Alkalosis induced by alpha-stat management: cause of neuronal injury after deep hypothermic perfusion.
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Seven healthy male subjects performed 10 maximal 6-s sprints, separated by 30-s recovery periods, on a non-motorized treadmill. On two occasions, separated by 3 days, the subjects ingested a solution of either sodium bicarbonate (NaHCO3; alkaline) or sodium chloride (NaCl; placebo), 2.5 h prior to exercise. The doses were 0.3 g kg-1 body mass for the alkaline treatment and 1.5 g total for the placebo, dissolved in 500 ml of water. The order of testing was randomly assigned. Pre-exercise blood pH was 7.43 +/- 0.02 and 7.38 +/- 0.01 for the alkaline and placebo trials respectively (P less than 0.01). Performance indices (i.e. mean and peak power outputs and mean and peak running speeds) were significantly reduced as a result of the cumulative effects of successive sprints, but not significantly affected by the treatments. However, the total work done (i.e. mean power output) in the alkaline condition was 2% higher than that achieved in the placebo condition. Post-exercise blood lactate concentrations were higher for the alkaline treatment than for the placebo condition (15.3 +/- 3.7 vs 13.6 +/- 3.0 mM respectively; P less than 0.01), but blood pH was similar in both conditions (alkaline: 7.15 +/- 0.13; placebo: 7.09 +/- 0.11). In both conditions, a relationship was found between post-exercise blood lactate and mean power output (alkaline: r = 0.82, P less than 0.01; placebo: r = 0.79, P less than 0.01). No significant differences were found in VE, VO2 and VCO2 between the two experimental conditions. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood, but has no effect on the power output during repeated bouts of brief maximal exercise.
Previous studies have shown that sodium bicarbonate ingestion prior to exercise may improve performance during repeated (interval) bouts. To examine the practical implications of such findings, seven collegiate swimmers participated in simulated swim competitions of multiple events following sodium bicarbonate (B) ingestion, placebo (P) ingestion and control (C--no ingestion) treatments. Each swimmer reported to the laboratory 1 h prior to the simulated competitions (72 h apart) and was randomly assigned to one of the three experimental treatments. Competition consisted of one relay (100 yards; 91.4 m) and two individual (200 yards; 182.8 m) swimming events with 20 min rest between events. Analysis of variance (ANOVA) with repeated measures revealed no significant differences in performance times as a result of the three treatments (P greater than 0.05). The results suggest that sodium bicarbonate ingestion prior to swim competition consisting of significant rest intervals between events is not an ergogenic procedure.
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Acute chloride depletion in rats is associated with the occurrence of an extensive cell damage in the mid-portion of the proximal convolutions which is followed by an excessive hyperplastic reaction of the renal epithelium; no other significant lesions were found by microdissection in either the tubules of the nephrons or the collecting system. Potassium deficiency is not essential to the development of this lesion but does increase the severity of the reaction. As in the case of potassium deficiency, chloride depletion predisposes to or exaggerates the structural alterations that accompany excess phosphate intake. The relations of the different structural changes in renal architecture that occur in various states of electrolyte imbalance are discussed as well as the relation of the lesions seen experimentally in the rat and monkey and clinically in man.
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Intraocular and intracranial pressures (IOP and ICP) were measured at four different arterial carbon dioxide tensions by direct continuous techniques in Rhesus monkeys during anaesthesia with halothane and nitrous oxide. Increases in IOP correlated significantly with PaCO2 ranging from 2.66 to 10.24kPa (P less than 0.001). Increases in ICP correlated significantly (P less than 0.001) with PaCO2 between 2.66 and 7.71 kPa, but plateaued thereafter. When PaCO2 was decreased rapidly, PaCO2, IOP and ICP decreased exponentially with similar half-times. The fast changes in IOP and ICP can probably be explained by an alteration of intraocular and intracranial blood volumes. IOP usually remained within the normal range, even at maximum PaCO2.
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