Lehmann, M. J., Lormes, W., Opitz-Gress, A., Steinacker, J. M., Netzer, N., Foster, C., & Gastmann, U. (1997). Training and overtraining: An overview and experimental results in endurance sports. Journal of Sports Medicine and Physical Fitness, 37, 7-17.

Overtraining is defined as "Training/competition to recovery imbalance." It primarily is caused by too little time for regeneration. Additional non-training stress sources, such as social, educational, occupational, nutritional, and travel factors and the monotony of training increase the risk of overtraining. Symptoms of overtraining are persistent performance incompetence, persistent high fatigue rating, altered mood state, increased rate of infections, and suppressed reproductive function.

This review considered three studies that evaluated effects on participants.

The ITV condition produced consistently depressed performances that persisted for a three-month period. On the other hand, the ITI study increased performances and did not produce an overtrained state. Its added rest period, greater variety of stimulation, and alternating hard and easy sessions better accommodated regeneration and the avoidance of monotony. [An opinion was offered by the authors that monotony might be just as critical in suppressing regeneration of an overtrained state as is training load.]

The ITE study confirmed what the authors had suspected, "that it seems easier to cause a performance decrease in athletes dependent on prolonged monotonous extensive training at a high training load than on intensified training of 1-2 hours per day." (pp. 9-10) In the ITE study, performances improved over the first three weeks but by week 6 performances and motivation were depressed despite the inclusion of extra regeneration weeks (microcycles).

Proposed Principle 1. An increased risk of staleness is likely after three weeks of intensified or prolonged monotonous endurance training.

Proposed Principle 2. If alternating hard and easy days is considered and at least two rest days (one per week) are included, there is only a risk of transient performance depression (overreaching) over periods of less than three weeks with an intensified high total training load.

The Autonomic Imbalance Hypothesis

The type of overtraining condition that results from endurance training can be described as an autonomic nervous system imbalance, where the parasympathetic nervous system dominates the sympathetic system. [This is not a new hypothesis: It was proposed by T. K. Cureton (1963; Review of studies to improve cardiovascular fitness at the Physical Fitness Research Laboratory, 1941-1963. Champaign, IL: University of Illinois) that when training was progressing well, the sympathetic nervous system was dominant promoting an athlete to be mildly aroused and vital (a condition labeled "sympatheticotonia"), but in overtraining the reverse occurs and "parasympatheticotonia" takes over.]

This condition is marked by a reduction in basal catecholamine excretion, which indicates a decrease in sympathetic intrinsic activity. However, that symptom only occurs when the overtrained state has progressed extensively. If one waited until this index was revealed then a difficult period and program of rehabilitation would be warranted.

Another "late" outcome of overtraining is elevated noradrenaline plasma levels. Unless overtraining studies progress to the stage where chronic and debilitating overtraining occurs these two hormonal factors might not be evident.

Observed overtraining-related reduced catecholamine sensitivity acts in a manner similar to what would result from using beta-blockers, that is, peripheral fatigue and depressed responses are evident.

Yet another symptom of overtraining is a decrease in neuromuscular excitability. This central nervous system feature is likely to occur "earlier" than the previous two "late" markers. The ITE study showed this decrease while no decrease in sensitivity to catecholamines had occurred.

These factors interfere with the ability to correctly stimulate the appropriate organs/musculature of the body to produce high-level performance movements.


". . . steps in a protective mechanism of target organs against pathological overload during the overtraining process, might be (I) a decrease in neuromuscular excitability, (II) a decreased cortisol release, (III) in parallel to slightly increased growth hormone release representing a shift to a more anabolic neuroendocrine responsibility (inhibition of catabolic stress), (IV) an inhibition of alpha-motoneuron activity, (V) a decrease in beta-adrenoreceptor density in advanced stages which cannot be overridden by an increased noradrenaline stress response, and (VI) a decrease in intrinsic sympathetic activity as reflected by a clearly reduced basal catecholamine excretion. All these mechanisms can be seen as impairment or inhibition of the transmission of ergotropic (catabolic) signals to target organs, which are complemented by intracellular protective mechanisms such as increased synthesis of heat shock proteins (HSP70), as observed in overtrained rowers." (p. 16)

Implication. If training loads are to be increased, the increase should come primarily from increased quality. Such changes have to be coupled with alternating hard and easy training sessions, at least one full day per week on no activity, and close monitoring of the athlete's response to ensure that regeneration is allowed to occur. Of prime importance, is the content of programming, which should be various and stimulating so as to avoid monotony. Such increases should not be planned for more than three weeks.

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