Definition, epidemiology, and pathogenesis of short-term overtraining (overreaching), long-term overtraining, and possibly resulting overtraining syndrome have already been described elsewhere (2,3,5,7,8,15,17,20,25,27,28,37). This overview focuses on long-term endurance overtraining, possibly resulting in overtraining syndrome, and the hypothesis of an underlying autonomic or neuroendocrine imbalance (15,17). An overall schematic presentation of factors likely to be related to the development of overtraining syndrome is given in Fig. 1.
From a clinical standpoint, Israel (15) distinguished between a parasympathetic or vagal type overtraining syndrome and a sympathetic type. The more frequently observed parasympathetic type may be called modern type of overtraining syndrome. It is characterized by persistent high fatigue ratings, apathy, altered mood state, persistent performance incompetence, altered immune, and reproductive function (4,5,10,20,25,27). According to anecdotal observations (15,27), the sympathetic or "classical" type overtraining syndrome is a less frequent problem in modern sports. It can be characterized by hyperexcitability, restlessness, and performance incompetence (15).
The parasympathetic type overtraining syndrome is assumed to be the consequence of an imbalance between long-term inappropriately high training volume in endurance sports and too little time for regeneration (besides other additional and more or less essential stress factors (5)). The sympathetic type overtraining syndrome may also be the consequence of such an imbalance but seems to be related to inappropriately intensive training sessions. This classification may be too simple and one-dimensional, as no sympathetic type overtraining syndrome was seen after intensive resistance (6) and after high-intensity endurance overtraining (26). Therefore, a sympathetic type overtraining syndrome may rather be the consequence of too much accompanying psycho-emotional stress, such as too many competitions and too many nontraining stress factors (social, educational, occupational, economical, nutritional, travel, and time stress).
ADDISON OR BASEDOW TYPE OVERTRAINING SYNDROME
From a clinical standpoint, the parasympathetic or vagal overtraining syndrome was also called Addison type, and the sympathetic was named Basedow type overtraining syndrome (15). Their clinical patterns were similar to adrenal insufficiency (Morbus Addison) and thyroidal hyperfunction (Morbus Basedow).
Hackney et al. (12) observed reduced resting thyroid stimulating hormone (TSH), total T3 and free T3 concentrations in mountaineers subsequent to a Mt. McKinley expedition. Reduced resting TSH concentrations, reduced exercise-related TSH levels (by 40-50%), and approximately 20% reduced thyroid-releasing hormone-stimulated pituitary release of TSH were also observed in an early stage of the overtraining syndrome (26). Probably dependent on methodical problems, these changes did not reach the level of significance and have first to be confirmed. Data that can be related to an altered thyroidal function in an advanced stage of an overtraining syndrome are lacking at present anyway. Besides lacking confirmation of altered thyroidal function, decreased TSH (and TT3, fT3) levels could point to reduced hypothalamic TRH and pituitary TSH release owing to inhibitory effects caused by long-term increased sympathetic nervous system activity, metabolism, and body core temperature during prolonged training periods (11).
Persson et al. (33) described a reduced ACTH-stimulated adrenal cortisol release in chronically fatigued horses. These data, however, could not be confirmed by Kuipers (19). Contrary to untrained controls, Wittert et al. (40) observed significantly increased ACTH plasma concentrations in ultramarathoners during an early morning period between 3 and 8. Cortisol plasma levels or 24-h renal cortisol excretions did not show any significant differences. This study was performed 3-5 d after completion of the 1-d New Zealand coast-to-coast marathon. Corresponding to the findings presented by Persson et al. (33) in chronically fatigued horses, the findings of Wittert et al. (40) may point to decreased adrenal responsiveness to ACTH in these ultra-endurance athletes. The decreased adrenal responsiveness can be the consequence of an overload during heavy preparatory training sessions before the ultramarathon, the ultramarathon stress itself, and incomplete regeneration. An incomplete regeneration may be assumed because a period of 3-5 d seems too short for complete regeneration. In this stage, the decreased adrenal responsiveness may still be compensated by increased ACTH levels (responses).
An approximately 60-80% higher pituitary corticotrop-in-releasing hormone (CRH)-stimulated ACTH response was also observed in experimentally overtrained athletes in an early stage of the overtraining syndrome (26). However, this increased response could no longer prevent a significantly reduced adrenal cortisol response compared to baseline. The findings lagged behind and were still amplified after 2 wk of incomplete regeneration (26,27). A decreased adrenal responsiveness was no longer completely compensated by increased pituitary ACTH response. In agreement with these findings, significantly (24) or tendentially (26) decreased exercise-related maximum cortisol levels were observed in overtrained distance runners (24) or recreational athletes (26) compared to baseline (397 ± 119 vs 502 ± 188 nmol/L, and 353 ± 39 vs 389 ± 166 nmol/L).
Barron et al. (1) additionally described a significantly decreased pituitary ACTH response related to insulin-induced hypoglycemia in overtrained distance runners. This was paralleled by clearly reduced adrenal cortisol response as also observed in chronically fatigued horses (33) and in overtrained human athletes (26,27). Besides the question of underlying different mechanisms (insulin-induced hypoglycemia vs CRH test), the findings of Barron et al. (1) additionally reflect a decreased hypothalamic and/or pituitary responsiveness, besides reduced adrenal responsiveness to ACTH. They also described a decreased pituitary release of growth hormone. This pattern may be characteristic of an advanced stage in the overtraining process. Recently, Gastmann et al. (9) also observed a reduced pituitary ACTH response to CRH in experienced road cyclists. This study was performed at the end of a heavy road pacing season after an additional 2-wk high-volume training stress without a preceding regeneration period.
Altogether, the majority of findings provide evidence of a reduced adrenal responsiveness to ACTH in the stage of overreaching or early overtraining syndrome. The reduced responsiveness is initially compensated by an increased pituitary ACTH response. However, it is no longer compensated in an early stage of a parasympathetic (Addison type) overtraining syndrome; the cortisol response decreases. A decreased hypothalamic/pituitary responsiveness (ACTH response) is added in an advanced stage of a parasympathetic overtraining syndrome (Fig. 2). There is additionally some evidence of a decreased pituitary release of thyroid-stimulating hormone (12,26); growth hormone release may be increased in an early stage (26,27) and decreased in an advanced stage of an overtraining syndrome (1).
At present, there is no valid experimental model of the genesis of the seldom observed sympathetic (Basedow type) overtraining syndrome. Because our knowledge concerning this type of overtraining syndrome mainly arises from anecdotal observations (15,27), the following sections therefore focus on the more common parasympathetic (Addison type) overtraining syndrome.
PARASYMPATHETIC TYPE OVERTRAINING SYNDROME AND BASAL RENAL CATECHOLAMINE EXCRETION
Basal renal (urinary) catecholamine excretion, the excretion of free catecholamines during overnight rest, is seen to reflect the intrinsic activity or tone of the sympathetic nervous system, as activating mechanisms are clearly reduced during night rest (18,22). Because noradrenaline concentrations in plasma and cerebrospinal fluid are quite similar (34,35), circulating and excreted noradrenaline may reflect the neuronal noradrenaline release in the brain.
Anecdotal observations in a top tennis player after too many matches, in track and road cyclists before the 1988 Games in Seoul (22,27), and during a follow-up of semiprofessional soccer players (22) give some support to Israel's hypothesis (15) of an autonomic imbalance and altered sympathetic nervous system activity in athletes suffering from parasympathetic type overtraining syndrome. The majority of these overtrained athletes showed an average 50-70% reduction in basal urinary catecholamine excretion. Such a finding was independently reported in soccer players by Naessens et al. (29). However, we believe this to be a "late" finding in the overtraining process during long-term high-volume training (22,27). Catecholamine excretion was negatively correlated to fatigue ratings (27) and showed normalization during a 2-3-wk regeneration period (22). There is also a negative correlation between basal catecholamine excretion and latency of REM sleep (r = −0.46; P < 0.01) in elite athletes (36). These correlations support the hypothesis that basal catecholamine excretion may reflect central mechanisms and that a clearly reduced basal catecholamine excretion may indicate central fatigue.
Altogether, there is some evidence that significantly reduced intrinsic activity of the sympathetic system, altered adrenal cortisol response, and potential alterations in thyroidal function can explain fatigue, demotivation, and performance incompetence in athletes suffering from a parasympathetic type overtraining syndrome. The decrease in sympathetic intrinsic activity is seen to depend on a negative feedback mechanism to increased concentration of circulating free catecholamines during prolonged heavy training sessions (Fig. 3). A plasma amino acid imbalance and altered brain neurotransmitter metabolism (30,31) is hypothesized to be involved in this process. An inhibitory effect of hypothalamic heat centers on hypothalamic sympathetic centers may have additional influence caused by increased body core temperature during prolonged training sessions.
PARASYMPATHETIC TYPE OVERTRAINING SYNDROME AND PLASMA CATECHOLAMINE LEVELS
During a prospective high-volume (moderate intensity) endurance overtraining study, final resting plasma norepinephrine (noradrenaline) levels before exercise and submaximum responses were significantly increased compared to baseline (23,24). Increased resting plasma norepinephrine levels were also observed by Hooper et al. (14) in overtrained elite swimmers. Increased submaximum norepinephrine responses were also described by Fry et al. (6) related to resistance overtraining. Increased plasma norepinephrine levels in overtrained athletes can indicate a loss in sensitivity of target organs to catecholamines, that is, a loss in training-dependent adaptation (32). But neither increased resting levels nor increased submaximum responses were observed after a 6-wk prospective high-intensity (moderate volume) overtraining study (26). Thus, inappropriately prolonged and monotonous daily training sessions may be an essential prerequisite for this loss in adaptation. Because catecholamine plasma clearance is not related to training (13), an increased response likely reflects an increased release and increased neuronal sympathetic activity because neuronal sympathetic activity is positively correlated to plasma norepinephrine levels (39,41).
A decreased intrinsic sympathetic activity (see above) as observed in the same affected athletes (23,24) and in other different groups of overtrained athletes (22,27,29) may not be seen as contradictory to increased submaximum plasma catecholamine responses, as plasma responses reflect acute stress-related changes in sympathetic activity rather than changes in intrinsic activity. Despite overtraining-related decreased intrinsic activity, stress-related responses are maintained and even amplified at identical absolute submaximum work load (27). From a common sense standpoint, this guarantees "flight or fight" even in fatigued subjects at least during early phases of overtraining. Related to a respective lowered absolute maximum work load in affected overtrained athletes, the final maximum plasma catecholamine responses were similar compared to baseline (23) or even decreased in more advanced stages of the overtraining process (17).
Increased plasma norepinephrine responses may also indicate the attempt to overcome overtraining-related peripheral or muscular fatigue. Because a decrease in β-adreno-receptors on blood cells was observed in swimmers and distance runners (16) subsequent to prolonged high-volume training periods, increased plasma norepinephrine stress responses can be explained as consequence to decreased β-adrenoreceptor density. The decrease in β-adrenoreceptor density can be seen as a protective mechanism underlying the loss in sensitivity of target organs to catecholamines. This mechanism can explain overtraining-related "peripheral" fatigue in athletes after prolonged periods of high-volume training. This is supported by also decreased β-adrenoreceptor-mediated metabolic and cardiac effects in affected athletes after high-volume overtraining (23)(Fig. 4). The increased submaximum plasma norepinephrine responses were related to decreased submaximum heart rate, blood glucose, lactic acid, and free fatty acid responses (Fig. 4).
This pattern is identical to that following administration of β-blockers (21). An overtraining-related down-regulation of β-adrenoreceptors can be seen as a consequence to an increased concentration of circulating free catecholamines during prolonged, heavy, daily training sessions. The complete pattern of decreased intrinsic sympathetic activity, decreased β-adrenoreceptor density, decreased β-receptor-mediated effects, and increased norepinephrine levels/responses can only be expected after prolonged periods of daily training sessions of more than 2-3 h but not at a training load of <1 h·d−1(Fig. 4). Thus, after a 6-wk high-intensity (but moderate volume) overtraining study, decreased blood glucose and compromised performance ability were also observed (26). However, this was not paralleled by decreased sympathetic intrinsic activity, by significantly increased submaximum plasma norepinephrine, and by a complete pattern of decreased heart rate, lactic acid, and free fatty acid responses (Fig. 4). Therefore, the first step in the endurance overtraining process might be a significant decrease in stored energy-rich substrates such as glycogen (3), which is amplified or removed by down-regulation of β-adrenoreceptors during inadequately prolonged daily training sessions. An overtraining-related down-regulation in β-adrenoreceptors can be seen as protecting mechanism of target organs against overload-dependent irreversible damage. The transmission of ergotropic or catabolic signals becomes adapted to the reduced functional state of fatigued target organs.
Parasympathetic overtraining syndrome can thus be thought of as an ultimate negative feedback response to sustained levels of arousal, whether from long-term heavy exercise or other issues. Given both by the volume of training undertaken by contemporary athletes and the general pace of life today, the ability to enforce a reduction in the net stress to the system is, in fact, very adaptive. The unique problem for athletes and their coaches is to provide appropriate regeneration before the athlete's body does it independently. In this regard, athletes and coaches must learn that performance incompetence and severe fatigue are symptoms to be respected, not problems to overcome.
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