Doping for Chess Performance
Abstract
Sighart Golf
During a chess game, the needed energy is first derived instantly from ATP and creatine-phosphate, then within a few seconds later from glycogen stores in brain, glycogen, muscle and liver and finally, 1-2 hours later from adipose tissue. Anaerobic oxidation of glucose-derivative from glycogen delivers energy 6 times faster than aerobic oxidation of glucose and oxidation of fatty acids; correspondingly, mental activity can perform as well 6 times faster as long as glycogen is available.
The mental profile of chess players correlates with cerebral processes such as attention, conflict solution, memory,
motivation and recognition, which together constitute a specific chess-domain expertise.
A chess player may compete best when a) regularly physical exercise is carried out to compete in strenuous chess tournaments and to stimulate mental cognition, b) super compensated glycogen is accumulated in brain, muscle and liver by corresponding nutrition and physical and mental activities, and c. an active mental disposition is available for complex brain tasks during chess by complementary treatment schemes e.g., cogni-tive enhancement (CE) by chesstraining with chess boards, chess books, building chess images, visual observation of chess games, vocational training with chess, metacognitive training, and additionally regular light physical stress.
An illicit improvement of brain performance for chess playing may be achieved by several measures:
1. Increase of O2 supply by therapy with erythropoietin (EPO) for chess tournaments at high altitudes and for
chess players with lung diseases
2. Increase of body glycogen by therapy with insulin
3. mental stimulation by caffeine
AAS, anabolic agents, amphetamines, nicotine and cocaine have no proven effect on quality of chess playing. Many steroid- and proteohormones such as cortisol, testosterone, ACTH, EPO, GH, hCG, IGF-I, Insulin, LH, present positive effects on brain development and cognition only when present in natural concentrations during development of brain. Pharmaceutical preparations show positive effects only at low baseline cognition. With elevated concentrations, these hormones present negative effects on mental cognition.
Actual CE drugs have effects only with persons at low cognitive baseline. With normal persons, CE is still below clinical significance.
Regular non-medical use of steroid and proteohormones in elevated concentrations and CE-drugs must also consider numerous side effects ranging from simple metabolic disturbances through cardiac problems to cognitive decline to tumorgenesis and sudden death.
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