The results of the present study suggest that supplementation with alpha-tocopherol, beta-carotene and ascorbic acid might partially account for the hormonal and enzymatic stress marker profile observed during habitual training activity of professional basketball players.

Professional basketball players of the First Spanish League (ACB) are highly trained athletes performing high training loads and competition sessions. As intense physical activity has been suggested to increase free radical production, we examined the effects of a vitamin antioxidant mixture on the degree of oxidative stress in these athletes. Subjects received either 600 mg alpha-tocopherol, 1,000 mg vitamin C and 32 mg beta-carotene, or a placebo over 32 days during a regular competition season. Plasma concentrations of alpha-tocopherol, vitamin C, beta-carotene, retinol, lipoperoxides (LPO), and the total antioxidant status (TAS) were analysed before and after treatment. Lipoperoxide plasma levels decreased significantly (p < 0.05) in the vitamin antioxidant supplemented group. The LPO/TAS ratio decreased about 15.3% in this group indicating a reduction in oxidative stress. Vitamin C dropped dramatically (p < 0.03, mean 15.4 micromol/L) in the placebo group leading to a marginal plasma vitamin C concentration (from 11 to less than 28 micromol/L). The results of this study suggest that the administered vitamin antioxidant mixture decreases oxidative stress and avoids the development of a marginal vitamin C status in professional basketball player during habitual training.

SUMMARYThe 'engine' of fetal metabolism generates heat (3-4 W kg-' in fetal sheep) which has to be dissipated to the maternal organism. Fetal heat may move through the amniotic/allantoic fluids to the uterine wall (conductive pathway; total conductance, 1-1 W 0C-' kg-') and with the umbilical arterial blood flow (convective pathway) to the placenta. Because resistance to heat flow is larger than zero fetal temperature exceeds maternal temperature by about 0 5°C (0.3-1°C). Probably 85 % of fetal heat is lost to the maternal organism through the placenta, which thus serves as the main 'radiator'. Placental heat conductivity appears to be extremely high and this may lead to impaired heat exchange (guinea-pig placenta). A computer simulation demonstrates that fetal temperature is essentially clamped to maternal temperature, and that fetal thermoregulatory efforts to gain thermal independence would be futile. Indeed, when the late gestational fetus in uter^o is challenged by cold stress, direct and indirect indicators of (non-shivering) thermogenesis (oxygen consumption, increase of plasma glycerol and free fatty acid levels) change only moderately. In prematurely delivered lambs, however, cold stress provokes summit metabolism and maximum heat production. Only when birth is imitated in utero (by cord clamping, external artificial lung ventilation and cooling) do thermogenic efforts approach levels typical of extra-uterine life. This suggests the presence of inhibitors of thermogenesis of placental origin, e.g. prostaglandins and adenosine. When the synthesis of prostaglandins is blocked by pretreatment with indomethacin, sheep fetuses react to intra-uterine cooling with vigorous thermogenic responses, which can be subdued by infusion of prostaglandin E2 (PGE2). Since the sheep placenta is known to produce sufficient amounts of PGE2, it seems that the placenta controls fetal thermogenic responses to some extent. This transforms the fetus into an ectothermic organism, and yet allows the newborn the full exploitation of thermoregulatory responses typical of endothermic animals.

Heat produced by the fetus exists to the mother by one of two principal routes: by fetal-maternal exchange in the placenta or through the fetal skin to the amniotic fluid and uterine wall. We measured heat conductances along each pathway to estimate the fraction of total heat exiting each route. Thermistors were placed in the fetal aorta, two different sites in the amniotic fluid, and in a maternal artery. Five days after surgery we injected a total of 280 ml of ice-cold saline into the two separate amniotic fluid sites during a 45-s interval and measured the temperature response for the next hour. After one or two such injections the fetus was killed to cut off umbilical blood flow, and the experiment was repeated to measure the heat fluxes in the absence of placental heat exchange. Experimentally obtained temperature curves were compared with the predictions of a mathematical model. Heat conductances of the skin and uterine wall, as well as the fetal heat production, were estimated in the model using least-squares parameter optimization. In 10 fetal lambs, weighing 3.73 +/- 0.40 (SE) kg, total fetal heat production averaged 3.75 +/- 0.33 W X kg-1. The heat conductance of the uterine wall, 6.6 +/- 0.8 W X degrees C-1, was lower than that of the fetal skin, 10.2 +/- 1.0, and of the placenta, 25.7 +/- 2.9 W X degrees C-1, temperature gradient. We estimated that 84.5% of total fetal heat production exists by fetal-maternal exchange in the placenta with the remaining 15.5% exiting through the fetal skin.

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Isolated cotylidons of human term placentas are perfused artificially on the fetal and maternal side. The relative transfer rates of radioactive labelled D-glucose, L-glucose, D-mannose and D-mannitol across the placenta are measured and the inhibition of these transports by phloretin is studied: 1. Transfer rates of D-glucose and D-mannose exceed that of L-glucose about 1.5-4 times. 2. Phloretin (10(-3) mol/l) decreases the transports of D-hexoses, whereas the transport of L-GLUCOSE REMAINS UNAFFECTED. 3. If the concentration of D-glucose is increased, the transport of D-mannose is inhibited competitively. 4. L-glucose and D-mannitol equal in transfer rates. These results show, that D-hexoses cross the human placenta by a specific carrier and by simple diffusion.

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