Acute Exhaustive Exercise Research Articles

The study of the differential expression of rats’ skeletal muscle proteome after acute high‐intensity exhaustive exercise

The study of the differential expression of rats’ skeletal muscle proteome after acute high‐intensity exhaustive exercise

Effect of maximal exercise on the short-term kinetics of zinc metabolism in sedentary men

Objective: To examine the effect of acute exhaustive exercise versus rest on short-term zinc kinetics in men. Design: Crossover design, wherein all subjects were their own control. Setting: University setting,...

Effects of acute exhaustive physical exercise upon glutamine metabolism of lymphocytes from trained rats

Transitory immunosupression is reported after intense exercise, especially after an increase in training overload and in overtraining. The influence of intense exercise on plasma hormones and glutamine concentration may contribute to this effect. However, the effect of such exercise-induced changes upon lymphocyte and glutamine metabolism is not known. We compared glutamine metabolism in lymphocytes in sedentary (SED) and trained rats. Rats from the moderate group (MOD) swam for 6 weeks, 1 h/day, in water at 32 ± 1 °C, with a load of 5.5% body weight attached to the tail. Animals from the exhaustive group (EXT) trained like MOD, with training increasing to 3 times 1 h a day during the last week, with 150 min rest between each bout. Animals were killed immediately after the last training bout. We observed reduced concentrations of plasma glucose ( p < 0.05), glutamine ( p < 0.05), glutamate ( p < 0.05) in EXT compared to SED. In MOD, decreases in glutamine ( p < 0.05) were observed. Analyzing lymphocyte metabolism, we observed an increase in lactate production and glutamine consumption ( p < 0.05) in MOD ( p < 0.05) compared to SED and a decrease in glutamine consumption ( p < 0.05) and aspartate production in EXT. An increase in the proliferative response of lymphocytes in MOD and EXT was also observed when stimulated by ConA and LPS similarly to SED. Acute exercise promoted decreased glutamine plasma concentration and changes in glutamine metabolism that did not impair lymphocyte proliferation in exhaustive trained rats.

Acute exhaustive exercise does not alter lipid peroxidation levels and antioxidant enzyme activities in rat hippocampus, prefrontal cortex and striatum

Although regular physical exercise is beneficial to the body, it is well known that exhaustive exercise causes oxidative stress in muscle. Recent studies suggest that regular moderate physical exercise has the beneficial effects on brain. However, there is little information regarding whether or not exhaustive exercise could generate oxidative stress in brain and the findings are conflicting. The aim of this study was to investigate the effects of exhaustive exercise on thiobarbituric acid reactive substances, as an indicator of lipid peroxidation, in the hippocampus, prefrontal cortex and striatum. Additionally we examined antioxidant enzymes activities, superoxide dismutase and glutathione peroxidase, to assess the effects of reactive oxygen species. Exhaustive exercise did not change superoxide dismutase and glutathione peroxidase enzyme activities and thiobarbituric acid reactive substances levels neither immediately (0 min) nor at 3, 6, 12, 24 and 48 h after the cessation of exercise in the brain. These results indicate that acute exhaustive exercise may not cause significant lipid peroxidation in the hippocampus, prefrontal cortex and striatum during the post-exercise period.

Effects of endurance training and acute exhaustive exercise on antioxidant defense mechanisms in rat heart

We investigated whether 8-week treadmill training strengthens antioxidant enzymes and decreases lipid peroxidation in rat heart. The effects of acute exhaustive exercise were also investigated. Male rats ( Rattus norvegicus, Sprague-Dawley strain) were divided into trained and untrained groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h day − 1 , 5 days week − 1 for 8 weeks. For acute exhaustive exercise, graded treadmill running was conducted. Malondialdehyde level in heart tissue was not affected by acute exhaustive exercise in untrained and trained rats. The activities of glutathione peroxidase and glutathione reductase enzymes decreased by both acute exercise and training. Glutathione S-transferase and catalase activities were not affected. Total and non-enzymatic superoxide scavenger activities were not affected either. Superoxide dismutase activity decreased by acute exercise in untrained rats; however, this decrease was not observed in trained rats. Our results suggested that rat heart has sufficient antioxidant enzyme capacity to cope with exercise-induced oxidative stress, and adaptive changes in antioxidant enzymes due to endurance training are limited.

EFFECTS OF ENDURANCE TRAINING ON ANTIOXIDANT DEFENSE MECHANISMS AND LIPID PEROXIDATION IN TESTIS OF RATS

Male rats were equally divided into trained rest (TR), trained exhaustive exercise (TE), untrained rest (UR), and untrained exhaustive exercise (UE). Endurance training consisted of treadmill running for 1.5 h/d, 5 days a week for 8 weeks reaching the speed of 2.1 km/h at the fortieth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km/h at 95th min, 10% uphill, continued until exhaustion. Testicular tissue malondialdehyde (MDA), antioxidant potential (AOP) levels, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST), glutathione reductase (GR) and catalase (CAT) activities were determined. There was a slight decrease, but not significant, in the SOD activity in UE group compared to TE and TR groups. Activity of GSH-Px decreased in the UE group compared to UR, TR and TE groups. Acute exhaustive exercise did not affect testicular tissue GSH-Px activity in trained rats. Testicular tissue GST activity of the UE group was similar to TE group, but lower than UR and TR groups. In UE group, testicular tissue AOP values were lower than UR, TR and TE groups. The oxidative effects of acute exhaustive exercise on the rat testis decreased with endurance training. Endurance training prevents oxidative injuries by eliminating oxygen radicals and inhibiting lipid peroxidation via preventing decreases in antioxidant enzyme activities.

L-Arginine attenuates xanthine oxidase and myeloperoxidase activities in hearts of rats during exhaustive exercise

The present study was to investigate the effects of l-arginine (l-Arg) supplementation on cardiac oxidative stress and the inflammatory response in rats following acute exhaustive exercise on a treadmill. Rats were randomly divided into four groups: sedentary control (SC); SC with l-Arg treatment (SC+Arg); exhaustive exercise (E); exhaustive exercise with l-Arg treatment (E+Arg). Rats in groups SC+Arg and E+Arg received a 2 % l-Arg diet. Rats in groups E and E+Arg performed an exhaustive running test on a treadmill at a final speed of 30 m/min, 10 % grade, at approximately 70-75 % VO2max. The results showed a significant increase in cardiac xanthine oxidase (XO) and myeloperoxidase activities and membrane lipid peroxidation endproduct (malondialdehyde; MDA) levels of exercised rats compared with SC rats. The increased cardiac XO activity and MDA levels in exercised rats were significantly decreased in exercised rats supplemented with l-Arg. Myocardial GSSG content increased whereas the GSH:GSSG ratio was depressed in exercised rats compared with SC rats. Cardiac GSSG levels significantly decreased, whereas total glutathione, GSH and the GSH:GSSG ratio increased in exercised rats supplemented with l-Arg compared with exercised rats. The activities of creatinine kinase (CK) and lactate dehydrogenase (LDH), and lactate, uric acid, and nitrite and nitrate levels in the plasma significantly increased in exercised rats compared with SC rats. The activities of plasma CK and LDH were significantly decreased in l-Arg-supplemented plus exercised rats compared with exercised rats. These findings suggest that l-Arg supplementation reduces the oxidative damage and inflammatory response on the myocardium caused by exhaustive exercise in rats.

Angiotensin II Inhibition Attenuates Postexercise Proteinuria in Rats

An important explanatory theory for the mechanism of postexercise proteinuria is that angiotensin II could be inhibited by angiotensin converting enzyme inhibitors. Because of the kininase effect of the angiotensin converting enzyme, it is unclear whether the kallikrein-kinin system contributes to the effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. The aim of this study was to evaluate any possible involvement of the kallikrein-kinin system in the therapeutic effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. We evaluated urinary protein levels in exhausted rats receiving an angiotensin converting enzyme inhibitor (enalapril) or an angiotensin II type I receptor antagonist (losartan). Enalapril (30 mg/kg/day, two days) or losartan (20 mg/kg/day, two days) were given to animals using an intragastric catheter. Urinary protein levels increased (41 %) in rats which were exhausted via treadmill running (p < 0.05). In animals that received drug treatment (enalapril or losartan), but did not exercise to exhaustion, urinary protein levels were not different from the control group. Urinary protein levels were found to be significantly lower (p < 0.05) in animals which performed acute exhaustive exercise after enalapril or losartan administration, compared to rats which were exhausted without drug administration. Inhibition of postexercise proteinuria by either enalapril or losartan suggested that angiotensin II plays an important role in postexercise proteinuria, however, it appears the kallikrein-kinin system is not involved in angiotensin converting enzyme inhibitors effect.

Endurance training attenuates exercise-induced oxidative stress in erythrocytes in rat

The aim of this study was to investigate whether endurance training reduces exercise-induced oxidative stress in erythrocytes. Male rats (n=54) were divided into trained (n=28) and untrained (n=26) groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h x day(-1), 5 days a week for 8 weeks, reaching the speed of 2.1 km x h(-1) at the fourth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km x h(-1) at the 95th min, 10% uphill, and was continued until exhaustion. Acute exhaustive exercise increased the erythrocyte malondialdehyde level in sedentary but not in trained rats compared with the corresponding sedentary rest and trained rest groups, respectively. While acute exhaustive exercise decreased the erythrocyte superoxide dismutase activity in sedentary rats, it increased the activity of this enzyme in trained rats. On the other hand, acute exhaustive exercise increased the erythrocyte glutathione peroxidase activity in sedentary rats; however, it did not affect this enzyme activity in trained rats. Erythrocyte glutathione peroxidase activity was higher in trained groups compared with untrained sedentary group. Neither acute exhaustive exercise nor treadmill training affected the erythrocyte total glutathione level. Treadmill training increased the endurance time in trained rats compared with sedentary rats. The results of this study suggest that endurance training may be useful to prevent acute exhaustive exercise-induced oxidative stress in erythrocytes by up-regulating some of the antioxidant enzyme activities and may have implications in exercising humans.

High antioxidant foods protect against oxidative stress during acute exhaustive exercise in athletes

High antioxidant foods protect against oxidative stress during acute exhaustive exercise in athletes

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.

Effects of Endurance Training on Three Superoxide Dismutase Isoenzymes in Human Plasma

The effects of endurance training and acute exhaustive exercise on plasma levels of three superoxide dismutase (SOD) isoenzymes and the ability of superoxide generation in neutrophils were studied. Eighteen healthy male students, aged 17–22 years, who volunteered for this study, underwent three months of endurance training in swimming or running. Before and after the training course, they performed acute exercise and blood samples were collected before and after this exercise. The endurance training significantly increased maximal oxygen uptake (V˙O2max) in all subjects. Neither the endurance training nor the acute exercise affected the plasma CuZn-SOD level. Acute exercise after the training, but not before the training, increased both the plasma Mn-SOD and extracellular SOD (EC-SOD) levels by 33.6 and 33.5%, respectively. The training decreased the EC-SOD level at rest by 22.2%. Acute exercise after the training, but not before the training, increased the plasma lipid peroxide level, suggesting higher oxidative stress in trained subjects during exhaustive exercise. The ability of neutrophils to generate superoxide was increased by the acute exercise, but induction of the superoxide was suppressed after training. These results indicate that EC-SOD levels were changed in a different manner from the CuZn-SOD and Mn-SOD: it was decreased by training but was increased by acute exercise, suggesting that endurance training increases the reserve of EC-SOD in tissues. The results also suggest the possibility of plasma EC-SOD assay as a new index of endurance training.

Effects of endurance training on tissue glutathione homeostasis and lipid peroxidation in streptozotocin-induced diabetic rats.

The aims of our study were to assess whether endurance training strengthens glutathione-dependent antioxidant defenses and decreases oxidative stress in experimental diabetes. Streptozotocin-induced diabetic rats were divided into trained and untrained groups, which were further divided into resting and acute exercise groups. Endurance training consisted of treadmill running for 8 weeks. For acute exhaustive exercise, graded treadmill running was conducted until exhaustion. Eight weeks' treadmill training increased the endurance, favorably decreased lipid peroxidation as measured by thiobarbituric acid reactive substances but not conjugated dienes levels in kidney and vastus lateralis muscle and upregulated glutathione peroxidase in red gastrocnemius muscle. However, it adversely decreased total glutathione level and glutathione peroxidase activity in kidney. Acute exhaustive exercise up-regulated glutathione peroxidase activity in liver. Endurance training did not prevent the increase in thiobarbituric acid reactive substances level in liver due to acute exhaustive exercise. Activities of glutathione disulfide reductase and glutathione S-transferase were not affected. Even though endurance training appeared to upregulate glutathione dependent antioxidant defense in skeletal muscle and to decrease lipid peroxidation in kidney and vastus lateralis muscle as measured by TBARS, our results suggests that beneficial effects of 8 weeks of endurance training are limited in this rat model of uncontrolled diabetes mellitus.

No effect of seasonal variation in training load on immuno‐endocrine responses to acute exhaustive exercise

This study was designed to examine the relationship between seasonal changes in training and competition load, and changes in leukocyte subsets, stress hormones, and interleukin-6 (IL-6) in response to a standardised bout of endurance exercise. In addition, changes in mood states were monitored. Ten male, international Nordic skiers, age 20-29, maximal oxygen uptake 70-82 ml x kg(-1) x min(-1) performed the same incremental treadmill tests to exhaustion at the same time of day (+/-1 h), during the competitive season (in-season HI test) and the recovery season (off-season LO test). The subject filled out a training and competition log (TC score) for three weeks prior to each test and a 65-item Profile of Mood State (POMS) test on arrival at the laboratory. Venous blood for haematological, hormonal, and IL-6 analysis was drawn before and at 0, 15, 30, 60, 120 and 240 min after the test. TC score was more than twice as high during the competitive season (16.0 +/- 3.9) compared to the off-season period (7.0 +/- 4.4). An ANOVA procedure for repeated measures showed no difference in exercise induced changes in concentrations of neutrocytes, lymphocytes, epinephrine, ACTH or cortisol between the in-season HI and off-season LO tests; however, norepinephrine and the IL-6 concentrations were elevated at the in-season HI test compared to the off-season LO test. There were no significant differences in POMS global mood score or sub-scores between the in-season HI and the off-season LO tests. Thus, in a group of elite Nordic skiers, we conclude that a doubling of the training and competition load during the winter season does not alter the leukocyte and stress hormone responses to an incremental exercise test to exhaustion.

No effect of seasonal variation in training load on immuno-endocrine responses to acute exhaustive exercise

No effect of seasonal variation in training load on immuno-endocrine responses to acute exhaustive exercise

Measurement of acute dynamic anaerobic muscle fatigue using a novel Fatigue Resistance Index

A variety of isokinetic fatigue protocols have been previously reported in the literature. The purpose of this study was to examine a new protocol to objectively quantify dynamic concentric and eccentric muscle performance in individuals, or in a multiple subject group, under conditions of acute exhaustive exercise. Pre-fatigue maximal peak torque (PT) and peri-fatigue PT values were measured in unilateral dominant leg quadriceps femoris of human subjects using an isokinetic dynamometer. The protocol was based on single-velocity (90°/s) reciprocal-mode concentric/eccentric (CON/ECC) contractions fixed at 35 repetitions per set. A novel Fatigue Resistance Index (FRI) was then calculated for each individual subject for both CON and ECC contractions. The group CON FRI (36.5±3.9% maximal force) was greater than group ECC FRI (26.9± 2.7% maximal force). This protocol and FRI permit comparisons between eccentric and concentric dynamic anaerobic muscle performances for a given individual subject, or for a group of subjects.

Heat Shock Protein Expression is Increased in Cardiac and Skeletal Muscles of Fischer 344 Rats After Endurance Training

Heat shock proteins (HSPs) are expressed when cells are exposed to various types of stress and they may provide protection against cellular insult. Previous data have shown increases in HSP expression following acute exhaustive exercise in rats (Locke et al. 1990, 1995; Salo et al. 1991) and humans (Liu et al. 1999); however, it is not known if chronic exercise will increase resting levels of HSPs. The purpose of this study was to determine if basal protein levels of HSP 72/73 and HSP 60 are increased in cardiac and skeletal muscle of endurance trained Fischer 344 rats. Heart, soleus (SOL) and lateral gastrocnemius (LG) muscles were removed and hearts were sectioned into left ventricle (LV), right ventricle (RV) and atria (AT). Endurance training improved myocardial citrate synthase activity by 88, 90 and 77% and cytochrome c oxidase activity by 58, 51 and 89% in LV, RV and AT, respectively. LV and RV oxidative enzyme activities were greater when compared to AT for both trained and untrained rats (P &lt; 0.05). HSP 72/73 expression was significantly greater (P &lt; 0.05) in LV, RV and SOL from endurance trained versus from control rats (26, 45 and 67%, respectively). HSP 60 was also increased (P &lt; 0.05) in LV, RV and SOL in trained relative to untrained rats. HSP 72/73 and HSP 60 were unchanged in AT and LG after training. These results indicate that endurance training increases the basal expression of stress proteins and this observation is consistent with the hypothesis that endurance training may activate a protective mechanism to stress.

Heat shock protein expression is increased in cardiac and skeletal muscles of Fischer 344 rats after endurance training.

Heat shock proteins (HSPs) are expressed when cells are exposed to various types of stress and they may provide protection against cellular insult. Previous data have shown increases in HSP expression following acute exhaustive exercise in rats (Locke et al. 1990, 1995; Salo et al. 1991) and humans (Liu et al. 1999); however, it is not known if chronic exercise will increase resting levels of HSPs. The purpose of this study was to determine if basal protein levels of HSP 72/73 and HSP 60 are increased in cardiac and skeletal muscle of endurance trained Fischer 344 rats. Heart, soleus (SOL) and lateral gastrocnemius (LG) muscles were removed and hearts were sectioned into left ventricle (LV), right ventricle (RV) and atria (AT). Endurance training improved myocardial citrate synthase activity by 88, 90 and 77% and cytochrome c oxidase activity by 58, 51 and 89% in LV, RV and AT, respectively. LV and RV oxidative enzyme activities were greater when compared to AT for both trained and untrained rats (P < 0.05). HSP 72/73 expression was significantly greater (P < 0.05) in LV, RV and SOL from endurance trained versus from control rats (26, 45 and 67%, respectively). HSP 60 was also increased (P < 0.05) in LV, RV and SOL in trained relative to untrained rats. HSP 72/73 and HSP 60 were unchanged in AT and LG after training. These results indicate that endurance training increases the basal expression of stress proteins and this observation is consistent with the hypothesis that endurance training may activate a protective mechanism to stress.

Vitamin E level changes in serum and red blood cells due to acute exhaustive exercise in collegiate women.

The purpose of this study was to investigate the change in vitamin E level in both serum and red blood cells (RBC) during exercise and to clarify the effect of vitamin E supplementation. Ten young sedentary female subjects received 200 mg D-alpha-tocopherol acetate daily for 1 wk after the initial exercise bout. After 1 wk of vitamin E supplementation, the same subjects repeated the same exercise. Before vitamin E supplementation, the alpha-tocopherol level in the serum (serum-alpha-tocopherol) did not change after exercise, but a significant decrease in the alpha-tocopherol level in RBC (RBC-alpha-tocopherol) was observed after exercise (p < 0.05). On the other hand, after vitamin E supplementation, the serum-alpha-tocopherol level decreased significantly after exercise (p < 0.05), while the RBC-alpha-tocopherol level was maintained after exercise. Furthermore, a negative correlation between the changes in serum- and RBC-alpha-tocopherol levels was observed only after vitamin E supplementation (r = 0.667, p < 0.05). The present results suggest that as RBC suffers oxidative stress, vitamin E in RBC is consumed to protect RBC from oxidative damage during exercise. These results also suggest that when there is a sufficient amount of vitamin E in the serum, vitamin E is shifted from the serum to RBC, resulting in a steady RBC-alpha-tocopherol level and a decrease in the serum-alpha-tocopherol level under oxidative stress such as exercise.

Lactate transport activity in rat skeletal muscle sarcolemmal vesicles after acute exhaustive exercise.

The effect of a single bout of exhaustive exercise on muscle lactate transport capacity was studied in rat skeletal muscle sarcolemmal (SL) vesicles. Rats were assigned to a control (C) group (n = 14) or an acutely exercised (E) group (n = 20). Exercise consisted of treadmill running (25 m/min, 10% grade) to exhaustion. SL vesicles purified from C and E rats were sealed because of sensitivity to osmotic forces. The time course of 1 mM lactate uptake in zero-trans conditions showed that the equilibrium level in the E group was significantly lower than in the C group (P < 0.05). The initial rate of 1 mM lactate uptake decreased significantly from 2.44 +/- 0.22 to 1.03 +/- 0.08 nmol. min(-1). mg protein(-1) (P < 0.05) after exercise, whereas that of 50 mM lactate uptake did not differ significantly between the two groups. For 100 mM external lactate concentration ([lactate]), exhaustive exercise increased initial rates of lactate uptake (219.6 +/- 36.3 to 465.4 +/- 80.2 nmol. min(-1). mg protein(-1), P < 0.05). Although saturation kinetics were observed in the C group with a maximal transport velocity of 233 nmol. min(-1). mg protein(-1) and a Michealis-Menten constant of 24.5 mM, saturation properties were not seen after exhaustive exercise in the E group, because initial rates of lactate uptake increased linearly with external [lactate]. We conclude that a single bout of exhaustive exercise significantly modified SL lactate transport activity, resulting in a decrease in 1 mM lactate uptake and was associated with alterations in the saturable properties at [lactate] above 50 mM. These results suggest that changes in sarcolemmal lactate transport activity may alter lactate and proton exchanges after exhaustive exercise.