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.

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 Po 2 corresponding to the training altitude. Methods: Erythropoietin levels were measured in 16 elite junior swimmers before and after 4 h exposure to normobaric hypoxia (Fio 2 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.

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 ( FiO(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.

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.

Physical activity is considered an important factor in attaining bone mass. However, the mechanisms by which exercise affects bone metabolism are not completely understood. The present study was performed to investigate the effects of aerobic and anaerobic exercise on bone turnover. Twenty healthy young males (aged 20 -29 years) were followed through an 8-week program of aerobic (n ‫؍‬ 10) and anaerobic training (n ‫؍‬ 10). Ten age-matched individuals served as controls. Serum bone-specific alkaline phosphatase (BAP), serum osteocalcin (OC), and urinary pyridinoline (Pyd) and deoxypyridinoline (Dpd) were determined as indices of bone metabolism. After 4 weeks of aerobic training, serum BAP and OC ( p < 0.01), and urinary Pyd ( p < 0.001) and Dpd ( p < 0.01) were significantly reduced. After 8 weeks, BAP and OC levels had returned to baseline values, whereas the urinary cross-link excretion remained low. In the anaerobic training group, elevated levels of BAP ( p < 0.05 vs. week 4), OC ( p < 0.05 vs. week 4), and Pyd ( p < 0.01 vs. week 0) were observed after 8 weeks of exercise. Changes in urinary Pyd and Dpd (week 0 vs. week 8) were positively correlated with changes in the mean power level in the Wingate test, a parameter of the anaerobic performance capacity (r ‫؍‬ 0.50 and r ‫؍‬ 0.55, p < 0.01, respectively). In the controls, no significant changes in biochemical markers were observed. We conclude that aerobic and anaerobic training excert different effects on bone metabolism. While aerobic training led to changes compatible with reduced bone resorption activity, anaerobic training seems to result in an overall accelerated bone turnover. Therefore, the impact of physical activity on bone turnover may depend on the kind of exercise performed. (J Bone Miner Res 1998;13:1797-1804)

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.

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.

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.