NaHCO3 Ingestion Research Articles

1086 EFFECT OF SODIUM BICARBONATE INGESTION ON EXHAUSTIVE RESISTANCE EXERCISE PERFORMANCE

Six weight trained males were studied prior to, during, and in recovery from exhaustive resistance exercise, 105 min after ingesting 300 mg.kg-1 of either a placebo or NaHCO3. The exercise test consisted of four sets of 12 repetitions with a fifth set to volitional fatigue on a Universal leg press machine at a resistance equaling approximately 70% of the subjects 1-repetition maximum. Arterialized venous blood was analyzed for lactate concentration, blood gas, and acid-base parameters. The ingestion of NaHCO3 produced a significant increase in resting pH (7.39 to 7.46), HCO3- (22.9 to 28.3 mEq.l-1), and oxygenated base excess (-1.3 to 4.4 mEq.l-1). With the completion of each exercise set, a progressive decline in the acid-base status of both groups was observed (pH set 1-5: NaHCO3, 7.40 to 7.31; placebo, 7.34 to 7.25; HCO3- set 1-5: NaHCO3, 25.3 to 17.9; placebo, 21.7 to 15.3 mEq.l-1; base excess set 1-5: NaHCO3, 3.7 to -7.1; placebo, -1.4 to -10.7 mEq.l-1); however, the NaHCO3 condition was significantly more alkaline than the placebo condition. Blood lactate concentration [La] progressively increased with the completion of each exercise set ([La] set 1-5: NaHCO3, 1.37 to 11.15; placebo, 1.31 to 9.81 mM); but were not significantly different between treatments. Repetitions performed in the final exercise set were not significantly different between groups (NaHCO3: 19.6 +/- 1.6, placebo: 18.2 +/- 1.1 repetitions).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sodium bicarbonate ingestion on anaerobic performance: a meta-analytic review.

Many researchers have investigated the effects of induced metabolic alkalosis, by ingestion of sodium bicarbonate, on anaerobic exercise performance. But the results have been inconsistent and often contradictory. The purpose of this review was to synthesize the varied findings using a meta-analytic approach. Twenty-nine investigations met our inclusion criteria. Results show that NaHCO3 ingestion clearly results in a more alkaline extracellular environment. The dosage, however, was only moderately related to the increase in pH and HCO3-. Overall, performance was enhanced but the range of effect sizes was large, -0.12 to 2.87. In studies that measured time to exhaustion, there was a mean 27 +/- 20% increase in duration. The treatment effect, however, was only weakly related to the degree of induced alkalosis. But in comparing the 19 studies that showed a positive treatment effect with the 16 that showed no effect, the former were associated with a greater increase in pH following ingestion of a somewhat larger dosage, and a greater decrease in pH with exercise.

Effect of acute sodium bicarbonate ingestion on excess CO2 output during incremental exercise.

The effect of bicarbonate ingestion on total excess volume of CO2 output (CO2 excess), due to bicarbonate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g.kg-1 body mass) of CaCO3 (control) and NaHCO3 (alkalosis). The resting arterialized venous blood pH (P < 0.05) and bicarbonate concentration ([HCO3-]b; P < 0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO3-]b, 29.4 (SD 1.5) mmol.l-1] than in the control [pH, 7.39 (SD 0.03); [HCO3-]b, 25.5 (SD 1.0) mmol.l-1]. The blood lactate concentrations ([la-]b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la-]b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol.l-1, P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol.l-1, P < 0.05] were found in AMA compared with the control. The CO2 excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml; P < 0.05]. The CO2 excess per body mass was found to be significantly correlated with both the increase of [la-]b from rest to 3 min after exercise (delta[la-]b; r = 0.926, P < 0.001) and with the decrease of [HCO3-]b from rest to 3 min after exercise (delta [HCO3-]b; r = 0.872, P < 0.001), indicating that CO2 excess per body mass increased linearly with both delta [la-]b and delta [HCO3-]b.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of metabolic alkalosis upon exercise metabolism in the thoroughbred horse

Six thoroughbred horses exercised on a motorised treadmill on two separate occasions at a speed of 11 or 12 m.s-1 for up to 2 min. 4 h prior to exercise each horse was given a 21 test solution of sodium bicarbonate (NaHCO3; 0.6 g.kg-1 body mass) or a control solution of water by nasogastric intubation, the order of administration of the two solutions was randomised. Blood samples (n = 15) were obtained before and during the 4 h after intubation, during exercise and for 30 min after exercise. NaHCO3 ingestion resulted in changes in pre-exercise acid-base status. The changes in blood lactate and base excess with exercise were greater after NaHCO3 administration; after 1 min of exercise in the case of lactate (P less than 0.05) and immediately after exercise in the case of base excess (P less than 0.05). Plasma ammonia levels were lower during (P less than 0.05) and immediately after (P less than 0.05) exercise following NaHCO3 ingestion. The peak change in plasma ammonia with exercise was also lower after NaHCO3 ingestion (P less than 0.05). Following exercise after NaHCO3 ingestion, five horses demonstrated lower muscle adenosine 5-triphosphate loss (P less than 0.05) and inosine 5-monophosphate formation (P = 0.05) and higher glycerol 3-phosphate formation (P less than 0.05). There is evidence to suggest that metabolic alkalosis may delay the onset of fatigue by decreasing the extent of adenine nucleotide loss during high-intensity exercise.

Effect of induced alkalosis on physical work capacity during arm and leg exercise.

The effect of NaHCO3 ingestion on work capacity was determined during moderately high intensity (80% [Vdot]O2 max) arm and leg exercise. Differences in the ergogenic effect of induced alkalosis between arm and leg exercise were also evaluated. Ten males underwent work capacity tests in three standardized modes; arms (A), Legs (L) and Arms + Legs (A + L). The head, chest and trunk were harnessed to a stabilizing backboard. Two hours prior to testing, subjects ingested 0·3 g kg−1 body weight of either NaHCO3 to induce alkalosis or CaCO3 as a placebo control. The six exercise trials were administered with a double blind design in counterbalanced order. Under alkalosis, work capacity increased (P<0·01) by 286 kg m for A, 1132kg m for L and 920 kg m for A + L. The magnitude of the increase in work capacity following induced alkalosis was greater for the A (13·20%) (P<0·05) and A + L (13·60%) (P<0·01) than the L (9·95%) modes. Differences were not found between the A and A + L modes. Blood acid-base and haemato...

Lowered cerebrospinal fluid sodium antagonizes effect of raised blood sodium on salt appetite.

Moderately Na-deficient sheep (i.e., Na deficit = 300-400 mmol) will correct their deficit when given hypertonic NaHCO3 solution to drink. Access to NaHCO3 was provided by bar press for 2 h only each day following 22 h of salivary loss from a parotid fistula. Each delivery by bar press provided 9 mmol of NaHCO3 and, of the 46.3 +/- 2.5 deliveries made and drunk in 2 h, 80-90% were made in the first 20 min. Ten minutes before access to NaHCO3 commenced an intracarotid infusion of 4 M NaCl at 1.6 ml/min for 30 min was initiated. This infusion reduced intake by approximately 80% and increased both plasma and cerebrospinal fluid sodium concentration (CSF[Na]). Intraventricular (ivt) infusion of 0.7 M mannitol in artificial CSF at 1 ml/h for 3 h begun 1 h before access to Na by bar press lowered CSF[Na] and approximately doubled voluntary Na intake. The combination of the two procedures resulted in NaHCO3 intake similar to base line. That is, the ivt infusion of 0.7 M mannitol counteracted the inhibition of Na appetite produced by the systemic infusion of hypertonic NaCl, and this was associated with attenuation of the effect of the systemic 4 M NaCl infusion on CSF[Na]. The results suggest that the effects of both the ivt and the systemic infusions are mediated via the same sensor system located within the neuropil.

Effect of acute induced metabolic alkalosis on 800-m racing time.

Six trained middle-distance runners wer studied under alkalotic (NaHCO3 ingestion), placebo (CaCO3 ingestion), and control conditions to determine the effect of an acute induced metabolic alkalosis on time to run an 800-m race. Pre-exercise, following NaHCO3 ingestion, pH and standard [HCO3-] were significantly higher. In the alkalotic condition, subjects ran faster (2.9 s) and the corresponding post-exercise values for blood [lactate] and extracellular H+ were higher than in the control and placebo conditions, suggesting an increased anaerobic energy contribution. These results support the speculation that the increase in extracellular buffering following NaHCO3 ingestion facilitated H+ efflux from the cells of working muscle, thereby delaying the decrease in intracellular pH and postponing fatigue. It is concluded that the ingestion of NaHCO3 by trained middle-distance runners prior to an 800-m race has an ergogenic benefit.

Consumption of sodium bicarbonate in water by steers fed varied all-concentrate diets.

Three experiments were conducted with rumen-fistulated Hereford steers fed all-concentrate diets in drylot with no bedding. Water containing NaHCO3 offered free choice together with untreated water was consumed in quantities equivalent to 10-day intakes of from 38 to 1852 gm. of NaHCO3 per steer among the different diets. After correction for temperature effects, significant (P<.05) differences in NaHCO3 intake occurred among the diets. In experiment 1, the lowest intake occurred on a diet which contained added NaHCO3; in experiment 2, the lowest intake occurred on a diet in which urea was the sole source of supplemental nitrogen; and in experiment 3, the lowest intake occurred on a diet which contained 5% molasses.

Ventilatory response to hypoxia and CO2 following CO2 exposure and NaHCO3 ingestion.

ArticleVentilatory response to hypoxia and CO2 following CO2 exposure and NaHCO3 ingestion.K H Falchuk, T W Lamb, and S M TenneyK H Falchuk, T W Lamb, and S M TenneyPublished Online:01 Mar 1966https://doi.org/10.1152/jappl.1966.21.2.393MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByVentilatory and integrated physiological responses to chronic hypercapnia in goats14 October 2018 | The Journal of Physiology, Vol. 596, No. 22A valiação da função respiratória na Síndrome de Apneia Obstrutiva do SonoRevista Portuguesa de Pneumologia, Vol. 2, No. 4-5Nasal Continuous Positive Airway Pressure in Decompensated Hypercapnic Respiratory Failure as a Complication of Sleep ApneaChest, Vol. 104, No. 3Effects of H+ versus CO2 on ventilation in the Pekin duckRespiration Physiology, Vol. 68, No. 2Integration of Respiratory Responses to Changes in Alveolar Partial Pressures of CO2 and O 2 and in Arterial pH1 January 2011Controversies in sleep-related breathing disordersLung, Vol. 164, No. 1Effect of perinatal hypercapnia on the adult ventillatory response to carbon dioxideRespiration Physiology, Vol. 57, No. 3Tests of ventilatory controlRESPIRATORY CONTROL IN CHRONIC OBSTRUCTIVE PULMONARY DISEASESClinics in Chest Medicine, Vol. 1, No. 1Severe hypercapnia associated with a non-respiratory alkalosisBritish Journal of Diseases of the Chest, Vol. 72Bicarbonate and the regulation of ventilationThe American Journal of Medicine, Vol. 57, No. 3Severe Hypercapnia Associated With Metabolic Alkalosis Due to Pyloric Stenosis25 March 2008 | Australian and New Zealand Journal of Medicine, Vol. 4, No. 4Comparison of three methods for quantitating respiratory response to hypoxia in manRespiration Physiology, Vol. 16, No. 1Development of the chemical control of breathing in the Virginia opossumRespiration Physiology, Vol. 14, No. 3ACID-BASE DIAGRAMSThe Lancet, Vol. 298, No. 7716Control of breathing in experimental anemiaRespiration Physiology, Vol. 10, No. 3Allgemeine Pathophysiologie der AtmungEffect of intravenous NaHCO3 on ventilation and gas exchange in normal manRespiration Physiology, Vol. 4, No. 2Carotid bodies, stimulus interaction, and ventilatory control in unanesthetized goatsRespiration Physiology, Vol. 1, No. 2 More from this issue > Volume 21Issue 2March 1966Pages 393-8 https://doi.org/10.1152/jappl.1966.21.2.393PubMed5934441History Published online 1 March 1966 Published in print 1 March 1966 Metrics

Respiration and cerebrospinal fluid pH in metabolic acidosis and alkalosis.

An acute base deficit of 5 mm/liter (metabolic acidosis) was induced in one normal man by an initial oral dose of 20 g NH4Cl and sustained for 5 days by administering 3 g every 6 hr. pHa (arterial) decreased from 7.42 to 7.34 in 4 hr. Ve (minute ventilation) increased from 6.2 to 8.4 liters/min, PaCOCO2 decreased from 40 to 37 mm Hg, CSF pH increased from 7.32 to 7.34, and the CO2 response curve shifted –2.8 mm Hg Pco2 without slope change. At 24 hr, CSF pH was 7.32, with CSF Pco2 and HCO3 – reduced to 42 mm Hg and 21.0 mEq/liter, respectively (control 49 mm Hg, 24 mEq/liter). Ve increased to 9.8 liters/min, arterial pH increased to 7.37, PaCOCO2 fell to 36 mm Hg, and the CO2 response curve was –5.0 mm Hg from control. After 6 days of acidosis, acute increase in pHa to 7.45 in 2 hr by NaHCO3 ingestion decreased Ve to 6.8 liters/min, increased PaCOCO2 to 39 mm Hg, decreased CSF pH to 7.30, and shifted the CO2 response curve back to control. Results of this study are consistent with the hypothesis that the peripheral chemoreceptors initiate and sustain alterations in Ve in metabolic abnormalities in the following manner: 1) acute acidosis increases Ve by stimulating the peripheral chemoreceptors; 2) the PaCOCO2 falls and CSF pH increases, decreasing medullary (H+) chemoreceptor activity; and 3) active transport across the blood-CSF barrier restores CSF pH and the medullary (H+) chemoreceptor activity to normal, causing a further increase in ventilation that partially compensates for the metabolic acidosis. medullary respiratory chemoreceptors; peripheral chemoreceptors; blood-brain barrier; active transport Submitted on July 27, 1964