1 Word count:5783 Distance Runners: Overtraining Manfred Lehmann1, Carl Foster2, Norbert Heinz1 and Joseph Keul1 1 University Medical Hospital, Department of Sports and Performance Medicine, Freiburg, Germany 2 Human Performance Laboratory, Milwaukee Heart Institute, Milwaukee, Wisconsin, USA Overtraining is ineffective training with too frequent, too prolonged, or too intense training sessions, with too little rest and regeneration. The training - recovery imbalance is the dominant factor; but additional stressors on the athlete, occupational, educational, social, nutritional, or endogenous cannot be discounted. Short-term overtraining (overreaching) lasting up to two weeks, has to be differentiated from long-term overtraining, since recovery is in direct temporal relationship to overtraining duration, and since supercompensation may be expected only subsequent to short- term and in no case after long-term overtraining. Long-term overtraining is characterized among others things by performance and competitive incompetence, persistent high fatigue ratings, lack of supercompensation, suppressed mood state, muscle soreness/stiffness, suppressed neuromuscular function, and different blood-chemical findings. The stale athlete is suffering from the overtraining syndrome (staleness). The "catabolic-anabolic dysbalance hypothesis", the "carbohydrate hypothesis", the "imbalanced 2 amino acid hypothesis", and the "sympathetic- parasympathetic dysbalance hypothesis" have been established to explain some of the underlying mechanisms. Etiological Aspects And Definition Of Overtraining The aim of an effective athletic training program in middle- and long-distance running is, as in all other sports, the adaptation to progressively increasing training loads in order to improve performance. Training methods during the last 50 years to cause this adaptation include: fartlek training, long slow distance (high mileage) training, interval training, lactate threshold training, periodization of training (cyclic training), with rest days and regeneration periods as essential components of the training programs (6,10). Overtraining represents an ineffective training program with too frequent, too prolonged, or too intensive training sessions, with too little rest and regeneration. That is, overtraining represents an imbalance between stress (training, competition, etc.) and recovery. Stress in this connection represents the sum of all training and non-training stress factors, such as social, educational, or occupational factors, particularly international travel, possibly combined with inadequate nutrition. This stress > recovery imbalance causes the so-called overtraining syndrome in affected athletes which is characterized by poor performance, mood state alterations and different physical findings (3,4,8,11,13,15,16,21,22,25) (Tab. 1). 3 Our knowledge of the etiology of the overtraining syndrome is based primarily on experience, single case observations, cross-sectional and longitudinal studies during regular training periods. There are few data from controlled overtraining studies, since training aimed at impairing function and reducing performance is self- contradictory. The motivation to train at a level capable of producing overtraining syndrome usually depends upon foreseeable competitive goals. Since the athlete can lose an entire competitive season to overtraining syndrome, willingness and motivation to produce overtraining syndrome for experimental purposes is unlikely. The border between adaptation as a result of training and a functional impairment with a loss of adaptation as a result of overtraining is fluid. This applies both to physiological and biochemical parameters, which explains the difficulty in recognizing overtraining on the basis of such parameters. A low iron or testosterone level can, for example, be present in both training-related improvement in performance and in a loss of adaptation due to overtraining. Interindividual variability in recovery potential, exercise capacity, stress tolerance and individually different non-training stress factors may explain the different vulnerability of athletes during identical training periods even with the same coach (21). Short-Term vs. Long-Term Overtraining Short-term overtraining lasting a few days up to two 4 weeks has to be differentiated from long-term overtraining over a period of weeks and months, since recovery is in direct relationship to the period of overtraining and since supercompensation appears to be possible only after short- term overtraining. Supercompensation in distance runners means the athlete can run faster for the same distance for an equivalent homeostatic disturbance following adaptation. Short-term overtraining up to a critical time period of approximately two weeks is characterized by training fatigue, by reduction or stagnation of the submaximum running performance (for example the running speed at a lactate concentration of 3 or 4 mmol.L-1), reduction of peak performance and transient competitive incompetence. The term OVERREACHING has been suggested as a useful alternative to using the term overtraining for two distinct meanings, that is for short- and long-term overtraining. Recovery from overreaching takes a matter of days up to two weeks. Overreaching is thus not usually a serious problem, unless the symptoms are not understood or recognized and the training load is increased in an attempt to overcome them. This may be fairly common, however, since the ordinary reaction of many athletes and coaches to a poor competition or training session is to increase the training load. Thus it may be hypothesized that many cases of overtraining syndrome are attributable to inappropriate responses to either accidental or deliberate overreaching. Figure 1 presents a generic model of the athlete's response to training, short-term overtraining (overreaching), long- term overtraining and tapering. Over-reaching must be 5 differentiated from the day-to-day fluctuation in performance and well-being, and also from overexertion complaints in individual muscle groups or so-called "local overtraining" (9,16,21,24). Overreaching can progress smoothly to long-term overtraining and the affected athlete suffers from the overtraining syndrome, also called STALENESS. Overtraining syndrome usually is observed when the training load is progressed too rapidly (Fig. 2). The prognosis with overtraining syndrome is not favorable, since complete recovery may take weeks or even months. The presence of a complete overtraining syndrome is, however, less common than the occurrence of more rudimentary forms (15,16,21). Overtraining syndrome is characterized by (a) a lack of supercompensation subsequent to tapering or a regeneration micro cycle, (b) the accumulation of training and non-training fatigue up to exhaustion, whereby a direct correlation has to be expected between a so-called symptom index (considering fatigue as the dominant symptom) and the weekly mileage (Fig. 3)., (c) by changes of the mood state to a more negative state, (d) by reduction or stagnation of the tempo-pace performance ability and (e) reduction of peak performance, (f) by accumulation of muscle soreness/stiffness and (g) competitive incompetence over weeks and months (Tab. 1). Fatigue in this context means that training load (mileage or intensity) which was previously tolerated must be reduced. Exhaustion or athlete's burn-out means that the training session must be terminated earlier than planned and previously tolerated or 6 has to be canceled (13,15,16,21). Disease must be ruled out in the evaluation of an apparent overtraining syndrome in the affected athlete. The question of parallels to the so-called Chronic Fatigue Syndrome, in which an Ebstein-Barr virus infection is assumed, may be an interesting speculation in this context, since "banal virus infections" are thought to promote an overtraining syndrome and since exercise of high intensity, frequency and long duration may be associated with adverse effects on immune function. This may in part be related to an impaired glutamine supply, a key fuel for cells of the immune system. Glutamine supply may be decreased by distance running, representing one aspect of the so-called "Imbalanced Amino Acid Hypothesis", suggested by Newsholme and coworkers (23). The finding of a decreased glutamine level could not, however, be confirmed in ten athletes performing the 1993 Colmar ultra triathlon (Table 2), as an example of extremely expanded endurance stress. Prevalence Of Overtraining Syndrome Recent research in elite distance runners has shown that 64% of the female and 66% of the male athletes had experienced overtraining syndrome at some point during their competitive careers (22), 21% of 14 elite swimmers were diagnosed as overtrained during a 6-month session (14), and 33% of the Indian national level basketball players were diagnosed as overtrained during a 6-week training camp (26). More than 50% of athletes of a soccer 7 team were diagnosed as suffering more or less from an overtraining syndrome subsequent to a 5-month competitive season (18). Overtraining cannot, therefore, be seen as a marginal problem in high-performance sports. Classical Vs. Modern Form Of Overtraining Syndrome Overtraining is not a by-product of modern endurance sports, but has been a well-known problem for years. The symptomatology, however, has gone from a pattern of excitation to one of depression or staleness with increasing training load. It has been suggested that the "classical" or so-called sympathetic form of the overtraining syndrome be differentiated from the "modern" or so-called parasympathetic form. These terms sympathetic or parasympathetic forms are descriptive; they are drawn from the clinical pattern, whereby pathophysiology and pathobiochemistry have not been sufficiently clarified. As synonyms, the likewise descriptive terms "basedowoid' and "addisonoid" forms are used. The former calls to mind a thyroid hyperfunction (Morbus Basedow), the latter an adrenal hypofunction (Morbus Addison). The main symptoms of the sympathetic form of overtraining syndrome are restlessness and excitation. Inhibition and depression are characteristic in the parasympathetic form, beside performance incompetence in both types. The sympathetic form is rare. When found, it is more present in so-called "anaerobic" types of sports of younger less, experienced athletes, whereas the parasympathetic form or staleness is 8 typically found in "aerobic" types of sports, such as distance running, swimming or cycling (15,16,21). Pathogenetic Aspects/Findings In Overtraining Syndrome (parasympathetic type of staleness) Overreaching is seen to be based only on so-called "peripheral fatigue". "Central fatigue" should be added in overtraining syndrome, that is, fatigue originating in the brain (central fatigue) or not (peripheral fatigue). The transition from peripheral to additional central fatigue is smooth and a clear delineation is only obvious retrospectively or for didactic reasons (15,12,21). Possible underlying mechanisms are summarized in Fig. 13. Mechanisms Underlying Peripheral Fatigue Metabolic Overload Incomplete recovery and premature fatigue of muscular motor units requiring an increase in nerve stimulation and recruiting of additional motor units is assumed in peripheral fatigue. This may be based partly on (a) the suppression of neuromuscular function, (b) on an afferent inhibitory proprio- and nociceptive influence on alpha- motoneuron activity, (c) on a decrease in beta- adrenoreceptor density (see below) and (d) on a reduction of muscular glycogen reserves and phosphocreatine caused by daily exhaustive training sessions and/or by additional nutritional carbohydrate deficit, underlying Costill's 9 carbohydrate hypothesis supposing a causative aspect of glycogen deficiency in the overtraining process (4,5,13). The muscular glycogen deficit is a cause of a suppressed lactate-exercise profile (Fig. 4) and in part of a decrease in the ratio of blood lactate concentration to ratings of perceived exertion (Fig. 5), whereas a hepatic glycogen deficit is seen to be the reason for a suppressed blood glucose-exercise-profile (Fig. 6) in overtrained athletes (9,24). The diagnostic relevance of blood-chemical parameters in overtraining syndrome, such as urea, electrolytes, muscle enzyme activity, hemoglobin, albumin, globulin, iron, ferritin levels, etc., is unclear. There is no single, simple blood-chemical parameter which can definitely prove the diagnosis of an overtraining syndrome, because similar changes in different blood-chemical parameters have been observed in overtrained as well as in non-overtrained athletes (15,16,17,19,21). Various systematic changes in blood-chemical parameters, as for example observed during a prospective and controlled 4-week high mileage overtraining study with already adapted middle- and long-distance runners, can however, be of significant adjuvant diagnostic relevance (Tab. 3). There is some evidence - with respect to distance running - that changes in blood-chemical parameters as indicators of metabolic overload have to be more expected during high mileage training than during threshold or interval training with a moderate total training volume (17). For further details concerning the mechanisms underlying changes in 10 different blood-chemical parameters see recently published review articles (3,5,11,13,15,16,21). Suppression Of Neuromuscular Function A suppression of neuromuscular function, that is, a loss in training-dependent neuromuscular adaptation (Fig. 7,8), may represent a further causative aspect of training fatigue. The suppressed neuromuscular function might be related to a "hyposensitization" of the neuromuscular synapses caused by chronic neuronal overstimulation with incomplete recovery (peripheral mechanism) and, for example, on inhibitory afferent proprio- and nociceptive signals from the overloaded tendon-muscle-joint system inhibiting the alpha-motoneuron activity (central mechanism). Such suppressed neuromuscular function as indicated by a hypoexcitability of affected muscles during the neuromuscular function test (Fig. 7,8) was, for example, observed subsequent to a 4-week high mileage overtraining session in distance runners (Fig. 7) as recently also confirmed during a 6-week threshold/interval overtraining period in moderately adapted athletes (Fig. 8). Decrease In ß-Adrenoreceptor Density A change in the hormone or neurotransmitter sensitivity of target organs, for example to catecholamines, must also be taken into consideration as an underlying factor in chronic peripheral fatigue in athletes with persistent high fatigue ratings. A decrease in ß- 11 adrenoreceptor density, isoproterenol stimulated cyclic-AMP activity, as well as in heart rate response can be demonstrated, (a) after incremental exhaustive ergometric cycling, (b) subsequent to a period of high mileage training in distance runners (approximately 1,450 ß- adrenoreceptors per cell), as compared to tapering (approximately 2,000 ß-adrenoreceptors per cell), or (c) during long-term IV-infusion of adrenergic agonists in a laboratory experiment (21). The possible effect of an overload-dependent decrease in ß-adrenoreceptor density in adapted athletes has to be understood as a loss in sympathetic adaptation, as if the subjects were taking beta-blocker drugs. Possible mechanisms underlying central fatigue The "imbalanced amino acid hypothesis" of Newsholme and coworkers (23) can explain some mechanisms which may underlie central fatigue in long-term overtraining. They found an altered balance of the plasma concentration of branched-chain amino acids (decreased) and free tryptophan (increased) - the precursor of 5-hydroxytryptamine - in distance running, that is also given for tyrosine and phenylalanine, the precursors of dopamine (Table 2), which can favor the entry of tryptophan and tyrosine into the brain, particularly in the hypothalamus. In addition, an increased concentration of 5-hydroxytryptamine and dopamine was detected in the brain of exhausted laboratory animals. An increased 5-hydroxytryptamine concentration may influence endocrine function with a suppression of endocrine axes. An increased dopamine concentration may 12 suppress the sympathetic neurotransmission via inhibitory dopaminergic D2-receptors and explain the more than 50% decrease in nocturnal urinary excretion of free catecholamines, as a possible indicator of the intrinsic sympathetic activity observed in overtrained middle- and long-distance runners (Fig. 2) and soccer players (Fig. 10), (18,19). Cardiopulmonary Findings Transient cardiac fatigue is considered possible directly after extreme prolonged exhaustive exercise (7). No evidence of an impaired cardiac function has, however, been found in the morning following nocturnal rest in overtrained middle- and long-distance runners who performed a 4-week high mileage training (Fig. 2) and in another group of moderately adapted athletes performing a 6-week high-intensity overtraining (Fig., 8), or in ten athletes subsequent to the 1993 Colmar ultra triathlon (Fig. 11). Resting heart rate is expected to decrease in the parasympathetic type of overtraining syndrome (staleness); a finding which is not to be expected in already adapted athletes with high vagal activity and resting heart rates of approximately 40 bpm; this should apply in analogy to blood pressure as well. An increase in resting heart rate was, on the other hand, observed in runners during over-reaching (8). Maximum heart rate, maximum oxygen uptake capacity, maximum lactate concentration are generally reduced in the state of an overtraining syndrome, just as is the peak performance 13 (15,16,21). The pulmonary vital capacity may be unchanged, the electrocardiogram is mostly normal in the athlete suffering from an overtraining syndrome, T-wave changes have, however, been observed (21). Neuro-Endocrine Findings The mosaic of neuro-endocrine findings in the state of over-reaching or overtraining syndrome is confusing and does not presently permit a consensus of assessment. What we need is an expansion of the experimental basis by prospective, experimental and controlled research. Barron et al. (2) found reduced cortisol, ACTH, growth hormone and prolactin release following insulin-induced hypoglycemia in four overtrained marathon runners. The pituitary LH, FSH, and prolactin release on LHRH and TRH did not differ, however, from that in well-trained athletes. Hypothalamic dysfunction (fatigue) with normal pituitary function is therefore assumed in the state of long-term overtraining. Keizer et al. (cited in Ref. 21) described reduced (a) CHR- dependent and (b) exercise-induced ß-endorphin release in over-reached endurance athletes subsequent to an 8-day exhaustive training period, indicating a decreased pituitary sensitivity to CRH. An increased pituitary sensitivity to CRH was observed, however, in six moderately adapted athletes subsequent to a 6-week threshold and interval training period (Fig. 9), combined with a reduced adrenal cortisol release (Fig. 12). This finding may indicate an increased pituitary sensitivity to CRH and decreased adrenal sensitivity to ACTH during long-term 14 overtraining. Reduced adrenal cortisol release on ACTH challenge has also been observed in chronically fatigued horses, but these results could not be confirmed by Kuipers (16). The plasma levels of free testosterone and cortisol have been suggested as indicators of anabolic and catabolic tissue activity. Adlercreutz and coworkers (1) have proposed an anabolic-catabolic imbalance during overtraining (anabolic-catabolic imbalance hypothesis) because they found a more than 30% decrease in the testosterone-cortisol ratio in long-distance runners following very intense training for one week. This hypothesis, however, is not without contradiction and requires further confirmation, since - for example - already low levels of free testosterone (approximately 40- 70 pmol/L) did not show any significant change in highly- adapted middle- and long-distance runners during a 4-week high mileage overtraining study (19), but decreased approximately from 62 to 42 pmol/L in 10 participants of the 1993 Colmar ultra triathlon as an example of extreme acute exhaustive endurance stress. A decrease in free testosterone concentration (from 105 to 85 pmol.L-1) was also observed, however, in moderately-adapted athletes during a 6-week threshold/interval overtraining study. Accordingly, an alteration of free testosterone concentration may depend on the initial concentration, on the level of adaptation the athletes have already reached and the extent of staleness or duration of exhaustive endurance stress in affected athletes. The mechanism 15 underlying the decrease in testosterone concentration may be based on a suppressed pituitary LH release caused by an increased ACTH and ß-endorphin release (Fig. 12) in the moderately-adapted athletes (2). It is unclear, however, whether this mechanism is also functioning in highly- adapted athletes. Neuro-Vegetative Findings The hypothesis of a neuro-vegetative dysfunction in the parasympathetic type of overtraining is supported by the finding of a 40-70% decrease in nocturnal urinary excretion of free catecholamines in overtrained distance runners and soccer players (18,19). Excretion increased again in athletes during the recovery period (Fig. 10). The nocturnal catecholamine excretion can be understood as an indicator of intrinsic sympathetic activity, since activating mechanisms of the neuro-vegetative axis, such as "central command", afferent nervous feedback from the working musculature, and metabolic or non-metabolic error signals must be reduced to a minimum during the nightly rest. There appears to be some evidence that a reduction of intrinsic sympathetic activity in the parasympathetic type of overtraining syndrome (staleness) is more likely a reason for a decrease in the activity level of affected athletes than an additional increase in vagal activity in already adapted athletes. The possible mechanism underlying the observed decrease in intrinsic sympathetic activity has already been discussed (see "Imbalanced Amino Acid Hypothesis"). 16 The increase in noradrenalin plasma level is greater in stale athletes at identical absolute submaximum work loads compared to baseline, indicating a loss in adaptation and in sensitivity to catecholamines (14,19,21). Both unchanged and reduced catecholamine levels have been observed at peak performance in stale athletes, the latter possibly due to a longer period of overtraining (21). Disturbance Of Mood State High volumes of training at high intensity are accompanied by a disturbance in the mood state to a more negative state; an improvement is seen during tapering (22); that is, mood state disturbances related in a "dose- response manner" to the training stimulus. Monitoring of the mood state may provide a potential method of preventing staleness. The mechanism underlying the change in mood state has also been seen in relation to an amino acid imbalance in stale or exhausted athletes with an increased brain 5-hydroxytryptamine concentration (23). Prevention Of Overtraining Syndrome Clearly, as long as athletes seek to improve their performance, overtraining will continue to be a problem. This problem is, however, similar to other risks that must be assumed by elite athletes whose life consists of pushing back the frontiers of human performance. Certainly, the training load - recovery imbalance is the dominant contributor to the likelihood of developing overtraining 17 syndrome. Other stressors on the athlete, occupational, educational, social, nutritional, or endogenous cannot be discounted. Organizers, managers, coaches and athletes have to accept that professional training requires a likewise professional cyclic regeneration and training control which cannot be left to chance. The task remains to develop sensitive and practicable screening systems - which may depend on the findings summarized in Table 1 - and to implement them in normal training. There is experimental evidence that high mileage training may be more likely to produce overtraining syndrome (17,19); but there are suggestions that high intensity training may be similarly disadvantageous. In order to minimize the risk of overtraining and injuries in distance runners, each training week should include a complete rest day. Tempo- pace, repetition or interval training (intensive training measurements) have to be compensated by an easy training day (extensive training at a lactate concentration of approximately 1-2 mmol.L-1). Training mileage can be increased 10-15 km every third week using 6-week cycle running programs or - in a more critical manner - every second and third week (so-called crash cycle) with the fourth week as regeneration cycle (approximately 50% mileage program of the first week), using 4-week cycle running programs. However, the fundamental problem is to find the adequate long-term training-regeneration balance in each individual runner. At the simplest level, on must use either periodic time trials, index workouts or laboratory evaluation to 18 document that the athlete is, in fact, progressing in his training. Certainly no athlete who is progressing is overtrained. In already-adapted athletes, failure to progress in training should be viewed as a clear sign of impending overtraining syndrome and should be respected as such. Given that the prognosis following development of overtraining syndrome is so unfavorable, prevention must have a high priority. In the future, with better understanding of the basic response to training and overtraining, perhaps a definitive marker of impending overtraining will allow objective control of training. However, at the present time, athletes and their coaches must rely on simple methods. 19 References 1. Adlercreutz, H., M. Harkonen, K. Kuoppasalmi, H. Naveri, H. Huthamieni, H. Tikkanen, K. Remes, A. Dessipris, and J. Karvonen. Effect of training on plasma anabolic and catabolic steroid hormones and their response during physical exercise. Int. J. Sports Med. 7, (Suppl): 27-28, 1986 2. Barron, J.L., T.D. Noakes, W. Levy, C. Smith, and R.P. Millar. Hypothalamic dysfunction in overtrained athletes. J. Clin. Endocrin. Metabol. 60:803-806, 1985 3. Budgett, R. Overtraining Syndrome. Br. J. Sports Med. 24:231-236, 1990 4. Costill, D.L. Inside Running. Benchmark Press Inc., Indianapolis, US: 123-132, 1986 5. Coyle, E.F. Carbohydrate feedings: effects on metabolism, performance and recovery. In: F. Brouns (ed.) Advances In Nutrition And Top Sport. Basel: Karger 1-14, 1991 6. Daniels, J. Training distance runners. A primer. Sports Science Exchange 1, 11 (1986) Gatorade Sports Science Institute 7. Douglas, P.S., M.L. O'Toole, W.D.R. Hiller, K. Hackney, and N. Reichek. Cardiac fatigue after prolonged exercise. Circulation 76:1206-1214, 1987 8. Dressendorfer, R.H. and C.E. Wade. The muscular overuse syndrome in long-distance running. Physician Sports Med. 11:116-120, 125-126, 1983 9. Foster, E., A.C. Snyder, N.N. Thompson, and K. Kuettel. Normalization of the blood lactate profile in athletes. Int. J. Sport Med. 9:198-200, 1988 10. Fry, R.D., A.R. Morton, and D. Keast. Periodisation of training stress - a review. Can. J. Sports Sci. 17:234- 240, 1992 11. Fry, R.D., A.R. Morton, and D. Keast. Overtraining in athletes; an update. Sports Med. 12:32-65, 1991 12. Griffith, R., R.H. Dressendorfer, and C.E. Wade. Testicular function during exhaustive endurance training. 20 Physician Sports Med. 18:54-64, 1990 13. Hacknes, A.C., S.N. Pearmann III, and J.M. Nowacki. Physiological profiles of overtrained and stale athletes. A review. Appl. Sports Physiol. 2:21-3, 1990 14. Hooper, S.L., L.T. Mackinnon, R.D. Gordon, and A.W. Bachmann. Hormonal responses of elite swimmers to overtraining. Med. Sci. Sports Exerc. 25:741-747, 1993 15. Israel, S. Zur Problematik des Übertrainings aus internistischer und leistungsphysiologischer Sicht. Medizin und Sport 16:1-12, 1976 16. Kuipers, H. and H.A. Keizer. Overtraining in elite athletes. Sports Med. 6:79-92, 1988 17. Lehmann, M., P. Baumgartl, C. Wieseneck, A. Seidel, H. Baumann, S. Fischer, U. Spöri, G. Gendrisch, R. Kaminski, and J. Keul. Training - overtraining: Influence of a defined increase in training volume vs. training intensity on performance, catecholamines and some metabolic parameters in experienced middle- and long- distance runners. Eur. J. Appl. Physiol. 64:169-177, 1992 18. Lehmann, M., W. Schnee, R. Scheu, W. Stockhausen, and N. Bachl. Decreased nocturnal catecholamine excretion. Parameter of an overtraining syndrome in athletes? Int. J. Sports Med. 13:236-242, 1992 19. Lehmann, M. U. Gastmann, K.G. Petersen, N. Bachl, A. Seidel, A.N. Khalaf, S. Fischer, and J. Keul. Training - overtraining. Performance and hormones after a defined increase in training volume vs. intensity in experienced middle- and long-distance runners. Br. J. Sports Med. 26:233-242, 1992 20. Lehmann, M., U. Gastmann, K.G. Petersen, A.N. Khalaf, K. Knizia, S. Fischer, L. Kerp, and J. Keul. Influence of 6-week training on pituitary function in recreational athletes. Br. J. Sports Med. 27 21. Lehmann, M. C. Foster, and J. Keul. Overtraining in endurance athletes. A brief review. Med. Sci. Sports Exerc. 25:854-862, 1993 22. Morgan, W.P. D.R. Brown, J.S. Raglin, P.J. O'Connor, and K.A. Ellickson. Psychological monitoring of 21 overtraining and staleness. Br. J. Sports Med. 21:107- 114, 1987 23. Newsholme, E.A., M. Parry-Billings, N. McAndrew, and R. Budgett. A biochemical mechanism to explain some characteristics of overtraining. In: F. Brouns (ed.) Advances In Nutrition And Top Sport. Basel: Karger, 79- 93, 1992 24. Snyder, A.C., A.E. Jenkendrup, M.K.G. Hesselbrink, H. Kuipers, and C. Foster. A physiological/psychological indicator of overreaching during intensive training. Int. J. Sports Med. 14:29-32, 1993 25. Stone, M.H., R.E. Keith, J.T. Kearney, S.J. Fleck, G.D. Wilson, and N.T. Triplett. Overtraining: A review of the signs, symptoms and possible causes. J. Appl. Sport Sci. Res. 5:35-50, 1991 26. Verma, S.K., S.R. Mahindroo, and D.K. Kansal. Effect of four weeks of hard physical training on certain physiological and morphological parameters of basketball players. J. Sports Med. 18:379-384, 1978 22 Table 1: Findings in overtraining syndrome (staleness) ___________________________________________________________ _ competition incompetence reduction in peak performance reduction/stagnation of tempo-pace performance persistent high fatigue ratings suppressed mood state lack of supercompensation suppressed blood glucose-exercise profile suppressed blood lactate-exercise profile suppressed lactate-perceived exertion ratio suppressed neuro-muscular function suppressed catecholamine sensitivity suppressed intrinsic sympathetic activity muscle soreness / stiffness adjuvant blood-chemical findings altered hypothalamic-pituitary function ___________________________________________________________ __ 23 Table. 2: Significant changes in serum amino acid concentration in 10 athletes during the 1993 Colmar ultra triathlon (percent of baseline) ___________________________________________________________ __ Asparagine - 18% Threonine - 22% Serine - 17% Glutamine - Proline - 56% Glycine - 27% Alanine - 29% Citrulline - 25% Valine - 24% Cystine + 38% Methionine + 24% n.s. Isoleucine - 28% Leucine - Tyrosine + 10% n.s. Phenylalanine + 12% Ornithine - 43% Lysine - 10% Histidine - 13% Arginine - 26% total Tryptophan - free Tryptophan + 74% ___________________________________________________________ n.s.: not significant; a) Hematocrit: - 10% 24 Tab. 3: Significant changes in different blood-chemical parameters (in percent of baseline) during a 4- week high mileage overtraining study in 8 middle- and long-distance runners (17,19). ___________________________________________________________ _ Peak Performance - 6% 4 LT Performance stagnation ___________________________________________________________ _ Leukocytes - 22% Hematocrit - 5% Serum Iron - 30% Serum Ferritin - 61% Prothrombin Time + 15% Serum Creatine Phosphokinase + 40% a) Serum Calcium - 5% Serum Triglycerides - 32% Total Serum Cholesterol - 10% VLDL Cholesterol - 32% LDL Cholesterol - 11% Serum Albumin - 14% Serum Free Fatty Acids BE - 26% Serum Free Fatty Acids ME - 19% Serum Glycerol ME - 20% Serum Glucose BE - 7% Serum Glucose SE - 9% Serum Glucose ME - 12% Blood Lactate ME - 23% Blood Ammonia BE - 30% Blood Ammonia SE - 27% Blood Ammonia ME - 42% ___________________________________________________________ __ a) noticeable but not significant change BE before, SE submaximal, ME maximal incremental exercise; not significant changes: blood hemoglobin, erythrocytes, platelets, transferrin, fibrinogen, urea, creatinine, GOT, GPT, yGT, sodium, potassium, magnesium 25 Figures Fig. 1: Schematic response pattern in training, overreaching and overtraining. As the training load increases, performance should improve from baseline (A). The magnitude of the response depends upon the load and will be suboptimal with too little training (B) and near the athlete's potential with an optimal training load (C). With reduced training (tapering), performance will be improved briefly, super-compensation will have occurred (B' and C'). During very heavy training consistent with overreaching (D), performance will decrease. However, if the training load is decreased, performance will again improve. There is some controversy whether the supercompensation following deliberate overreaching will be to levels below (D') or above (D'') those achieved during tapering following optimal training (C'). If overreaching is at too great a level, continued for too long, or is combined with other stressors on the athlete - social, occupational, educational, travel - performance will continue to decline as overtraining syndrome emerges (E). Fig. 2: Scheme (above) of a four-week mezo cycle training session in distance running (1 mezo cycle - 4 micro cycles, each lasting one week, including one rest day), and average mileage during a four- week high mileage overtraining study (below) in eight middle-and long-distance runners (17,19). Fig. 3: Correlation between a symptom index (including fatigue as the dominant symptom) and the weekly mileage during a four-week high mileage overtraining study (17,19); (index 1, no symptoms; 2, mild; 3, moderate; 4, severe symptoms). 26 Fig. 4: Blood lactate responses to increased running velocity in an already-adapted athlete during a period of heavy training (closed circles) compared to baseline (open circles). Rather than the apparent, and favorable, right shift of the curve (from 16.5 to 18.0 km . hr-1) at a blood lactate concentration of 4 mmol/L, these results demonstrate a downshift that is at least partially attributable to muscle glycogen depletion. This problem can partially be compensated for by "normalizing" the curve to the peak lactate during maximum exercise. Adapted from Foster et al. (9). Fig. 5: Schematic response pattern of the ratio of blood lactate to rating of perceived exertion during submaximum exercise at a velocity of approximately 4 mmol/L and a rating of perceived exertion 4 (somewhat hard). Beyond some threshold of training load, blood lactate will be systematically depressed, probably secondary to muscle glycogen depletion. The rating of perceived exertion will either be unchanged or increased at the same time, leading to a decreased ratio. It may be hypothesized that lactate/RPE ratios outside the normal range of variation are indicative of overreaching and of the need of an increased regeneration phase in the athlete's training. Adapted from Snyder et al. (24). Fig. 6: Suppressed blood glucose-exercise profile after a six-week threshold/interval overtraining period (_) com-pared to baseline (_) or a subsequent 3- week recovery period (_) in six moderately- adapted athletes (20). Fig. 7: Suppressed neuro-muscular function 27 (hypoexcitability) of the M. vastus medialis ( ) after a four-week high mileage overtraining (STU) as compared to baseline ( ) and to the control study (STI, above) in eight to nine middle- and long-distance runners as indicated by significantly higher minimum electrical impulses (I) that can produce a single contraction of the muscle at different impulse durations from 0.1 to 10 ms. Fig. 8: Suppressed neuro-muscular function (hypoexcitability) of the M. vastus medialis after (Day 42) a six-week threshold/interval overtraining as compared to baseline (Day 0) or Day 21 in six moderately-adapted athletes, as indicated by significantly higher minimum electrical impulses (I) that can produce a single contraction of the muscle at different impulse durations of 0.1 to 100 ms (20). Fig. 9: A six-week training program is presented schematically in the upper part of this picture with an increase in training load during micro cycles 2 and 3 (week 2 and 3) and a regeneration cycle during week 4 followed by a further progression in training load. A six-week threshold/interval overtraining study in six moderately-adapted athletes is represented below. The training load of the threshold training (_) was increased from 90% (week 1) to 99% (week 6) of the baseline 4 mmol lactate performance, the training load of interval training (_) was increased from 117% (week 1) to 127 and 126% (week 3 and 4), and had to be decreased again to 111% (week 6) of the baseline 4 mmol lactate performance due to fatigue (20). Fig. 10: Behavior of nocturnal urinary adrenaline (A), 28 noradrenalin (NA), and dopamine (DA) excretion in athletes of a soccer team during competitive season and winter break with a significant decrease in early November likely due to overtraining, and a significant re-increase during the regeneration period in mid- to late December (median values and 50% range of confidence). Fig. 11: Echocardiographically determined resting cardiac shortening fraction (SF) and ejection fraction (EF) in eight middle- and long-distance runners before and after a 4-week high mileage overtraining study (°), in six moderately-adapted athletes before and after a 6-week threshold/interval overtraining study (_), and in ten adapted athletes before and after the 1993 Colmar ultra triathlon (_). Fig. 12: Possible mechanism underlying decrease in free serum testosterone and spermatogenesis: *) as experimentally demonstrated (20), **) according to Griffith et al. (12). Fig. 13: Possible mechanisms underlying peripheral and central fatigue during long-term overtraining; a) overload of muscle-tendon-joint system; b) nociceptive and proprioceptive impulses. (Adrenal overload: see Fig. 12).