotherapy provides higher weight reduction and fat mass loss in obesity treatment. It also seems to have further beneficial effects on leptin re
sistance, as indicated by decreases in leptin levels expressed per kilogram of fat mass.
The relationships between exercise and metabolites as well as between exercise and sarcoplasmic reticulum function were studied in gastrocnemius muscle of ovariectomized-trained rats. Prolonged moderate-intensity exercise, treadmill up-hill run for 90 min with a 10° incline, decreased the muscle glycogen content. Exercise until exhaustion further lowered the glycogen concentration to 13 % of the control, together with a significant decrease of ATP and glucose-6-phosphate concentrations. Also, Ag+-induced Ca2+release, measured in whole muscle homogenate, showed a 30 % reduction on exhaustion, while Ca2+ uptake was unaffected by this exercise. ATPase activities, of both homogenate and SR vesicles, and Ca2+ transport in the latter preparation were not altered on exhaustion. It could be concluded from these results that muscular fatigue in ovariectomized rats after aerobic exercise is caused by the change in energy supply and Ca2+ release from the SR, this latter possibly due to metabolites generated by the exercise., I. Gigli, L. E. Bussmann., and Obsahuje bibliografii
The effect of exercise on oxidant stress and on alterations in antioxidant defense in elderly has been investigated extensively. However, the impact of regularly performed long-term physical activity starting from adulthood and prolonged up to the old age is not yet clear. We have investigated the changes in the activities of antioxidant enzymes – superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) – and lipid peroxidation in various tissues of rats which had performed (old-trained) or had not performed (old-control) regular swimming exercise for one year. These animals were compared with young-sedentary rats. Increased lipid peroxidation was observed with ageing in all tissues (heart, liver, kidney, striated muscle) and swimming had no additional effect on this elevation of lipid peroxidation. Heart and striated muscle SOD activites, and striated muscle CAT activity increased as a consequence of ageing, whereas kidney and liver CAT activities, as well as GPx activities in kidney, liver, lung and heart were significantly decreased compared to young controls. Lung and heart SOD, liver CAT activities as well as GPx activities in liver, lung and heart were increased significantly in rats which performed exercise during ageing, compared to the old-control group. These findings suggest that lifelong exercise can improve the antioxidant defense in many tissues without constituting any additional oxidant stress.
The purpose of the present study was to investigate the effect of short-term endurance training on plasma total antioxidant status (TAS) and on in vitro platelet aggregation and ATP release. Blood samples were collected from the abdominal aorta of rats following short-term treadmill exercise (25 m/min, 0 % grade, 30 min) for three consecutive days, as well as in non-exercised control group. Platelet aggregation and platelet ATP release were evaluated by impedance and bioluminescence techniques, respectively. Plasma TAS was measured spectrophotometrically. Plasma TAS was higher and ADP-induced platelet ATP release was lower in the short-term training group with respect to the control group (p<0.001). Significant negative correlation (r = -0.56, p<0.05) was found between plasma TAS and ADP-induced platelet ATP release. Neither ADP- and collagen-induced maximum aggregation rate nor collagen-induced platelet ATP release were significantly different between the groups. According to these results, short-term training caused an alteration in platelet functions limited to the secretion response, which may be related to the oxidant/antioxidant balance changes favoring the antioxidants. The improved plasma total antioxidant capacity was possibly sufficient to prevent exercise-induced oxidative damage, and the adaptive response of platelets might be associated with enhanced antioxidant status.