Possible involvement of plasma antioxidant defences in training-associated decrease of platelet responsiveness in humans

The aim of this study was to evaluate in sedentary individuals the effects of a 20-week exercise training program on ex vivo platelet responsiveness and the possible involvement of plasma antioxidant defences in relation to the mechanisms controlling platelet sensitivity. A statistically significant decrease in ADP- and collagen-evoked platelet aggregation was observed after physical training together with an increase in plasma total antioxidant capacity (TEAC), superoxide dismutase activity, and high-density lipoprotein cholesterol (HDL-C) concentration. Additionally, a rise in lag time for in vitro low-density lipoprotein (LDL) oxidation as well as a decreased plasma level of secondary products of lipid peroxidation were observed after training, and the values for lag time were significantly correlated with TEAC and HDL-C. Nitrate/nitrite (NO_x) content both in plasma and in platelet cytosol was significantly enhanced at the end of the training period and a significant positive correlation was found between plasma and intraplatelet NO_x values. Furthermore, intraplatelet NO_x content was positively correlated with HDL-C levels. The findings of the current study suggest that the improvement of antioxidant defences induced by moderate regular exercise may be involved in desensitising blood platelets most likely through the inhibition of LDL oxidation and the simultaneous enhancement of plasma and intraplatelet NO_x bioavailability and HDL-C level.     

Post-exercise platelet activation--aggregation and release in relation to dynamic exercise

Relatively scarce information is found on the period immediately following physical stress, with special reference to human platelet activity. This, in connection with earlier observations of an increase in platelet release products and hyperaggregability following surgical stress, has initiated the present study. We studied platelet function in eight healthy non-mediated volunteers during and 1 h after cycle exercise of submaximal intensity. ADP-induced platelet aggregability was enhanced in the last minute of exercise followed by a decreased aggregability 1 h after. Adrenaline-induced platelet aggregation showed the same attenuation after exercise but no change during work. The release products beta-thromboglobulin and serotonin in plasma showed significant increases after exercise. This is taken as evidence of an enhanced platelet activity following exercise. A normal stress-response, measured as increase in cyclic AMP in plasma, was observed. In conclusion, platelets are activated following moderate exercise and it seems valid to include the post-exercise period in future studies.     

Prolonged platelet activation in individuals with elevated blood pressure in response to a moderate exercise challenge

We examined the magnitude of 20-min moderate exercise-induced platelet activation in 50 volunteers with normal ( n =31) or elevated blood pressure (EBP; n =19). Blood was drawn before, immediately after, and 25 min after exercise. Antibody-staining for platelet activation markers, P-selectin, and fibrinogen receptors was done with and without adenosine diphosphate (ADP) stimulation in whole blood for flow cytometric analyses. Exercise led to increases in percent aggregated platelets and percent platelets expressing P-selectin or PAC-1 binding ( p s≤.001). This increase in percent platelets expressing P-selectin continued even after a 25-min rest only in the EBP group ( p ≤.01) accompanied by an increase in percent of aggregated platelets ( p ≤.05). Although ADP stimulation led to increased platelet activation at rest, it was attenuated following exercise, even among EBP individuals. A moderate exercise challenge induced prolonged platelet activation in individuals with EBP but attenuation in activation to further stimulation by an agonist. Findings suggest that a recovery period after physical stress appears critical in individuals with high BP regarding platelet activation and aggregation, which can lead to an acute coronary syndrome in vulnerable individuals.     

The effect of exercise on platelet beta-adrenoceptor function and platelet aggregation in healthy human volunteers

Plasma levels of adrenaline and noradrenaline, platelet cyclic-AMP (cAMP) content, platelet aggregation, platelet release of beta-thromboglobulin, and platelet factor 4 and serum content of thromboxane B2(TXB2) and 6-keto-PGF1 alpha were measured in 12 healthy male volunteers (age 38-72, mean 54.2 years) who were tested at rest and immediately after five min light cycle exercise. The plasma levels of adrenaline and noradrenaline increased significantly after exercise (P less than 0.01). The platelet cAMP level was not changed by exercise. The functional capacity of platelet beta-adrenoceptors, determined as cAMP production after beta-adrenoceptor stimulation in vitro, decreased highly significantly after exercise in all 12 volunteers (P less than 0.01). No alteration was observed in platelet aggregation induced by adrenaline or in platelet release of beta-thromboglobulin or platelet factor 4. No change was observed in the serum levels of TXB2 and 6-keto-PGF1 alpha. In conclusion: light cycle exercise results in a decreased functional capacity of platelet beta-adrenoceptors, but has no effect on platelet aggregation or platelet release. This might indicate a concomitant and equal decreased functional capacity of platelet alpha-adrenoceptors.     

Quantitative assessment of nitric oxide in rat skeletal muscle and plasma after exercise

Nitric oxide (NO), a short-lived vasoactive substance that has multiple physiological functions, is also involved in skeletal muscle physiology. This work examines the levels of nitrate (the metabolic end-product of NO) in muscle and plasma after different exercise protocols: namely acute, eccentric, cardiac stress and training. Plasma nitrate levels were augmented after strenuous exercise and did not change after training. The vastus intermedius and the gastrocnemius, both oxidative muscles, showed the highest concentrations of cytosolic nitrate after strenuous exercise. NO levels varied, depending on the fibre type, and this may correlate well with the specific contractile function performed. Electronic Publication     

Platelet aggregation and strenuous exercise

1. Platelet aggregation in the Chandler's tube has been found to be increased in a group of normal male and female volunteers who undertook strenuous physical exercise. This coincided with acceleration of the ;intrinsic' blood clotting system and a rise in fibrinogen. The rise in fibrinogen occurred despite increased fibrinolysis.2. The study confirms the sensitivity of the platelet aggregation system to changes in the ;intrinsic' clotting mechanism. Acceleration of this system in this study resulted from a physiological cause and produced accelerated aggregation in the coagulation-affected phase.     

Fish diet and physical fitness in relation to membrane and serum lipids,prostanoid metabolism and platelet aggregation in female students

Summary The effects of a 14-week fish diet and exercise programme on lipid metabolism and platelet aggregation in healthy female students (n=99) were studied. The subjects were divided into four groups: a control group, a fish diet group (3.5 meals containing fish per week, 0.9 g n-3 fatty acids per day), an exercise group (at least three training sessions per week) and a combined fish diet and exercise group. The proportion of n-3 fatty acids increased at the expense of n-6 fatty acids in platelets and erythrocyte ghosts in the fish diet groups. Serum triglyceride concentrations tended to decrease in the fish diet and exercise groups and a significant decrease was found in the combined fish diet and exercise group (13%, P<0.05). No significant changes took place in the other serum lipid and apolipoprotein concentrations. Platelet production of thromboxane B₂, plasma 6-keto-PGF₁ concentrations and adenosine 5diphosphate (ADP)-induced platelet aggregation also remained unchanged in all groups during the study. However, an inverse correlation was found between physical fitness (maximal oxygen uptake and maximal exercise intensity) and serum triglycerides, total cholesterol, low density lipoprotein cholesterol and platelet aggregation. This suggests that improved physical fitness is related to beneficial changes in serum lipid concentrations and to a decreased aggregation tendency of platelets. The responses of the female subjects to a fish diet were smaller when compared to earlier studies on male subjects. This suggests that there are sex differences in the efficiency of n-3 fatty acids in modifying lipid metabolism.     

肝缺血预处理保护作用与一氧化氮/内皮素-1系统有关

目的:研究一氧化氮/内皮素-1(NO/ET-1)失衡与肝缺血再灌注(I/R)损伤的关系以及肝缺血预处理(IPC)对NO/ET-1系统的调节作用。方法:采用鼠肝I/R模型,比较I/R组和IPC+I/R组NO/ET-1系统的变化情况及其与肝I/R损伤的关系。用RT-PCR检测再灌注2h内肝组织中是否有诱生性一氧化氮合酶(iNOS)mRNA表达。结果:再灌注急性期血浆NO代谢产物(NO₂^-/NO₃^-)降低、ET-1升高致NO/ET-1比值降低,血浆ALT、AST、LDH、TNF-α含量及肝组织丙二醛(MDA)含量增高,而肝组织ATP含量降低,肝损伤加重;肝IPC的保护作用与其升高NO₂^-/NO₃^-、降低ET-1,升高NO/ET-1比值有关;在上述肝组织中未测出有iNOSmRNA表达。结论:肝I/R损伤与NO/ET-1失衡有关,IPC对I/R急性期肝的保护作用可能是通过对NO/ET-1系统的调节作用而介导的,此时NO来源于原生性一氧化氮合酶(cNOS)而非iNOS。     

Platelet function during thrombolytic therapy with anistreplase

Platelets are likely to play a role during thrombolytic therapy of acute myocardial infarction, but their exact involvement is not fully understood at present. The effects of thrombolytic agents on platelet function have mainly been studied using in vitro experiments and results are rather controversial; data from in vivo studies are rare. We studied 10 patients with acute myocardial infarction, who were treated with intravenous anistreplase. Use of aspirin or other anti-platelet drugs were not allowed. Before and after thrombolysis, blood was collected for determining ex vivo platelet aggregation and platelet factor 4, β-thromboglobulin and thromboxane-B₂ in plasma. Immediately after anistreplase, the aggregation of platelets was significantly inhibited: aggregation induced by ADP decreased to 67±36% (mean±SD) of pretreatment (P<0.05), by arachidonic acid to 29±29% (P<0.005) and by collagen to 58±46% (P<0.05). The aggregation defect was transient; after 6–12h aggregation had returned to normal. Then, a significant stimulation of ADP-induced aggregation became apparent, lasting until 24–48h after thrombolysis; possibly this was mediated by heparin. The platelet proteins and thromboxane-B₂ were significantly elevated before thrombolysis and showed a steady decrease after anistreplase. In the first phase of anistreplase therapy, we found no indications of platelet activation. Additional in vitro studies confirmed these findings. Antibodies to streptokinase did not affect platelet function in these patients.     

Specific training improves skeletal muscle mitochondrial calcium homeostasis after eccentric exercise

There is limited understanding of the mitochondrial adaptation following repeated eccentric exercise bouts, a model resulting in muscle adaptation known as the repeat bout effect. It was hypothesized that downhill training would reduce mitochondrial calcium content (MCC) post an acute eccentric bout with concurrent improvements in mitochondrial respiratory function. Thirty-four Sprague–Dawley rats were divided into four groups: control (N), control with acute eccentric exercise (N _ecc), trained control (X) and trained with acute eccentric exercise (X _ecc). Training for X and X _ecc consisted of 30 min per day for five consecutive days of downhill treadmill running. The acute eccentric exercise bout was a ?14° treadmill exercise for 90 min performed 2 weeks after the training period. Animals were killed 48 h post-exercise. Isolated mitochondria from the red quadriceps allowed for the measure of mitochondrial respiratory indices and MCC. Calpain activity and heat shock protein 72 expression (HSP72) were also measured. MCC dramatically increased following the acute bout of eccentric exercise in N _ecc (p < 0.001), but did not change in X _ecc. Mitochondrial respiratory function tended to be slightly depressed in N _ecc (state 3 respiration, p = 0.053; respiratory control ratio, p = 0.098) and unaltered in X _ecc. Previous training altered the calpain and heat shock protein response to an acute bout of eccentric exercise. The results suggest that downhill exercise training improves mitochondrial calcium homeostasis following an acute bout of prolonged eccentric exercise and may stabilize mitochondrial respiratory function. These improvements coincide with a reduction in calpain activity and heat shock protein upregulation.     

Influence of training on markers of platelet activation in response to a bout of heavy resistance exercise

Recent connections between platelet activity and cardiovascular disease have raised questions of whether platelet function varies in exercising individuals. Resistance training has been linked to a possible reduction in hyper-aggregability of platelets, especially following acute strenuous exercise. The present investigation was designed to explore the effects of an acute resistance exercise test on the primary hemostatic system in both resistance-trained (RT) and untrained (UT) individuals. Ten RT (five men and five women; age, 26.0 ± 4.5 years; height, 175.12 ± 8.54 cm; weight, 79.56 ± 13.56 kg) and ten UT (five men and five women; age, 26.4 ± 6.2 years; height, 170.31 ± 7.45 cm; weight 67.88 ± 16.90 kg) individuals performed an Acute Exhaustive Resistance Exercise Test (AERET; six sets of ten repetitions of squats at 80 % of the 1-Repetition Maximum (RM)). Blood samples were obtained before, immediately after, and at 15, 60, and 120 min following the AERET. Blood samples were analyzed for platelet count, von Willebrand factor antigen (vWF:Ag), beta-thromboglobulin (β-TG), and platelet factor 4 (PF4). B-TG showed significant differences (p < 0.05) between RT and UT at +15 and +60 min. Both groups showed a main effect for time in platelet count, vWF, and β-TG following the AERET, whereas PF4 remained unchanged. All blood variables returned to baseline 120 min after exercise. Compared with UT, RT demonstrated reduced platelet activation in response to an acute bout of heavy resistance exercise. Reduced platelet activation may be attributed to training status, as shown by a reduction in plasma concentrations of B-TG in the RT group.     

Strenuous exercise increases plasmatic and urinary leukotriene E4 in cyclists.

The purpose of this study was to investigate plasma and urinary levels of leukotriene (LT) and the changes in pulmonary function induced by strenuous exercise in highly trained cyclists (HT) with mild exercised-induced hypoxemia (EIH). METHOD: Nine HT and five untrained subjects (UT) performed a 30-min exercise at 78% of their VO2peak. Leukotriene E4 (LTE4) was assayed in plasma and urine. Pulmonary function tests and pulmonary diffusion capacity (DLCO) were examined before and after exercising. Ear arterialized blood gases were assessed at rest and during exercise. RESULTS: The mean drop in partial oxygen pressure was 15 mmHg in HT during exercise; and the DLCO decreased by 7.5% following exercise. No significant changes were found in forced vital capacity or forced expiratory flows. LTE4 levels increased significantly in HT following exercise: urinary LTE4 was 42.9 +/- 6.3 ng.mmol-1 creatinine at rest and 66.3 +/- 11.9 ng.mmol-1 creatinine 2 hrs after exercise, and plasma LTE4 rose from 528 +/- 91 pg.mL-1 at rest to 897 +/- 123 pg.mL-1 after exercise. By contrast, urinary LTE4 level was unchanged in the UT group. Among the HT group, there was no significant correlation between urinary LTE4 changes and PO2, air flow rates, or DLCO changes. CONCLUSION: These results suggest that strenuous exercise induces an increase of LTE4 release in highly trained cyclists with mild EIH. These changes in LTE4 levels were not related to significant impairment of lung function.     

17Beta-estradiol rapid stimulation of rat aorta NOS activity is prevented by oestrogen deficiency

OBJECTIVES: The purpose of this study was to determine the effects of chronic oestrogen deficiency on rat aorta rapid response to 17beta-estradiol treatment. METHODS: Rat aortic strips (RAS) were isolated from Wistar female rats of three different groups: rats 6-7-month old with normal oestrogen levels (NER); aged rats, 24-month old, with low oestrogen levels (LER); and young rats after 2 months of bilateral ovariectomy (OVX). Platelet aggregation was measured after incubation of RAS in a platelet rich plasma by addition of 10 microM ADP. NO production by RAS was measured by 3H-citrulline technique. RESULTS: RAS obtained from NER treated with 17beta-estradiol produced an inhibition of platelet aggregation specific for ovarian hormones, since testosterone was devoid of any effect. In aortic tissue isolated from male rats no increment in nitric oxide (NO) production was found. RAS from LER and OVX treated with 1-10 nM failed to induce a significant inhibition of platelet aggregation compared with NER (5 and 17%; 6 and 20% vs. 45 and 77% inhibition of platelet aggregation respect to control, respectively). In contrast to NER, 5 min treatment of LER and OVX aortic tissue with 1 nM 17beta-estradiol did not incremented NO production (NER 1.14 vs. 2.3 (P < 0.05); LER 1.14 vs. 1.42; OVX 1.24 vs. 1.52 pmol NO per mg protein). CONCLUSIONS: These results suggest that chronic oestrogen deprivation impairs the inhibition of platelet aggregation and suppresses the rapid stimulation of aortic NOS induced by acute 'in vitro' treatment with 17beta-estradiol.     

Adrenergic control of post-exercise metabolism

After strenuous exercise there is a sustained increase in resting O₂ consumption. The magnitude and duration of the excess post-exercise O₂ consumption (EPOC) is a function of exercise intensity and exercise duration. Some of the mechanisms underlying the rapid EPOC component (<1 h) are well defined, while the mechanisms causing the prolonged EPOC component (>1 h) are not fully understood. It has been suggested that β-adrenergic stimulation is of importance for the prolonged component. There is an increased level of plasma adrenaline and noradrenaline during exercise, and it is shown that catecholamines stimulate energy expenditure through β-adrenoceptors. After exercise an increased fat oxidation and an increased rate of triglyceride fatty acid (TG–FA) cycling may account for a significant part of the prolonged EPOC component. These processes may be stimulated by catecholamines. However, the return of plasma concentration of catecholamines to resting levels after exercise is more rapid than the return of O₂ uptake. But plasma concentration of catecholamines may be an insensitive indicator of sympathetic activity, since the clearance rate of catecholamines is high. Also, the sensitivity to catecholamines may be increased after exercise. A decreased post-exercise O₂ uptake has been shown when β-blockade is administered in dogs before the exercise bout. In a pilot study in humans, administration of β-antagonist after exercise did not seem to change EPOC.     

Platelet adhesion and aggregation on polyethylene: effect of exhaustive exercise

The aim of the present study was to evaluate the effect of an exhaustive exercise on platelet adhesion and aggregation on polyethylene (PE) in relation to changes in plasma cortisol concentration in order to ascertain the effect of physical stress response in the blood-contacting properties of polymeric materials. Twelve healthy sedentary subjects, six males and six females, were studied. Each subject performed an exercise test on a bicycle ergometer at intensity corresponding to 70% VO2 max until exhaustion. One month after the exercise session, each subject participated in a control rest session. In both sessions, blood samples were drawn every 5 min for cortisol, lactate, hemoglobin, and hematocrit determinations and every 15 min for evaluation of platelet adhesion and aggregation. Individual comparisons between the rest and exercise cortisol patterns identified three categories of cortisol responders to exercise: positive responders (C +, showing higher concentrations during exercise than during rest), negative responders (C -, showing lower concentrations during exercise than during rest), and nonresponders (NR, showing similar concentrations during exercise and rest). The results revealed that C + had lower platelet adhesion and aggregation scores during exercise than during rest; moreover C - had higher scores than C + and NR during exercise. The results obtained demonstrated no effects of sex or exercise on either cortisol plasma levels or platelet adhesion and aggregation on PE surface. With regard to cardiovascular risk, the results suggest that exercise favorably affects platelet functions when mechanisms of metabolic adaptation to prolonged muscular work, expressed by a cortisol increase, are activated during exercise.     

Increase in immune activation, vascular endothelial growth factor and erythropoietin after an ultramarathon run at moderate altitude

The present study was performed to investigate the effects of exhaustive long lasting exercise at moderate altitude on the time course of serum immunomodulatory peptides, vascular endothelial growth factor (VEGF) and serum erythropoietin (EPO). Thirteen well trained runners participated at the Swiss Alpine Marathon of Davos (distance 67 km, altitude difference 2300 m). Interleukin-6 was significantly elevated in the first 2h after the run. In contrast, tumor necrosis factor-alpha and both soluble tumor necrosis factor-a receptors I and II were increased after exercise termination and showed sustained serum concentrations the following days. Neopterin, a serum marker for the activation of the cellular immune system, was increased until day two after the run. Immediately after the run VEGF was significantly elevated and further increased 2.4-fold until day five post exercise (p = 0.005). EPO was also increased after exercise but reached its maximum 2 h after the run (2-fold increase; p = 0.004) and decreased thereafter. The main findings of our study are that prolonged strenuous exercise at moderate altitude induced a significant long lasting increase in serum VEGF and EPO which was accompanied by an activation of the immune system.     

Effects of ketanserin,a selective 5-HT2 serotonergic antagonist,on the secondary recruitment of human plateletsin vitro

Ketanserin, a selective 5-HT₂ serotonergic receptor antagonist, reducesin vitro the release-associated human platelet aggregation induced by threshold concentrations of collagen and curtails the second wave of aggregation/release induced by critical concentrations of ADP in particular and, to a lesser extent, of 1-epinephrine. Its inhibitory effect on the second waves becomes more pronounced when the reaction is already attenuated by moderate cyclo-oxygenase inhibition with esculetin, by yohimbine or by propranolol. The first wave of aggregation induced by ADP or 1-epinephrine is not affected.Such an inhibition of secondary platelet recruitment by ketanserinin vitro may be due to an inhibition of the 5-HT₂ receptor-mediated amplifying effects of platelet-released 5-HT or to a non-specific interference with the platelet membrane, reducing the release of mediators from the platelets.Reduction of the increased plasma BTG levels in patients after ketanserin may result from such release-inhibiting mechanisms.     

Trained versus untrained men: different immediate post-exercise responses of pituitary adrenal axis

The hypothalamo-pituitary-adrenal axis is involved throughout the exercise-recovery cycle. Nevertheless, differences in hormone responses during early recovery between sedentary and endurance trained subjects are not well known. The aim of this preliminary study was to monitor plasma cortisol and adrenocorticotropic hormone (ACTH) concentrations both during and after the end of running exercise performed by four endurance trained adults (marathon men) compared to four sedentary subjects. Two parameters, i.e. intensity and duration, were changed on 4 consecutive days. The 1^st day (D₀) was spent in the laboratory: all blood samples were obtained at rest to determine diurnal variations of each hormone. On the following days (D₁–D₄) the subjects exercised: D1 and D2 brief (20 min), light (50% maximal heart rate HR_max, D₁) or strenuous (80% HR_max, D₂), D₃ and D₄ prolonged (120 min), light (D₃) or strenuous (D₄). In both groups, neither brief (D₁, D₂) nor prolonged light exercise (D₃) induced any significant variation in plasma ACTH or cortisol concentrations. Plasma ACTH and cortisol concentrations increased only if the exercise was intense and prolonged (D₄). The training factor did not modify the intensity or duration thresholds for the activation of the pituitary-adrenocortical response to exercise in the conditions of our experiment. However, during immediate recovery from the four exercise regimens, the plasma ACTH concentrations of the marathon men were constantly above the values of the sedentary subjects, although plasma cortisol concentration remained similar in both groups. As an indirect means of evaluating the relationships between ACTH and cortisol we compared the areas under the cortisol and ACTH curves (AUC) from 0.5 to 3.5h during recovery from D₁ to D₄ compared to D₀ at the same time. Cortisol AUC were similar in the sedentary subjects and marathon men although the ACTH AUC were different in the sedentary subjects and marathon men, suggesting a change in the pituitary-adrenal relationship at some yet indeterminate level. During the immediate recovery from exercise whatever its intensity, the magnitude of the ACTH response was increased in the trained subjects but with a reduced effect upon its target, the adrenal glands. This phenomenon has not been described in the literature. Two non-exclusive phenomena may be involved, i.e. a decreased adrenal sensitivity to ACTH stimulation, and/or a decreased hypothalamo-pituitary axis sensitivity to cortisol negative feedback.     

Changes in salivary antimicrobial peptides,immunoglobulin A and cortisol after prolonged strenuous exercise

The aim of the present study was to examine whether amount of oral antimicrobial components, human β-defensin-2 (HBD-2), cathelicidin (LL-37), and immunoglobulin A (IgA), might be affected by prolonged strenuous exercise. Ten young male volunteers either exercised on recumbent ergometer at 75% [(V)\dot]\textO_2max \dot{V}{\text{O}}_{{2\max }} for 60 min (exercise session) or sat quietly (resting session). Saliva samples were obtained at 60-min intervals during sessions for measurements of saliva antimicrobial components (HBD-2, LL-37, and IgA), saliva cortisol and osmolality. Saliva flow rate was decreased and saliva osmolality was increased during the 60-min exercise. Saliva HBD-2 and LL-37 concentrations and secretion rates were increased during and after the exercise, whereas saliva IgA concentration and secretion rates were decreased after the exercise. Saliva cortisol was increased during and after the exercise. The areas under the curve of the time courses of saliva levels of HBD-2 and LL-37 were negatively correlated with those of cortisol levels in saliva. The present findings suggested that a single bout of prolonged strenuous exercise caused a transient increase in the oral HBD-2 and LL-37 levels.     

Erythrocyte membrane fluidity and indices of plasmatic oxidative damage after acute physical exercise in humans

Optimal levels of membrane fluidity are essential for numerous cell functions including cell growth, solute transport and signal transduction. Since exercise enhances free radical production, our aim was to evaluate in healthy male subjects the effects of an acute bout of maximal and submaximal exercise on the erythrocyte membrane fluidity and its possible relation to the oxidative damage overproduction due to exercise. Subjects (n = 34) performed three cycloergometric tests: a continuous progressive exercise, a strenuous exercise until exhaustion and an acute bout of exercise at an intensity corresponding to 70% of maximal work capacity for 30 min. Venous blood samples were collected before and immediately after these exercises. Erythrocyte membrane fluidity was assessed by fluorescence spectroscopy. Plasma malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA) concentrations and carbonyl content of plasmatic proteins were used as an index of lipid and protein oxidation, respectively. Exercise produced a dramatic drop in the erythrocyte membrane fluidity as compared to resting time, but this was not accompanied by significant changes in the plasmatic MDA and 4-HDA concentrations. The highest erythrocyte membrane rigidity was detected immediately after strenuous exercise until exhaustion was performed. Protein carbonyl levels were higher after exhaustive exercises than at rest. Continuous progressive and strenuous exercises until exhaustion, but not submaximal workload, resulted in a significant enhanced accumulation of carbonylated proteins in the plasma. These findings are consistent with the idea that exercise exaggerates oxidative damage, which may contribute, at least partially, to explain the rigidity in the membrane of the erythrocytes due to acute exercise.