Overtraining is a process of excessive exercise training in high-performance athletes that may lead to overtraining syndrome. Overtraining syndrome is a neuroendocrine disorder characterized by poor performance in competition, inability to maintain training loads, persistent fatigue, reduced catecholamine excretion, frequent illness, disturbed sleep and alterations in mood state. Although high-performance athletes are generally not clinically immune deficient, there is evidence that several immune parameters are suppressed during prolonged periods of intense exercise training. These include decreases in neutrophil function, serum and salivary immunoglobulin concentrations and natural killer cell number and possibly cytotoxic activity in peripheral blood. Moreover, the incidence of symptoms of upper respiratory tract infection increases during periods of endurance training. However, all of these changes appear to result from prolonged periods of intense exercise training, rather than from the effects of overtraining syndrome itself. At present, there is no single objective marker to identify overtraining syndrome. It is best identified by a combination of markers, such as decreases in urinary norepinephrine output, maximal heart rate and blood lactate levels, impaired sport performance and work output at 110% of individual anaerobic threshold, and daily self-analysis by the athlete (e.g. high fatigue and stress ratings). The mechanisms underlying overtraining syndrome have not been clearly identified, but are likely to involve autonomic dysfunction and possibly increased cytokine production resulting from the physical stress of intense daily training with inadequate recovery.
Overtraining is a process of excessive exercise training that may, if left unchecked, lead to a condition termed ‘overtraining syndrome’. Overtraining syndrome is characterized by persistent fatigue, poor performance in sport despite continued training, changes in mood state and neuroendocrine factors and frequent illness, such as upper respiratory tract infection (URTI).1, 2 Overtraining syndrome reflects the body’s inability to adapt to cumulative fatigue resulting from daily, intense exercise training that is not balanced with appropriate and sufficient rest.
Recovery from overtraining syndrome may require weeks to months of complete rest or greatly reduced exercise training. The term ‘overreaching’ describes a qualitatively similar state to overtraining syndrome, but is less severe and resolved within days to weeks. Other terms previously used to describe overtraining syndrome include ‘burnout’ and ‘staleness’. It is only within the past few years that, in the research literature, the process of overtraining has been differentiated from the resultant conditions of overtraining syndrome or overreaching. Overtraining syndrome has several parallels with chronic fatigue syndrome and clinical depression, in particular persistent fatigue, mood state disturbances, and muscle soreness.3, 4
Overtraining is of great importance to the high performance athlete. Prolonged periods of persistent fatigue interfere with optimal preparation for major events, such as World Championships or the Olympics. Inconsistent or poor performance at critical times in an athlete’s career may influence selection for representative teams, lead to loss of sponsorship or income from government and private sources and possibly cause the athlete to prematurely retire from sport.
Models to study overtraining syndrome in athletes
Two general models are used to study responses to overtraining in athletes. In one model, athletes may be assessed at various times throughout a competitive season, usually lasting 3–8 months. Physiological and psychological responses are then compared for each athlete between periods of high and low training intensity, or between athletes showing symptoms of overtraining syndrome and those considered well-trained (without symptoms). The advantage of this model is that athletes are studied in their ‘natural’ environment, without manipulating the normal training regimen. The disadvantage is that it is difficult to control for possible confounding variables, such as illness, travel, dietary changes, competition stress and seasonal variability.
In the other model, training is intentionally intensified for up to 4 weeks. For ethical reasons, 4 weeks is considered the maximum time that athletes can withstand intensification of already high training loads.5, 6, 7 By the definitions given earlier, any resultant condition should be called overreaching rather than overtraining, because, by definition, 4 weeks is too short to induce overtraining. Performance in a sport-specific task (e.g. time to complete a given distance) and physiological and psychological variables are compared from before and after intensified training or, less frequently, between athletes showing symptoms of overreaching and those considered well-trained. This model permits better control of confounding variables listed earlier. However, there is much variability in the responses of the athletes to intensified training; that is, some athletes improve without deleterious effects, while others show signs of overreaching.8 Moreover, the increases in training load are usually much higher than usual and do not reflect the athletes’ normal training regimen. Despite these limitations, both models provide useful information for identifying indicators and understanding mechanisms underlying overtraining syndrome.
Prevalence of overtraining and impact on performance
The prevalence of overtraining syndrome is difficult to estimate, because it requires surveying large groups of athletes from diverse sports over long periods of time. Moreover, the term overtraining elicits a strong reaction from coaches and athletes, who are often reluctant to identify particular athletes as overtrained. Nevertheless, it is a term widely recognized among high-performance athletes across virtually all sports. It is estimated that, at any given time, between 7 and 20% of all athletes may exhibit symptoms of overtraining syndrome.9, 10, 11 The prevalence varies by sport and is thought to be highest in endurance sports requiring high volume intense training, such as swimming, triathlon, road cycling, rowing and, to a lesser extent, distance running. Except for distance running, high performance athletes in these sports frequently train for 4–6 h each day, 6 days per week for several months without appreciable time off. It is believed that the imbalance between excessively large volumes of training without adequate rest and recovery leads to overtraining syndrome. It is instructive that the sports most likely to cause overtraining, as noted earlier, are body mass-supported; that is, except for distance running, the body is supported by equipment or water. Risk of musculoskeletal injury limits training volume in weight-bearing activities, such as distance running, and, consequently, the incidence of overtraining may be lower than in other endurance sports. It is important to emphasize, however, that there are few empirical data to unequivocally support this claim. Overtraining also occurs in ‘power’ sports, such as weight lifting and judo.12, 13
The incidence of overreaching is easier to identify in studies using the short-term intensified training model (discussed earlier). Studies using this model have reported that 30–100% of athletes exhibit symptoms of overreaching after intensified training lasting 10 days to 4 weeks.5, 6, 7, 8, 14, 15 In these studies, symptoms appear after training volume is increased by 40–100%; generally, the larger and more abrupt the increase in training load, the higher the incidence of symptoms. These studies show that, given a sufficiently rigorous training regimen, most if not all high-performance athletes will exhibit symptoms of overreaching over the short term. As noted earlier, however, such dramatic increases in training volume are not natural for these athletes.
A decrement in performance despite continued training is the most obvious objective indicator of overtraining syndrome. Decrements in competitive performance of 1–20% have been documented.7, 8, 9, 14, 16, 17 In elite sport, continued performance is expected and any decrement in performance, no matter how small, can be catastrophic to the athlete who has invested years working toward a major competition such as the Olympics. For example, in the 100 m sprint, a performance decrement of 1% (about 0.1 s for men) may mean the difference between finishing in medal contention or not. In swimming, only a 4–5% difference separates times required to qualify to compete in the Olympics from world record times. In addition to performance decrements during competition, overtraining syndrome is frequently associated with an inability to train effectively, that is, to maintain the rigorous daily training regimen required to compete an a international level. Besides overtraining syndrome, there are many possible causes of substandard performance and the inability to train, such as illness, anaemia, dietary insufficiency and poor psychological preparation; poor performance by itself is inadequate as an indicator of overtraining syndrome.
Symptoms of overtraining
There are many purported signs and symptoms of overtraining syndrome, although few have been consistently documented to be reliable and valid indicators of the syndrome. Identifying clear symptoms of overtraining is important for two reasons. First, from a practical viewpoint, athletes and coaches wish to identify as early as possible the athlete moving toward overtraining syndrome so that training may be altered before performance deteriorates. Second, from a scientific viewpoint, clearly identifying the symptoms of overtraining syndrome gives direction to the search for underlying mechanisms (discussed further later).
At present, the only physiological variables consistently documented to occur with overtraining syndrome include:
A variety of other purported physiological indicators of overtraining have not been clearly supported by the research literature. These include elevated early morning heart rate, haematological changes, such as low serum ferritin levels, changes in hormones, such as blood concentrations of testosterone and cortisol, frequent URTI, loss of body mass and reduced maximal oxygen consumption (VO2max).
Psychological changes also accompany overtraining syndrome,9, 10, 11, 16 including changes in mood state as indicated on the Profile of Mood States (POMS),21 apathy and loss of motivation, loss of appetite, irritability or depression and sleep disturbances.
There are many possible factors that contribute to or cause overtraining syndrome. The observation that overtraining occurs across a wide spectrum of sports involving different exercise modes suggests that there is a commonality of contributing factors. It is generally accepted that the following factors, at minimum, contribute to overtraining syndrome22:
Sudden increase in training volume and/or intensity.
Heavy competition schedule.
Lack of periodization or programmed recovery in training schedule.
Monotonous training program.
High self-reported stress levels, regardless of whether they are directly related to training.
Several experimental models of overreaching show that a sudden increase in training volume induces signs and symptoms such as poor performance, high fatigue levels, sleep disturbances, mood state changes, altered catecholamine output and persistent muscle soreness.5, 6, 7, 8, 15, 19 In a study on distance runners, doubling training volume elicited signs and symptoms such as 7% performance decrement, fatigue and muscle soreness.6 In contrast, in the same study, a similar group of runners did not exhibit symptoms after increasing training intensity while maintaining volume. In elite swimmers already training at a high intensity, progressively increasing training volume by 10% each week for 4 weeks induced symptoms, such as high fatigue levels, sleep disturbances and poor performance, in one-third of the athletes7. In physically fit special armed forces personnel, after 10 days of twice daily, maximal running all subjects reported symptoms, such as inability to maintain training load, nausea, muscle soreness and irritability15. It appears that athletes already training at high intensity cannot tolerate sudden increases in training volume for more than a few days without exhibiting symptoms of overreaching. Because, for ethical reasons, these studies were not extended beyond a few weeks, it can only be speculated that maintaining such training regimes without adequate rest is likely to lead to the more serious overtraining syndrome.
Athletes often maintain daily log books, in which details of training distance/duration, intensity and performance are recorded; the athlete’s perception of adaptation to training may also be included. If given space to write their own subjective feelings about their adaptation to training, overtrained athletes frequently write comments such as ‘heavy legs’, ‘can’t get going’, or ‘feeling flat’.8, 15, 16 Measures of well-being, such as fatigue levels, quality of sleep, perceived stress levels and muscle soreness, may also be quantified on a daily basis.5, 9, 15, 16 High self-reported stress levels have been shown to be predictive of overtraining16 and overreaching,8 even when the sources of stress do not directly relate to the rigours of training. In a study of elite swimmers followed over a 6 month season, in those swimmers later identified as overtrained, high stress levels were observed 4–6 weeks before performance deteriorated and other symptoms appeared.16 Athletes experience stress relating to finances, time management, study and relationships with family and significant others, all of which can be adversely affected by the rigours of training for 4–6 h per day. These data suggest that high perceived stress levels may contribute to the subsequent development of symptoms of overreaching or overtraining syndrome, although the mechanism by which this may occur is not yet clear.
Changes in physiological and neuroendocrine variables during overtraining
Overtraining syndrome is associated with changes in several physiological variables, in particular physical work capacity, maximal heart rate, blood lactate variables and skeletal muscle glycogen concentration. Decrements in physical work capacity may involve endurance exercise capacity (i.e. ability to perform exercise for prolonged periods) and/or muscular strength, depending on the type of athlete and training. For example, endurance exercise capacity is most affected in endurance athletes, such as swimmers or distance runners,5, 6, 9 whereas muscular strength declines in power athletes, such as weightlifters12, 23 and judo athletes.13 The individual anaerobic threshold (IAT), or the work rate associated with an exponential rise in blood lactate level, is a consistent predictor of endurance exercise performance. The onset of blood lactate accumulation reflects the exponential rise in lactate output from skeletal muscle. High lactate levels in skeletal muscle lower pH, inducing fatigue via inhibition of metabolic pathways, in particular anaerobic glycolysis, limiting the rate of ATP resynthesis. Time to volitional fatigue at a work rate equivalent to 110% of IAT declines by approximately 20–30% in overtrained athletes,18 suggesting impairment in the capacity to maintain high intensity work, a crucial requirement of virtually all sports.
Athletes and coaches often use early morning heart rate (EMHR) as an indicator of overtraining syndrome, although most of the empirical evidence has failed to find any change in EMHR in overtrained athletes.5, 6, 9, 19 In contrast, there is good evidence that maximal heart rate (MHR) declines by 5–10 b.p.m.5, 6, 19, 20 Lower maximal blood lactate concentration also accompanies overtraining syndrome5, 6, 19 and is thought to reflect a reduction in catecholamine-induced stimulation of glycogenolysis (use of muscle glycogen to produce ATP required by high-intensity exercise) within skeletal muscle. Decreased maximal heart rate and blood lactate concentrations are consistent with the belief that overtraining syndrome is a neuroendocrine disorder (discussed further later).24, 25, 26 Low muscle glycogen concentration has also been associated with overtraining14 and would explain reduced maximal blood lactate levels and comments by athletes reporting ‘heavy legs’. However, symptoms of overreaching also appear despite maintenance of muscle glycogen levels,19 suggesting that this is not a consistent outcome of or contributing factor to overtraining syndrome.
Overtraining syndrome has been associated with alterations in neuroendocrine factors, in particular urinary excretion of NEp. For example, Lehmann et al. have observed progressively declining overnight urinary NEp excretion in male distance runners during 4 weeks of intensified training that resulted in clear symptoms of overreaching; NEp excretion was significantly correlated with self-reported symptoms.5, 6 In another study in which training was intensified over 4 weeks in swimmers, urinary NEp excretion was significantly lower in overreached compared with well-trained swimmers.8 In the latter study, low NEp excretion appeared before the onset of symptoms, suggesting that neuroendocrine changes may precede, and possibly contribute to, subsequent development of symptoms. Changes in urinary NEp levels during training and tapering (reduced training before major competition) also predict performance during competition.27 Although the concentrations in the blood of testosterone and cortisol, and their ratio, fluctuate in response to training stress, most evidence does not support a role for these changes in the aetiology of overtraining syndrome8, 9, 15.
Changes in immunological variables during overtraining
Athletes and coaches associate overtraining with frequent illness, especially URTI. As discussed in more detail in other papers in this special supplement, endurance athletes experience a high incidence of URTI during intense training and after major competition. Also as discussed in other papers in this supplement, a single bout of acute intense exercise may suppress immune parameters for several hours afterwards. Moreover, there is evidence that high-performance athletes demonstrate mild suppression of a host of immunological parameters. One unanswered question is whether such immune suppression results from overtraining syndrome itself, or rather from the long-term stress of intense daily exercise training, regardless of whether such training leads to symptoms of the syndrome. Table 1 provides a brief summary of the responses of various immune parameters to intense training and overtraining.
Upper respiratory tract infections and overtraining
There are surprisingly few studies to directly address the issue of incidence of URTI in overtrained athletes,7, 28, 29 despite the well-accepted belief that overtrained athletes are susceptible to illness. In one study of 24 competitive swimmers, training was intensified over 4 weeks, resulting in eight (33%) of the swimmers showing symptoms of overreaching.7 Of the 24 swimmers, 10 (42%) exhibited self-reported symptoms of URTI during the 4 weeks. Unexpectedly, the rate of URTI among the overreached swimmers (one of eight, or 12.5%) was significantly lower than that in the well-trained swimmers (nine of 16, or 56%). It has been suggested that increased risk of URTI may not necessarily accompany overtraining/overreaching, but may instead be a consequence of intense training in all athletes. It has later been suggested that the higher rate of URTI among the well-trained swimmers (i.e. those who did not become overreached) may have protected against overreaching.30 That is, the appearance of mild symptoms of URTI may have caused these swimmers to consciously or subconsciously ease their training loads for a few days, providing sufficient rest to prevent overreaching. In another study, again on elite swimmers, no association was found between incidence of URTI and increasing training volume and intensity over an 8 month season.28 However, another study of 25 athletes has found that a high proportion of illnesses occur when training exceeds thresholds identified for individual athletes, based on a combination of training volume and monotony.29
Thus, the few studies published directly on this issue do not support the concept that overtraining syndrome itself is associated with an increased risk of URTI. There is, however, good evidence showing increased risk of URTI among endurance athletes and a dose–response relationship between training volume and incidence of URTI (discussed by others in this special supplement). Taken together, it appears that, in athletes, both overtraining syndrome and URTI result from a common cause: excessive training with insufficient rest and variety of training. The risk of URTI is elevated in athletes during periods of intense training, regardless of whether such training leads to symptoms of overtraining syndrome.
Effects of overtraining/overreaching on leucocyte number and function
Resting peripheral blood leucocyte number is generally clinically normal in athletes, even during intense training and overtraining.8, 15, 16, 31 No differences have been reported in leucocyte number between elite swimmers identified as overtrained compared with well-trained swimmers.16 In contrast, leucocyte number has been shown to progressively decline to clinically low values (from 4.9 to 4.2 × 109/L) in a short-term overreaching study in which training volume was doubled over 4 weeks in distance runners.6 Interestingly, this decline was observed only when training volume (distance) and not intensity (pace) increased. It is currently unknown whether there are any clinical consequences of a decline in peripheral blood leucocyte number and whether it reflects simply a redistribution of cells between peripheral blood and other lymphoid compartments or, alternatively, an increase in cell turnover. There is evidence that acute intense exercise may cause apoptosis in peripheral blood leucocytes,32 but it is unclear whether this contributes to changes in circulating cell number.
Lymphocyte number and function Resting peripheral blood lymphocyte number also appears to be relatively unaffected by intense training and overtraining.8, 15, 31, 33, 34 Two studies have noted transient decreases in lymphocyte number during the initial stages (2–4 weeks) of intensified training;8, 34 in both studies, this was attributed to declines in CD3+ CD4+ number. However, cell counts had normalized by the end of the intensified training periods (4–8 weeks), suggesting only temporary perturbation of these cell counts that is unlikely to be of biological significance. Peripheral blood lymphocyte counts are clinically normal in athletes showing symptoms of overtraining or overreaching.8, 15, 33
In contrast to the relatively stable number of cells in the circulation, lymphocytes may be activated by periods of intense exercise training.15, 33, 35 For example, expression of CD122 (high-affinity IL-2 receptor) was higher on resting CD8+ and CD16/CD56+ cells in distance runners compared with matched non-runners.35 A significant increase in CD25 (low-affinity IL-2 receptor) expression has been observed in cells obtained over 10 days of intense running training that caused overreaching, despite no changes in lymphocyte or CD3+ cell number.15 The ability of lymphocytes to respond to mitogenic challenge in the standard in vitro assay appears to be unchanged or possibly enhanced by intense training.36 It is unclear if there is any biological significance of this apparent activation of peripheral blood lymphocytes during intense training.
Neutrophil number and function Neutrophils appear to be the type of leucocyte most affected by prolonged periods of intense exercise training, although few studies have measured neutrophil function in athletes specifically classified as overtrained or overreached. Lower resting and post-exercise neutrophil activity has been reported in athletes from a variety of sports compared with non-athletes or within the same athletes across different phases of the training cycle.28, 37, 38 For example, Smith et al.37 first noted significantly lower neutrophil activation (opsonized zymosan (OZ)-stimulated reactive oxygen species (ROS) production) in neutrophils isolated at rest and up to 6 h after 60 min exercise in trained cyclists compared with matched non-athletes. In elite swimmers, resting neutrophil activity (OZ-stimulated ROS production, expressed per cell) declined progressively during a 12 week intense training period.28 The lowest values were observed during the phase of highest training intensity, and activity was partially recovered during a subsequent rest phase. In another study, neutrophil phagocytic activity (latex bead ingestion) and activation (ROS production) were shown to be significantly lower at rest and 24 h after a standard maximal exercise test during intense compared with moderate training in distance runners, and compared with matched non-athletes.38 These data suggest that downregulation of neutrophil function may occur in response to prolonged periods of intense exercise training. The biological significance of such changes is not currently known, although it has been speculated that downregulation of neutrophil function reflects an adaptive response to chronic inflammation resulting from tissue microtrauma elicited by daily intense exercise.39 In the study on swimmers, declining neutrophil activation was not correlated with the appearance of URTI over 12 weeks of intense training.28
Natural killer cell number and function Peripheral blood NK (CD16+/56+) cell number and percentage are generally normal in athletes, although NK cytotoxic activity (NKCA) may be higher at rest in athletes compared with non- athletes.40 There are, at present, no studies describing NK cell number and function in athletes classified as overtrained or overreached. Natural killer cell number may decrease during short-term (1–4 weeks)15, 41 and long-term (7 months)31 intense training. For example, CD56+ cell number declined more than 40% during 10 days of intense running training in physically fit military personnel; values remained low for 5 days recovery training (light exercise).15 In another study, NK (CD16+/56+) cell number and percentage declined by 30–40% after 7 months intense swim training and were 20–30% lower than in age-matched non-athletes.31 Both NK cell number and NKCA declined over 4 weeks intensified training in swimmers that did not lead to symptoms of overreaching41. These changes in NK cell number and percentage occurred despite no changes in other cell counts.15, 31, 41 The reasons for and biological significance of such changes in NK cell number and possibly function are not known at present. Acute intense prolonged exercise causes transient suppression of NKCA, lasting at least 6 and perhaps more than 12 h.42, 43 Elite athletes often train twice per day and it is possible that NK cell number and function require an extended time to recover from each session of intense exercise.
Most comparisons between athletes and clinical norms show that resting serum Ig levels are normal in athletes. There are, however, recent reports suggesting clinically low serum Ig levels during intense training in some athletes. For example, serum IgA, IgG and IgM concentrations were significantly lower throughout a 7 month training season in elite swimmers compared with age-matched non-athletes.31 In these swimmers, serum IgA, IgG, IgM, and IgG2 levels were in the lowest 10th percentile for their age population. Low values could not be attributed to differences in relative or absolute B or T cell numbers. Despite the low serum Ig levels, the ability to produce antibody in response to antigenic challenge is normal in swimmers44 and triathletes.45
Because of the seemingly high incidence of URTI among athletes, much attention has focused on the mucosal immune system response to intense exercise training, using salivary IgA concentration as a marker. Low resting salivary IgA concentration has been reported in some elite athletes.31, 46, 47 Salivary IgA levels decline during prolonged periods of intense exercise training31 and IgA concentration is lower in overtrained compared with well-trained swimmers.48 Low salivary IgA concentration is predictive of the subsequent appearance of symptoms of URTI over the short49 and long term.46, 47 For example, lower IgA1 levels early in the training season have been correlated with the number of URTI episodes throughout the season; IgA2 levels were also clinically low in these swimmers.47 To date, salivary IgA concentration is the only immune parameter to be directly associated with the appearance of URTI.46, 47, 49
Glutamine, the most abundant amino acid in the body, is required for normal function by lymphocytes and monocytes. Glutamine is released from skeletal muscle during physical stress, such as exercise and other trauma, and is an important substrate for gluconeogenesis in the liver. Low plasma glutamine concentration has been associated with overtraining syndrome.50 It has been speculated that lymphocyte function may be compromised by low glutamine availability, possibly increasing susceptibility to infection in overtrained athletes. When various biochemical and immunological parameters were measured in overtrained athletes, low plasma and skeletal muscle glutamine concentrations were the only variables to distinguish athletes with symptoms from healthy athletes or clinical norms.51 However, 26 weeks of glutamine supplementation has had no effect on the incidence of URTI or peripheral blood lymphocyte counts, despite significantly increased plasma and muscle glutamine concentrations over this time.52 In another study, plasma glutamine concentrations declined progressively over 10 days of intense running training that resulted in symptoms of overreaching.53 Despite the low plasma glutamine levels, however, all other immune parameters (e.g. cell counts, lymphocyte activation markers) increased or remained unchanged. In a study on swimmers, when training intensity was progressively increased over 4 weeks, plasma glutamine concentration remained unchanged in swimmers diagnosed as overreached; over the 4 weeks values increased in the well-trained athletes and were 20% higher than in overreached swimmers.7 However, plasma glutamine levels were not significantly different between swimmers who developed symptoms of URTI and those who remained healthy. Thus, although plasma glutamine concentration may decline in some instances of overtraining, there is little evidence to link this decline with immune suppression. It is thought that decreasing plasma glutamine levels may more closely reflect metabolic events, such as glycogen depletion, metabolic acidosis and increased protein degradation in skeletal muscle as a result of intense prolonged exercise on a daily basis.2, 54, 55
Mechanisms underlying overtraining syndrome
It is unlikely that the diverse symptoms of overtraining syndrome, which appear in such a variety of athletes, can be explained by a single mechanism. As mentioned earlier, neuroendocrine changes may underlie many of the effects and symptoms of overtraining, such as poor performance, lowering of maximal heart rate and blood lactate levels, mood state changes and decrements in muscular strength.24, 25, 26 It has been proposed that the physical stress of intense exercise training initially causes elevation of stress hormone levels, such as catecholamines and glucocorticoids.24, 26 Persistently elevated stress hormone levels may then lead to disturbed sensitivity and/or number of adrenergic receptors, alterations in other hormones, such as insulin and pituitary hormones, and changes in muscle metabolism, which may ultimately lead to autonomic dysfunction. Several studies have provided evidence that alterations in sympathoadrenal activity occur during overtraining, such as reduced urinary output and increased or decreased plasma concentration of catecholamines,5, 6, 8, 9, 56 altered baroreflex-mediated responses to changes of body position57 and changes in adrenergic receptor sensitivity58
A hypothesis has recently been proposed implicating cytokines as mediators of overtraining syndrome.4 It has been suggested that repetitive, high volume exercise with inadequate rest causes injury (microtrauma) to joints, muscles and connective tissue. This injury in turn activates monocytes to produce and release inflammatory cytokines such as IL-1β, IL-6 and TNF-α. These cytokines would then initiate a ‘whole-body’ response, involving chronic systemic inflammation, ‘sickness behaviour’, suppressed immune function and mood state changes. It has also been suggested that these responses fit the third stage of Seyle’s general adaptation syndrome, that is, related more to recovery and survival from, rather than adaptation to, stress. Because inflammatory cytokines may also activate the hypothalamic-pituitary-adrenal axis, it has been further suggested that cytokine release may underlie neuroendocrine changes observed in overtraining syndrome. Inflammatory cytokines such as IL-1β and IL-6 are released after prolonged exercise, such as running or cycling,4 but there are, at present, no studies measuring cytokine levels in overtrained athletes. Obviously, further experimental work is needed to provide more evidence supporting or refuting these hypotheses.
Preventing overtraining syndrome
Overtraining syndrome may have potentially devastating effects on an athlete’s career and prevention is of utmost importance. Because the best indicators of overtraining syndrome, poor performance and persistent fatigue, occur too late to be of benefit to the athlete, coaches and athletes are interested in early indicators or predictors that may appear before the onset of serious symptoms. Prevention requires a carefully planned training program that includes regular monitoring by coaches and the athletes themselves to assess adaptation to training over both the short and long term.
Measures suggested to prevent overtraining include:22
Early identification and monitoring of susceptible athletes.
Minimizing known effects, such as sudden increases in training loads, inadequate dietary intake and too frequent competition.
Programming recovery training and rest days into the training cycle.
Tools for monitoring the athlete’s response to training must be both valid and convenient to use on a daily basis. As discussed earlier, there are few reliable and valid objective physiological and psychological indicators of the syndrome and certainly none that stand alone to clearly identify the overtrained athlete. For routine monitoring, the best and most cost-effective variables include a combination of measures, such as performance, heart rate after a standardized maximal effort, work accomplished at 110% IAT and some form of self-analysis by the athlete of his/her adaptation to training (e.g. POMS, daily measures of well-being). Although urinary catecholamine output seems to be a valid indicator, it is neither cost-effective nor convenient for routine monitoring. There appears to be individual variability in the threshold of training leading to overtraining syndrome,8, 16, 29 a factor often considered in developing a long-term training program for individual athletes. Daily monitoring of self-analysis measures, such as the athlete’s perception of training adaptation, stress levels, fatigue, quality of sleep and muscle soreness, may be effective in identifying susceptible athletes before the appearance of other symptoms.9, 16 Moreover, self-analysis measures also correlate with urinary catecholamine excretion,5, 6 providing an inexpensive and non-invasive method of estimating physiological responses. Immunological parameters do not, at present, appear to be useful in monitoring overtraining, although salivary IgA concentration may be of value in predicting susceptibility to URTI among high-performance athletes.46, 47, 49