Training and overtraining: an overview and experimental results in endurance sports.
Overtraining can be defined as "training-competition > > recovery imbalance", that is assumed to result in glycogen deficit, catabolic > anabolic imbalance, neuroendocrine imbalance, amino acid imbalance, and autonomic imbalance. Additional non-training stress factors and monotony of training exacerbate the risk of a resulting overtraining syndrome. Short-term overtraining called overreaching which can be seen as a normal part of athletic training, must be distinguished from long-term overtraining that can lead to a state described as burnout, staleness or overtraining syndrome. Persistent performance incompetence, persistent high fatigue ratings, altered mood state, increased rate of infections, and suppressed reproductive function have been described as key findings in overtraining syndrome. An increased risk of overtraining syndrome may be expected around 3 weeks of intensified/prolonged endurance training at a high training load level. Heavy training loads may apparently be tolerated for extensive periods of time if athletes take a rest day every week and use alternating hard and easy days of training. Persistent performance incompetence and high fatigue ratings may depend on impaired or inhibited transmission of ergotropic (catabolic) signals to target organs, such as: (I) decreased neuromuscular excitability, (II) inhibition of alpha-motoneuron activity (hypothetic), (III) decreased adrenal sensitivity to ACTH (cortisol release) and increased pituitary sensitivity to GHRH (GH release) resulting in a counter-regulatory shift to a more anabolic endocrine responsibility, (IV) decreased beta-adrenoreceptor density (sensitivity to catecholamines), (V) decreased intrinsic sympathetic activity, and (VI) intracellular protective mechanisms such as increased synthesis of heat-shock proteins (HSP 70) represent a complex strategy against an overload-dependent cellular damage.
Lehmann
M J
MJ
Department of Sports Medicine, University Medical Hospital Ulm.
Lormes
W
W
Opitz-Gress
A
A
Steinacker
J M
JM
Netzer
N
N
Foster
C
C
Gastmann
U
U
D000311:Adrenal Glands / Q000503:physiopathology; D000324:Adrenocorticotropic Hormone / Q000502:physiology; D000339:Affect / Q000502:physiology; D000596:Amino Acids / Q000378:metabolism; D001341:Autonomic Nervous System / Q000503:physiopathology; D002055:Burnout, Professional / Q000209:etiology; D002395:Catecholamines / Q000502:physiology; D005221:Fatigue / Q000209:etiology; D006003:Glycogen / Q000378:metabolism; D013007:Growth Hormone-Releasing Hormone / Q000502:physiology; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D019382:Human Growth Hormone / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007239:Infections / Q000209:etiology; D009046:Motor Neurons / Q000502:physiology; D009469:Neuromuscular Junction / Q000503:physiopathology; D009490:Neurosecretory Systems / Q000503:physiopathology; D010807:Physical Endurance / Q000502:physiology*; D010902:Pituitary Gland / Q000503:physiopathology; D011597:Psychomotor Performance / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D012098:Reproduction / Q000502:physiology; D012307:Risk Factors; D013177:Sports / Q000502:physiology*; D013312:Stress, Physiological / Q000503:physiopathology; D013315:Stress, Psychological / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D013577:Syndrome
D000596:Amino Acids; D002395:Catecholamines; D006360:Heat-Shock Proteins; D011943:Receptors, Adrenergic, beta; D019382:Human Growth Hormone; D000324:Adrenocorticotropic Hormone; D006003:Glycogen; D013007:Growth Hormone-Releasing Hormone; D006854:Hydrocortisone