Time Course of Blood Bicarbonate and pH Three Hours After Sodium Bicarbonate Ingestion

2008 ◽  
Vol 3 (2) ◽  
pp. 240-242 ◽  
Author(s):  
Michael J. Price ◽  
Malkit Singh

This study examined the increase in blood pH and bicarbonate concentration after ingestion of a standard sodium bicarbonate solution. Peak blood pH and bicarbonate concentration occurred between 60 and 90 minutes. Values decreased over the remainder of the ingestion period although still elevated above preingestion levels.

2021 ◽  
Author(s):  
Josh W Newbury ◽  
Matthew Cole ◽  
Adam L Kelly ◽  
Richard J Chessor ◽  
Andy Sparks ◽  
...  

Background: Contemporary research suggests that the optimal timing of sodium bicarbonate (NaHCO 3 ) should be based upon an individual time in which bicarbonate (HCO 3 – ) or pH peaks within the blood. However, the mechanisms surrounding acidosis on exercise performance are contested, therefore it is plausible that the ergogenic effects of NaHCO 3 are instead a result of an increased strong ion difference (SID) following ingestion. Since the post-ingestion time course of the SID is currently unknown, the purpose of this study was to investigate the pharmacokinetics of the SID in direct comparison to HCO 3 – and pH. Methods: Twelve highly trained, adolescent swimmers (age: 15.9 ± 1.0 yrs, body mass: 65.3 ± 9.6 kg) consumed their typical pre-competition nutrition before ingesting 0.3 g?kg BM -1 NaHCO 3 in gelatine capsules. Capillary blood samples were then taken during quiet, seated rest on nine occasions (0, 60, 75, 90, 105, 120, 135, 150, and 165 min post-ingestion) for the assessment of time course changes in HCO 3 – , pH, and the SID. Results: On a group mean level, no differences were found in the time in which each variable peaked within the blood (HCO 3 – = 130 ± 35 min, pH = 120 ± 38 min, SID = 96 ± 35 min; p = 0.06). A large effect size was calculated between the timing of peak HCO 3 – and the SID  ( g = 0.91), however, suggesting that a difference may occur between these two measures in practice. Conclusions: A time difference between peak HCO 3 – and the SID presents an interesting avenue for further research since an approach based upon individual increases in extracellular SID has yet to be investigated. Future studies should therefore compare these dosing strategies directly to elucidate whether either one is more ergogenic for exercise performance.


PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0248456
Author(s):  
Josh W. Newbury ◽  
Matthew Cole ◽  
Adam L. Kelly ◽  
Richard J. Chessor ◽  
S. Andy Sparks ◽  
...  

The timing of sodium bicarbonate (NaHCO3) supplementation has been suggested to be most optimal when coincided with a personal time that bicarbonate (HCO3–) or pH peaks in the blood following ingestion. However, the ergogenic mechanisms supporting this ingestion strategy are strongly contested. It is therefore plausible that NaHCO3 may be ergogenic by causing beneficial shifts in the strong ion difference (SID), though the time course of this blood acid base balance variable is yet to be investigated. Twelve highly trained, adolescent swimmers (age: 15.9 ± 1.0 years, body mass: 65.3 ± 9.6 kg) consumed their typical pre-competition nutrition 1–3 hours before ingesting 0.3 g∙kg BM-1 NaHCO3 in gelatine capsules. Capillary blood samples were then taken during seated rest on nine occasions (0, 60, 75, 90, 105, 120, 135, 150, 165 min post-ingestion) to identify the time course changes in HCO3–, pH, and the SID. No significant differences were found in the time to peak of each blood measure (HCO3–: 130 ± 35 min, pH: 120 ± 38 min, SID: 98 ± 37 min; p = 0.08); however, a large effect size was calculated between time to peak HCO3– and the SID (g = 0.88). Considering that a difference between time to peak blood HCO3– and the SID was identified in adolescents, future research should compare the ergogenic effects of these two individualized NaHCO3 ingestion strategies compared to a traditional, standardized approach.


1983 ◽  
Vol 245 (4) ◽  
pp. F433-F442 ◽  
Author(s):  
D. C. Batlle ◽  
K. Itsarayoungyuen ◽  
M. Downer ◽  
R. Foley ◽  
J. A. Arruda ◽  
...  

This study examined urinary acidification shortly after recovery from chronic hypocapnia induced by hypoxemia. Distal acidification was evaluated by measuring the urinary PCO2 and urine-blood PCO2 difference (U-B PCO2) when blood PCO2 had returned to normal. In posthypocapnic rats, maximal alkalinization of the urine by acute sodium bicarbonate loading failed to increase urine PCO2 and U-B PCO2 to the level of posthypoxemic control rats and normal control rats with comparable blood pH and urine bicarbonate concentration. To test the hypothesis that decreased distal hydrogen ion secretion in posthypocapnic rats resulted from intracellular alkalosis secondary to protracted hypocarbia, posthypocapnic rats were exposed to hypercapnia of brief duration (30 min) and prolonged duration (120 min) in an attempt to restore distal acidification to normal. In posthypocapnic rats, hypercapnia of brief duration was associated with a significant increase in urine PCO2 and a fall in urine pH. Prolonged hypercapnia resulted in a marked increase in urine PCO2 and a further fall in urine pH. At any urinary bicarbonate concentration, however, the urine PCO2 and U-B PCO2 posthypocapnic rats exposed to hypercapnia were still significantly lower than in normal control rats identically subjected to prolonged hypercapnia and with comparable blood PCO2 and blood pH. Our findings indicate that distal acidification after abrupt recovery from chronic hypocapnia is decreased as if the kidneys were still under the influence of sustained hypocapnia. These findings could not be ascribed to extracellular alkalemia but could be explained by postulating that decreased urinary acidification resulted from persistence of cell alkalinity secondary to the accumulation of non-CO2 buffers generated during protracted hypocarbia. Alternatively, factors other than cell pH could mediate the adaptive decrease in distal hydrogen ion secretion of posthypocapnic rats.


2014 ◽  
Vol 1058 ◽  
pp. 213-216 ◽  
Author(s):  
Guang Xu ◽  
Jin Hu ◽  
Yu Tian Wang

Iridium trichloride hydrate and acetyl acetone were used as raw materials, Tris – acetylacetonate - iridium (III) was synthesis by the method of solutions - precipitating method. Composition and structure of obtained organic complex were investigated by means of Elemental Analysis, IR, 1HNMR and UV-vis. Effect of sodium bicarbonate solution concertation on the synthesis yield also been studied. The results demonstrated that two oxygen atoms in acetyl acetone form chelated hexatomic ring with iridium ions. The highest yield was 19.9% when the concentration of sodium bicarbonate was 0.56mol/l.


2012 ◽  
Vol 7 (2) ◽  
pp. 152-160 ◽  
Author(s):  
Amelia J. Carr ◽  
Gary J. Slater ◽  
Christopher J. Gore ◽  
Brian Dawson ◽  
Louise M. Burke

Purpose:The aim of this study was to determine the effect and reliability of acute and chronic sodium bicarbonate ingestion for 2000-m rowing ergometer performance (watts) and blood bicarbonate concentration [HCO3−].Methods:In a crossover study, 7 well-trained rowers performed paired 2000-m rowing ergometer trials under 3 double-blinded conditions: (1) 0.3 grams per kilogram of body mass (g/kg BM) acute bicarbonate; (2) 0.5 g/kg BM daily chronic bicarbonate for 3 d; and (3) calcium carbonate placebo, in semi-counterbalanced order. For 2000-m performance and [HCO3−], we examined differences in effects between conditions via pairwise comparisons, with differences interpreted in relation to the likelihood of exceeding smallest worthwhile change thresholds for each variable. We also calculated the within-subject variation (percent typical error).Results:There were only trivial differences in 2000-m performance between placebo (277 ± 60 W), acute bicarbonate (280 ± 65 W) and chronic bicarbonate (282 ± 65 W); however, [HCO3−] was substantially greater after acute bicarbonate, than with chronic loading and placebo. Typical error for 2000-m mean power was 2.1% (90% confidence interval 1.4 to 4.0%) for acute bicarbonate, 3.6% (2.5 to 7.0%) for chronic bicarbonate, and 1.6% (1.1 to 3.0%) for placebo. Postsupplementation [HCO3−] typical error was 7.3% (5.0 to 14.5%) for acute bicarbonate, 2.9% (2.0 to 5.7%) for chronic bicarbonate and 6.0% (1.4 to 11.9%) for placebo.Conclusion:Performance in 2000-m rowing ergometer trials may not substantially improve after acute or chronic bicarbonate loading. However, performances will be reliable with both acute and chronic bicarbonate loading protocols.


2021 ◽  
Vol 26 (2) ◽  
pp. 137-143
Author(s):  
S. N. Gromova ◽  
N. A. Guzhavina ◽  
E. A. Falaleeva ◽  
E. P. Kolevatykh ◽  
А. V. Elikov ◽  
...  

Relevance. A wide variety of oral care products is available nowadays. Sometimes aggressive advertising rather than doctor’s advice determines our patients’ choice. In our research, we provide evidence of the clinical use of toothpaste containing fluoride and sodium bicarbonate.Materials and methods. During four weeks, we followed up a group of students who used the toothpaste containing 1400 ppm fluoride and 67% aqueous sodium bicarbonate solution. The clinical, biochemical and microbiological tests and saliva crystallization score assessed the characteristics stated by the manufacturer.Results. The statistically significant correlation between all studied criteria is evidence of the effectiveness of the toothpaste. In addition to the significant remineralization and antiplaque effect, biochemical and microbiological tests confirmed the anti-inflammatory effect of the toothpaste. An immediate cleaning effect was observed after the first brushing as well as in long-term use.Conclusion. Improvement of oral hygiene indices and reduction of periodontal inflammation confirmed the successful result of the comprehensive treatment of chronic gingivitis.


2016 ◽  
Vol 41 (4) ◽  
pp. 354-361 ◽  
Author(s):  
Matthew F. Higgins ◽  
Susie Wilson ◽  
Cameron Hill ◽  
Mike J. Price ◽  
Mike Duncan ◽  
...  

This study evaluated the effects of ingesting sodium bicarbonate (NaHCO3) or caffeine individually or in combination on high-intensity cycling capacity. In a counterbalanced, crossover design, 13 healthy, noncycling trained males (age: 21 ± 3 years, height: 178 ± 6 cm, body mass: 76 ± 12 kg, peak power output (Wpeak): 230 ± 34 W, peak oxygen uptake: 46 ± 8 mL·kg−1·min−1) performed a graded incremental exercise test, 2 familiarisation trials, and 4 experimental trials. Trials consisted of cycling to volitional exhaustion at 100% Wpeak (TLIM) 60 min after ingesting a solution containing either (i) 0.3 g·kg−1 body mass sodium bicarbonate (BIC), (ii) 5 mg·kg−1 body mass caffeine plus 0.1 g·kg−1 body mass sodium chloride (CAF), (iii) 0.3 g·kg−1 body mass sodium bicarbonate plus 5 mg·kg−1 body mass caffeine (BIC-CAF), or (iv) 0.1 g·kg−1 body mass sodium chloride (PLA). Experimental solutions were administered double-blind. Pre-exercise, at the end of exercise, and 5-min postexercise blood pH, base excess, and bicarbonate ion concentration ([HCO3−]) were significantly elevated for BIC and BIC-CAF compared with CAF and PLA. TLIM (median; interquartile range) was significantly greater for CAF (399; 350–415 s; P = 0.039; r = 0.6) and BIC-CAF (367; 333–402 s; P = 0.028; r = 0.6) compared with BIC (313: 284–448 s) although not compared with PLA (358; 290–433 s; P = 0.249, r = 0.3 and P = 0.099 and r = 0.5, respectively). There were no differences between PLA and BIC (P = 0.196; r = 0.4) or between CAF and BIC-CAF (P = 0.753; r = 0.1). Relatively large inter- and intra-individual variation was observed when comparing treatments and therefore an individual approach to supplementation appears warranted.


1977 ◽  
Vol 69 (1) ◽  
pp. 173-185
Author(s):  
C. M. Wood ◽  
B. R. McMahon ◽  
D. G. McDonald

Exhausting activity results in a marked and immediate drop in blood pH which gradually returns to normal over the following 6h. The acidosis is caused largely by elevated Pco2 levels, which vary inversely with pH. Blood lactate concentration increases slowly, reaching a maximum at 2--4h post-exercise, and contributes significantly to the acidosis only late in the recovery period. The slow time course of lactic acid release into the blood permits temporal separation of the peak metabolic acidosis from the peak respiratory acidosis. Evidence is presented that a metabolic acid other than lactic also makes a modest contribution to the pH depression during the recovery period.


1988 ◽  
Vol 255 (4) ◽  
pp. F690-F698 ◽  
Author(s):  
R. J. Roman ◽  
M. L. Kaldunski ◽  
A. G. Scicli ◽  
O. A. Carretero

The influence of kinins and angiotensin II on the regulation of renal cortical and papillary blood flow and sodium and water excretion was examined in rats. Superficial cortical and papillary blood flows were measured using a laser-Doppler flowmeter. Papillary blood flow increased 50% after enalaprilat (60 micrograms/kg) and phosphoramidon (5.5 micrograms.kg-1.min-1) were given along with 0.3 M sodium bicarbonate solution to inhibit degradation of kinins and enhance urinary kallikrein activity. Infusion of a kinin antagonist, D-Arg-Hyp-Thi-D-Phe-bradykinin (5 micrograms/min), returned papillary blood flow to control levels. Urine flow and sodium excretion increased after the administration of the kininase inhibitors and sodium bicarbonate, while glomerular filtration rate (GFR) and outer cortical blood flow were unaltered. The kinin antagonist did not alter sodium and water excretion in rats receiving the kininase inhibitors and bicarbonate. Administration of the kinin antagonist alone lowered papillary blood flow by 20%, without affecting outer cortical blood flow or GFR. Urine flow decreased and urine osmolality increased after the rats received the kinin antagonist, but sodium excretion remained unaltered. To assess the role of angiotensin II in the control of papillary blood flow, kinin receptors were blocked by infusion of an antagonist, and the effects of enalaprilat and saralasin were studied. Papillary blood flow increased after blockade of the angiotensin II system in rats receiving the kinin antagonist. These results indicate that the kallikrein-kinin and renin-angiotensin systems participate in the regulation of papillary blood flow.


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