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The general practice of altitude training is widely accepted as a means to enhance sport performance despite a lack of rigorous scientific studies. For example, the scientific gold-standard design of a double-blind, placebo-controlled, cross-over trial has never been conducted on altitude training. Given that few studies have utilised appropriate controls, there should be more scepticism concerning the effects of altitude training methodologies. In this brief review we aim to point out weaknesses in theories and methodologies of the various altitude training paradigms and to highlight the few well-designed studies to give athletes, coaches and sports medicine professionals the current scientific state of knowledge on common forms of altitude training. Another aim is to encourage investigators to design well-controlled studies that will enhance our understanding of the mechanisms and potential benefits of altitude training.

Increased plasma levels of vascular endothelial growth factor (VEGF) due to lower levels of its soluble receptor (sFlt-1) had been suggested to cause vasogenic brain edema and thereby to cause the symptoms of acute mountain sickness (AMS). We tested this hypothesis after active ascent to high altitude. Plasma was collected from 31 subjects at low altitude (100 m) before (LA1) and after (LA2) 4 weeks of aerobic exercise training in normobaric hypoxia or normoxia, and one night after ascent to high altitude (4559 m). Training modalities (hypoxia or normoxia) did not influence VEGF- and sFlt-1-levels. Therefore, data of both training groups were analyzed together. After one night at 4559 m, 18 subjects had AMS (AMS+), 13 had no AMS (AMS-). In AMS+ and AMS-, VEGF was 110 ± 75 (SD) pg/ml vs. 104 ± 82 (p = 0.74) at LA1, 63 ± 40 vs. 73 ± 50 (p = 0.54) at LA2, and 88 ± 62 vs. 104 ± 81 (p = 0.54) at 4559 m, respectively. Corresponding values for sFlt-1 in AMS+ and AMS- were 81 pg/ml ± 13.1 vs. 82 ± 17 (p = 0.97), 79 ± 11 vs. 80 ± 16 (p = 0.92) and 139 ± 28 vs. 135 ± 31 (p = 0.70), respectively. Absolute values or changes of VEGF were not correlated and those of sFlt-1 slightly correlated with AMS scores. These data provide no evidence for a role of plasma VEGF and sFlt-1 in the pathophysiology of AMS. They do, however, not exclude paracrine effects of VEGF in the brain.

The purpose of the study was to test the hypothesis that myofiber recruitment is enhanced when whole-body vibration (WBV) is added to squat training. In a randomized cross-over design, 14 recreationally active men were subjected to 2 sessions consisting of 5 sets of 10 squats with external load, performed either on a vibration platform (whole-body vibration squatting [WBVS]) or conventionally without WBV (CON). Electromyographic (EMG) activity of the right vastus lateralis muscle was continuously recorded during WBVS and CON. The integrated EMG values were normalized to the EMG activity recorded during measurement of the maximal voluntary contraction force (MVC) on an isometric leg press at the beginning of each training session. Capillary lactate concentration was determined before and repeatedly after the squatting exercise. Overall mean normalized and integrated EMG (nIEMG) activity during WBVS (62 ± 4% MVC) was significantly (p < 0.001) higher compared with CON (47 ± 2% MVC). There was a tendency for nIEMG to increase during the 5 sets of 10 squats performed as WBVS (p = 0.089), whereas there was a significant (p < 0.001) decrease in nIEMG during CON. Whole-body vibration squatting induced a significantly (p < 0.001) larger increase in capillary lactate than CON (3.03 ± 0.32 vs. 1.60 ± 0.30 mmol · L(-1), p < 0.001). The increased myoelectric activity and the enhanced exercise-induced increase in capillary lactate concentration during WBVS provide evidence for augmented recruitment of muscle tissue when WBV is added to exhaustive squatting exercise.

When ventilating large volumes of air during exercise, airway fluid secretion is essential for airway function. Since these are impaired in cystic fibrosis and exercise-induced asthma, it was the aim of this study to determine how exercise affects airway Na(+) and Cl(-) transport and whether changes depend on exercise intensity. Nasal potential was measured in Ringer's solution, with amiloride to block Na(+) transport, and in low chloride-containing isoproterenol to assess Cl(-) channels. Nasal potential was measured at rest and during submaximal and maximal bicycle ergometer exercise in individuals with cystic fibrosis, exercise-induced asthma and controls. At rest, nasal potential was significantly higher in cystic fibroses than in the others. Maximal exercise decreased nasal potentials in cystic fibrosis and controls but not in exercise asthma. Submaximal exercise decreased nasal potentials only in cystic fibrosis. Cl(-) transport was not affected. Our results indicate that nasal potentials and Na(+) transport were decreased by maximal exercise in healthy and cystic fibrosis, whereas submaximal exercise decreased potentials in cystic fibrosis only. Exercise did not affect nasal potentials in asthmatics. Decreased reabsorption during exercise might favour airway fluid secretion during hyperpnoea. This protective effect appears blunted in patients with exercise-induced asthma.

Abnormalities of baseline hemostatic variables have been related to a hypercoagulable state in patients with chronic heart failure (CHF). Given that physical exercise leads to an activation of coagulation physiologically, this study addressed the question of whether the exercise-induced hemostatic activation is enhanced in patients with CHF. Ten patients with dilated cardiomyopathy (ejection fraction < 40%) and 10 healthy individuals (matched for sex, age and body mass index) were subjected to a maximal exercise test on a bicycle ergometer. Healthy subjects performed a second exercise test at a submaximal intensity level, in which oxygen consumption (VO2) was adjusted to the peak oxygen consumption (VO2peak) of the corresponding patient. Exercise testing had only marginal effects on markers of thrombin formation in patients and healthy individuals alike. In patients with CHF, exercise-induced changes in fibrinopeptide A, an index of fibrin formation, paralleled those observed in controls after submaximal exercise whereas most pronounced changes occurred in healthy subjects after maximal exercise. Plasmin-antiplasmin complexes increased almost three-fold with maximal exercise in both groups, thus indicating a marked formation of plasmin. Maximal physical exercise does not induce an exaggerated formation of thrombin and fibrin in CHF patients. The fibrinolytic response to exercise in terms of plasmin formation is not compromised in patients with dilated cardiomyopathy.

Introduction: Repeated short-term exposures to a severe degree of hypoxia, alternated with similar intervals of normoxia, are recommended for performance enhancement in sports. However, scientific evidence for the efficiency of this method is controversial with regard to anaerobic performance. Therefore, we conducted a randomized, double-blind, placebo-controlled study to investigate the effects of this new method on both anaerobic and aerobic performance., Methods: During 15 consecutive days, 20 endurance-trained men (V O2max (mean +/- SD) 60.2 +/- 6.8 mL x kg(-1) x min(-1)) were exposed each day to breathing (through mouthpieces) either a gas mixture (11% O2 on days 1-7 and 10% O2 on days 8-15; hypoxia group, N = 10) or compressed air (control group, N = 10), six times for 6 min, followed by 4 min of breathing room air for a total of six consecutive cycles. Before and after the treatment, an incremental cycle ergometer test to exhaustion and the Wingate anaerobic test were performed to assess aerobic and anaerobic performance., Results: Hypoxic treatment did not improve peak power or mean power during the Wingate anaerobic test, nor did it affect maximal oxygen uptake (V O2max), maximal power output (Pmax), lactate threshold or levels of heart rate (HR), minute ventilation (V E), oxygen uptake (V O2), or blood lactate concentration at the submaximal workloads during the ergometer test. Maximal lactate concentration (Lamax) after the tests and HRmax and maximal respiratory exchange ratio (RERmax) during the ergometer test were not significantly different between groups at any time., Conclusion: The results of this study demonstrated that 1 h of intermittent hypoxic exposure for 15 consecutive days has no effect on aerobic or anaerobic performance.

The use of oral contraceptives (OC) is associated with an increased risk of thrombosis, suggesting OC exert procoagulant and/or antifibrinolytic effects. Given that physical exercise physiologically leads to an activation of blood coagulation and fibrinolysis, this study tested the hypothesis that OC might compromise the fibrinolytic response to exercise. Fibrinolytic variables were measured in 10 women (24 +/- 2 years) using OC (a formulation containing 30 micro g ethinylestradiol and 150 micro g desogestrel) and in 11 women without OC (mean +/- SD, 27 +/- 3 years) before, during and after a 1-h run on a treadmill at a velocity corresponding to an oxygen demand of 75-80% of maximum (anaerobic threshold). Exercise testing gave rise to considerable increases of tissue-type plasminogen activator antigen by seven-fold to eight-fold in women taking and not taking OC alike. In the presence of unchanged plasma levels of plasminogen activator inhibitor-1, exercise-induced release of tissue-type plasminogen activator led to enhanced plasmin formation with respect to plasmin-antiplasmin complexes, rising by (mean +/- standard error) 701 +/- 77 ng/ml (P < 0.001) in women using OC and by 695 +/- 117 ng/ml (P < 0.001 versus baseline; NS versus OC users) in controls. The fibrinolytic response to intensive physical exercise is preserved in women using OC and is similar to women not using OC.

Exercise-induced hyperinsulinism (EIHI) is a recently described entity characterised by recurrent episodes of hypoglycaemia induced by physical exercise. The index patient for this disorder and a matched control were subjected to aerobic and anaerobic exercise tests on a cycle ergometer. Aerobic exercise was performed at an intensity of 60% of the respective 4 mmol/l lactate threshold (40 min). Anaerobic exercise with an intensity corresponding to 130% VO2max lead to exertion within 2-3 min and elicited comparable maximal lactate levels in both subjects (10-11 mmol/l). The patient experienced a massive increase in insulin from 34 to 649 mU/l after the anaerobic test, and a lower increase in insulin from 27 to 79 mU/l during the aerobic test. Insulin concentration remained unchanged during both tests in the control. Epinephrine increased in the EIHI patient, which was probably a counterregulatory response to hypoglycaemia. The activity of lactate dehydrogenase of the index patient in isolated leukocytes as well as the response to inhibition of oxamate was normal. The hypothesis of abnormal transport or metabolism of lactate/pyruvate in the beta-cells of patients with EIHI was further supported by the parallel increase of lactate and insulin in this study elicited in particular by anaerobic exercise.

Heart rate monitoring and lactate measurements are used to control exercise intensity during training at moderate altitude although there is some uncertainty about hypoxia-induced changes in these parameters at equivalent submaximal exercise intensities compared to normoxia. To study the influence of acute normobaric hypoxia (FiO2 0.15) on heart rate and performance at the individual anaerobic lactate threshold (IAT), at the 4 mmol x l(-1) threshold (AT) and at an intensity requiring 80 % of VO2max measured in the respective environment, 20 endurance-trained male athletes performed an incremental treadmill test in normoxia and normobaric hypoxia. During exercise in normobaric hypoxia, heart rate and velocity were significantly (p < 0.001) reduced with a wide individual variation at the IAT (range: - 1 to - 17 min(-1), - 0.3 to - 3.5 km x h(-1)), at the AT (- 2 to - 13 min(-1), - 0.2 to - 3.3 km x h(-1)) as well as at an intensity requiring 80 % of VO2max (0 to - 18 min(-1), - 1.1 to - 3.7 km x h(-1)). Relative VO2 at the lactate thresholds expressed as a percentage of VO2max was not significantly different compared to normoxia (86 +/- 6 % vs. 84 +/- 5 %, IAT; 90 +/- 5 % vs. 88 +/- 6 %, AT), but also showed a considerable individual variation. In conclusion, heart rate and performance have to be reduced individually to a varying extent during exercise in a hypoxic environment in order to achieve an equivalent intensity compared to exercise in normoxia.

Physical exercise leads to minor activation of blood coagulation, which appears to be balanced by a concomitant activation of the fibrinolytic system. The mechanisms underlying this physiological phenomenon are still unknown. To evaluate the role of oxidative stress for exercise-induced activation of coagulation, we investigated if supplementation with alpha -lipoic acid (LA) as an antioxidant reduces the hemostatic response to exercise. Ten young men (age, 25 +/- 4 years; maximal oxygen consumption [V o 2 max], 61 +/- 6 mL/(kg min) [mean +/- SD]) were subjected to a 1-hour run on a treadmill at a velocity corresponding to an oxygen demand of 75% to 80% of maximum (anaerobic threshold). Exercise testing was repeated in the same subjects after supplementation with LA (1200 mg/d PO) for 10 days. Molecular markers of thrombin (prothrombin fragment 1 + 2, thrombin-antithrombin complexes) and fibrin formation (fibrinopeptide A) as well as markers of the fibrinolytic activity (tissue-plasminogen activator, plasmin-antiplasmin complexes, d -dimers) and of lipid peroxidation (malondialdehyde) were determined before and immediately after exercise. Supplementation therapy with LA had no effect on hemostatic and fibrinolytic variables either at rest or in response to exercise. Likewise, concentrations of malondialdehyde at rest and after exercise were not influenced by LA. In summary, the hemostatic response to exercise is not affected by supplementation with LA in young healthy male individuals. The role of oxidative stress for exercise-induced activation of coagulation has to be defined in further studies.

Purpose: The aim of the present study was to find out if the determination of the individual anaerobic threshold (IAT) during incremental treadmill tests in normoxia and acute normobaric hypoxia (FiO2 0.15) defines equivalent relative submaximal intensities in these environmental conditions., Methods: 11 male middle and long distance runners performed a 1-h treadmill run in normoxia and hypoxia at the intensity of the IAT determined in the respective environment with measurement of lactate, glucose, heart rate, catecholamines, ventilatory parameters, and rate of perceived exertion (RPE)., Results: During the 1-h treadmill runs, speed was significantly reduced in hypoxia compared with normoxia (12.8 +/- 0.7 vs 14.7 +/- 0.7 km x h(-1)). Relative intensity expressed as a percentage of VO(2max) was similar in both environments (82-83% on the average) and elicited comparable lactate steady states [LaSS, 2.5 +/- 0.7 - 3.4 +/- 1.1 mmol x L(-1) (normoxia), 2.7 +/- 0.8 - 3.6 +/- 1.0 mmol x L(-1) (hypoxia) after 10 and 60 min, respectively] and glucose levels, but significantly reduced heart rate in hypoxia by 5 beats x min(-1) on the average. A steady state was also found for the ventilatory parameters. Plasma epinephrine and norepinephrine levels were similar in both environments. RPE was significantly lower after 40-60 min of exercise in hypoxia., Conclusions: Relative intensities in normoxia and acute hypoxia are equivalent when endurance exercise is performed with the running speed at the IAT determined in the respective environment. The heart rate-blood lactate relationship, however, is changed in hypoxia and relative submaximal exercise intensity is higher in acute hypoxia when training is performed with similar heart rate as in normoxia.

Aims: In order to investigate the muscular adaptations to a novel form of strength training, 18 male untrained subjects performed 4 weeks of low resistance-high repetition knee extension exercise., Methods: Nine of them trained on a conventional weight resistance device (Leg curler, CON/ECC group), with loads equivalent to 30% of the concentric one-repetition maximum (1RM) for both the concentric and eccentric phase of movement. The other nine trained on a newly developed computer-driven device (CON/ECC-OVERLOAD group) with the concentric load equivalent to 30% of the concentric 1RM and the eccentric load equivalent to 30% of the eccentric 1RM., Results: Training resulted in significantly (P < or = 0.05) increased peak torque and a tendency (P=0.092) to increased muscle cross-sectional area for the CON/ECC-OVERLOAD but not the CON/ECC group, while strength endurance capacity was significantly (P < or = 0.05) increased in the CON/ECC group only. RT-PCR revealed significantly increased myosin heavy chain (MHC) IIa and lactate dehydrogenase (LDH) A mRNAs, a tendency for increased MHC IIx mRNA (P = 0.056) and high correlations between the changes in MHC IIx and LDH A mRNAs (r=0.97, P=0.001) in the CON/ECC-OVERLOAD group., Conclusions: These results indicate a shift towards a more type II dominated gene expression pattern in the vasti laterales muscles of the CON/ECC-OVERLOAD group in response to training. We suggest that the increased eccentric load in the CON/ECC-OVERLOAD training leads to distinct adaptations towards a stronger, faster muscle.

In the healthy individual intensive physical exercise leads to a minor activation of blood coagulation that appears to be balanced by a concomitant activation of the fibrinolytic system. This study tested the hypothesis that vigorous exercise might give rise to an exaggerated activation of coagulation in subjects with resistance to activated protein C (APC). Molecular markers of thrombin (prothrombin fragment 1 + 2, thrombin-antithrombin III complexes) and fibrin formation (fibrinopeptide A), as well as markers of the fibrinolytic activity (plasmin-antiplasmin complexes, D-dimers), were determined in nine asymptomatic male individuals with APC resistance [age, 18 +/- 3 years; maximal oxygen consumption, 56.7 +/- 2.7 ml/kg per min (mean +/- standard deviation)] and in nine male control subjects (age, 19 +/- 4 years; maximal oxygen consumption, 56.2 +/- 3.2 ml/kg per min) after 1 h of running to exhaustion. Baseline levels of prothrombin fragment 1 + 2 were higher in individuals with APC resistance than in controls [0.67 +/- 0.06 nmol/l (mean +/- standard error) versus 0.48 +/- 0.01 nmol/l; P < 0.05]. In response to exercise, hemostatic variables significantly increased in both groups to a similar small extent. Likewise, exercise-induced changes of fibrinolytic variables in subjects with APC resistance paralleled those observed in controls. In summary, exhaustive running in subjects with APC resistance does not provoke an abnormal hemostatic or fibrinolytic response, suggesting that vigorous exercise does not imply an increased risk for thrombosis in young male subjects with APC resistance.

We investigated whether similar increments in venous plasma norepinephrine (NE) concentration caused by exercise and by intravenous NE infusion will elevate plasma norepinephrine sulfate (NES) to similar concentrations. In randomized order venous plasma NE concentration was elevated to similar concentrations by bicycle exercise (BE; 65% VO(2)max) and by intravenous NE infusion at rest (INF; 0.14 microg/min/kg). N = 11 subjects participated in the study. Increments in plasma NE and the area under curve of plasma NE were similar during BE (11.2 +/- 1.3 nM; 411 +/- 23 nM/min; means +/- S.E.) and INF (12.6 +/- 1.9 nM; 429 +/- 27 nM/min). Plasma NES was significantly elevated to similar concentrations with BE (from 5.7 +/- 1.0 to 8.5 +/- 1.3 nM) and with INF (from 5.6 +/- 0.9 to 8.9 +/- 1.0 nM). Plasma NE and NES concentration during control conditions remained unchanged. Heart rate decreased significantly to 43 +/- 1 beats/min with INF and increased significantly to 162 +/- 3 beats/min with BE. Systolic blood pressure increased with both, INF and BE (155 +/- 3 mmHg; 179 +/- 6 mmHg, respectively). Present findings firstly show that intravenously infused NE is sulfoconjugated in humans, indicating that a major part of NE is sulfoconjugated in blood or at sites easily accessible from blood. Secondly, plasma NE may be a useful additional marker for NES release.

In healthy individuals, prolonged intensive physical exercise leads to an activation of blood coagulation that results in the formation of thrombin and fibrin. This study investigated whether oxidative stress during intensive physical exercise induces tissue factor (TF) via activation of the redox-responsive transcription factor nuclear factor-kappaB (NF-kappaB). Twelve young men performed a standardized 1-h maximal run on a treadmill that gave rise to significant increases of markers of thrombin and fibrin formation. The ratio of intracellular reduced to oxidized glutathione as measured by HPLC decreased from 23.3 +/- 10.7 to 14.2 +/- 6.5 (P < 0.05), indicating the generation of free radicals during exercise. Electrophoretic mobility shift assays from nuclear extracts of peripheral blood mononuclear cells revealed that exercise testing increased NF-kappaB (p50/p65) binding activity to a NF-kappaB consensus sequence by 105 +/- 68% (P < 0.01) but did not affect NF-kappaB (p65/c-Rel) binding to a nonconsensus-kappaB-like site present in the TF promoter. Consistently, there was no exercise-induced increase in TF expression as demonstrated by TF-specific immunofluorescence staining and ELISA. Thus selective activation of NF-kappaB (p50/p65) during intensive physical exercise does not result in the expression of TF, suggesting that the TF-dependent pathway in peripheral blood mononuclear cells does not account for exercise-induced formation of thrombin and fibrin.

Objective: In the present study we investigated whether plasma catecholamine (CA) responses to short-term severe exercise (SX) are affected by different training regimen and whether this test will increase plasma catecholamine sulfates., Methods: Nine anaerobically (ANTA) and eight aerobically trained male athletes (ATA) performed a severe treadmill exercise test (SX) at similar oxygen demands, leading to exhaustion within 2-3 min., Results: The anaerobic contribution to energy supply was higher in ANTA than in ATA as indicated by the higher maximal accumulated oxygen deficit (37.5+/-3.5 vs. 22.7+/-4.4 mL x kg(-1) x min(-1)) (means +/- SE) (P<0.009) and blood lactate concentration after exercise (19.4+/-2.4 vs. 15.0+/-1.9 mmol x L(-1)) (P<0.005). In both groups plasma norepinephrine (NE), norepinephrine sulfate (NE-S), epinephrine (EPI), and epinephrine sulfate (EPI-S) increased significantly (P<0.05) during exercise with higher increments (P<0.05) in ANTA than in ATA (NE: 87.5+/-9.7 vs. 60.8+/-7.1 nmol x L(-1), P<0.034; EPI: 16.6+/-3.3 vs. 6.9+/-1.2 nmol x L(-1), P<0.009)., Conclusion: Data suggest that during this type of exercise the sympathoadrenergic system is more activated in ANTA than in ATA and seems related to the higher anaerobic contribution to energy supply in ANTA. The short duration of SX was sufficient to increase plasma NE-S and EPI-S concentration.

The aim of the study was to test the hypothesis that iron supplementation in well-trained non-iron-depleted athletes leads to an enhanced increase of total body hemoglobin (TBH) during training at moderate altitude. Therefore, the members of the national German boxing team were randomly assigned to treatment with ferrous-glycine-sulfate (1335 mg equivalent to 200mg elementary iron daily) or with placebo during 18 days of endurance training at moderate altitude (1800 m). Before and after altitude training TBH was determined by CO-rebreathing, measures of exercise performance were determined with an incremental treadmill test. Before, during and after the stay at moderate altitude erythropoietin (Epo), reticulocytes (Retics) and parameters of iron metabolism were measured in venous blood. The results show that TBH did not change significantly in the placebo-group and even slightly, but significantly decreased in the iron-treated group. However, there was a significant increase of Epo and Retics in both groups during training at moderate altitude whereas parameters of iron metabolism remained unchanged. VO2max did not change either. To test whether a training-induced hemolysis, an increased urinary iron excretion or gastrointestinal blood loss could explain the unexpected drop of TBH we tested most of the boxers again during a similar training camp at low altitude (400-1000 m) to obtain measures of hemolysis, urinary iron excretion and occult hemoglobin loss with the stools. Although there were signs of an increased erythrocyte turnover no iron loss could be observed. We conclude that 18 days of endurance training at an altitude of 1800 m does not lead to an increase of TBH in non-iron-depleted athletes with and without iron supplementation.

We tested the hypothesis that measurement of plasma catecholamine sulphate concentration after exercise reflects the overall activation of the sympathoadrenergic system during the whole period of repeated bouts of short-term exercise. A group of 11 male athletes performed two exercise tests at similar average power outputs consisting of three sets each. The tests either started with one set of three very intense sprints (95% of maximal running speed) followed by two sets of three less intense sprints (85% of maximal running speed; HLX) or vice versa (LHX). Similar mean areas under the curve of free noradrenaline (NA) during HLX and LHX [622 (SEM 13) v.s. 611 (SEM 14) nmol x l(-1) min) as well as similar mean heart rates [143 (SEM 9) v.s. 143 (SEM 8) beats x min(-1)] indicated comparable sympathetic activation during both exercise tests. Even so, plasma concentration of free NA was still significantly higher at the end of LHX than of HLX [35.7 (SEM 3.5) v.s. 22.5 (SEM 2.1) nmol x l(-1), respectively], i.e. when exercise ended with the more intense set of sprints. Plasma noradrenaline sulphate (NA-S) increased with exercise intensity showing higher mean increments after the first set of HLX compared to LHX [1.83 (SEM 0.42) v.s. 1.18 (SEM 0.29) nmol x l(-1); P<0.05]. However, after the end of HLX and LHX, increments in plasma NA-S were similar [4.52 (SEM 0.76) v.s. 4.06 (SEM 0.79) nmol x l(-1)], suggesting that NA-S response changed in parallel with the overall activation of the sympathetic nervous system during repeated bouts of short-term exercise. The results supported the hypothesis that measurement of plasma NA-S immediately after repeated bouts of short-term exercise reflects overall activation of the sympathetic nervous system during prolonged periods of this type of exercise.

Purpose: The present study was conducted to evaluate the role of the duration of exercise and the impact of the exercise type for exercise-induced activation of coagulation., Methods: Eleven male triathletes were subjected to stepwise maximal (17 min) and 1-h maximal exercise in swimming, cycling, and running. Changes of hemostatic variable sand of plasma thrombomodulin, a marker of endothelial cell activation, were monitored., Results: Irrespective of the type of exercise, alterations in markers of thrombin (prothrombin fragment 1 + 2, thrombin-antithrombin III complexes) and fibrin formation (fibrinopeptide A) were more pronounced after 1-h exercise than after stepwise maximal exercise. Hemostatic parameters rose to the highest levels after running resulting in substantial fibrin formation as indicated by fibrinopeptide A increasing from 1.33 ng.mL-1 to 2.25 ng.mL (P < 0.05) after 1-h exercise testing. Significant changes of plasma thrombomodulin were detected exclusively after running with increases from 38.2 ng.mL-1 to 44.2 ng.mL-1 (1 h, P < 0.01)., Conclusions: The data demonstrated that prolonged exercise is necessary for exercise-induced activation of coagulation resulting in thrombin and fibrin formation and suggested that endothelial cell activation possibly due to mechanical factors associated with running might play a role.

To examine the relationship between exercise intensity and activation of coagulation and fibrinolysis, we measured markers of thrombin, fibrin, and plasmin formation in 12 male subjects (mean 24+/-4 yr (SD)) before and after running on a treadmill for 1 h at two different intensities corresponding to moderate (82% maximal heart rate (HR), 68% VO2max) and very heavy (94% maximal HR, 83% VO2max) exercise. During moderate exercise plasma levels of tissue plasminogen activator (t-PA) antigen rose from 3.7+/-0.5 (mean+/-SE) to 14.6+/-1.8 ng x mL[-1] (P < 0.01) and of plasmin-alpha-antiplasmin (PAP) complexes from 2.1+/-0.3 to 4.2+/-0.7 nmol x L[-1] (P < 0.01), whereas prothrombin fragment 1+2 (PTF1+2), thrombin-antithrombin III (TAT) complexes and fibrinopeptide A (FPA) did not change significantly. In response to very heavy exercise, mean plasma levels of t-PA antigen and PAP complexes exceeded the upper limit of normal values 2.5- (P < 0.01) and two-fold (P < 0.01), respectively, while significant increases of plasma levels of PTF1+2 (P < 0.01), TAT (P < 0.05), and FPA (P < 0.01) occurred within the range of normal. We conclude that in healthy young individuals, exercise-induced activation of coagulation is well balanced by activation of the fibrinolytic system, since moderate exercise results in increased plasmin formation only, while at very heavy exercise generation of plasmin seems to exceed that of thrombin and fibrin.

Catecholamine (CA) response to hypoxic exercise has been investigated during severe hypoxia. However, altitude training is commonly performed during mild hypoxia at submaximal exercise intensities. In the present study we tested whether submaximal exercise during mild hypoxia compared to normoxia leads to a greater increase of plasma concentrations of CA and whether plasma concentration of catecholamine sulphates change in parallel with the CA response. A group of 14 subjects [maximal oxygen uptake, 62.6 (SD 5.2) ml*min(-1)*kg(-1) body mass] performed two cycle ergometer tests of 1-h duration at the same absolute exercise intensities [191 (SD 6) W] during normoxia (NORM) and mild hypoxia (HYP) followed by 30 min of recovery during normoxia. Mean plasma concentrations of noradrenaline ([NA]), adrenaline ([A]), and noradrenaline sulphate ([NA-S]) were elevated (P <0.01) after HYP and NORM compared with mean resting values and were higher after HYP [20.9 (SEM 3.1), 2.2 (SEM 0.24), 8.12 (SEM 1.5) nmol . 1(-1), respectively] than after NORM [(13.7 (SEM 0.9), 1.5 (SEM 0.14), 6.8 (SEM 0.7) nmol . 1(-1), respectively P <0.01]. The higher plasma [NA-S] after HYP (P <0.05) were still measurable after 30 min of recovery. From our study it was concluded that exercise at the same absolute submaximal exercise intensity during mild hypoxia increased plasma CA to a higher extent than during normoxia. Plasma [NA-S] response paralleled the plasma [NA] response at the end of exercise but, in contrast to plasma [NA], remained elevated until 30 min after exercise.

To examine whether exercise-induced thrombin formation is accompanied by increased in vivo plasmin formation, we measured molecular markers and neoantigens of the hemostatic system in 10 male subjects (mean 29 yr. range 19-38) before, immediately after, and 2, 8, and 21 h after a triathlon lasting 128-163 min. Thrombin-antithrombin (TAT) complexes, fibrinopeptide A (FPA), and tissue plasminogen activator (t-PA) antigen were maximally increased immediately after exercise and decreased thereafter rapidly. Prothrombin fragment 1 + 2 (PTF1 + 2), fibrin degradation products (FbDP) and plasmin-antiplasmin (PAP) complexes rose to a similar extent 0 and 2 h after exercise decreased thereafter. The maximal levels of PTF1 + 2, TAT, FPA, and FbDP were 1.5-, 2.1-, 1.8-, and 1.9-fold above baseline, respectively. This investigation shows that strenuous prolonged exercise leads to a moderate activation of blood coagulation resulting in thrombin and fibrin formation which is accompanied by a greatly enhanced plasmin generation. It is concluded that the hemostatic of healthy individuals is well kept in balance when stimulated by prolonged strenuous exercise.

In 13 middle-aged, moderately trained men (40-60 yr) we investigated the influence of anaerobic training on immunological parameters measured at rest. The 4 week anaerobic training program (two 30-min sessions weight lifting and one interval training per week; lactate levels 4-6 mM and 8-10 mM, respectively), caused a significant increase of the mean arm muscle force by 7% (handgrip test, p < 0.05). Evaluation of lymphocyte subsets was performed by means of three-colour immunofluorescence analysis (FACS). After 4 weeks of training we found a significant reduction of the CD4+ T-cell counts by 15% (p < 0.05) paralleled by a fall of naive cells (CD3+/CD4+/CD45RA+) by 16%, which, however, was statistically not significant. While percentages of CD3+ lymphocytes decreased significantly by 6% (p < 0.001), absolute numbers of CD3+ T-lymphocytes were not detectably affected and also the relative ratio of CD8+ T-cell subsets, i.e. the ratio of suppressor vs cytotoxic T-cells (CD3+/CD8+/CD11b+, CD3+/CD8+/CD11b- respectively) remained unchanged. Likewise the serum concentrations of the soluble CD8 and CD4 antigen (sCD8/sCD4) as determined by sandwich enzyme immunoassays were found to be unaffected. We conclude that 40-60 years old healthy human subjects performing anaerobic training experience on average a significant decrease of circulating CD4+ T-lymphocytes, while other parameters including the activation parameters sCD8 and sCD4 remained unchanged.

Concentrations of thrombin-antithrombin III (TAT) complexes in plasma were previously reported to be increased after a 100-km run, while fibrinopeptide A (FPA) concentration remained unchanged. Thus, antithrombin III appears to neutralize thrombin generated during running and prevents fibrin formation. To determine the clinical relevance of these findings, we compared the effects of exhaustive running (1 h, n = 10) on the plasma concentrations of prothrombin fragments F1 and F2, TAT, FPA, and beta-thromboglobulin with the effects of recreational jogging (1 h, n = 10) and exhaustive bicycling on an ergometer (1 h, n = 8). Prothrombin fragments F1 and F2 and TAT concentrations increased significantly in each group. The most significant increase in TAT concentration was measured in the running group (from 1.72 +/- 0.49 to 3.61 +/- 1.03 ng/ml, P < 0.001). The best correlation was found between the postexercise TAT and lactate concentrations (r = 0.62, n = 28, P < 0.001). Mean FPA concentrations after exercise did not exceed normal values in any of the three groups analyzed. An increase in beta-thromboglobulin concentration was measured in the running and in the cycling group. Thus, thrombin is formed, in particular, when associated with anaerobic metabolism, and platelets are activated during high-intensity exercise.

A possible contribution of exercise to the fluid retention associated with acute mountain sickness (AMS) was investigated in 17 mountaineers who underwent an exercise test for 30 min on a bicycle ergometer with a constant work load of 148 +/- 9 (SE) W at low altitude (LA) and with 103 +/- 6 W 4-7 h after arrival at 4,559 m or high altitude (HA). Mean heart rates during exercise at both altitudes and during active ascent to HA were similar. Exercise-induced changes at LA did not differ significantly between the eight subjects who stayed well and the nine subjects who developed AMS during a 3-day sojourn at 4,559 m. At HA, O2 saturation before (71 +/- 2 vs. 83 +/- 2%, P less than 0.01) and during exercise (67 +/- 2 vs. 72 +/- 1%, P less than 0.025) was lower and exercise-induced increase of plasma aldosterone (617 +/- 116 vs. 233 +/- 42 pmol/l, P less than 0.025) and plasma antidiuretic hormone (23.8 +/- 14.4 vs. 3.4 +/- 1.8 pmol/l, P less than 0.05) was greater in the AMS group, whereas exercise-induced rise of plasma atrial natriuretic factor and changes of hematocrit, potassium, and osmolality in plasma were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Physical exercise causes shortening of activated partial thromboplastin time (aPTT) and euglobulin clot lysis time. To investigate whether this activation of coagulation and fibrinolysis leads to in vivo thrombin or plasmin action after long distance running, 19 well trained male runners (36-65 years) were examined 5 to 53 min after termination of a 100 km race and 5 days later after at least 1 day without physical exercise. Compared to the control examination aPTT was decreased (30.2 +/- 2.8 vs 35.3 +/- 3.0 sec) and the following parameters were increased after the race: beta thromboglobulin (40 +/- 16 vs 23 +/- 7 ng/ml), thrombin-antithrombin III (TAT) complexes (5.5 +/- 3.4 vs 2.3 +/- 0.7 microgram/l), the fibrin(ogen) degradation products fragment E (57 +/- 15 vs 35 +/- 7 ng/ml) and B beta 15-42 (8.5 +/- 2.5 vs 6.5 +/- 2.5 ng/ml) (all p values less than 0.001). Platelet count, platelet factor 4, fibrinoepetide A (FPA) and haematocrit did not change significantly. Increased TAT complexes and unchanged FPA suggest that the generated thrombin was fully inactivated by antithrombin III (AT III) and did therefore not give rise to fibrin formation. The small increase of fibrin(ogen) degradation products indicates a minor in vivo activity of the fibrinolytic system. This investigation demonstrates the importance of AT III in the regulation of haemostasis in activated blood coagulation.

To test the hypothesis that severe hypoxia during low-resistance/high-repetition strength training promotes muscle hypertrophy, 19 untrained males were assigned randomly to 4 weeks of low-resistance/high-repetition knee extension exercise in either normoxia or in normobaric hypoxia (FiO2 0.12) with recovery in normoxia. Before and after the training period, isokinetic strength tests were performed, muscle cross-sectional area (MCSA) measured (magnetic resonance imaging) and muscle biopsies taken. The significant increase in strength endurance capacity observed in both training groups was not matched by changes in MCSA, fibre type distribution or fibre cross-sectional area. RT-PCR revealed considerable inter-individual variations with no significant differences in the mRNA levels of hypoxia markers, glycolytic enzymes and myosin heavy chain isoforms. We found significant correlations, in the hypoxia group only, for those hypoxia marker and glycolytic enzyme mRNAs that have previously been linked to hypoxia-specific muscle adaptations. This is interpreted as a small, otherwise undetectable adaptation to the hypoxia training condition. In terms of strength parameters, there were, however, no indications that low-resistance/high-repetition training in severe hypoxia is superior to equivalent normoxic training. [ABSTRACT FROM AUTHOR]