Overtraining & Overreaching Among Elite Athletes : Physiological Consequences & Implications for Training Design
by Matt Cole (1999)
Introduction
Overtraining manifests as a result of an imbalance between training and recovery e.g. chronic overwork or increased training loads and possibly reduced recovery associated with increased training frequency (Fry, Morton, & Keast, 1991; Kuipers, 1997; O'Toole, 1998). The syndrome appears to originate at the hypothalamus (Kuipers & Keizer, 1988; Keizer, 1998). The resulting neuroendocrine dysfunction in turn can compromise the immune system, cardiovascular system, nervous system, the balance between anabolic and catabolic function, carbohydrate and lipid metabolism, as well as induce chronic fatigue (Budgett, 1998; Kreider, Fry, & O'Toole, 1998; Kuipers & Keizer, 1988; Stone et al., 1991).
These physiological consequences coupled with prolonged deterioration of performance may interrupt a competitive season, sacrifice an upcoming season, or worse, cause the premature termination of the athlete's career (Fry, Morton, & Keast, 1992; Kreider et al., 1998). Hence, various periodization schemes have been developed in accordance with Selye's general adaptation syndrome (GAS) in an attempt to curve the onset of overtraining, while still optimizing performance gains (Bompa, 1994; Fry et al., 1992; Matveyev & Giljatsova, 1991; Matveyev, 1992; Morton, 1991, 1997; Wathen, 1994).
Nonetheless, overtraining is still a phenomenon not entirely understood and difficult to diagnose early on. That is while a host of symptoms and markers have been observed no signal diagnostic test is available to detect the onset of overtraining (Budgett, 1998; Fry et al., 1991). This is in part due to the fact that not all symptoms/markers are always present and at times have been contradictory (O'Toole, 1998). Furthermore, there is some indication that symptoms of overtraining may manifest differently in endurance athletes compared to those athletes competing in highly anaerobic events (Kreider et al., 1998). Moreover, among anaerobic, or rather strength and power athletes, symptoms appear to vary between high volume overtraining and high intensity overtraining (Fry & Kraemer, 1998)
It is intention of this paper to review the current literature on overtraining and overreaching pertaining to both the endurance athlete and strength and power athlete. Physiological consequences and training implications will be examined.
Different terminology and definitions have been noted in the literature e.g. chronic fatigue syndrome, overtraining syndrome, overtraining, burn out, and staleness (Budgett, 1991; Kreider et al., 1998; Kuipers & Keizer, 1988; Stone et al., 1991). Therefore, for the purposes of this paper the following definitions will be used. The definitions of overtraining and overeaching are those adopted by Kreider et al. (1998) and similar to those of Kuipers and Keizer (1988).
Overtraining: The accumulation of training and nontraining stress resulting in a long-term decrement in performance capacity with or without related physiological and pyschological signs and symptoms of overtraining in which recovery may take from several weeks to a number of months.
Overreaching: The accumulation of training and nontraining stress resulting in a short-term decrement in performance capacity with or without related physiological and pyschological signs and symptoms of overtraining in which recovery may from several days to a several weeks.
Stress: A host of non-specific physiological responses of an organism induced by exposure to one or more diverse stressors.
Stressor: One of many distinct agents that will elicit stress when exposed to an organism.
Cumulative fatigue: A progressive build up of fatigue when training sessions are intersped with intervals that do not allow full neuromuscular recovery.
The General Adaptation Syndrome
Selye (1976) demonstrated that an organism would react to a variety of diverse stressors, including muscular work, with a number of non-specific responses (stress). However, that is not to say that the stressors themselves would not induce specific responses as well. In fact, Selye states that these specific responses invariably modify the stress response, as do endogenous (i.e. athlete's genetics) and exogenous (i.e. hormone treatment) conditioning factors.
The general adaptation syndrome (GAS) may manifest in three stages (Selye, 1976). The first stage, referred to as the alarm reaction, is characterized by the discharge of catecholamines from the adrenal cortex, depleting its storage of secretory granules. Moreover, at the hypothalamus nervous stimuli induce the emission of corticotropic hormone releasing factor (CRF). CRF then elicits the release of adrenocorticotropic hormone (ACTH) at the anterior pituitary, which in turn induces the secretion of glucocorticoids, including cortisol, at the adrenal cortex (Selye). The discharge of sympathetic neurons and secretion of catecholamines is the more immediate response; the release of cortisol follows in later part of the alarm stage and may act to dampen the acute response (Standford & Salmon, 1993).
However, because the alarm state cannot be maintained indefinitely, a stage of resistance follows in which adaptation occurs and the organism re-establishes physiological homeostasis (Selye, 1976). Anabolism and an enlarged adrenal cortex rich in secretory granules characterize this stage. If continued exposure to the stressor is of relatively smaller amounts, resistance/adaptation will continue and the organs will return to normal (Selye). Yet, if the exposure to the stressor continues at the same high level over a prolonged period, the adaptation incurred will deteriorate after several months and symptoms of the alarm reaction stage will reappear (Standford & Salmon, 1993). This is the stage of exhaustion in which symptoms may become irreversible leading to pathology and even death of the organism (Selye).
Overtraining
While the overtraining syndrome is generally not considered fatal or its symptoms irreversible, it has been described as a stress response consistent to Selye's general adaptation syndrome (Kraemer, Bradley, & Nindl, 1998; Kuipers & Keizer, 1988; Stone et al., 1991).
Within the sport science literature two general types of overtraining have been differentiated based upon impaired autonomic function: the sympathetic and parasympathetic syndrome (Fry, Morton, & Keast, 1991; Kuipers & Keizer, 1988; Lehmann et al., 1998; Stone et al., 1991). The sympathetic syndrome (table 1) is characterized by increased sympatheic tone at rest (Kuipers, 1997). Resting heart rate, recovery heart rate, resting blood pressure, recovery blood pressure, basal metabolic rate may all be elevated (Kuipers & Keizer, 1988). During exercise heart rate and oxygen uptake may be greater at a given workload (Kuipers & Keizer). A decreased free testosterone: cortisol ratio may be present via an increase in restinig cortisol and/or a decrease in resting testosterone yielding a catabolic state (Kuipers & Keizer, 1988; Stone et al., 1991).
Down regulation of circulating cortisol and elevation of serum testosterone is of prime importance for the effective anabolic/adaptive processes to occur during recovery following progressive overload type training sessions (Fry et al., 1991). Prolonged elevated resting cortisol levels and depressed testosterone may delay and hamper the efficiency of these processes during recovery. Moreover, continued training in the presence of incomplete recovery of the balance between anabolic and catabolic hormones may compound impaired recovery and further deterioration (Kuipers & Keizer, 1988).
Additional traits of the sympathetic syndrome (table D1) include decreased appetite, decreased body mass, a negative nitrogen balance, decreased maximal plasma lactate, disturbed sleeping patterns, increased irritability, and increased incidence of infection or illness.
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Table D1. Characteristics of Sympathetic and Parasympathetic Overtraining Syndromes (presented characteristics from Kuipers & Keizer, 1988; Lehmann et al., 1998; Stone et al., 1991).
|
The Sympathetic Type: Associated Characteristics |
The Parasympathetic Type: Associated Characteristics |
|
-Decreased Performance -Elevated resting heart rate -Increased heart rate at given work load -Retarded recovery heart rate -Increased resting blood pressure -Retarded recovery blood pressure -Increased basal metabolic rate -Weight loss -Negative nitrogen balance -Elevated serum cortisol -Decreased serum testosterone -Decreased free testosterone: cortisol ratio -Sense of fatigue at rest -Disturbed sleep patterns -Decreased appetite -Decreased maximal plasma lactate -Increased irritability -Increased incidence of infections |
-Decreased Performance -Decreased resting heart rate -Normal or decreased exercise heart rate -Normal or quicker recovery heart rate -Decreased resting blood pressure -Increased time spent in sleep -Hypoglycemia -Decreased maximal plasma lactate during exercise -Decreased plasma lactate during exercise -Apathetic behavior -Fatigue manifests early on during exercise -Depressed endrocrine response to stressors -Suppressed neuromuscular excitability -Suppressed catecholamine sensitivity -Suppressed sympathetic intrinsic activity
|
The parasympathetic syndrome (table D1) is characterized by suppressed sympathetic activity and parasympathetic activity dominant both at rest and during exercise. Resting heart rate and blood pressure are decreased, while recovery heart rate may be normal or quicker (Kuipers & Keizer, 1988). Plasma lactate levels can be decreased at all levels of exercise and accompanied by hypoglycemia (Fry et al., 1991). Apathy and increased time spent sleeping are common (Stone et al., 1991). Moreover, there appears to be an overall depressed neuroendrocine response to all types of stressors as well as suppressed neuromuscular excitability and catecholamine sensitivity (Lehmann et al., 1998).
The suppressed neuroendocrine activity, for example, has been characterized by a depressed response of ACTH, cortisol, growth hormpne (GH), and prolactin to insulin induced hypoglycemia (Barron, Noakes, Levy, Smith, & Millar, 1985) and dampened response/sensitivty of the adrenals to ACTH (Lehmann, Foster, Dickhuth, & Gastmann, 1997; Kuipers & Keizer, 1988). In addition, exercised induced amenorrhea in female athletes is thought to result from diminished pituitary secretion via altered hypothalamic regulation of gonadtrophin (Fry et al., 1991).
Occurance of the parasympathetic syndrome appears to predominate among endurance athletes, while the sympathetic syndrome is more common among strength and power athletes (Kuipers, 1997; Lehmann, 1997). Alternatively, it has also been postulated that the parasympathetic syndrome may represent an advanced state of overtraining and may be preceded by the sympathetic form (Kuipers & Keizer, 1988). This hypothesis has yet to be validated, however. Nonetheless, it is not uncommon for sympathetic type symptoms to be reported among endurance athletes (Fry et al., 1991). And such a progressive sequence of overtraining symptoms would correspond to the general adaptation syndrome with the sympathetic syndrome representing a prolonged systemic stress response and the parasympathetic syndrome evident of exhaustion of the neuroendocrine system (Fry et al., 1991; Stone et al., 1991).
The Immune Response
Empirical observation has associated overtraining with increased incidence of infection, suggesting a training induced suppression of the immune system (Kuipers & Keizer, 1998). Diminished immunoglobulin (Ig) and glutamine levels have both been suspected of contributing to a compromised immune system (Budgett, 1998).
In an extensive review by Mackinnon (1998) of immune responses of overtrained and well-trained athletes exposed to high volume training, it was indicated that a suppressed immune system might manifest in the absence of overeaching/overtraining. That is a decreased Ig, which has been associated with increased incidence of upper respiratory tract infection, has been noted in diverse groups of well-trained athletes. This hypothesis is supported by Mackinnon and Hopper (1995) who found 9 out of 10 cases of upper respiratory tract infection were among the well trained swimmers, while seven of the eight overtrained swimmers did not exhibit infection.
Chronically depressed serum glutamine levels have been observed in overtrained athletes (Parry-Billings, Budgett, Koutedakis, & Blomstrand, 1992; Rowbottom, Keast, & Morton, 1996). This, combined with the fact that glutamine is required for synthesis of immune cells (lymphocytes and macrophages), has yielded the hypothesis that suppressed glutamine release may compromise the immune system, specifically impaired lymphocyte activity (Rowbottom et al.). However, the literature has not supported this thus far (Mackinnon, 1998).
In contrast to overtrained athletes, plasma glutamine has been shown to progressively increase over 9 months in well-trained triathletes (Rowbottom, Keast, Garcia-Webb, & Morton, 1997). This study also showed that plasma glutamine was moderately correlated with performance (r = .365).
Still, glutamine's possible relationship to immunosuppression and performance remains unclear[1] and further investigation is required.
In addition, the regulation of the immune system is extremely complex and subject to influence of the neuroendorcine system (Fry et al., 1991). Therefore, altered hormonal output likely plays a major role in immunosuppression associated with overreaching and overtraining (Mackinnon, 1998). Cortisol and catecholamines are in particular, suspect (Fry et al., 1991; Kuipers & Keizer, 1998), yet this area is largely unexplored (Fry et al., 1991).
Overtraining & the Endurance Athlete
Regarding the endurance athlete, it has been suggested that training volume, rather than intensity, is the primary training factor involved in the development of overtraining with these athletes (Hopper, Mackinnon, Gordon, & Bachmann, 1993; Hopper, Mackinnon, Howard, Gordon, & Bachmann, 1995; Lehmann, 1998). However, published case studies of chronically overtrained athletes are rare and for ethical reasons investigation into this area has been over relatively short periods (1-6 weeks). What follows is a review of some of the more recent literature in which training volume was increased with endurance athletes.
Increased Volume
Lehmann et al. (1991a, 1991b) investigated increased volume in two studies utilizing middle and distance runners. In the first study the training volume of eight distance runners was increased progressively over a 4-week training regimen. Total increment in training volume amounted to approximately 100% (85.9 Km/wk - 174.6 Km/wk). Training consisted of long duration monotonous runs 7d/wk.
Results showed a depressed heart rate prior to exercise at submaximal and maximal workloads. Total running distance on the treadmill increment test was reduced. Running velocity at 4 mmol lactate concentration threshold plateaued. Nocturnal urinary norepinephrine decreased, however exercise induced norepinephrine and epinephrine response increased at the same workload. Furthermore, as figure 1 shows, there was a continuous increase on the complaint index (training log indicators of fatigue), which correlated with the decrease in norepinephrine (r = -.52)
Figure D1. Relationship between complaint index (4 point scale) and basal nocturnal urinary norepinephrine (r = -.52) in response to progressive increase in training volume (Lehmann et al., 1997).
The authors suggested that parasympathetic type of overtraining developed in most of the athletes taking part in the study. Yet, the increased catecholamine response to exercise appeared contradictory[2] to the rest of the observed symptoms (Lehmann, 1991a). However, an increase the norepinephrine response to exercise - in the presence of a depressed heart rate - is strongly suggestive of a reduced sensitivity of ß2 adrenoreceptors to catecholamines (Lehmann, 1998).
Body mass, blood pressure, and resting heart rate were not good indicators of overtaining and their decreases have been absent among other overtained endurance athletes (Fry, Morton, Garcia-Webb, Crawford, & Keast, 1992; Hopper et al, 1993, 1995; Synder, Kuipers, Cheng, Servais, & Fransen, 1995). Fry et al. (1991) suggested that the time course of symptoms is variable and that some symptoms may disappear while others emerge. Considering the length of the study (4-weeks), it is possible that some symptoms had yet to develop.
The follow up study conducted one year later failed to induce overtraining (Lehmann et al., 1992a, 1992b). Lehmann and colleagues again progressively increased volume over a 4-week training regimen. Training consisted of high intensity type training and long runs. Mondays 6-10 400 meter intervals were performed with a 3-minute active rest interval. Wednesday 6-10 high speed 1000 meter intervals were performed with the same 3-minute rest interval. Friday one 8000-10000 meter speed endurance run was performed. Tuesday and Thursday training was composed of long duration runs which were only modestly increased over the study (52.5km/wk - 62Km/wk). Sunday served as an "off" day. Seven of the eight distance runners from the previous study and two middle distance runners served as the subjects.
The subjects increased their running velocity at 4 mmol lactate concentration threshold and total distance on the increment test. Tolerance of the training program and the observed performance gains were contributed to the prescribed "off" day, a non-monotonous training protocol, and a lower overall training volume compared to the first study (Lehmann et al., 1992a, 1992b).
In a longitudinal study conducted by Urhausen, Holger, Gabriel, and Kindermann (1997), 17 endurance athletes (cyclists and triathletes) were monitored over 19 months during periods of normal and overtraining. Each athlete was assessed five times over the course of the study (every 3-5 months). Subjects trained according to their individual programs, however they increased their training at the appropriate times.[3]
Results showed that time to exhaustion on an incremental cycle ergometer test was depressed by 27% when they were overtrained compared to when they were well trained. Maximal power on a 30s Windgate test plateaued. Maximal heart rate and plasma lactate was decreased during exercise. Moreover, there was a marked blunted response in maximal ATCH, GH, and insulin following exhaustive exercise with a tendency for the same in cortisol. However, there was no difference between overtrained and well-trained states on free catecholamines, nocturnal urinary norepinephrine[4], blood glucose, resting heart rate, resting serum growth hormone, sex hormone binding globulin, testosterone, cortisol, and luteinizing hormone (Urhausen et al., 1997).
The authors concluded that parasympatheic overtraining did not fully manifest, but rather the observed symptoms were indicative of overreaching. This is likely since the subjects were asked only to increase their training protocols for 2-3 weeks prior to the assigned overtraining test periods. Furthermore, the athletes were able to continue to train and recover before the normal state testing periods.[5]
In comparison Kuipers and Keizer (1988) reported a case of a chronically overtrained cyclist who had developed the parasympathetic syndrome. The subject suffered from prolonged under performance, had a resting heart rate of 38bpm, and recovery required six months.
Considering the presented data it appears that 2-4 weeks of unaccustomed training volume is sufficient to induce overreaching in endurance athletes. Yet, the degenerative process appears to be accelerated to overtraining via prolonged training on consecutative days and/or a more dramatic increase in volume.[6] Furthermore, increases in training volume may be better tolerated with a variation of the training stimulus and prescribed "off" days dispersed across the microcycle (Lehmann et al, 1992a).
Overtraining & The Strength & Power Athlete
The majority of the published information regarding overtraining pertains to the endurance athlete, while little research is able on the strength and power athlete. This is especially true for athletic populations engaged in intensive resistance training programs. Still, from the available literature it appears that both increased volume and prolonged high intensity training can contribute to overreaching and overtraining among these athletes.
Increased Volume
Mackinnon and colleagues (Mackinnon, Hooper, Jones, Gordon, & Bachman, 1997) measured 16 immunological, hematological, and hormonal variables in 24 elite swimmers (100 m & 200 m specialists) before, during and at the conclusion of 4 weeks increased training volume. Training was composed of both sport specific training and dry land resistance training of which the total volume was increased approximately 10% per week over the 4 weeks. Training intensity and frequency (6d/wk) were held constant.
The authors diagnosed 8 of the 24 swimmers as overreached. However, of the 16 variables[7] measured, only nocturnal urinary norepinephrine differed significantly between the overreached and the well-trained swimmers. Furthermore, the decreased nocturnal urinary norepinephrine was observed to be present 2-4 weeks prior to the appearance of overreaching symptoms, further suggesting impaired neuroendocrine function may precede and contribute to overreaching and overtraining (Table D2).
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Table D2. Nocturnal Urinary Norepinephrine of well Trained and Overeached Elite Swimmers (modified from Mackinnon et al., 1997)
|
Noc. Urinary NEPI (nmol/mmol creatinine) |
T1 (Wk 0) |
T2 (Wk 2) |
T3 (wk 4) |
|
Well Trained (n=16)
|
14.7 Mean 1.8 SD |
12.3 Mean 0.7 SD |
12.7 Mean 1.1 SD |
|
Overreached (n=8) |
8.2 Mean 0.8 SD |
10.0 Mean 1.2 SD |
7.0 Mean 0.6 SD |
Note. Overreached swimmers had a lower urinary norepinephrine excretion than the well-trained swimmers from the onset. The possibility was suggested that the athletes which developed overreaching symptoms during the study may have been predisposed to overreaching via non-physical stressors and/or individual variation of work capacity/tolerance of the training protocol used prior to the study: 28.5 Km/wk (in pool) + 151.2 min/wk resistance training over 6d/wk. SD = standard deviation.
In an earlier study (Callister, Callister, Fleck, & Dudley, 1989) training volume was progressively increased over 10 weeks among elite judo athletes. Training consisted of judo specific training, interval training (track and cycle ergometer sprints), and resistance training. Phase one of the training (week 1-4) served as baseline period of initial training volume. In phase two (weeks 5-8) volume of both the interval and resistance training was increased by 50%. In phase three (weeks 9-10) interval and resistance training volume was reduced back to that of phase one, while judo specific training increase by 100% (figure D2).
Figure D2. Schematic representation of the manipulation of training volume of judo specific training, resistance training, and interval training over 10 weeks.
While performance decrements were observed, the authors concluded that the athletes did not develop overtraining, but rather were overreaching. That is, no changes were observed in resting heart rate, exercise heart rate (submaximal), maximal heart rate, post exercise blood lactate, resting blood pressure, aerobic capacity, and aerobic power.
Changes in the performance parameters, and their time course, were specific to the variable. Isokinetic (60, 90, 180, 240, & 300 d/s) strength for both the forearm and knee flexors and extensors increased in phase one, plateaued in phase two, and decreased in phase three. However, total 300 m interval time (3 x 300 m) declined across both phase one and two and plateaued in phase three. Vertical jump was unchanged while total 50 m interval time (5 x 50 m) actually increased in phase three. Hence, the study indicated that different performance parameters will respond to 6 weeks of increased volume of training in a variable way depending upon the nature of the training increased and the nature of the performance parameter.
Increased Intensity
Several attempts to induce overreaching through persistent low volume high intensity resistance training had been attempted (Fry, Kraemer, Lynch, Triplett, & Kozeriris, 1994a; Fry et al., 1994b; Webber et al., 1996). Of these, only one study (Fry et al., 1994b) elicited a significant decrease in a training mode specific 1RM measure. However, the others studies have important implications because they did elicit decrements in other performance parameters.
Fry et al. (1994a) used a 8 x 1 @ 95% 1RM 5d/wk protocol for 3 weeks, utilizing a machine exercise that mimicked the parallel squat. Results showed that while 1RM gains were observed on the training exercise, significant decreases were observed on the 9.1 m and 36 m sprints, as well as isokinetic knee extensions (1.05 rad/s).
Similar findings were reported by Webber et al (1996) who used a 2 x 1 @ 95% 1RM + 3 x 90% 1RM 3d/wk protocol for 3 weeks. Both 9.1 m sprint and peak isokinetic squat (.20 m/s) declined, while 1RM back squat and 36.5 m sprint showed a marked plateau.
Taken together these studies indicate that prolonged high intensity training can adversely effect performance parameters, while specific training module 1RM is maintained.
Fry et al. (1994b) established a model for high relative intensity overreaching with the 10 x 1 @ 100% 1RM 6d/wk protocol. That is, this protocol induced a significant decrease in 1RM strength on the training module (squat machine). Moreover, decrements were also observed on isokinetic knee extensions at .53 & 5.24 rad/s.
Comparison of maximal voluntary and maximal stimulated isometric force indicated that the primary site of maladaptation was in the periphery, rather than central (Fry et al., 1994b). However, muscle damage was not indicated by excessive circulating creatine kinase (CK) levels.
This is contrary to Koutedakis et al. (1995) who examined 10 overtrained Olympic athletes (predominately endurance athletes) in a similar fashion and discounted the peripheral component and contributed strength decrements to impaired neural drive.
While these low volume high intensity protocols may not reflect typical training regimens, they have effectively demonstrated that prolonged high intensity resistance training can adversely effect a number of performance parameters. And while low volume high intensity training is not usually performed in isolation, it is often included along with a higher volume of more moderate intensity training. Hence, high volume training and high intensity training can be expected to interact as separate stressors (Fry, 1998). Mistakes in the prescription of either volume and/or intensity can result in performance decrements.
Neuroendocrine Response.
In a thorough review by Fry and Kraemer (1997), the authors noted that the neuroendocrine profile of high intensity resistance overtrained athletes is unlike that of high volume resistance overtraining.[8] That is, there is no evidence that pituitary regulation of testosterone, cortisol, and growth hormone are altered. Resting catecholamines also appear to be unaltered. However, there is a dramatic increase in catecholamine response to exercise (Fry, 1998), characteristic of the sympathetic syndrome. Although, others symptoms associated with the sympathetic syndrome e.g. increased resting heart rate and isomonia have been absent (Fry & Kraemer). Therefore, the increase in the acute catecholamine response may represent the first in a theoretical continuum of symptoms of this form of overtraining (Fry & Kraemer).
The Intentional Use of Overreaching
Overreaching is occasionally intentionally prescribed to induce a delayed, yet superior, performance gain (Fry & Stone, 1998; Kraemer, Bradley, & Nindl, 1998; Kuipers & Keizer, 1988). These designs, referred to as shock or crash microcycles in the literature (Fry, Morton, & Keast, 1992; Kukushkin, 1983), involve sharp increases in both volume and intensity, accompanied by an increase in frequency, over a period of 1-3 weeks (Fry & Stone, 1998). Initially, however, performance is decreased and the performance gains are only realized after an unloading microcycle or several weeks later upon returning to normal training loads (Fry & Stone, 1998). However, the effectiveness of these designs are purely empirical and have yet to be validated in well controlled studies.
Prevention & Intervention
Monotony of training has been associated with a plateaus in performance, and for some, is accepted as an additional contributor to overtraining in addition to chronic overwork, excessive increases in training loads, and reduced recovery (Kuipers & Keizer, 1998; Lehmann et al., 1998; Stone et al., 1991). The use of periodization methodology in the design of training regimens attempts to counter these factors, while still ensuring optimal performance gains.
Training Design
Variation of the training stimulus via varying the type of training and/or the loadings across the microcycle eliminates monotony of training. The use of prescribed "off" days within the microcyle is thought to enhance recovery and tolerance to demanding training regimens from week to week. This is complemented with the use of an unloading or regeneration microcycle at the conclusion of a mesocycle, which theoretically allows any cumulative fatigue to dissipate before the commencement of the next mesocycle (Bompa, 1994). Thus, the unloading microcycle also is an opportunity test athletes in such a way that a normal acute/or cumulative training fatigue and be distinguished from more chronic fatigue or decrement in performance (Fry et al., 1991, 1992). Moreover, unloading microcycles provide regular short intervals in which the athlete is not under a constant demand to adapt. Recall that even though an organism has demonstrated adaptation to a stressor, if exposure to that stressor is continued to the same degree over a prolonged period, the acquired adaptation will begin to deteriorate after several months (Selye, 1976).
While periodization methodology is theoretically sound and its effectiveness accepted by many, periodization is still as much an art as it is a science. Future investigations may help to uncover the optimal frequency of unloading for a number of types of training and loading scenarios within the confines of individual variation in work capacity.
An additional concern in training design is the influence of external non-physical stressors on the athlete. It is widely accepted that these external stressors compound the problem of overtraining by interacting with the imposed training stressors to effectively reduce the training threshold at which overreaching/overtraining manifests (Budgett, 1998; Kreider et al., 1998; Lehmann et al., 1997). Therefore a reduction in training volume may be warranted when an athlete's exposure to these external stresssors is particularly intense.
Monitoring
With no one diagnostic test available to detect overreaching and/or overtraining, regular monitoring of a set of variables is recommended (Fry et al., 1991). Performance parameters, sense of fatigue, and mood state profiling are ideal, however recording changes in body mass, heart rate and sleep patterns may be useful as well.
Depressed nocturnal urinary norepinephrine has been observed in a diverse group of overeached/overtrained athletes (Lehmann, Schnee, Scheu, Stockhausen, & Bachl, 1992; Mackinnon et al., 1997; Naessens, Chandler, Kibler, & Driessens, 1996) and may develop early on before the onset of overreaching symptoms (Mackinnon et al.). Therefore, it appears to be a promising marker.
It has been suggested that a drop in nocturnal catecholamine excretion of 50% or more may constitute overtraining (Lehman, Schee et al., 1992), while a decrease in norepinephrine of 40% or has been suggested to be indicative of overreaching and a 60% decrease characteristic of overtraining (Naessens et al.). Nonetheless, further validation is warranted.
Conclusions
In conclusion, overtraining appears to originate at the hypothalamus (Keizer, 1998). While the sympathetic syndrome is believed to predominate among strength and power athletes and the parasympathetic syndrome dominant among endurance athletes (Kuipers, 1997, Lehmann et al., 1997), this appears to be a simplistic view of a complex phenomenon. In fact the resulting form of the neuroendocrine dysfunction and its consequences, have yet to be determined to be an effect of the type of training, the age of the athlete, an interaction with non-physical external stressors, or the stage of overtraining.
Immune suppression, which has been associated with overtraining, appears to occur among well-trained endurance athletes complying with demanding training programs (Mackinnon, 1998). The severity of immune suppression among these two populations requires further investigation.
Incorporating periodization methodology into the design of training regimens is believed effective (Bompa, 1994, Kuipers & Keizer, Fry et al., 1991, 1992) and is in line with Selye's GAS. However, the optimal loadings and optimal frequency of regeneration or unloading microcycles have yet to be elucidated.
A marked declined in nocurtanal urinary norepinephrine is a potential marker of overreaching and overtraining, which may manifest early on before the onset of overeaching symptoms (Mackinnon et al., 1997). Additional studies might attempt to further validate this measure with an even more diverse athletic population.
Serum catecholamine response to exercise can show a marked rise in some forms or phases of overtraining (Lehman et al., 1992a; 1992b; Fry & Kraemer, 1997), while chronically overtrained athletes with the parasympathetic syndrome can show symptoms characteristic of adrenal exhaustion.
Plasma glutamine has been suggested as a marker for overtraining because depressed levels have been observed in overtrained athletes (Parry-Billings et al., 1992; Rowbottom et al., 1996). However, depressed levels were not evident in overreached swimmers (Mackinnon et al., 1996). Moreover, glutamine's relationship to immnuosuppression and/or performance is not yet understood.
Finally, increased volume[9] appears to be the primary training factor contributing to overtraining in endurance athletes (Hooper et al., 1993, 1995; Lehmann et al., 1998). Yet, prolonged high intensity training may also contribute to decrements in performance with strength and power athletes (Callister et al., 1989; Fry et al., 1994a; Webber at al., 1996).
In the case of resistance training, high relative intensity overtraining may induce declined in performance measures e.g. sprint acceleration and/or speed, while 1RM strength is maintained (Fry et al., 1994a; Webber at al., 1996). Hence, 1RM testing may fail to detect a compromised performance parameter.
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[1] Depressed serum glutamine has been hypothesized to play a role in the development of central fatigue (Guezennec, 1996).
[2] Increased norepinephrine response was later reproduced (Hopper et al., 1993; 1995).
[3] Training stressors were increased via increased training loads and increased training frequency or number of competitions.
[4] There was a noted difference in the urine sampling method compared to the Lehmann et al. (1991a, 1991b) study.
[5] Two athletes spontaneously developed overtraining during this period, which was contributed non-training stressors.
[6] Due to the individualization of the programs in the Urhasen et al. (1997) study and lack of reported absolute training volumes, direct comparisons to Lehmann et al (1992a,1992b) are difficult.
[7] These included resting plasma cortisol, testosterone, T/C ratio, norepinephrine, hematocrit, hemoglobin, mean red cell volume (MCV), and various immune cell counts.
[8] The neuroendocrine profile of high volume resistance overtrained athletes is purportedly similar to that of high volume endurance overtrained athletes (Fry & Kraemer, 1997).
[9] Accompanied with increased volume via increased frequency is reduced recovery.
