The purpose of the current investigation was to determine whether sodium citrate enhances endurance cycling performance and, if so, what dosage(s) produces this effect. Eight trained [peak power output: 362 (48) W; power:weight: 5.1 (0.4) W x kg(-1), mean (SD)] male cyclists were requested to complete four, 40-km time-trials, each separated by 3-7 days, on their own bicycles, mounted on a Kingcycle ergometer. To mimic the stochastic nature of cycle road races, the time-trials included four 500-m, four 1-km and two 2-km sprints. The experimental conditions involved the ingestion of three dosages of sodium citrate dissolved in 400 ml water: 0.2 g x kg(-1), 0.4 g x kg(-1) and 0.6 g x kg(-1) body mass (b.m.) and a placebo (calcium carbonate, 0.1 g x kg(-1) b.m.). Subjects were asked to complete both the sprints and total distance in the fastest time possible. Venous blood samples were collected before, as well as at 10-km intervals during the trials for the analysis of plasma lactate and glucose concentrations and for the measurement of blood pH and PCO2 levels. Immediately before, as well as during exercise, pH was significantly higher in the group ingesting the highest citrate dose (range 7.36-7.45) compared to the placebo (range 7.31-7.39) and the two lower citrate dosages. Despite this, no significant differences in power output (P = 0.886) or time taken to complete the 40 km (P = 0.754) were measured between the four trials. The average performance times (in min:s, with SD in parentheses) and average power output (in W) for the 40-km time-trials were: 58:46 (5:06) [265 (62) W], 60:24 (6:07) [251 (59) W], 61:47 (5:07) [243 (44) W] and 60:02 (5.05) [255 (55) W] for the 0.2, 0.4, 0.6 g x kg(-1) b.m. sodium citrate and placebo trials, respectively. There were also no significant differences measured between treatments in terms of time, power output, speed or heart rate during the 500-m, 1-km and 2-km sprints. The ingestion of increasing sodium citrate dosages before exercise produced dose-dependent changes in pH, base excess and HCO3- concentrations before and during the 40-km time-trial. However, these changes influenced neither the time-trial time nor the sprinting performance times.

Skeletal muscle buffering capacity (beta mtitr) was determined in soleus (type I) and superficial vastus (type II) muscles of 16 Long-Evans rats with differing levels of spontaneous activity and in 11 sedentary control rats. beta mtitr was 24% higher (P < 0.001) in superficial vastus muscle than in soleus muscle (268 +/- 50 vs. 216 +/- 30 mumol H+ g muscle dry wt-1 pH unit-1) (mean +/- SD). There was no relationship between beta mtitr and mean weekly running distance amongst spontaneously running rats, nor was beta mtitr any greater in these rats than in a group of sedentary control rats. Protein to wet wt ratio was 31% higher (P < 0.0001) in the superficial vastus muscle when compared with soleus muscle (22.04 +/- 3.74 vs. 16.77 +/- 3.00 mg protein, 100 mg wet wt muscle-1), but there was no relationship between protein to wet wt ratio and running distance. Initial muscle homogenate pH (pHi) was lower in superficial vastus muscle compared with soleus muscle (6.36 +/- 0.25 vs. 6.63 +/- 0.16). Running rats had a significantly lower pHi in both soleus and superficial vastus than sedentary controls. There was an exponential relationship between weekly running distance and pHi in both the superficial vastus muscle (r = -0.86. P < 0.001) and the soleus muscle (r = -0.73, P < 0.01). Citrate synthase activity correlated with weekly running distance in superficial vastus muscle (r = 0.66, P < 0.01) but not in soleus muscle. The results confirm a higher beta mtitr in the type II superficial vastus muscle when compared with the predominantly type I soleus muscle. We suggest that this may be partly the result of a higher protein concentration in type II muscle. Future studies measuring beta mtitr in mixed muscle (e.g. human vastus lateralis) should report fibre type composition.

1. Pregnant rats were fed either low (<1 p.p.m.) Zn or control (40p.p.m. Zn) diets from day 10 of gestation. They were killed at intervals during the last 96h preceding the normal time for onset of parturition, and differences in plasma progesterone, oestradiol-17, and ovarian 20a-hydroxysteroid dehydrogenase were assessed. 2. Gestation was prolonged in Zn-deficient rats. 3. Although the preparturient decline in plasma progesterone began at the same time in all groups, at term, plasma progesterone concentration in Zn-deficient rats remained significantly higher than in normal females. 4. Induction of ovarian 20a-hydroxysteroid dehydrogenase activity was delayed by about 8h by Zn deficiency. This delay was not observed if prostaglandin F2. was injected previously. 5. The results suggest a Zn-dependent step(s) in uterine synthesis and/or release of prostanoids.Zinc was first reported to be required for normal parturition in the rat by Apgar (1968a). Female rats fed a diet containing 1 p.p.m. or less of Zn beginning on the first day after mating displayed loss of appetite and lethargy. Harderian-gland pigment often accumulated on the face and paws. Delivery was difficult and prolonged and accompanied by excessive bleeding, and most of the neonates were abandoned and placentae were left unconsumed. Further studies (Apgar, 1968b(Apgar, , 1970(Apgar, , 1972(Apgar, , 1973(Apgar, , 1975(Apgar, , 1976(Apgar, , 1977aGombe et al., 1973) showed that such effects were relatively specific to Zn deficiency and were not induced by restriction either of total food intake (pair-feeding) or

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