Decreased nocturnal catecholamine excretion: parameter for an overtraining syndrome in athletes?

The effectiveness of high performance training should be examined at short intervals in order to recognize overtraining promptly. Field or laboratory tests can usually not be performed with such frequency. Easy-to-measure biological, training-relevant parameters are being sought to use in their place. Since the importance of the sympathetic nervous system for adaptation of stress and the relationship between physical training and the activity of the sympathetic nervous system are well accepted, and since an impairment of the sympathetic nervous system is assumed in an overtraining syndrome, we examined the relevance of nocturnal "basal" urinary excretion of free catecholamines with respect to its practical application: 1. during a pilot study (training of road and track cyclists before the 1988 Olympic Games in Seoul), 2. through a 4-week prospective, experimental study in 1989 and 1990 (middle- and long-distance runners), 3. during the competitive season and winter break of a soccer team between August 1990 and April 1991. The following hypothesis was made: An overtraining or exhaustion syndrome in athletes may usually be accompanied by at least a 50% decrease in basal dopamine, noradrenaline and adrenaline excretion. When training is effective or the athletes are not exhausted, the decrease of the excretion rate--with the exception of dopamine--is more likely to be lower (noradrenaline, adrenaline). Generalization of these results requires further expansion of the experimental basis.     

Does overtraining exist? An analysis of overreaching and overtraining research

Athletes experience minor fatigue and acute reductions in performance as a consequence of the normal training process. When the balance between training stress and recovery is disproportionate, it is thought that overreaching and possibly overtraining may develop. However, the majority of research that has been conducted in this area has investigated overreached and not overtrained athletes. Overreaching occurs as a result of intensified training and is often considered a normal outcome for elite athletes due to the relatively short time needed for recovery (approximately 2 weeks) and the possibility of a supercompensatory effect. As the time needed to recover from the overtraining syndrome is considered to be much longer (months to years), it may not be appropriate to compare the two states. It is presently not possible to discern acute fatigue and decreased performance experienced from isolated training sessions, from the states of overreaching and overtraining. This is partially the result of a lack of diagnostic tools, variability of results of research studies, a lack of well controlled studies and individual responses to training.The general lack of research in the area in combination with very few well controlled investigations means that it is very difficult to gain insight into the incidence, markers and possible causes of overtraining. There is currently no evidence aside from anecdotal information to suggest that overreaching precedes overtraining and that symptoms of overtraining are more severe than overreaching. It is indeed possible that the two states show different defining characteristics and the overtraining continuum may be an oversimplification. Critical analysis of relevant research suggests that overreaching and overtraining investigations should be interpreted with caution before recommendations for markers of overreaching and overtraining can be proposed. Systematically controlled and monitored studies are needed to determine if overtraining is distinguishable from overreaching, what the best indicators of these states are and the underlying mechanisms that cause fatigue and performance decrements. The available scientific and anecdotal evidence supports the existence of the overtraining syndrome; however, more research is required to state with certainty that the syndrome exists.     

Training practices and overtraining syndrome in Swedish age-group athletes

Heavy training in combination with inadequate recovery actions can result in the overtraining/staleness syndrome and burnout. Even young and aspiring elite athletes develop staleness. The aim was therefore to determine the incidence and nature of staleness, and its association with training behavior and psychosocial stressors in young elite athletes. A sample of 272 individuals from 16 sports completed questionnaires on training, staleness, and psychosocial stress and 37% reported being stale at least once. The incidence rate was higher for individual sports (48%) compared with team (30%) and less physically demanding sports (18%). Stale athletes reported greater perceptual changes and negatively elevated mood scores in comparison to healthy athletes. Staleness was distinguished from burnout on the basis of motivational consequences; 41 % of the athletes lost their motivation for training, which in turn indicates a state of burnout. Further, 35 % of the athletes reported low satisfaction with time spent on important relationships, 29% rated the relationship with their coach as ranging from very, very bad to only moderately good. The results indicate that staleness is a widespread problem among young athletes in a variety of sports, and is not solely related to physical training, but also to non-training stressors.     

Monitoring and titrating symptoms : a science-based approach to using your brain to optimise marathon running performance

A key challenge to optimising marathon running performance is to train with adequate frequency, duration and intensity as well as get enough recovery to optimise biological adaptations underlying performance. Some marathon runners train inadequately and underperform, while others perform poorly because they become injured or develop staleness in response to overtraining. Staleness, a depression-like syndrome, could plausibly be caused by overtraining-induced molecular and cellular changes in brain circuits involved in depression or other related mood states such as anger, fatigue, vigor and confusion. The central thesis of this paper is that easily assessed resting and/or exercise symptoms, valid markers of either difficult-to-access, expensive-to-assess or unmeasurable brain circuits, can be used to optimise marathon running performance by helping to avoid either inadequate training or excessive training resulting in staleness. Available models of human performance and relevant data, admittedly incomplete at the present time, suggest that marathon runners may benefit from systematically using symptom responses to training in order to aid in adjusting training loads for the purpose of optimising training. As this approach is better linked with neuroscience and neuroimaging findings, it could be refined and prove to be useful for elite as well as non-elite marathon runners.     

Autonomic adaptations to intensive and overload training periods: a laboratory study

PURPOSE: Looking for practical and reliable markers of fatigue is of particular interest in elite sports. One possible marker might be the autonomic nervous system activity, known to be well affected by physical exercise and that can be easily assessed by heart rate variability. METHODS: We designed a laboratory study to follow six sedentary subjects (32.7 +/- 5.0 yr) going successively through 2 months of intensive physical training and 1 month of overload training on cycloergometer followed by 2 wk of recovery. Maximal power output over 5 min (Plim5'), VO(2) and standard indices of heart rate variability were monitored all along the protocol. RESULTS: During the intensive training period, physical performance increased significantly VO(2peak) : +20.2%, < 0.01; Plim5': +26.4%, < 0.0001) as well as most of the indices of heart rate variability (mean RR, Ptot, HF, rMSSD, pNN50, SDNNIDX, SDNN, all < 0.05) with a significant shift in the autonomic nervous system toward a predominance of its parasympathetic arm (LF/HF, LFnu, HFnu, < 0.01). During the overload training period, there was a stagnation of the parasympathetic indices associated to a progressive increase in sympathetic activity (LF/HF, < 0.05). During the week of recovery, there was a sudden significant rebound of the parasympathetic activity (mean RR, HF, pNN50, rMSSD, all < 0.05). After 7 wk of recovery, all heart rate variability indices tended to return to the prestudy values. CONCLUSION: Autonomic nervous system status depends on cumulated physical fatigue due to increased training loads. Therefore, heart rate variability analysis appears to be an appropriate tool to monitor the effects of physical training loads on performance and fitness, and could eventually be used to prevent overtraining states.     

Overtraining in athletes. An update

Overtraining appears to be caused by too much high intensity training and/or too little regeneration (recovery) time often combined with other training and nontraining stressors. There are a multitude of symptoms of overtraining, the expression of which vary depending upon the athlete's physical and physiological makeup, type of exercise undertaken and other factors. The aetiology of overtraining may therefore be different in different people suggesting the need to be aware of a wide variety of parameters as markers of overtraining. At present there is no one single diagnostic test that can define overtraining. The recognition of overtraining requires the identification of stress indicators which do not return to baseline following a period of regeneration. Possible indicators include an imbalance of the neuroendocrine system, suppression of the immune system, indicators of muscle damage, depressed muscle glycogen reserves, deteriorating aerobic, ventilatory and cardiac efficiency, a depressed psychological profile, and poor performance in sport specific tests, e.g. time trials. Screening for changes in parameters indicative of overtraining needs to be a routine component of the training programme and must be incorporated into the programme in such a way that the short term fatigue associated with overload training is not confused with the chronic fatigue characteristic of overtraining. An in-depth knowledge of periodisation of training theory may be necessary to promote optimal performance improvements, prevent overtraining, and develop a system for incorporating a screening system into the training programme. Screening for overtraining and performance improvements must occur at the culmination of regeneration periods.     

Fatigue and underperformance in athletes: the overtraining syndrome

The overtraining syndrome affects mainly endurance athletes. It is a condition of chronic fatigue, underperformance, and an increased vulnerability to infection leading to recurrent infections. It is not yet known exactly how the stress of hard training and competition leads to the observed spectrum of symptoms. Psychological, endocrinogical, physiological, and immunological factors all play a role in the failure to recover from exercise. Careful monitoring of athletes and their response to training may help to prevent the overtraining syndrome. With a very careful exercise regimen and regeneration strategies, symptoms normally resolve in 6-12 weeks but may continue much longer or recur if athletes return to hard training too soon.


     

Brain serotonin reuptake did not change during one year in overtrained athletes

Brain 5-HT neurotransmission has been described to be down-regulated in depressed people, and also suspected to be changed in overtraining state, the consequence of long-term physical overloading and stress in athletes. We studied brain serotonin (5-HT) transporter binding i.e., 5-HT reuptake with the specific radioligand (123-I-labelled 2beta-carbomethoxy-3beta[4-iodopenyl]-nortropane, Nor-beta-CIT), and with single photon emission tomography (SPET) in severely overtrained athletes and their controls at the baseline and after a one-year recovery period. Twelve overtrained (6 women and 6 men, mean age 27 yrs, range 16 - 39 yrs) and 11 healthy (6 women, 5 men, 26 yrs, 20 - 39 yrs) athletes were examined. Overtrained athletes 1) had suffered from an unexplained decrement in physical performance and fatigue for several weeks to many months and continued to have the same symptoms even after a recovery time of weeks to months, 2) had been examined to be otherwise healthy, and 3) had a suitable training history for overtraining. Nor-beta-CIT SPET was acquired 5 min, and 3, 6, and 24 h after the injection of the radioligand. 5-HT reuptake in ml/ml in midbrain (raphe nuclei) was calculated as (midbrain - cerebellum)/cerebellum. According to two-way analysis of variance, no changes inside the groups or group differences in 5-HT reuptake were found. Male athletes had significantly higher 5-HT reuptake than female athletes at the baseline (p = 0.034). The overtrained athletes were moderately depressed, while their scores in standardized Hamilton and Montgomery-Asberg Depression Rating Scales were 16 +/- 2 (mean +/- SEM, range 8 - 29) and 17 +/- 2 (7 - 28), respectively. In the CA, the scores were 6 +/- 1 (range 2 - 18) and 6 +/- 2 (1 - 19), respectively. 5-HT reuptake did not correlate with the depression scores either in the whole group or in the OA. The finding of the present study does not support the idea of long-term changes in 5-HT neurotransmission in overtraining state, in this case serotonin reuptake in midbrain, the regulating area of brain serotonin neurotransmission. Furthermore, depression of overtrained athletes may be its own variant having no correlation with 5-HT reuptake in midbrain. Sex may have effect on chronic stress response at the brain level in athletes, which may be a confusing factor in the overtraining studies, and has to be taken into consideration in the future.     

Heart rate variability, blood pressure variability, and baroreflex sensitivity in overtrained athletes.

OBJECTIVE: To assess the effects of abruptly intensified physical training on cardiovascular control. DESIGN: Retrospective longitudinal study. SETTING: Research laboratory. PARTICIPANTS: Ten healthy athletes (5 men and 5 women) from track and field as well as triathlon. INTERVENTIONS: A 2-week training camp, including daily stepwise increasing cycling tests, running of 40 minutes, and additional cycling of 60 minutes. MAIN OUTCOME MEASUREMENTS: Time and frequency domain parameters of resting heart rate and blood pressure variability (HRV and BPV) and baroreflex sensitivity (BRS), before, during, and after the training camp. RESULTS: We found significantly reduced HRV during the training camp (mean beat-to-beat interval: 1042 [937 to 1194] ms vs. 933 [832 to 1103] ms vs. 1055 [947 to 1183] ms, P < 0.01; root-mean-square of beat-to-beat interval differences: 68 [52 to 95] ms vs. 52 [38 to 71] ms vs. 61 [48 to 78] ms, P < 0.05). Further, BRS was significantly reduced: 25.2 (20.4 to 40.4) ms/mmHg vs. 17.0 (12.9 to 25.7) ms/mmHg vs. 25.7 (18.8 to 29.1) ms/mmHg, P < 0.05. These effects disappeared at a large degree after 3 to 4 days of recovery. CONCLUSION: Abruptly intensified physical training results in an altered autonomic cardiovascular activity towards parasympathetic inhibition and sympathetic activation that can be monitored by means of HRV and BRS analyses and might provide useful markers to avoid the overtraining syndrome.     

Training-overtraining. A prospective, experimental study with experienced middle- and long-distance runners.

Overtraining may be one frequent cause of stagnation or decrease in performance capacity of athletes. Israel (19) differentiates between addisonoid (parasympathetic) and basedowoid (sympathetic) overtraining, characterized by inhibition or excitation. We tried to induce an overtraining syndrome in 8 experienced middle- and long-distance runners, based on an increase in training volume from an average 85.9 km (week 1) to 115.1 km (week 2) and 143.1 km (week 3) to 174.6 km per week (week 4). The influence of this training on cardiovascular, metabolic and hormonal parameters was examined with special respect to plasma and urinary catecholamines. Laboratory testing including graded treadmill running was performed on the days 0, 14 and 28. Training was held six days each week, with nearly 30 km per day in the fourth week. A stagnation in endurance performance capacity (running velocity at the aerobic-anaerobic transition range) and a decrease in maximum working capacity were observed in 6 and a stagnation in 2 of the 8 sportsmen, indicated by a decrease in total running distance from 4719 + 912 m to 4361 + 788 m during incremental treadmill ergometry. The sportsmen could neither improve nor could they even approximately reach their personal records during the subsequent competitive season. Subjective complaints, classified on a four-point scale, increased from 1.2 (week 1) to 3.2 in week 4. Glucose, lactate, ammonia, glycerol, free fatty acids, albumin, LDL, VLDL cholesterol, hemoglobin level (transient), leukocytes, and heart rate (before and during exercise) decreased significantly. Urea, creatinine, uric acid, GOT, GPT, gamma-GT, serum electrolytes (except phosphate and calcium) remained constant at the measuring times, CPK was elevated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Night heart rate variability during overtraining in male endurance athletes

AIM: The purpose of the study was to examine whether an unaccustomed increase in training volume would result in characteristics changes in heart rate variability (HRV), in order to determine if this marker can be used to diagnose overtraining. METHODS: Nine experienced endurance athletes increased their usual amount of training by 100% within 4 weeks. Night ECG was recorded before (baseline) and after (OVER) this period of overload, and after 2 weeks of recovery (REC). RESULTS: We diagnosed overtraining in 6 subjects using both physiological and psychological criteria. No difference was noted in heart rate for night periods (56+/-12, 55+/-10 and 53+/-15 bpm, respectively; p>0.05). We found no significant changes of LF/HF (1.10+/-0.92, 0.96+/-0.57 and 0.59+/-0.43, respectively; p>0.05) or HF expressed in normalized units (54.81+/-20.12, 53.81+/-11.35 and 66.15+/-15.12%, respectively; p>0.05). CONCLUSION: In the conditions of the present study, HRV during sleep does not seem to be a valid marker of overtraining in male endurance athletes. Before concluding to the uselessness of this tool in the monitoring of the syndrome, longitudinal studies with elite or sub-elite athletes are needed to determine if spontaneously developed overtraining results in the same response.     

Overtraining syndrome.

This review discusses the overtraining syndrome which is characterized by fatigue and underperformance precipitated by stress of training. Other stresses, depression and an increased susceptibility to infections may be important. Treatment requires rest and a stress management program over 3 months.     

Place de l'interrogatoire dans le diagnostic de surentraînement

Objectives. – This literature review highlights the importance of medical interview in the early diagnosis of overtraining syndrome. We propose an analytic process consisting to specify with the athlete his answers to the self-administered overtraining questionnaire proposed by the French Sport Medicine Society.Topics. – The first step consists to ensure the long-term alteration of sport performance. This feature is a prerequisite to define an overtraining syndrome. This decrease in sport performance must be paralleled to an eventual increase in the training load. In a second step a chronic fatigue must be evidenced and characterized allowing to verify its specificity to overtraining and the absence of underlying disease. The third step aims to confirm the diagnosis of overtraining assessing the presence of physical and psychological symptoms frequently reported in the literature. The last step consists in seeking favoring factors and/or triggers linked to the sport practice, to the close environment of the athlete, or to personal factors. These factors may allow identifying the causes of overtraining and their relief.Future prospects. – Practically, we suggest to undertake this medical interview in depth in order to specify with the athlete his answers to the short self-administered overtraining questionnaire proposed by the French Sport Medicine Society (SFMS), a screening tool, integrating most of the items discussed in this article. Based on this literature review and on the different works performed by the memberships of the SFMS, the article proposed in the following, summarizes this analytic process. The latter is concluded by the position stand of the SFMS on the role of medical interview in early diagnosis of overtraining syndrome.     

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.     

Chronic fatigue syndrome: an update

The chronic fatigue syndrome is characterised by a fatigue that is disproportionate to the intensity of effort that is undertaken, has persisted for 6 months or longer, and has no obvious cause. Unless there has been a long period of patient- or physician-imposed inactivity, objective data may show little reduction in muscle strength or peak aerobic power, but the affected individual avoids heavy activity. The study of aetiology and treatment has been hampered by the low disease prevalence (probably <0.1% of the general population), and (until recently) by a lack of clear and standardised diagnostic criteria. It is unclear how far the aetiology is similar for athletes and nonathletes. It appears that in top competitors, overtraining and/or a negative energy balance can be precipitating factors. A wide variety of other possible causes and/or precipitating factors have been cited in the general population, including psychological stress, disorders of personality and affect, dysfunction of the hypothalamic-pituitary-adrenal axis, hormonal imbalance, nutritional deficits, immune suppression or activation and chronic infection. However, none of these factors have been observed consistently. The prognosis is poor; often disability and impairment of athletic performance are prolonged. Prevention of overtraining by careful monitoring seems the most effective approach in athletes. In those where the condition is established, treatment should aim at breaking the vicious cycle of effort avoidance, deterioration in physical condition and an increase in fatigue through a combination of encouragement and a progressive exercise programme.     

Elucidating the unexplained underperformance syndrome in endurance athletes : the interleukin-6 hypothesis

The unexplained underperformance syndrome (UPS), previously known as the overtraining syndrome (OTS), has been defined as a persistent decrement in athletic performance capacity despite 2 weeks of relative rest. It has been proposed that UPS may be caused by excessive cytokine release during and following exercise causing a chronic inflammatory state and 'cytokine sickness'. This article extends that hypothesis by proposing that time-dependent sensitisation could provide a model through which the aetiology of UPS may be explained. In this model, the principal abnormal factors in UPS are an increased production of and/or intolerance to interleukin (IL)-6 during exercise. Strategies to attenuate the IL-6 response to exercise that may also reduce an athlete's susceptibility to UPS are proposed.     

Resolution of Postural Orthostatic Tachycardia Syndrome After CT-Guided,Percutaneous T2 Ethanol Ablation for Hyperhidrosis

Postural orthostatic tachycardia syndrome is characterized by orthostatic intolerance. Orthostasis (or other mild physical stress) triggers a cascade of inappropriate tachycardia, lightheadedness, palpitations, and often fainting. The underlying defect is sympathetic dysregulation of the heart, which receives its sympathetic tone from the cervical and upper thoracic sympathetic ganglia. Primary hyperhidrosis is also thought to be the result of sympathetic dysregulation. We present the case of a patient treated with CT-guided, percutaneous T2 EtOH sympatholysis for craniofacial hyperhidrosis. The patient also suffered from postural orthostatic tachycardia syndrome for many years and was unresponsive to treatment. Immediately after sympatholysis, the patient experienced resolution of both craniofacial hyperhidrosis and postural orthostatic tachycardia syndrome.     

Intense endurance training on heart rate and blood pressure variability in runners.

Physical training with incomplete recovery times can produce significant fatigue. A study of cardiovascular responses showed that there is a sympathetic and a parasympathetic form of fatigue. PURPOSE: The purpose of this experimentation was to measure the effects of intense endurance training on autonomic balance through a spectral analysis study of the heart rate (HR) and systolic blood pressure (SBP). METHODS: Eight elite runners were tested twice: after a relative rest period (RRP) of 3 wk and after an 12-wk intense training period (ITP) for endurance. At the end of each phase, the subjects were tested by means of a VO2max test and a tilt-table test. RESULTS: The resting heart rate (HR) variability was lower (P < 0.001) in the intensive training phase. Likewise, there were differences in the low-frequency (0.04-0.150 Hz; LF) and high-frequency (0.150-0.500 Hz; HF) components and the LF/HF ratio of the HR spectral analysis. The LF spectral power was significantly lower in the supine position (P < 0.05) during ITP. Upright tilting was accompanied by a 22.6% reduction in HF values during the rest period, whereas in ITP the HF spectral power rose by 31.2% (P < 0.01) during tilt, characterizing a greater parasympathetic system control. Sympathetic control represented by the LF/HF ratio regressed markedly (P < 0.01) in response to the tilt test in ITP. CONCLUSIONS: The spectral analysis of SBP in the high frequencies shows that the changes in cardiac parameters are coupled with a decrease in sympathetic vasomotor control (-18%) and a reduction in diastolic pressure (-3.2%) in the response to the tilt test at the end of ITP. Spectral analysis could be a means of demonstrating impairment of autonomic balance for the purpose of detecting a state of fatigue that could result in overtraining.     

Circulating cell-free DNA: an up-coming molecular marker in exercise physiology

The phenomenon of circulating cell-free DNA (cfDNA) concentrations is of importance for many biomedical disciplines including the field of exercise physiology. Increases of cfDNA due to exercise are described to be a potential hallmark for the overtraining syndrome and might be related to, or trigger adaptations of, immune function induced by strenuous exercise. At the same time, exercise provides a practicable model for studying the phenomenon of cfDNA that is described to be of pathophysiological relevance for different topics in clinical medicine like autoimmune diseases and cancer. In this review, we are summarizing the current knowledge of exercise-based acute and chronic alterations in cfDNA levels and their physiological significance. The effects of acute exercise on cfDNA concentrations have been investigated in resistance exercises and in continuous, stepwise and interval endurance exercises of different durations. cfDNA concentrations peaked immediately after acute exercise and showed a rapid return to baseline levels. Typical markers of skeletal muscle damage (creatine kinase, uric acid, C-reactive protein) show delayed kinetics compared with the cfDNA peak response. Exercise parameters such as intensity, duration or average energy expenditure do not explain the extent of increasing cfDNA concentrations after strenuous exercise. This could be due to complex processes inside the human organism during and after physical activity. Therefore, we hypothesize composite effects of different physiological stress parameters that come along with exercise to be responsible for increasing cfDNA concentrations. We suggest that due to acute stress, cfDNA levels increase rapidly by a spontaneous active or passive release mechanism that is not yet known. As a result of the rapid and parallel increase of cfDNA and lactate in an incremental treadmill test leading to exhaustion within 15-20 minutes, it is unlikely that cfDNA is released into the plasma by typical necrosis or apoptosis of cells in acute exercise settings. Recently, rapid DNA release mechanisms of activated immune-competent cells like NETosis (pathogen-induced cell death including the release of neutrophil extracellular traps [NETs]) have been discovered. cfDNA accumulations might comprise a similar kind of cell death including trap formation or an active release of cfDNA. Just like chronic diseases, chronic high-intensity resistance training protocols induced persistent increases of cfDNA levels. Chronic, strenuous exercise protocols, either long-duration endurance exercise or regular high-intensity workouts, induce chronic inflammation that might lead to a slow, constant release of DNA. This could be due to mechanisms of cell death like apoptosis or necrosis. Yet, it has neither been implicated nor proven sufficiently whether cfDNA can serve as a marker for overtraining. The relevance of cfDNA with regard to overtraining status, performance level, and the degree of physical exhaustion still remains unclear. Longitudinal studies are required that take into account standardized and controlled exercise, serial blood sampling, and large and homogeneous cohorts of different athletic achievement. Furthermore, it is important to establish standardized laboratory procedures for the measurement of genomic cfDNA concentrations by quantitative real-time polymerase chain reaction (PCR). We introduce a new hypothesis based on acute exercise and chronic exposure to stress, and rapid active and passive chronic release of cfDNA fragments into the circulation.     

Biochemical aspects of overtraining in endurance sports: a review

Top-level performances in endurance sports require several years of hard training loads. A major objective of this endurance training is to reach the most elevated metabolic adaptations the athlete will be able to support. As a consequence, overtraining is a recurrent problem that highly-trained athletes may experience during their career. Many studies have revealed that overtraining could be highlighted by various biochemical markers but a principal discrepancy in the diagnosis of overtraining stems from the fact that none of these markers may be considered as universal. In endurance sports, the metabolic aspects of training fatigue appear to be the most relevant parameters that may characterise overtraining when recovery is not sufficient, or when dietary habits do not allow an optimal replenishment of substrate stores. From the skeletal muscle functions to the overall energetic substrate availability during exercise, six metabolic schemes have been studied in relation to overtraining, each one related to a central parameter, i.e. carbohydrates, branched-chain amino acids, glutamine, polyunsaturated fatty acids, leptin, and proteins. We summarise the current knowledge on these metabolic hypotheses regarding the occurrence of overtraining in endurance sports.