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PubMed2004

Metabolic effects of induced alkalosis during progressive forearm exercise to fatigue.

Metabolic alkalosis induced by sodium bicarbonate (NaHCO(3)) ingestion has been shown to enhance performance during brief high-intensity exercise. The mechanisms associated with this increase in performance may include increased muscle phosphocreatine (PCr) breakdown, muscle glycogen utilization, and plasma lactate (Lac(-)(pl)) accumulation. Together, these changes would imply a shift toward a greater contribution of anaerobic energy production, but this statement has been subject to debate. In the present study, subjects (n = 6) performed a progressive wrist flexion exercise to volitional fatigue (0.5 Hz, 14-21 min) in a control condition (Con) and after an oral dose of NaHCO(3) (Alk: 0.3 g/kg; 1.5 h before testing) to evaluate muscle metabolism over a complete range of exercise intensities. Phosphorus-31 magnetic resonance spectroscopy was used to continuously monitor intracellular pH, [PCr], [P(i)], and [ATP] (brackets denote concentration). Blood samples drawn from a deep arm vein were analyzed with a blood gas-electrolyte analyzer to measure plasma pH, Pco(2), and [Lac(-)](pl), and plasma [HCO(3)(-)] was calculated from pH and Pco(2). NaHCO(3) ingestion resulted in an increased (P < 0.05) plasma pH and [HCO(3)(-)] throughout rest and exercise. Time to fatigue and peak power output were increased (P < 0.05) by approximately 12% in Alk. During exercise, a delayed (P < 0.05) onset of intracellular acidosis (1.17 +/- 0.26 vs. 1.28 +/- 0.22 W, Con vs. Alk) and a delayed (P < 0.05) onset of rapid increases in the [P(i)]-to-[PCr] ratio (1.21 +/- 0.30 vs. 1.30 +/- 0.30 W) were observed in Alk. No differences in total [H(+)], [P(i)], or [Lac(-)](pl) accumulation were detected. In conclusion, NaHCO(3) ingestion was shown to increase plasma pH at rest, which resulted in a delayed onset of intracellular acidification during incremental exercise. Conversely, NaHCO(3) was not associated with increased [Lac(-)](pl) accumulation or PCr breakdown.

Adenosine Triphosphatases↗
PubMed2002

Characterisation of the calcium paradox in the isolated perfused pigeon heart: protection by hypothermia, acidosis and alkalosis.

The aim of the present investigation was to examine the conditions inducing a calcium paradox in the isolated perfused pigeon heart. Loss of mechanical and electrical activity, creatine phosphokinase and total protein release were used to define cell damage. Perfusion was performed at 36, 38, 40 and 42 degrees C and calcium deprivation lasted 5, 10, 20 or 40 min. At low temperatures even prolonged calcium depletion failed to induce a calcium paradox. After a 40 min calcium depletion at normal body temperature (42 degrees C) ventricular activity ceased and a major contraction occurred followed by an increase in resting tension. During the 20-min reperfusion period the release of creatine phosphokinase was 267.18 +/- 0.8 IU/g of dry wt and the total amount of protein loss was 109.3 +/- 1.0 mg/g of dry wt, while lower temperatures resulted in a decreased loss of protein and creatine phosphokinase. Using two different Tyrode's perfusion buffers instead of normal bicarbonate ones, a protection of the pigeon heart against the induction of this phenomenon was observed. Furthermore, acidosis as well as alkalosis protected the heart as estimated by the significant recovery of electromechanical activity, and the quite low total protein and creatine phosphokinase losses. The results of this study suggest that the basic mechanisms and damaging effects of calcium overloading are common in mammalian and pigeon hearts.

Acidosis↗
PubMed2002

Electrocardiographic QT prolongation and sudden death in renal hypokalemic alkalosis.

A 3-year-old boy was found to have a mixed tubulopathy with hypokalemia (1.9 mmol/l), alkalosis (blood pH 7.51, plasma carbon dioxide pressure 46 mm Hg, plasma bicarbonate 35.7 mmol/l) and hypophosphatemia (1.21 mmol/l). An electrocardiogram disclosed a prolonged heart rate corrected QT interval of 490 ms. The boy was put on potassium chloride, phosphate and nonsteroidal anti-inflammatory agents. With this treatment plasma phosphate normalized and plasma potassium increased up to 3.0-3.3 mmol/l. Three years later the child, who did not have history of gastroesophageal reflux or epileptic convulsions, suddenly died during sleep. The cause of death could not be determined through gross examination of the body. The history of hypokalemia, the QT-prolongation, the sudden death and the failure to assess the cause of death through gross examination of the body suggest that death was caused by an arrhythmia secondary to hypokalemia.

Alkalosis↗
PubMed1983

Stereological-ultrastructural study of pancreatic B cells in metabolic alkalosis.

The secretion of insulin in response to glucose and the changes in the B cell at the ultrastructural level were studied in rat pancreas perfused at pH 7.4 and 7.8 with different concentrations of glucose. Raising the extracellular pH from 7.4 to 7.8 significantly inhibits glucose-induced insulin secretion. Coincidentally, morphometric studies showed significant evidences of low secretory activity in B cells from pancreas submitted to high glucose stimulation under alkalosis, namely lower number of emiocytotic figures and microtubules as well as a decrease in the volume density of the granular endoplasmic reticulum and the Golgi complex. On the other hand, a significant increment in the number of images of granulolysis was also demonstrated. These secretory and ultrastructural results confirm the inhibitory effect of pH 7.8 upon B cell secretory activity induced by glucose. Moreover, they lend further support to the role of intracellular hormone degradation as a regulator of B cell insulin content.

Alkalosis↗
PubMed1989

Acute metabolic alkalosis during haemodialysis.

A 32-year-old woman developed acute metabolic alkalosis during haemodialysis due to dialysate with a very high bicarbonate concentration. This was subsequently discovered to have been caused by the reversed connection of bicarbonate and acid concentrate containers to the entry ports of the Monitral 'S' machine and to failure of the pH meter. Recommendations are made to prevent this potentially fatal accident.

Acute Disease↗
PubMed1996

Relative role of alkalosis and sodium ions in reversal of class I antiarrhythmic drug-induced sodium channel blockade by sodium bicarbonate.

BACKGROUND: Hypertonic sodium salts are used to treat sodium channel-blocking drug cardiotoxicity. The relative roles of alkalinization and increased sodium concentration ([Na+]o) for various drugs are incompletely known. METHODS AND RESULTS: The effects of four class I drugs on action potential characteristics of canine Purkinje fibers at equieffective concentrations (disopyramide 30 mumol/L, mexiletine 80 mumol/L, flecainide 7 mumol/L, imipramine 5 mumol/L) were studied in the presence of normal Tyrode solution and one altered solution (increased [Na+]o, increased bicarbonate concentration, or both) in each experiment. Combined increases in sodium and bicarbonate concentration significantly reduced the depressant effects of flecainide, imipramine, and mexiletine on phase 0 upstroke (Vmax) but did not alter the effects of disopyramide. The effects of sodium bicarbonate were entirely due to alkalinization in the case of imipramine, but both alkalinization and increased [Na+]o contributed to the interaction with flecainide and mexiletine. The reversal of Vmax depression by increased [Na+]o and pH was due in part to hyperpolarization. In addition, alkalosis directly reversed the hyperpolarizing shift in Vmax inactivation caused by flecainide and imipramine without altering the shift caused by disopyramide and mexiletine. CONCLUSIONS: Increases in sodium bicarbonate concentration reverse the effects of class I antiarrhythmic drugs to a varying extent, with drug-specific contributions of the sodium and bicarbonate moiety. The molecular basis for this drug specificity remains to be elucidated, but it has important potential implications for the use of hypertonic sodium salts to treat cardiotoxicity caused by sodium channel-blocking drugs.

Alkalosis↗
PubMed1985

Effect of mechanical ventilator mode on tendency towards respiratory alkalosis.

The question whether assist-control ventilation (A/C) results in more frequent or more severe respiratory alkalosis than intermittent mandatory ventilation (IMV) is often raised. We prospectively compared the respiratory rates and arterial blood tensions of 18 critically ill patients with respiratory failure of diverse causes who were mechanically ventilated for 1 h with each of these ventilatory modes. Each patient served as his own control. We found that after 1 h of IMV the average pH was 7.42 +/- 0.2 (mean +/- SEM), after 1 h of A/C the pH was 7.45 +/- 0.01 (p less than 0.005), the average PaCO2 during IMV was 40.7 +/- 1.8, the average PaCO2 during A/C was 37.9 +/- 1.6 (p less than 0.001), the average respiratory rate during IMV was 21 +/- 2.0, and the average respiratory rate during A/C was 15 +/- 2.0 (p less than 0.001). One patient became alkalemic (pH 7.55) during A/C. These pH and PaCO2 changes were not associated with any adverse clinical sequelae. We conclude that the responsible physician should be guided by factors other than control of pH in choosing the mode of mechanical ventilation for most patients.

Adult↗
PubMed1972

The effects of acidosis and alkalosis on the metabolism of glutamine and glutamate in renal cortex slices.

Studies of the metabolism of glutamine and glutamate by renal cortex slices from acidotic, alkalotic, and control rats were performed. 88-95% of the glutamine and 104-115% of the glutamate taken up from the medium could be accounted for by the products found. Acidosis increased glutamine uptake and conversion to ammonia, CO(2), glucose, lactate, pyruvate, lipid, and protein. The increase in glutamine conversion to ammonia after acidosis could be completely accounted for by the associated increase in its conversion to glucose, glutamate, lactate, and pyruvate. When glutamate metabolism was examined, acidosis did not affect substrate uptake but did increase its conversion to ammonia, glucose, lactate, CO(2), and lipid. The increase in (14)CO(2) from U-(14)C-glutamine and U-(14)C-glutamate found with cortex slices from acidotic animals could be explained by the CO(2) production calculated to be associated with the enhanced conversion of these substrates to other products during acidosis. (14)CO(2) production from 1.2-(14)C-acetate was found to be significantly increased in alkalosis rather than acidosis. These studies suggest that in the rat, the rate at which glutamine is completely oxidized in the Krebs cycle is not a factor regulating renal ammonia production. A comparison of the effects of acidbase status on glutamine and glutamate metabolism suggests that either glutamine transport or glutamine transaminase activity are significantly increased by acidosis.

Acidosis↗
PubMed1984

Segmental chloride and fluid handling during correction of chloride-depletion alkalosis without volume expansion in the rat.

To determine whether chloride-depletion metabolic alkalosis (CDA) can be corrected by provision of chloride without volume expansion or intranephronal redistribution of fluid reabsorption, CDA was produced in Sprague-Dawley rats by peritoneal dialysis against 0.15 M NaHCO3; controls (CON) were dialyzed against Ringer's bicarbonate. Animals were infused with isotonic solutions containing the same Cl and total CO2 (tCO2) concentrations as in postdialysis plasma at rates shown to be associated with slight but stable volume contraction. During the subsequent 6 h, serum Cl and tCO2 concentrations remained stable and normal in CON and corrected towards normal in CDA; urinary chloride excretion was less and bicarbonate excretion greater than those in CON during this period. Micropuncture and microinjection studies were performed in the 3rd h after dialysis. Plasma volumes determined by 125I-albumin were not different. Inulin clearance and fractional chloride excretion were lower (P less than 0.05) in CDA. Superficial nephron glomerular filtration rate determined from distal puncture sites was lower (P less than 0.02) in CDA (27.9 +/- 2.3 nl/min) compared with that in CON (37.9 +/- 2.6). Fractional fluid and chloride reabsorption in the proximal convoluted tubule and within the loop segment did not differ. Fractional chloride delivery to the early distal convolution did not differ but that out of this segment was less (P less than 0.01) in group CDA. Urinary recovery of 36Cl injected into the collecting duct segment was lower (P less than 0.01) in CDA (CON 74 +/- 3; CDA 34 +/- 4%). These data show that CDA can be corrected by the provision of chloride without volume expansion or alterations in the intranephronal distribution of fluid reabsorption. Enhanced chloride reabsorption in the collecting duct segment, and possibly in the distal convoluted tubule, contributes importantly to this correction.

Absorption↗
PubMed1991

Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis.

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.

Acidosis, Respiratory↗
PubMed2000

Syndrome of hypokalemic metabolic alkalosis and hypomagnesemia associated with gentamicin therapy: case reports.

Nephrotoxicity, as evidenced by renal insufficiency is a well-known consequence of gentamicin therapy. We report two patients with gentamicin-induced syndrome of hypokalemic metabolic alkalosis and hypomagnesemia. Both had complete recovery of renal tubular function after cessation of antibiotic therapy. These cases emphasize the need to routinely monitor patients receiving gentamicin therapy for electrolyte abnormalities to avoid potential morbidity.

Acute Kidney Injury↗
PubMed1982

Cystic fibrosis presenting with chronic electrolyte depletion, metabolic alkalosis and hyperaldosteronism.

A five month old infant who presented with failure to thrive and was found to have severe electrolyte depletion, metabolic alkalosis and hyperaldosteronism is described. The diagnosis of cystic fibrosis was made by demonstrating abnormal sweat electrolytes and pancreatic insufficiency. It is important to exclude cystic fibrosis in any infant presenting with this biochemical abnormality.

Alkalosis↗
PubMed2003

Pre-HD dilution acidosis, without post-HD contraction alkalosis in uremic patients.

The aim of this study was to verify if the degree of pre-HD acidosis and its correction post-HD is related to body fluid expansion during the interdialytic period. Twelve uremic patients without major problems, with stable hematocrit, with regular and similar HD-session characteristics, but widely varying amounts of body fluid expansion in the interdialytic period were included. Blood samples were collected from arterial line pre- and post-HD, anaerobically in heparinized syringes, for determination of HCO3-, pH and PaCO2 (radiometer Copenhagen ABL 300 Acid-Base Laboratory), in two similar HD-sessions for each patient (12 patients, 24 HD-sessions). The percentage (%) of body weight gain in the interdialytic period was also estimated. For each patient, the mean value of parameters studied in the two HD-sessions was used for the evaluation of findings. According to mean values (+/-SD) of HCO3-, pH and PaCO2 Pre-HD (18.26+/-1.99 mmol/L, 7.31+/-0.03, 36.27+/-2.5 mmHg respectively) and post-HD (26.37+/-1.7, 7.43+/-0.03, 38.43+/-2.10 respectively) patients are acidotic pre-HD and slightly alkalemic post-HD. Correlation between the percentage (%) of interdialytic body weight gain (IBWG) and the values of HCO3-, pH and PaCO2, Pre-HD (r=-0.814, p<0.001; r=-0.931, p<0.001; r=0, 100 NS; respectively) and post-HD (r=-0.958, p<0.001; r=-0.937, p<0.001; r=-0.504 NS; respectively) indicates a significant and negative relationship of IBWG% with HCO3- and pH pre- and post-HD, but not with PCO2. In conclusion, the negative relationship of IBWG% with HCO3- and pH pre- and post-HD indicates that the body fluid expansion during the interdialytic period contributes to a dilutional acidosis pre-HD, but not to a contraction alkalosis post-HD, by the elimination of fluid during the HD-session.

Acid-Base Equilibrium↗
PubMed2004

Induced metabolic alkalosis affects muscle metabolism and repeated-sprint ability.

PURPOSE: The purpose of this study was to assess the effects of induced metabolic alkalosis, via sodium bicarbonate (NaHCO3) ingestion, on muscle metabolism and power output during repeated short-duration cycle sprints. METHODS: : Ten active females (mean +/- SD: age = 19 +/- 2 yr, VO2max = 41.0 +/- 8.8 mL x kg x min ) ingested either 0.3 g x kg NaHCO3 or 0.207 g x kg of NaCl (CON), in a double-blind, random, counterbalanced order, 90 min before performing a repeated-sprint ability (RSA) test (5 x 6-s all-out cycle sprints every 30 s). RESULTS: Compared with CON, there was a significant increase in resting blood bicarbonate concentration [HCO3] (23.6 +/- 1.1 vs 30.0 +/- 3.0 mmol x L ) and pH (7.42 +/- 0.02 vs 7.50 +/- 0.04), but no significant difference in resting lactate concentration [La] (0.8 +/- 0.2 vs 0.8 +/- 0.3 mmol x L ) during the NaHCO3 trial. Muscle biopsies revealed no significant difference in resting muscle [La], pH, or buffer capacity (beta(in vitro)) between trials (P > 0.05). Compared with CON, the NaHCO3 trial resulted in a significant increase in total work (15.7 +/- 3.0 vs 16.5 +/- 3.1 kJ) and a significant improvement in work and power output in sprints 3, 4, and 5. Despite no significant difference in posttest muscle pH between conditions, the NaHCO3 trial resulted in significantly greater posttest muscle [La]. CONCLUSIONS: As NaHCO3 ingestion does not increase resting muscle pH or beta(in vitro), it is likely that the improved performance is a result of the greater extracellular buffer concentration increasing H efflux from the muscles into the blood. The significant increase in posttest muscle [La] in NaHCO3 suggests that an increased anaerobic energy contribution is one mechanism by which NaHCO3 ingestion improved RSA.

Adult↗
PubMed2005

Effects of induced metabolic alkalosis on prolonged intermittent-sprint performance.

PURPOSE: Previous studies have shown that induced metabolic alkalosis, via sodium bicarbonate (NaHCO3) ingestion, can improve short-term, repeated-sprint ability. The purpose of this study was to assess the effects of NaHCO3 ingestion on a prolonged, intermittent-sprint test (IST). METHODS: Seven female team-sport athletes (mean +/- SD: age = 19 +/- 1 yr, VO2peak = 45.3 +/- 3.1 mL x kg(-1) x min(-1)) volunteered for the study, which had received ethics clearance. The athletes ingested two doses of either 0.2 g x kg(-1) of NaHCO3 or 0.138 g x kg(-1) of NaCl (placebo), in a double-blind, random, counterbalanced order, 90 and 20 min before performing the IST on a cycle ergometer (two 36-min "halves" of repeated approximately 2-min blocks: all-out 4-s sprint, 100 s of active recovery at 35% VO2peak, and 20 s of rest). Capillary blood samples were drawn from the ear lobe before ingestion, and before, during, and after each half of the IST. VO2 was also recorded at regular intervals throughout the IST. RESULTS: Resting plasma bicarbonate concentration ([HCO3-]) averaged 22.6 +/- 0.9 mmol x L(-1), and at 90 min post-ingestion was 21.4 +/- 1.5 and 28.9 +/- 2.8 mmol x L-1 for the placebo and NaHCO3 conditions, respectively (P < 0.05). Plasma [HCO3-] during the NaHCO3 condition remained significantly higher throughout the IST compared with both placebo and pre-ingestion. There was a trend toward improved total work in the second (P = 0.08), but not first, half of the IST after the ingestion of NaHCO3. Furthermore, subjects completed significantly more work in 7 of 18 second-half, 4-s sprints after NaHCO3 ingestion. CONCLUSIONS: The results of this study suggest that NaHCO3 ingestion can improve intermittent-sprint performance and may be a useful supplement for team-sport athletes.

Adult↗
PubMed1975

Hypokalemia and metabolic alkalosis resulting from overuse of magnesium oxide.

A 23 year old woman had taken large doses of magnesium oxide (up to 20 to 30g per day) initially for habitual constipation and later for idiopathic edema instead of diuretics, until the concealed abuse was discovered. During the abuse she showed hypokalemia and metabolic alkalosis. When the ingestion was stopped, the electrolyte imbalance recovered within two weeks.

Adult↗
PubMed1991

An unusual cause of respiratory alkalosis.

A 56-year-old man with a longstanding tracheostomy presented to the hospital with upper GI bleeding and was found to have a profound respiratory alkalosis. The cause of this patient's involuntary hyperventilation was hiccuping complicated by the absence of glottic closure.

Alkalosis, Respiratory↗