Distance Runners Overtraining - Sportscience

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       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
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  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).

				
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