The described functional alterations of pituitary-adrenal axis and sympathetic system can explain persistent performance incompetence in affected athletes.
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.
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.
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 [ig thyrotropin releasing hormone (TRH), 100 [tg gonadotrophin-releasing hormone (GnRH), 100 [tg corticotrophin releasing hormone (CRH), 50 [tg 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, folliclestimulating 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.
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