INTRODUCTION: Strength training for heart patients seemed not to be indicated until recently. There was fear that this kind of training could lead to malignant ventricular arrhythmia and to inappropriate blood pressure increase. This opinion is changing, however, since cross-sectional strength studies with heart patients showed no increased risks, even for patients with severe heart failure. METHODS: We examined 20 patients (10 in a training group, 10 in a control group) with stable coronary heart disease, 6 or more months after acute incidence, such as myocardial infarction, PTCA or heart surgery. The left ventricular function was slightly to moderate reduced (shortening fraction minimum 0.24). All patients had an echocardiography, a bicycle ergometer test, VO2 max test, a double leg press under ECG and bloodpressure monitoring, additionally blood samples were taken. The training group underwent a normal fitness training for 3 months, twice a week. The training was performed under the supervision of a physician and an experienced physiotherapist. The training consisted of 10 different exercises for shoulder, chest, arm muscles, leg extensors and flexors and abdominal muscles. During the first 4 weeks patients trained with 10 repetitions per exercise with 50% pmax, in the following 4 weeks with 2 series each of 10 repetitions per muscle group, respectivly 3 series in the last 4 weeks. The control group participated once a week (1h) in a regular coronary sports group and trained on their own (log book). RESULTS: During the whole strength training there was no cardiovascular or orthopedic problem. The left ventricular function and the end-diastolic diameter remained unchanged in both groups. There was a clear improvement in the bicycle ergometer in the training group. Cholesterol and triglyceride level decreased slightly. The control group showed no clear improvement. CONCLUSION: Our study shows that strength-endurance training under controlled conditions could be recommended for heart patients with good to moderate decreased LV function.

807 To evaluate training-related alterations in the hypothalamo-pituitary-adrenocortical system as a possible indicator of overtraining and regeneration, we performed CRH stimulation tests in 7 junior amateur cyclists (age 17±1 yrs, height 179±2 cm, body mass 64±5 kg, VO2max 56±7 ml*kg⁁−1*min⁁−1) after a synchronisation cycle of 2 weeks (B; median 435 km*wk⁁−1, 50%ROC 226-561) following a hard and long-lasting training/competition season of 8 month, after 2 weeks of to 52 % reduced cycling volume (I), and after 3 more weeks of to 42 % reduced training (F) compared to B, respectively. Baseline resting ACTH (median 4.8 pmol × l⁁−1, 50%ROC 2.9-6.0) and cortisol levels (median 257 mmol × 1⁁−1, 50%ROC 229-441) were in the normal range with an appropriate release in the CRH stimulated pituitary-adrenal function test. After the first 2 weeks of only slight training reduction (I), cortisol release was only ∼50 % by over 70 % CRH release on an in total elevated level of these hormones. Only when the training volume was further reduced for 3 more weeks (F), ACTH and cortisol resting levels and release returned to similar values as at baseline. In conclusion, the organism seems to react to overload, which was also reflected by a reduced or stagnating performance in graded cycle ergometer tests and 10-km outdoor time trials, with hyposensitivity of target organs as a protection against possible damage. The duration necessary for recovery after prolonged and intensive training/competition periods should be rather more than 2 weeks than less with only low-intensity, low-volume activities.

Background. Aim was to answer the question whether resting laboratory parameters are suitable for monitoring intensive endurance training at moderate energetic demands. This was designed since markers of overtraining at high energetic demands, e.g. mild anemia,leukopenia, iron deficiency, reduced serum albumin, glucose, triglyceride, triglyceride-rich cholesterol (LDL, VLDL), free fatty acid, increased plasma noradrenaline levels, and decreased basal catecholamine excretions were recommended.Methods. A prospective 6-wk, 6-dys/wk intensive steady state and interval cycle ergometer training of 40-60 min/dy was performed. Total load was about 6-time pretraining activities followed by a 2-wk, 2-hour/wk regenerative training period. Six recreational athletes (VO(2)max 51.5+/-4.5 ml.kg(-1).min(-1)) participated and finished the study. A large pattern of resting hematological, blood-chemical, and hormonal parameters was tested regarding suitability for monitoring overtraining.Results. After 3 wks, submaximum and maximum performance were significantly increased, stopped improving between wk 3 and 6, or deteriorated. No supercompensation occurred after regeneration, but a decrease in work output. Lack of progression and supercompensation, and decreased maximum work output indicate a critical stage in the training process.Conclusions. All examined resting laboratory parameters failed to reflect this critical stage except for a significant decrease in serum glucose, ferritin, and free fatty acid concentrations.

PURPOSEThe parasympathetic, Addison type, overtraining syndrome represents the dominant modern type of this syndrome. Beside additional mechanisms, an autonomic or neuroendocrine imbalance is hypothesized as underlying.METHODS/RESULTSSeveral findings support this thesis. During heavy endurance training or overreaching periods, the majority of findings give evidence of a reduced adrenal responsiveness to ACTH. This is compensated by an increased pituitary ACTH release. In an early stage of the overtraining syndrome, despite increased pituitary ACTH release, the decreased adrenal responsiveness is no longer compensated. The cortisol response decreases. In an advanced stage of overtraining syndrome, the pituitary ACTH release also decreases. In this stage, there is additionally evidence for decreased intrinsic sympathetic activity and sensitivity of target organs to catecholamines. This is indicated by decreased catecholamine excretion during night rest, decreased beta-adrenoreceptor density, decreased beta-adrenoreceptor-mediated responses, and increased resting plasma norepinephrine levels and responses to exercise. However, this complete pattern is only observed subsequent to high-volume endurance overtraining at high caloric demands.CONCLUSIONThe described functional alterations of pituitary-adrenal axis and sympathetic system can explain persistent performance incompetence in affected athletes.

BACKGROUND:Objective of this study was to get more insight in hematology, biochemistry, and endocrinology of ultra-endurance exercise, to improve knowledge in this field, supplementation, and medical care of affected athletes.METHODS:A large body of individual hematological, biochemical, and endocrinological parameters was analyzed in the blood taken from ultra-athletes before and after completing the 1993 Colmar ultra triathlon covering 7.5 km swimming, 360 km cycling, and approximately 85 km running.PARTICIPANTS:Nine experienced ultra-athletes participated in the study. A follow-up was not possible since the athletes left Colmar within 24 hrs after the contest.RESULTS:The athletes finished the ultra-contest at rankings 4, 5, 7, 8, 9, 11, 18, 22, 23 in a total time between 23:38:53 and 27:54:30 hr:min:sec. Their final body mass (68.6 +/- 1 kg) was significantly lower than at baseline (71.9 +/- 4.2 kg). Non of the athletes made use of medical care. Data after this contest reflect mild hyponatremia, intravascular hemolysis, increased triglyceride turnover, acute-phase reaction, hyperaldosteronemia 2061 +/- 1013 pmol.L-1), hypercortisolemia 971 +/- 486 nmol.L-1), hyper-growth-hormonemia (median 6.8 ng.ml-1), hypoinsulinemia, hypo-free-testosteronemia (42 +/- 17 pmol.L-1), protein catabolism, depressed testicular function, oliguria, and muscle cell leakage.CONCLUSIONS:In our opinion, data presented do not reflect any acute health risks in healthy athletes who are well prepared and carefully supplied during such a contest.

1289 It is important in rowing training to improve force and endurance capacity. The endurance capacity was traditionally considered to be more dependent on muscle fiber type I while force development more on type II. However, muscle fibers have been currently proven to contain heterogeneous contractile proteins which may determine force or endurance capacity. This study was designed to investigate muscular adaptation to a 4-week-training on the protein level (myosin heavy chain I and II, i.e. MHC I and II, and actin). Ten well trained rowers were enrolled in the study. The training program was divided into 4 phases with emphasis on force development, high intensive endurance and rowing specifically endurance training, and World Championships, respectively. Muscle samples were taken from M. vastus lateralis before training and at end of each training phase by fine needle biopsy. Protein analysis was performed by standard Western blot with specific antibodies, and followed by densitometry. Actin increased during training and decreased after the Championship. MHC II increased clearly and reached its peak level after the force training phase and decreased gradually during the endurance training. During endurance (including sports specific) training, MHC I increased progressively and reached its maximum level. In conclusion, force training leads to increase of MHC II while endurance training to MHC I increment. The dynamic changes of contractile proteins can be observed during a relative short training period, which may provide useful information for evaluation of training strategies.

The minimal rectangular current pulse that produces a single contraction of reference muscles at different pulse durations has been recommended as a marker of the neuromuscular excitability (NME) of skeletal muscles. NME is improved in well-trained, non-fatigued endurance athletes and deteriorates after prolonged heavy exercise and high-volume overtraining. The hypothesis was tested that a deterioration in NME also indicates an early stage in the overtraining process during high-intensity endurance training. Six subjects participated for 40–60 min per day in a 6-week, 6-days-per-week, intensive, steady-state and interval training program using a cycle ergometer. Training was stopped each day on volitional exhaustion. On day 7 of each week training was of low intensity for about 30–40 min. Submaximum and maximum power output were significantly increased after 3 weeks, but there was no further improvement, rather a deterioration after week 6 compared to week 3. Even after 2 weeks of regeneration no supercompensation was evident, rather a decrease in maximum power output. NME was slightly improved after 3 weeks, but deteriorated after 6 weeks, and was again normalized after 2 weeks of regeneration. The discrepancy between normalization of NME and still-deteriorated performance ability after 2 weeks of regeneration reflects additional significant, and probably central mechanisms that explain persistent performance incompetence. Deterioration in NME may indicate an early stage in the overtraining process during high-volume as well as high-intensity endurance overtraining, but normalization does not necessarily indicate sufficient regeneration.

To exclude overload during recreational bicycle hiking 10 CHD patients with moderate LVD (61±5ys,EF 53±6%;EC 2.0±0.5watts·kg1)7.3±3.9 ys after heart attack and 8 healthy controls (61±25 ys,EF 61%;EC 2.4±0.4 watts·kg-1) performed a bicycle ride covering 5 sections of 5 - 7 kms with a 5-10 min-break after each section, (total distance 31.5 kms, average velocity 16.4 kms·h-1, temperature 25-31°C; humidity 34-51%). The day before, 5/3/2 patients finished a graded ergometric test because of fatigue/dyspnea/coronary insufficiency. Measured variables during field test: Total pattern of hematological and blood-chemical parameters(before/after); blood pressure, blood lactate, serum glucose levels(before/each break/after); urinary catecholamine excretion (during the ride vs. 24 h-control period); ECG (continuously). Results: Maximum responses for HR amounted to 92±14 (CHD) vs. 109±15 bpm (controls), for RR to 131/80±15/11 (CHD) vs. 133/78± 18/10 mm Hg, for lactate to 1.86±0.38 (CHD) vs. 2.34±1.03mmol·L-1. Average glucose levels decreased in both groups. Moderate increases in catecholamine excretion, HC values, fibrinogen levels and decreases in triglycerides (TG, VLDL, LDL) were observed in both groups. Echo/Dopplercardiographic parameters didn't show any significant change. Conclusions: Cardiac and metabolic overload can be excluded in the examined patients.

The hypothesis was tested that changes in resting hematological, blood-chemical, and endocrinological parameters can indicate an early stage in the overtraining process during high-intensity endurance training as earlier described for such parameters during high-volume training. 6 subjects(25±1 ys, VO2max 52±5 ml·ml-1·kg-1) participated 40-60 mins per day in a “6 week-6 days per week” high-intensity steady state (90-96% of 4LT) and interval training (117-127% of 4LT) using a cycle ergometer, which stopped each day on muscular exhaustion. On day 7 each week, training was regenerative. Total training was about 5 to 7-times their usual activities, followed by 2 weeks of regeneration. Submaximum and maximum power output were significantly increased after 3 weeks, stopped improving between weeks 3 and 6 or deteriorated. No supercompensation was evident after regeneration, rather a decrease in maximum power output, which points to an early stage in the overtraining process. An extensive pattern of hematological, blood-chemical, and endocrinological parameters, including urea, cortisol, free testosterone, catecholamines etc, failed to reflect this early stage in the overtraining process, except for serum ferrtin and glucose levels.

Introduction. `Sleep high - training low' (SHTL) has reportedly an effect to improve physical performance and this effect is assumed to be increase of oxygen delivery. However, the cardiac function which may contribute to oxygen delivery, has not been studied. This study was designed to investigate the effect of SHTL on cardiac functions. Methods. 21 healthy well-trained thiathlon athletes, aged 21±5 yrs, were divided into SHTL- and SL-group (11 and 10, respectively). Performing the same training program at sea level for 2 weeks, the subjects of SL-group lived at sea level, while those of SHTL-group stayed at an altitude of 1950m (>12h/day). Doppler echocardiography was performed at rest at sea level before and immediately after the training program. Results. The diameters of left atrium, aortic root and end-diastolic left ventricle did not change after the training program, and there was no significant difference between both groups. After the training the left ventricular end-systolic diameter of SHTL-group decreased by 10.6%(P<0.05) while that of SL-group did not change. In SHTL-group shortening fraction and ejection fraction increased from 33.5% to 38.5% and 61.9% to 75.9%, respectively, and the ratio of pre-ejection period to left ventricular ejection time was reduced by 18.2% (P<0.01), while those of SL-group did not change significantly. The peak flow velocity of early filling (E) and late filling (A) as well as E/A did not change significantly, no difference between both groups. Conclusion. Two-week SHTL did not clearly affect the diastolic functions but improved systolic functions significantly, which probably as a result from an improved ventricular contractibility.

Introduction: Since glucose is the main fuel for muscular work, reduced levels of blood glucose during exercise may affect performance. This study was designed to examine wether the suppressed blood glucose is accompanied by reduced performance. Methods: Following 3 days of recovery, 54 well trained rowers(aged 18 ± 1 yr., weight 77 ± 10 kg and height 186 ± 8 cm) performed an incremental test to exhaustion on a Concept II rowing ergometer before and after a training camp (22-26 days, 3.06 ± 0.17 h training/day). Lactate [La] and glucose [Glc] were measured electrochemically from capillary blood samples. From the plot of La and Glc versus performance lactic threshold at 4 mmol/l [LAT] and performance at minimal Glc [PGlmin] rsp. [Glcmin] were estimated using spline functions. Results: Maximum performance and the performance at LAT increased after the training (404.3 ± 66.6 W to 415.6 ± 69.2 W and 301.9 ± 56.5 W to 325.8 ± 59.2 W, rsp. p<0.01). During exercise, Glcmin decreased from 4.25 ± 0.64 mmol/l to to 3.59 ± 0.46 mmol/l (p<0.01) after the training, while corresponding performance increased from 253.9 ± 68.6 W to 319.5 ± 77.3 W (p<0.01). Glc at end of exercise decreased from 5.81 ± 0.92 mmol/l to 4.65 ± 1.03 mmol/l (p<0.01). Conclusion: A suppressed blood glucose curve during exercise is not accompanied by a reduced performance. These findings probably result from an improved utilization of glucose.

The hypthesis was tested, that a deterioration in NME of stressed skeletal muscles indicates an early stage in the overtraining process also during high-intensity endurance training as earlier shown for high-volume endurance training. As marker of NME, the minimal rectangular current pulse was used which produces a single contraction of muscle fibers at different pulse durations. 6 subjects (26 ± 1 ys; VO2max 52±5 ml·kg-1min-1) participated 40-60 min per day in a“6 week-6 days per week” intensive steady state (90-96% of 4LT) and interval cycle ergometer training (117-127% of 4LT) which stopped each day on muscular exhaustion. On day 7 each week, training was regenerative. Submaximum and maximum power output were significantly increased after 3 weeks, stopped improving between weeks 3 and 6 or deteriorated. Even after 2 weeks of regeneration no supercompensation was evident, rather a decrease in maximum power output. NME was slightly improved after 3 weeks, deteriorated after 6 weeks, and improved again during regeneration. Conclusion: Deterioration of NME may also indicate an early stage in the overtraining process during high-intensity endurance training.

The hypothesis was tested that high-volume endurance training can be monitored using hematological and blood-chemical parameters as markers of an early stage in the overtraining process. Eight experienced distance runners participated in a prospective, experimental, controlled study. The study consisted of an unaccustomed average 103% increase in training volume (ITV) within 4 weeks (average final volume: 174.6 km per week). A year later, 9 runners performed the additional 4-week control study that consisted of an unaccustomed average 152% increase in intensive training measures (ITI). Average total volume amounted to 61.7 km (week 1) and 84.7 km (week 4). Seven athletes participated in both studies. Simultaneously to performance diagnostics, a comprehensive pattern of hematological and blood-chemical parameters was determined. During ITV, submaximum running performance was improved after 2 weeks, stopped improving between week 3 and 4; maximum performance did not increase rather was decreased after week 4 compared to baseline as indication of an early stage in the overtraining process. During ITI, submaximum and maximum running performances increased continuously. In contrast to ITI, the following parameters decreased significantly during ITV: White blood cell count, serum iron, ferritin, VLDL-(very low density lipoproteins), LDL (low density lipoproteins)-cholesterol, albumin, resting and maximum free fatty acid, maximum lactate, resting, submaximum and maximum glucose, summed amino acid, resting, submaximum and maximum ammonia concentrations, whereas prothrombin time increased significantly. During high-volume endurance training a multifactorial and longitudinal approach considering either a performance incompetence and an individually different range of symptoms and alterations in hematological and blood-chemical parameters can help to recognize an early stage in the overtraining process.

Overtraining can be defined as "training-competition > > recovery imbalance", that is assumed to result in glycogen deficit, catabolic > anabolic imbalance, neuroendocrine imbalance, amino acid imbalance, and autonomic imbalance. Additional non-training stress factors and monotony of training exacerbate the risk of a resulting overtraining syndrome. Short-term overtraining called overreaching which can be seen as a normal part of athletic training, must be distinguished from long-term overtraining that can lead to a state described as burnout, staleness or overtraining syndrome. Persistent performance incompetence, persistent high fatigue ratings, altered mood state, increased rate of infections, and suppressed reproductive function have been described as key findings in overtraining syndrome. An increased risk of overtraining syndrome may be expected around 3 weeks of intensified/prolonged endurance training at a high training load level. Heavy training loads may apparently be tolerated for extensive periods of time if athletes take a rest day every week and use alternating hard and easy days of training. Persistent performance incompetence and high fatigue ratings may depend on impaired or inhibited transmission of ergotropic (catabolic) signals to target organs, such as: (I) decreased neuromuscular excitability, (II) inhibition of alpha-motoneuron activity (hypothetic), (III) decreased adrenal sensitivity to ACTH (cortisol release) and increased pituitary sensitivity to GHRH (GH release) resulting in a counter-regulatory shift to a more anabolic endocrine responsibility, (IV) decreased beta-adrenoreceptor density (sensitivity to catecholamines), (V) decreased intrinsic sympathetic activity, and (VI) intracellular protective mechanisms such as increased synthesis of heat-shock proteins (HSP 70) represent a complex strategy against an overload-dependent cellular damage.

The hypothesis was tested that unaccustomed high-volume training goes along in distance runners with an alteration in markers of beta-Adrenoreceptor(b-AR) function, since down-regulated b-AR have been described after high-volume endurance training. 8 marathoners participated in a “4 week-100% increase in training volume study” (ITV), and a year later 9 in a “4 week-150% increase in training intensity study” (ITI); 7 participated in both studies. ITV (i) did not improve submaximum performance, and (ii) decreased maximum performance, whereas ITI improved submax. and max. performances. ITV-related performance deterioration and increased fatigue ratings point to an early stage in the overtraining process. As markers of b-AR function, (iii) blood lactate, (iv) serum glucose, (v) free fatty acids levels, and (vi) heart rate responses were significantly lower at final graded treadmill testing compared to baseline. This pattern went along with (vii) higher plasma noradrenaline responses pointing to an increased but frustrating noradrenaline release and decreased sensitivity to catecholamines. Since the total pattern (i-vii) agreed completely with experimental results in athletes taking beta-blockers, high-volume endurance overtraining is equal to partial beta-Adrenoreceptor blockade.

The hypothesis was tested, that a deterioration in NME is prevented during prolonged heavy exercise by carbohydrate supplementation, since NME of stressed muscles deteriorates during prolonged heavy exercise and high-volume and high-intensity overtraining. As marker of skeletal muscles' NME, the minimal rectangular current pulse was used, that produces a single contraction of muscle fibers at different pulse durations. 6 cyclists (24.8 ± 3.9 ys, 392 ± 38 Watts maximum power output) participated in a double-blind, randomized, controlled study. Prolonged exercise consisted of 2 hours cycling, first hour at 75% of 4 mmol lactate performance (4LT), second at 65% of 4LT, followed by a standardized 30 min break and a final ramp test to discriminate degree of exhaustion. Saccharose was supplemented (15 g in 0.3 L water; saccharose test) or not (only water; control test) at baseline, and after 30, 60, and 90 mins. Ramp test performance was significantly higher in the saccharose test 388 ± 34 Watts) compared to control test (342± 0 Watts). As expected, NME of vastus medialis muscle deteriorated in the control test. Deterioration was completely prevented in the saccharose test. These results indicate that deterioration in NME during prolonged heavy exercise may be related may be related to a deterioration in energy flux rate dependent on decrease in glycogen supplies.

To test the overtraining-related "imbalanced amino acid hypothesis" (19), the influence of an unaccustomed average 103 %.4 wk-1 increase in training mileage (ITV) on performance and on serum levels of individual amino acids (AAs) was examined in distance runners and controlled by an unaccustomed average 152%.4 wk-1 increase in tempo-pace and interval runs (ITI). Two mmol.l-1 lactate performance (2 LP) increased, 4 LP stagnated and total running distance (TD) decreased in the incremental test during ITV--which may indicate an ITV-dependent overtraining--in contrast to an ITI-related increase in 2 LP, 4 LP and TD. The summed serum AAs decreased in ITV (2744 +/- 534 vs 2933 +/- 663 umol.l-1; p < 0.05) in contrast to an ITI-related increase (3541 +/- 657 vs 3252 +/- 885 umol.l-1; p < 0.05) with an average 29% higher final summed AAs concentration during ITI (p < 0.05). During ITV 12 individual AAs decreased by 6-17%, 8 remained constant and 3 increased (Cys, Met, fTrp) by 6-19%, as opposed to an ITI-related increase in 16 AA by 6-55%. The observed ITV-related changes in serum AAs profile were smaller than after completing contests as a marathon, a 100 km-run or an ultra-triathlon. It may be concluded that the observed small changes in AAs profile or AAA/BCAA and AA/LNAA ratios only represent an epiphenomenon without recognizable influence on incremental test performance, since increases in fTrp/LNAA ratios (+28% in ITV vs +45% in ITI) were found to be related both to performance impairment (ITV) and improvement (ITI).

This study was designed to test the hypothesis that the arm muscles are fatigued prior to the leg muscles in rowing exercise. 13 well-trained male rowers performed 2.5 min rowing ergometry with maximal voluntary effort at a frequency of 20 strokes/min. The surface electromyographic (EMG) activity was measured from the dominant M. biceps brachii (BB) and M. vastus lateralis (VL) with silver chloride electrodes 8 cm apart and a sampling frequency of 1000 Hz. The values taken from the 1st and last 30 seconds (30s) were averaged for median frequency (MF), mean power frequency (MPF) and root mean square (RMS) of the EMG amplitude and maximal power output (Pmax). The results show that between the 1st and last 30s of rowing, Pmax decreased significantly by 27 Watts (from 417 to 390 Watts, P=0.01). While MF and MPF of BB decreased significantly from 1st to last 30s (7.2%, P<0.03 and 6.7%, P<0.01, respectively), MF and MPF of VL kept constant (1.3% and 1.0%, respectively, NS). Additionally, RMS of BB showed a trend of an increase by 9.8% (P=0.08) while it of VL remained unchanged (0.7%, P=0.5). Since a decrease of MF and MPF and an increase of RMS are the electromyographic phenomena of muscular fatigue and these were found in BB but not in VL in the present study, it can be concluded that the decrease of Pmax in the last 30s can be contributed to fatigue in arm muscles prior to leg muscles in rowing exercise.

Since we failed to induce an overtraining syndrome in distance runners by 150%*4wks-1 increase in intens. training (ratio ext./intens. training:5.8,3.2,3.1,2.7, wk 1 - 4), we tried it again in 6 less experienced athletes (26.1±1 ys; VO2max 51.5±4.5 ml) by 6 wk bic.erg.training (average ext./ intens.train.ratio:0.17). Results: During graded exercise, performance was increased in wk 3 (+36%) at 2 mmol lactate(P2), decreased in wk 6 (-9% vs wk 3), and after 2 wks of recovery (-11% vs wk 3); P4 was increased in wk 3 (+8%, stagnated in wk 6, and after recovery; total work (summed time*watt) was increased in wk 3 (+8%), stagnated in wk 6, and decreased after recovery (-8% vs baseline). Since glucose-exercise curce in wk 6, after recovery, and glucose response to iv-noradrenaline were suppressed, P2, P4 may have been overestimated (decreased glycogen stores). Suppressed performance and neuromusc. excitab., lack of supercompensation, may indicate an early overtraining stage. The only significant haemotological or blood-chemical change was a decrease in ferritin (-26% in wk 6, -67% vs baseline after recovery). Conclusion: Less adapted athletes may be at risk to get overtrained during monotonous, intensive, non-cyclic training of more than 3 wks with ext./intens.train.ratio << 1. Haematological, blood-chemical parameters, or basal catechol.excr. were not suitable to monitore such a training at a daily caloric demand of 2815±647kcal.