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Blood Hormones as Markers of Training Stress and Overtraining

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Summary

An imbalance between the overall strain experienced during exercise training and the athlete’s tolerance of such effort may induce overreaching or overtraining syndrome. Overtraining syndrome is characterised by diminished sport-specific physical performance, accelerated fatiguability and subjective symptoms of stress. Overtraining is feared by athletes yet there is a lack of objective parameters suitable for its diagnosis and prevention.

In addition to the determination of substrates (e.g. lactate, ammonia and urea) and enzymes (e.g. creatine kinase), the possibilities for monitoring of training by measuring hormonal levels in blood are currently being investigated.

Endogenous hormones are essential for physiological reactions and adaptations during physical work and influence the recovery phase after exercise by modulating anabolic and catabolic processes. Testosterone and cortisol are playing a significant role in metabolism of protein as well as carbohydrate metabolism. Both are competitive agonists at the receptor level of muscular cells. The testosterone/cortisol ratio is used as an indication of the anabolic/catabolic balance. This ratio decreases in relation to the intensity and duration of physical exercise, as well as during periods of intense training or repetitive competition, and can be reversed by regenerative measures. Correlations have been noted with the training-induced changes of strength. However, it seems more likely that the testosterone/cortisol ratio indicates the actual physiological strain in training, rather than overtraining syndrome.

The sympatho-adrenergic system might be involved in the pathogenesis of overtraining. Overtraining appears as a disturbed autonomic regulation, which in its parasympathicotonic form shows a diminished maximal secretion of catecholamines, combined with an impaired full mobilisation of anaerobic lactic reserves. This is supposed to lead to decreased maximal blood lactate levels and maximal performance. Free plasma adrenaline (epinephrine) and noradrenaline (norepinephrine) may provide additional information for the monitoring of endurance training. While prolonged aerobic exercise conducted at intensities below the individual anaerobic threshold lead to a moderate rise of sympathetic activity, workloads exceeding this threshold are characterised by a disproportionate increase in the levels of catecholamines. In addition, psychological stress during competitive events is characterised by a higher catecholamines to lactate ratio in comparison with training exercise sessions. Thus, the frequency of training sessions with higher anaerobic lactic demands or of competition, should be carefully limited in order to prevent overtraining syndrome.

In the state of overtraining syndrome and overreaching, respectively, an intraindividually decreased maximum rise of pituitary hormones (corticotrophin, growth hormone), cortisol and insulin has been found after a standardised exhaustive exercise test performed with an intensity of 10% above the individual anaerobic threshold. This disturbed stress-response corresponds to findings with insulin-induced hypoglycaemia in overtraining suggesting an impaired hypothalamic regulation.

However, the role of hormones in the recovery phase and their effect on the receptor and intracellular level remain to be better established. Reference values indicating a ‘normal’ exercise tolerance as well as easier and less expensive laboratory methods are still lacking. External factors influencing the hormonal blood levels require well-standardised sampling conditions which are often difficult to realise in the training environment. The impaired exercise-induced maximal increase of selected hormones and the potential consideration of the psychological stress component by hormonal measurements, however, represent interesting basic findings which encourage future investigations.

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Urhausen, A., Gabriel, H. & Kindermann, W. Blood Hormones as Markers of Training Stress and Overtraining. Sports Med. 20, 251–276 (1995). https://doi.org/10.2165/00007256-199520040-00004

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