The physiological and ventilatory responses to repeated 60 s sprints following sodium citrate ingestion
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CONTRIBUTORS:
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JOURNAL:
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YEAR:
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1994
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PUB TYPE:
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Journal Article
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SUBJECT(S):
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SPRINTING; SODIUM; DOPING; ACID-BASE-EQUILIBRIUM; LACTATE; RESPIRATION; ERGOGENIC-AID
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DISCIPLINE:
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No discipline assigned
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HTTP:
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LANGUAGE:
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English
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PUB ID:
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103-366-418
(Last edited on
2002/02/27 18:45:01 US/Mountain)
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SPONSOR(S):
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ABSTRACT:
This study examined the influence of sodium citrate on changes in selected blood, ventilatory and performance variables in response to intermittent sprint exercise. Eight moderately active male students completed three tests over a 6 day experimental period. The first test involved incremental exercise to determine VO2max, while the second and third tests were identical in nature and involved five 60 s sprints cycling against 0.075 kg kg-1 body mass (BM); each of the five sprints was separated by 5 min passive seated recovery. Three days separated the VO2 max test and first interval test, while a further 3 days elapsed between the first and second interval tests. Ninety minutes prior to each interval test, the subjects consumed either a solution of sodium citrate (0.5 g kg-1BM) or a placebo solution (1 g of calcium carbonate and 4 mg of sodium chloride). These were randomly administered in a double-blind crossover procedure so that every subject consumed each solution prior to the interval test over the 6 day period. Measured of work, VE, VO2, VCO2, post-exercise plasma lactate, and changes in both venous blood pH and venous blood bicarbonate (HCO3) were measured during each interval test. Although analysis of variance failed to identify differences in performance between the two solutions, both exercise VCO2 and changes in venous blood HCO3 were higher in the citrate condition (P less than 0.05). In addition, both peak post-exercise plasma lactate concentrations and post-exercise venous blood pH were significantly higher following citrate ingestion. Although these data are consistent with greater clearance of lactate and H plus from the active muscle cells following citrate ingestion, performance between the two trials was the same. Nausea experienced by all but one subject following citrate ingestion emerged as the most likely factor negating the ergogenic potential of the sodium citrate. The data have shown that citrate ingested prior to five 60 s sprints induced significant changes in selected ventilatory and blood variables but failed to influence work output.
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