Monitoring intensive endurance training at moderate energetic demands using resting laboratory markers failed to recognize an early overtraining stage.

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 (VO2max 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.

Autonomic imbalance hypothesis and overtraining syndrome.

PURPOSE: The 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/RESULTS: Several 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. CONCLUSION: The described functional alterations of pituitary-adrenal axis and sympathetic system can explain persistent performance incompetence in affected athletes.

Overtraining and the BCAA hypothesis.

The purpose of this review was to give an answer to the question whether there are convincing data to support the hypothesis of an amino acid imbalance as one possible mechanism to explain overtraining syndrome. Animal studies point to an enhanced synthesis of the neurotransmitter 5-hydroxytryptamine through an amino acid imbalance at the blood-brain barrier with a preferable tryptophan uptake into the brain, resulting in premature fatigue. Human studies, however, show contradictory results, mainly because of nonstandardized methodology, so that a final conclusion cannot be made at present. BCAA supplementation in addition to standard carbohydrate ingestion during sustained exercise seems to be of no eminent advantage to delay fatigue. The overall results concerning the BCAA hypothesis to explain overtraining are inconclusive and require more controlled experimental research.

Ultra-triathlon-related blood-chemical and endocrinological responses in nine 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.

Influence of an unaccustomed increase in training volume vs intensity on performance, hematological and blood-chemical parameters in distance runners.

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.

Training and overtraining: an overview and experimental results in endurance sports.

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.

Monitoring high-intensity endurance training using neuromuscular excitability to recognize overtraining.

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.

Unaccustomed high-mileage vs intensity training-related changes in performance and serum amino acid levels.

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).

Serum amino acid concentrations in nine athletes before and after the 1993 Colmar ultra triathlon.

The amino acid imbalance hypothesis should explain the fatigue originating in the brain during sustained exercise or over-training as a branched-chain (BCAA)/aromatic amino acids (AAA) imbalance with increased brain tryptophan uptake and 5-hydroxytryptamine synthesis. The serum amino acid profile was determined in 9 ultra-triathletes before and after completing the 1993 Colmar ultra-triathlon to additionally analyse the extent of this amino acid imbalance during such an extreme prolonged contest lasting more than 23 hours. The summed serum concentration of 25 amino acids decreased by 18% from 3962 +/- 846 to 3255 +/- 694 umol.l-1 likely reflecting a catabolic state of the organism with a decrease in 18 individual amino acids by 9-56%, an increase in cystine (+38%), methionine (+24%), tyrosine (+10%), phenylalanine (+12%), free tryptophan (+74%), and constant glutamine, leucine and total tryptophan levels. Since plasma volume increased by approximately 7.6% with a 3.3 kg body mass decrease in the athletes during the ultra triathlon, a decrease in intra-cellular water with an extra-cellular fluid increase is hypothesized. This decrease in cellular hydration state is seen as a protein-catabolic signal.

Unaccustomed high mileage compared to intensity training-related neuromuscular excitability in distance runners.

The influence of a 4-week unaccustomed average 103% mileage increase (ITV, increase in training volume; n = 8; average baseline mileage 85.9 km.week-1, final mileage 174.6 km.week-1) on performance and neuromuscular excitability (NME) was tested in experienced distance runners and controlled 1 year later by a 4-week unaccustomed average 152% increase in tempo-pace and interval-runs (ITI, increase in training intensity; n = 9; baseline 9 km.week-1 final 22.7 km.week-1) with an average total mileage of 61.7 km.week-1 (week 1) to 84.7 km.week-1 (week 4). Seven athletes participated in ITV as (week 4). Seven athletes participated in ITV as well as in ITI. During incremental treadmill test performance at a lactate concentration of 2 mmol.1-1 (2 LP) increased, and at 4 mmol.1-1 (4 LP) performance did not change, whereas total running distance (TD) during the incremental test decreased in ITV compared to an increase in 2 LP, 4 LP and TD during ITI which may indicate that there was an ITV-related overtraining. The NME of the reference muscles vastus medialis and rectus femoris deteriorated in ITV (day 28 compared to 0) compared to constant values during ITI, reflecting an ITV-related overload of neuromuscular structures.

Influence of 6-week, 6 days per week, training on pituitary function in recreational athletes.

The influence on pituitary function of 6 weeks of training on 6 days a week was examined in six recreational athletes. Endurance training on a bicycle ergometer for 31-33 min was performed on 4 days each week at 90-96% (weeks 1-3) and 89-92% (weeks 4-6) of the 4 mmol lactate thresholds determined on day 0 and day 21, respectively, with interval training of 3-5 x 3-5 min in addition on 2 days a week at 117-127% and 115-110%, respectively. Determination of the serum hormone levels and a combined pituitary function test (200 micrograms thyrotropin releasing hormone (TRH), 100 micrograms gonadotrophin-releasing hormone (GnRH), 100 micrograms corticotrophin releasing hormone (CRH), 50 micrograms growth hormone releasing hormone (GHRH)) were made before training, after 6 weeks of training and after another 3 weeks of recovery. Training increased performance at 2 mmol lactate by 25%, at 4 mmol by 12%, and maximum performance by approximately 12%. The releasing hormone-stimulable prolactin, thyroid stimulating hormone (TSH) and somatotrophic hormone (STH) synthesis-secretion capacity remained unchanged, the adrenocorticotrophic hormone (ACTH) was increased after training. Cortisol release was reduced, follicle-stimulating hormone (FSH)-synthesis-secretion capacity was increased after training, and the luteinizing hormone (LH)-synthesis-secretion capacity reduced. This had no influence on base or exercise-induced serum hormone levels (cortisol, aldosterone, insulin, prolactin, FSH, LH, TSH, ACTH, ADH and STH), which showed no dependence on training, except for free testosterone which showed a decreasing trend (P < 0.10) of 19-25% and post-exercise ACTH which showed an increasing trend of 33% (P < 0.10). Conditioning (cortisol sensitivity and ACTH response) or adaptation (FSH and LH responses) to changed testosterone serum levels and altered spermatogenesis is discussed.

Training-overtraining: performance, and hormone levels, after a defined increase in training volume versus intensity in experienced middle- and long-distance runners.

Performance and hormones were determined in eight middle- and nine long-distance runners after an increase in training volume (ITV, February 1989) or intensity (ITI, February 1990). Seven runners participated in both studies. The objective was to cause an overtraining syndrome. The mean training volume of 85.9 km week-1 increased within 3 weeks to 176.6 km week-1 during ITV and 96-98% of training volume was performed as long-distance runs at mean(s.d.) 67(8)% of maximum capacity. Speed endurance, high-speed and interval runs averaging 9 km week-1 increased within 3 weeks to 22.7 km during ITI, and the total volume increased from 61.6 to 84.7 km. A plateau in endurance performance and decrease in maximum performance occurred during ITV, probably due to overtraining, with performance incompetence over months. Nocturnal catecholamine excretion decreased markedly (47-53%), contrary to exercise-related plasma catecholamine responses, which increased. Resting and exercise-related cortisol and aldosterone levels decreased. Improvement in endurance and maximum performance occurred during ITI indicating a failure to cause an overtraining syndrome in ITI. Decrease in noctural catecholamine excretion was clearly lower (9-26%), exercise-related catecholamine responses showed a significant decrease, cortisol and aldosterone levels remained almost constant, exercise-related prolactin levels decreased slightly. There were no differences in insulin, C-peptide, free testosterone, somatotropic hormone (STH), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH), tri-iodothyronine (T3) and thyroxine (T4). The decrease in nocturnal catecholamine excretion during ITV might indicate a decrease in intrinsic sympathetic activity in exhausted sportsmen. But it remains open whether this reflected a central nervous system incompetence.

Heart rates, cardiac arrhythmia, lactate levels and catecholamine excretions in CHD patients during cross-country skiing.

We examined cross-country skiing-related strain in 10 less experienced postinfarction patients, performing a skiing test, covering a distance of approximately 7 km in 90 min. Heart rates, cardiac arrhythmia, lactic acid levels and catecholamine excretions were determined as strain indicators. The patients' exercise capacity, estimated during graded ergometric cycling, was 2.1 +/- 0.4 watts.kg-1, indicating a nearly age-appropriate submaximum performance ability. They had suffered myocardial infarction 2.8 +/- 0.7 years previously, participated regularly in a rehabilitation program for at least one year, and they did not show coronary insufficiency or significant cardiac dysrhythmias during laboratory testing under their usual medications. They went cross-country skiing during a 4-day instruction period and subsequently performed a cross-country skiing test on the 5th day. Mean skiing-related heart rates (124 +/- 9 bpm) and adrenaline excretions (124 +/- 88 pmol.min-1) corresponded on average to an exercise level of 1.85-2.0 watts.kg-1 during laboratory testing, and mean noradrenaline excretions (586-343 pmol.kg-1) and lactate concentrations (3.83 +/- 2.18 mmol.l-1) to a level of 1.48-1.73 watts.kg-1. Cardiac dysrhythmias were observed in a moderate number of 6-8 SVES, 9 to 12 VES and 4 to 7 couplets of VES per 1000 beats during cross-country skiing. The present results point to a comparatively high cardiovascular strain in less experienced postinfarction patients during a cross-country skiing test at an intensity level thought to be moderate.

[Differential diagnosis: physiologic-pathologic hypertrophy of the heart. A case report]. / Zur Differentialdiagnose: physiologische-pathologische Hypertrophie des Herzens. Ein Fallbericht.

We report on a 52-year-old asymptomatic patient, whom we have examined regularly since 1981. The principal finding is a marked terminal negativity of the T-wave in the extremities and left precordial chest leads in the electrocardiogram with regression at high exercise levels. The patient engages intensively in sports (running, cross-country skiing, gymnastics). His performance capacity is above normal at 4.5 (1981) and 3.8 watts/kg body weight (1988). The echographically determined left ventricular muscle mass (LVM) increased from 2.1-2.3 g/kg body weight to 2.9 g/kg, the end-diastolic thickness of the septum from 9 to 13, and the posterior wall from 8 to 12 mm. In physiological cardiac hypertrophy (athlete's heart), a LVM of 2.9 g/kg is not unusual, whereby the end-diastolic wall thickness does not, exceed 10 to 11 mm and the mass-volume ratio (LVM/end-diastolic ventricular volume) remains constant (about 1.2 g/ml) in contrast to the 1.75 g/ml in our patient. Thermodilution catheter examination of the heart showed a pathological increase in mean pulmonary capillary pressure (26 mm Hg) under exercise as an indication of impaired left-ventricular function. Normal myocardial scintigraphy (resting and exercise) and a lack of symptoms permit the exclusion of relevant coronary heart disease. We diagnosed non-obstructive hypertrophic cardiomyopathy. The problems of differentiating between physiological and pathological cardiac hypertrophies are discussed.

[Follow-up study of 48 athletes with stage I hypertension with and without pharmacotherapy]. / Verlaufsbeobachtung bei 48 Sportlern mit Hypertonie im Stadium I mit und ohne Pharmakotherapie.

We found in an earlier investigation that the frequency of hypertension is considerably lower among male athletes than in a random sample of the general population. The cases of hypertension in younger athletes are primarily hypertension stage I (WHO). We followed up on the question of the course of hypertension stage I and the possibility of spontaneous remission. For this, we observed 28 nonmedicated patients with hypertension stage I for 4.2 +/- 2.3 years, 20 patients undergoing drug therapy for 2.5 +/- 1.3 years, and 12 healthy athletes for 4.2 +/- 2.2 years. Under drug therapy, as expected, there was a normalization of both basic and exercise blood pressures. Fifty percent of patients without drug therapy showed remission of the elevated basic and exercise pressures after 2 to 3 years; 50% had an unchanged high pressure or deterioration. The transition of hypertension WHO stage I to stage II with regard to left ventricular hypertrophy could be ruled out echocardiographically in patients with a favorable course (remission). However, there was a tendency in this direction among patients with the least favorable course.

[Behavior of heart rate, blood pressure, lactate, glucose, noradrenaline and adrenaline level in coronary heart disease patients in the course of light swimming stress]. / Verhalten von Herzfrequenz, Blutdruck, Laktat-, Glukose-, Noradrenalin- und Adrenalinspiegel bei KHK-Patienten während leichter Schwimmbelastungen.

In previous investigations, we have been able to demonstrate that healthy individuals and CHD patients with normal exercise capacity experience changes in cardiovascular parameters, metabolism and sympathetic activity during light swimming exercise, changes which are not observed in seated bicycle ergometry at an exercise level of less than 2 W/kg-1. We have now examined 12 post-infarction patients (54.3 +/- 6 years) with limited exercise capacity (1.2 +/- 0.3 W/kg-1), who have been participating in physical therapy for 29 months (median time) under continuous medication. The examination comprised incremental seated bicycle ergometry and, approximately 60 min later, light swimming (2 to 3 x 2 min; speed v = 0.33 +/- 0.02 m.s-1; T = 28 degrees C). The changes in heart rate, blood pressure, lactate, glucose, adrenaline and noradrenaline levels during the swimming exercise were equivalent in mean value to ergometry at the 100 W level. Three patients had to discontinue swimming before the scheduled time, due to considerable arrhythmias. Three other patients stopped swimming because of subjective overexertion. The exercise reaction was less favorable among those unaccustomed to swimming than among regular swimmers.

[Catecholamine behavior, adrenoreceptor density of intact cells and sensitivity to catecholamines in a patient with orthostatic hypotension]. / Katecholaminverhalten, Adrenorezeptorendichte an intakten Zellen und Katecholaminempfindlichkeit bei einer Patinetin mit orthostatischer Hypotonie.

We evaluated sympathetic nervous system function in a patient with primary orthostatic hypotension. Plasma catecholamine levels--except for dopamine levels--and urinary catecholamine excretion were decreased, alpha-adrenoreceptor responsiveness to noradrenaline and beta-adrenoreceptor responsiveness to isoproterenol were increased according to increased beta-2-adrenoreceptor density on intact polymorphonuclear leukocytes. Alpha-2-adrenoreceptor density on intact platelets and adrenaline-induced platelet aggregation in vitro, however, were unchanged. We evolved a therapeutic regimen with fludrocortisone, propranolol, and dihydroergotamine that allowed the patient to resume nearly a regular degree of mobility.

[Primary orthostatic hypotension]. / Primäre orthostatische Hypotonie. Ein Fallbericht.

We studied a 25-year-old man suffering from primary orthostatic hypotension whose blood pressure decreased to 65/45 mm Hg during orthostasis and to 95/70 mm Hg during ergometric exercise (50 and 100 watt), and whose heart rate responses were inadequate. Resting catecholamine levels were within the normal range and did not show any significant increase related to orthostasis or to ergometric exercise. Hypersensitivity was observed to low doses of intravenous noradrenaline and isoproterenol. Specific binding of 3H-Yohimbine to intact platelets revealed a normal number of alpha-2-adrenoreceptors in agreement with the adrenaline-induced platelet aggregation in vitro, which was, however, in contrast to hypersensitivity to noradrenaline. Specific 3H-Dihydroalprenolol binding to intact polymorphonuclear leucocytes revealed an increased beta-2-adrenoreceptor density in agreement with hypersensitivity to Isoproterenol. Prescription of Fludrocortison improved orthostatic hypotension.