Classical altitude training was shown to cause an increase in total body hemoglobin (THB) if a certain "dose of hypoxia" is reached (moderate altitude ≥2000 m, duration ≥3 weeks). PURPOSE: To find out if already at low altitude an increase in erythropoiesis and in TBH can be induced when repetitive training camps are used. METHODS: 8 elite 400 m and 800 m runners (4 males, 4 females, 22.6±2.6 yrs, 180±11.2 cm, 67.6±11.4 kg) performed training camps in South Africa (1300 m) and Namibia (1650 m) for 20 and 22 days, interspersed by 19 days of sea-level training. A control group (CG) of 9 young well-trained runners (6 males, 3 females, 19.7±2.4 yrs, 178±5.7 cm, 66.3±11.2kg) performed comparable sea-level training. TBH was determined with the optimised CO-rebreathing method (typical error 2.5% in our hands) before and after each training camp as well as Erythropoietin (EPO), soluble Transferrin Receptor (sTfR) and Ferritin from venous blood samples. In the altitude training group (AG) EPO, sTfR and Ferritin were also repeatedly measured during the training camps. Athletes with low ferritin values received iron supplementation. RESULTS: Repeated Measures ANOVA revealed a significant (p = 0.05) increase in THB by 5.1% (0.2-13.6%) from 806±214 g to 850±235 g in the course of the 2 altitude training camps while THB remained unchanged in CG (from 770±126 g to 798±140 g, p = 0.243). During training in South Africa, EPO was significantly (p = 0.05) increased by 28% on days 10 and 17 compared to the value measured before altitude training, while in Namibia, EPO was significantly increased by 33-45% on days 2, 10 and 17 compared to the values measured after altitude training. STfR was significantly (p = 0.05) increased on day 17 of both altitude training camps by about 24% and after the training camps by about 8% while ferritin significantly decreased at the beginning of the first altitude training camp and remained slightly decreased compared to the value before altitude training. In CG, a slight, but significant decrease in sTfR was observed at the end of the study, while ferritin remained unchanged. CONCLUSION: Repetitive training at low altitude (1300-1650 m) induces an increase in erythropoiesis and, apparently, might also cause a consecutive augmentation of TBH. Supported by the Bundesinstitut für Sportwissenschaft (HA1VF070106/07)

BACKGROUND AND PURPOSE:The evidence for traumatic brain injury in amateur boxers is controversial. Hypothetically, sudden acceleration of the head due to the impact of the blow during the boxing fight might result in diffuse axonal injury or contusion. We wanted to determine whether cerebral microhemorrhages occur more often in amateur boxers than in nonboxers.MATERIALS AND METHODS:In 42 male, classical amateur boxers and in 37 healthy, nonboxing male volunteers we performed cranial MR imaging at 3T. The study protocol included a transverse dual spin-echo MR imaging sequence, a 3D sagittal magnetization-prepared rapid acquisition of gradient echo sequence, a coronal T2*-weighted sequence, and an axial time-of-flight MR angiography sequence. MR imaging data were made anonymous before 2 neuroradiologists independently evaluated the images. In addition, the following risk factors were assessed: total numbers of fights and knockouts, weight division, and duration of boxing. We compared the group proportions of microhemorrhages with Fisher test of exact probability.RESULTS:There was a statistically higher prevalence of cerebral microhemorrhages in the group of boxers (3 of 42; 7.1%) than in nonboxing persons (0 of 37; 0%). This difference was not statistically significant, however (P = .2479; Fisher exact test).CONCLUSION:Although we detected more microhemorrhages in amateur boxers than in nonboxing persons, this difference did not prove to be significant.

While there is some controversy whether anaerobic capacity might be improved after altitude training little is known about changes in anaerobic capacity during hypoxic exposure in highly trained athletes. PURPOSE To find out if acute exposure to moderate hypoxia affects anaerobic capacity in endurance-trained athletes. METHODS 18 male middle-/long-distance runners and triathletes (23.9 ± 3.9 yrs, 182 ± 6 cm, 70.8 ± 6.7 kg, VO2max 68.1 ± 4.3 ml · kg-1 · min-1) performed two supra- VO2max treadmill tests with the same speed, one in normoxia and one on a separate day after a 4 h exposure to normobarc hypoxia (FiO2 0.15). Maximal accumulated oxygen de.cit (MAOD) was determined as described by Medbø et al. (1988). Capillary blood samples from the earlobe were drawn at rest and repeatedly during 15 min of recovery for measurement of lactate and ammonia. RESULTS MAOD showed a tendency (p = 0.061) to be increased in hypoxia by 9 % on the average while maximal capillary lactate (12.8 ± 2.0 vs. 13.7 ± 2.1 mmol · L−1, p = 0.036) and maximal capillary ammonia concentration (95 ± 49 vs. 121 ± 42 μmol · L−1, p = 0.008) were significantly decreased. The reduction in time to exhaustion (144 ± 33 vs. 203 ± 55 s, p <0.001) was significantly correlated to the decrement in oxygen uptake during exercise in hypoxia (R = 0.797, p <0.001). CONCLUSION The slight increase in MAOD shows that performance during exhaustive supra-VO2max exercise in moderate hypoxia is not impaired by changes in anaerobic capacity. Supported by the Bundesinstitut für Sportwissenschaft (VF0408/01/01/2000–2001)

'The training-induced adaptation in muscle aerobic potential was blunted when training was performed during hypoxic conditions at the same relative intensity as during normoxia'. There is an ongoing controversial discussion as to whether altitude training with living and training in a hypoxic environment can cause a larger improvement in sea-level performance than equivalent training in normoxia. Besides an augmentation of total haemoglobin mass, due to the hypoxia-induced increase in erythropoiesis, enhanced muscular adaptations to endurance training in hypoxia are considered as possible mechanisms for making hypoxia an additional training stimulus. Bakkman et al., in this issue, show that hypoxia is not an additional stimulus for muscular aerobic adaptation. On the contrary, in their study, there were no changes in the activity of citrate synthase (CS) and in state 3 mitochondrial activity in biopsy samples obtained from the vastus lateralis muscles following 4 weeks of endurance training in hypoxia, although with 4 weeks of normoxic training, these variables were significantly increased (CS) or showed a tendency to be increased (state 3 mitochondrial activity). The study was performed with one-legged endurance exercise, training one leg in normoxia and the other leg in hypobaric hypoxia with equivalent relative intensity. These findings therefore suggest that adaptation of muscle oxidative function might even be impaired if endurance training is performed in hypoxia with the same relative intensity compared with normoxia and might therefore contribute to detraining, which was occasionally observed in elite athletes after altitude training.

Strength can be effectively trained by combined concentric/eccentric dynamic muscle actions in single- or multiple joint exercises performed with free weight or using training machines. For strength development, a variation of training load, repetition numbers and velocity as well as rest intervals is recommended. After onset of strength training, there is a rapid initial increase in strength due to neural adaptations. Adaptive changes of the exercised skeletal muscles, such as hypertrophy and an increase in the percentage area of fast type IIA-fibres, only take place following at least several weeks of training. These morphological muscular adaptations are caused by mechanical and/or metabolic stress of the exercised skeletal muscles and by hormonal regulation which, on the molecular level, lead to alterations of translation and transcription as well as to proliferation and incorporation of satellite cells. The results of some recently-published controlled studies suggest that two newly-developed strength training regimens might increase and modify neural and morphological adaptations. Computer-guided strength training with eccentric overload (desmodromic training) seems to increase the recruitment of fast muscle fibres during strength training, leading to distinct adaptations towards a faster muscle phenotype. Application of vibration during strength training apparently increases the neuromuscular adaptations and thereby causes acute strength and power enhancement and increased training effects. However, there still is a lack of controlled studies for desmodromic training as well as for vibration training, and additional investigations are needed before recommendations can be made for these training methods.

Neonatal myosin heavy chain (MHCneo) in small muscle fibers is considered a marker for early stages of muscle fiber development and was observed in biopsies from the trapezius muscles of power lifters (Kadi et al. 1999). PURPOSE: To find out if mRNA and protein expression of MHCneo are increased in the vastus lateralis muscle after maximum quadriceps strength training. METHODS: Vastus lateralis muscle biopsies were obtained from 26 strength-trained male athletes before and after 6 weeks of 3x/wk knee extension exercise, either in conventional concentric/eccentric mode (CON/ECC group, 24.5 ± 4.2yrs, 184 ± 7 cm, 80.5 ± 7.8 kg) or concentric/eccentric-overload mode (CON/ECC+ group, 24.1 ± 3.6 yrs, 185 ± 7cm, 80.0 ± 8.4 kg). MHCneo-mRNA was determined by quantitative RT-PCR and related to 18S rRNA. Transverse serial sections were stained for myofibrillar ATPase (pH 4.7) and histochemically using antibodies directed against i) MHCneo, ii) the neural cell adhesion molecule (NCAM, CD56) which is expressed in satellite cells, iii) MHC I, and iv) MHC II by single or double staining techniques. RESULTS: MHCneo mRNA was increased in 6 out of 15 subjects (p = 0.005) after CON/ECC+ and in 4 out of 11 subjects (n.s.) after CON/ECC training. MHCneo immunoreactive, small and intermediate-sized fibers were found only after training in biopsies with increased MHCneo-mRNA (5 CON/ECC+, 3 CON/ECC) and accounted for 4.4 ± 6.8 % (1–23%) of all analysed fibers (310 ± 140). Doublestaining revealed an exclusive colocalization of MHCneo and NCAM as well as MHC I and MHC II immunoreactivity. CONCLUSIONS: Both, the appearance of fibers coexpressing MHCneo and NCAM and the simultaneous increase in MHCneo-mRNA in biopsies from the vastus lateralis muscle after 6 weeks of heavy resistance training suggest the formation of new muscle fibers from activated satellite cells. Supported by the Bundesinstitut für Sportwissenschaft (VF 07/05/66/2004-2005)

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.

Objectives: Inter-individual variations in sea level performance after altitude training have been attributed, at least in part, to an inter-individual variability in hypoxia induced erythropoiesis. The aim of the present study was to examine whether the variability in the increase in total haemoglobin mass after training at moderate altitude could be predicted by the erythropoietin response after 4 h exposure to normobaric hypoxia at an ambient Po2 corresponding to the training altitude. Methods: Erythropoietin levels were measured in 16 elite junior swimmers before and after 4 h exposure to normobaric hypoxia (Fio2 0.15, ∼2500 m) as well as repeatedly during 3 week altitude training (2100–2300 m). Before and after the altitude training, total haemoglobin mass (CO rebreathing) and performance in a stepwise increasing swimming test were determined. Results: The erythropoietin increase (10–185%) after 4 h exposure to normobaric hypoxia showed considerable inter-individual variation and was significantly (p<0.001) correlated with the acute erythropoietin increase during altitude training but not with the change in total haemoglobin mass (significant increase of ∼6% on average). The change in sea level performance after altitude training was not related to the change in total haemoglobin mass. Conclusions: The results of the present prospective study confirmed the wide inter-individual variability in erythropoietic response to altitude training in elite athletes. However, their erythropoietin response to acute altitude exposure might not identify those athletes who respond to altitude training with an increase in total haemoglobin mass.

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.

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.

Resistance training was shown to increase muscle fiber cross sectional area (FCSA) and the type IIA fiber area. In addition, an increased mean FCSA after endurance training in normobaric hypoxia was reported by Desplanches et al. (Pflügers Arch., 1993). PURPOSE To investigate if hypoxia accentuates the effects of strength endurance training and if these changes are accompanied by changes in gene expression of different myosin heavy chain (MHC) isoforms. METHODS 19 male untrained subjects were randomly assigned to low resistance, high repetition knee extension exercise, 3x/wk for 4 weeks, either in normoxia (NORM, n = 9, 24.3±2.5 yrs, 179.3±8.4 cm, 72.9±9.0 kg) or in normobaric hypoxia (FiO2 0.12, HYP, n = 10, 25.1±2.9 yrs, 183.5±5.1 cm, 77.0±9.0 kg). Before and after training isokinetic strength tests were performed and muscle biopsy samples were taken from the right vastus lateralis muscle. Fiber types and FCSA were determined on microscopic images of ATPase stained cross sections. RT-PCR was used for the quantitation of MHC mRNA. RESULTS No differences between NORM and HYP were found for any of the parameters. The training led to increased strength endurance capacity (about 9 %) in both groups. FCSA and MHC mRNAs did not change significantly. The percentages of type IIA fibers showed a tendency to increase with corresponding decrease of type I. Relative changes in type IIA and I fiber areas correlated with changes in the respective MHC mRNAs (r = 0.634, p = 0.027 and r = 0.683, p = 0.015). A positive correlation was evident between the relative IIA fiber area and strength endurance capacity after training (r = 0.728, p = 0.005). CONCLUSION Severe normobaric hypoxia does not accentuate the effects of strength endurance training on fiber type distribution and FCSA. The observed changes are accompanied by changes in MHC gene expression. Supported by DFG and Bundesinstitut für Sportwissenschaften

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 ( F iO 2 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.

Results reported by Desplanches et al. (Pfügers Arch., 1993) suggest that strength endurance training performed in normobaric hypoxia with recovery in normoxia leads to a greater increase in muscle cross sectional area (CSA) than equivalent normoxic training. To find out whether hypoxia is an additional factor for the development of muscle hypertrophy 19 male subjects were randomly assigned to a 4wk weight resistance training of the quadriceps femoris performed 3x/wk as low resistance, high repetition knee extension exercise either in normobaric hypoxia (FiO2O 0.12, HYP, n = 10, 25.1 ± 2.9 yr, 183.5 ± 5.1 cm, 77.0 ± 9.0 kg) or in normoxia (NORM, n = 9, 24.3 ± 2.5 yr, 179.3 ± 8.4 cm, 72.9 ± 9.0 kg) after a 3wk lead-in training in normoxia. After the 4wk training period there was a significant (p < 0.05) increase of strength endurance capacity (SEC) measured as the work performed in an all-out-test on an isokinetic device (50 repetitions, 180°s−1) from 56.0 ± 11.4 to 60.5 ± 10.6 J/kg in HYP and from 59.6 ± 7.3 to 64.7 ± 7.2 J/kg in NORM. However, CSA of the quadriceps femoris determined with magnetic resonance imaging increased significantly (p < 0.05) only in NORM from 86.2 ± 13.4 to 89.2 ± 15.0 cm2 (HYP 89.3 ± 11.0 to 90.4 ± 11.0 cm2). There were no significant differences between HYP and NORM in the described changes. The results show that strength endurance training in hypoxia does not have greater effects on SEC or CSA than equivalent training in normoxia. Supported by Bundesinstitut für Sportwissenschaft, VF 0407/01/04/98

PURPOSE The purpose of this study was to find out whether iron repletion leads to an increase in red blood cell volume (RBV) and performance capacity in iron-deficient nonanemic athletes. METHODS 40 young elite athletes (13-25 yr) with low serum ferritin (< 20 microg.L-1) and normal hemoglobin (males > 13.5 g.dL-1, females > 11.7 g.dL-1) were randomly assigned to 12-wk treatment with either twice a day ferrous iron (equivalent to 2 x 100 mg elemental iron) or with placebo using a double blind method. Before and after treatment, hematological measures and parameters of iron status were determined in venous blood. RBV, blood volume (BV), and plasma volume (PV) were measured by CO rebreathing. For determination of the aerobic and anaerobic capacity (maximal accumulated oxygen deficit, MAOD), the athletes performed an incremental as well as a highly intensive treadmill test. RESULTS After 12 wk, ferritin levels were within the normal range in the iron-treated group (IG) with a significant (P < 0.001) mean increase by 20 microg.L-1 opposed to a slight nonsignificant decrease in the placebo group (PG). RBV did not change significantly in either group nor did any of the hematological measures. However, only in IG there were significant increases in VO2max and in O2 consumption in the MAOD test. MAOD and maximal capillary lactate concentration remained unchanged in both treatment groups. CONCLUSIONS The results indicate that in young elite athletes with low serum ferritin and normal hemoglobin concentration iron supplementation leads to an increase in maximal aerobic performance capacity without an augmentation of RBV.

Although it is well known that athletes have considerably larger blood volumes than untrained individuals, there is no data available describing the blood volume variability among differently trained athletes. The first aim of the study was to determine whether athletes from different disciplines are characterized by different blood volumes and secondly to what extent the blood volume can possibly limit endurance performance within a particular discipline. We investigated 94 male elite athletes subdivided into the following 6 groups: downhill skiing (DHS), swimming (S), running (R), triathlon (TA), cycling junior (CJ) and cycling professional (CP). Two groups of untrained subjects (UT) and leisure sportsmen (LS) served as controls. Total hemoglobin (tHb) and blood volume (BV) were measured by the CO-rebreathing method. In comparison to UT (mean +/- SD: tHb 11.0 +/- 1.1 g/kg, BV 78.3 +/- 7.9 ml/kg) tHb and BV were about 35 - 40 % higher in the endurance groups R, TA, CJ, and CP (e. g. in CP: tHb 15.3 +/- 1.3 g/kg, BV 107.1 +/- 7.0 ml/kg). Within the endurance groups we found no significant differences. The anaerobic discipline DHS was characterized by very low BV (87.6 +/- 3.1 ml/kg). S had an intermediate position (BV 97.4 +/- 6.1 ml/kg), probably because of the immersion effects during training in the water. VO(2)max was significantly related to tHb and BV not only in the whole group but also in all endurance disciplines. The reasons for the different BVs are an increased adaptation to training stimuli and probably also individual predisposing genetic factors.

OBJECTIVEIn 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.METHODSNine 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.RESULTSThe 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).CONCLUSIONData 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.