This study was designed to measure the electroencephalogram (EEG) after exercise with increasing intensity. In a field test with increments in running velocity a 2-min EEG was recorded, together with blood lactate concentration and heart rate, after each stage. An individual protocol was used, with up to six stages of running to ensure comparability of exercise intensity among the subjects, in each of 19 athletes (17 men, 2 women) experienced in leisure-time running. The exercise consisted initially of three running stages of aerobic exercise intensity without blood lactate accumulation followed by stages with an increase of lactate concentration. The protocol of the field test led to a progressive increase in cortical activity directly after the stages without blood lactate accumulation mainly in the delta frequency band, followed by theta and alpha-1 frequency band, and less pronounced in the alpha-2 and in the beta frequency bands. After the stages with an onset and further increase of blood lactate accumulation significant decreases in the beta-2, beta-1 and alpha-1 frequency bands occurred predominantly in temporal (T3, T4, T5, and T6) and occipital (O1, and O2) electrode positions, indicating a stage-by-stage decrease of activity. This decrease may be explained by feed-back from working muscle, via afferents to the cortex from intero- and proprio-receptors and affective processes. This could suggest that through a higher running intensity indicated by an onset of blood lactate accumulation metabolic and mechanical changes led to alterations within the afferent systems influencing the level of cortical activity.

The influence of increased training on the sympathoadrenergic system was investigated. Moderately trained male subjects (n = 15) increased their training within 10 wk by 60%; eight of the subjects increased their training volume, and seven increased their training intensity. Before and after the training, an exhaustive treadmill exercise was carried out. Acute treadmill exercise increased beta-adrenergic receptor number on mononuclear lymphocytes, isoproternol-stimulated cAMP production, and plasma catecholamine concentration. The increase of receptor number can at least partially be explained by a changed lymphocyte composition at rest and after exercise. After training, the exercise-induced increase of beta-adrenergic receptor number was significantly blunted, and the exercise-induced increase of the isoproternol-stimulated cAMP production per beta-receptor was enhanced. Subjects who experienced increased symptoms of physical discomfort and/or mood changes showed an enhanced cAMP production after training. These findings point to an altered regulation of the receptor and postreceptor mechanisms as an effect of a 10-wk period of hard training.

To investigate the influence of taurine and caffeine containing drinks and physical stress on the cortical movement-preparation, the readiness potentials or "Bereitschaftspotentiale" (BPs), preceding voluntary self-placed pedalling movements, were examined after different states of exhaustion on an ergometer. 15 (13 right-handed) healthy men, aged between 22-30, participated in a randomised, cross over, double-blind, placebo controlled study. BPs were averaged out of artefact free EEG-segments from more than 90 triggered events, measured at 17 electrodes of the 10:20 system. With increasing effort the BPs were enlarged differently depending on the drink consumed. In placebo trials after exhaustive exercise premovement negative potential curves could be seen even in frontal areas. With caffeine the BPs increased after lower workload, achieving a level, which was reached in the placebo trials only after submaximal physical activation. Furthermore a significant shortening of premovement-brain-potentials in frontal and parietal regions could be seen in the caffeine trials at rest. Taurine admixture seems to inhibit this effects.