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PubMed1991

Adaptations to chloride-depletion alkalosis.

The systemic and renal adaptations for the maintenance and correction of metabolic alkalosis generated by chloride depletion (CDA) are the focus of this review. The hypothesis that extracellular fluid (ECF) volume expansion is essential for the correction of CDA is refuted, while the concept that Cl- repletion is necessary and sufficient for correction is developed. Contraction of ECF volume probably can occur as a consequence of CDA. The principal mechanisms by which the kidney corrects CDA appear to reside primarily in the collecting duct, which is endowed with the anion exchange mechanisms and the capacity to effect the necessary changes in body anion composition. Although the remainder of the collecting duct is undoubtedly important in this response, the cortical segment appears to have the paramount role since it can either absorb or secrete HCO3-. Alterations in the delivery of Cl- or HCO3- to the collecting duct may also be important but changes in glomerular filtration rate appear to have a minor role. Major unanswered questions in the pathophysiology of CDA are the manner in which exogenous Cl- repletion is detected and the kidney is signaled to excrete HCO3- and the cellular mechanisms by which this is accomplished in the various nephron segments.

Adaptation, Physiological↗
PubMed1978

Characterization of distal hydrogen ion secretion in acute respiratory alkalosis.

The effect of acute respiratory alkalosis (ARA) on distal nephron H+ secretion was evaluated by measuring urine-to-blood (U-B) Pco2 in dogs with highly alkaline urine (urine pH greater than 7.8). ARA led to a significant decrease in U-B Pco2 and in urine HCO3 concentration; urine pH, however, increased significantly, indicating that the decrease in urine Pco2 was of greater magnitude than the decrease in urine HCO3 concentration. For any given urine HCO3 concentration urine Pco2 was lower (i.e., urine pH was higher) in ARA than in controls. Administration of tris(hydroxymethyl)aminomethane (Tris) during ARA resulted in a significant increase in U-B Pco2 to control values. In animals with moderately alkaline urine (urine pH 6.4--7.4) and high urine PO4 concentration, ARA resulted in a significant decrease in UB-Pco2 and urine PO4 concentrations. Neutral PO4 infusion in these dogs resulted in an increase in urine PO4 concentration and U-B Pco2 to control levels. These data demonstrate that ARA results in a significant decrease in U-B Pco2 that is not solely attributable to changes in urine HCO3 concentration. The observation that Tris and PO4 infusion during ARA raises U-B Pco2 to control levels suggests that the ability to secrete H+ is intact.

Alkalosis, Respiratory↗
PubMed1979

Effect of arsenite on renal tissue slice metabolism in chronic metabolic acidosis and alkalosis.

Tissue slices prepared from renal cortex of littermate dogs with chronic metabolic acidosis or alkalosis were incubated in media with or without arsenite and containing 1 mM L-[14C]glutamine or [1,5-14C]citrate. The presence of arsenite increased the concentration of alpha-ketoglutarate in slices by 5--20 times the values found without this inhibitor. alpha-Ketoglutarate concentrations in acidotic slices were 40% or more greater than those in alkalotic ones when arsenited was present. 14C incorporation into alpha-ketoglutarate was also increased manyfold by arsenite with either labeled glutamine or citrate as substrate. 14CO2 production from labeled glutamine by over 90% and from labeled citrate by over 75%; the difference between 14CO2 production by acidotic and alkalotic slices was greatly reduced or eliminated by arsenite. These results suggest that in chronic metabolic acidosis metabolism of both glutamine and citrate is stimulated at a site or sites preceding formation of alpha-ketoglutarate.

Acidosis↗
PubMed1983

Chloride-depletion alkalosis with a normal extracellular fluid volume.

Current concepts hold that volume expansion is essential to the correction of chloride-depletion alkalosis (CDA) with chloride repletion in a permissive role. In this scheme, intranephronal fluid reabsorption would be redistributed with increased delivery to the distal nephron where the provided chloride is readily reabsorbed and the limited capacity for bicarbonate reabsorption would promote bicarbonate excretion and correction of CDA. In a model of CDA produced by peritoneal dialysis against 0.15 M NaHCO3, we have shown complete correction of CDA within 24 h without volume expansion by either oral isotonic sodium or chloride salts with 70 mM chloride and despite an obligatory bicarbonate load and negative sodium and potassium balance. During correction of CDA without volume expansion in rats by intravenous isotonic fluids containing 80 mM chloride, fractional fluid and chloride reabsorptions in the proximal convoluted tubule and in the loop segment of superficial nephrons were not different from controls but chloride reabsorption was enhanced in the collecting duct segment and probably within the distal convolution. Despite no differences in serial hematocrits, blood pressure, and measured plasma volume, kidney and nephron glomerular filtration rate (GFR) were reduced in CDA and returned to normal upon recovery 24 h later.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗
PubMed1984

Renal handling of phosphate during acute respiratory acidosis and alkalosis in the rat.

Clearance experiments were performed in acutely thyroparathyroidectomized rats to evaluate the renal handling of phosphate during respiratory acidosis (R ACID) and alkalosis (R ALK) in rats fed either a normal (0.7%) or low (0.07%) phosphate diet for 4 days. Different acid-base states were achieved by varying the mixture of carbon dioxide in the inspired air. Each group received graded infusions of phosphate to control for differences in plasma phosphate (PPi) and to determine the maximum transport capacity of phosphate reabsorption (TmPi/GFR). In rats fed a normal phosphate diet, PPi and the fractional excretion of phosphate (FEPi) were significantly greater in R ACID than in R ALK. However, there were no differences between R ACID and R ALK when FEPi was evaluated as a function of the PPi, and values for TmPi/GFR during R ACID were not different from those during R ALK. In rats fed low phosphate diet, PPi during R ACID was significantly greater than during R ALK, yet FEPi was less than 1% in all groups due to an adaptive increase in TmPi/GFR. Further, the TmPi/GFR was similar irrespective of the acid-base state. We conclude that acute respiratory acid-base changes do not alter the intrinsic capacity of the kidney to reabsorb phosphate.

Acidosis, Respiratory↗
PubMed1985

Effects of metabolic acidosis, alkalosis, and dietary hydrogen ion intake on phosphate transport in the proximal convoluted tubule.

Early proximal convoluted tubules were perfused in vivo with equilibrium Ringer buffered at pH 7.65 and 6.5 to characterize phosphate absorption due to changes in extracellular and intracellular hydrogen ion concentration. Phosphate absorption is normally greater from intraluminal pH 7.65 compared with pH 6.5 in thyroparathyroidectomized rats with fractional phosphate excretion of 0.5%. Metabolic alkalosis produced by bicarbonate infusion in rats ingesting normal amounts of phosphate (45 mg/day) resulted in an increase in overall renal phosphate reabsorption (fractional phosphate excretion 0.3%). The Jmax and Km values were: pH 7.65, 33.67 +/- 13.49 pmol X min-1 X mm-1, and 1.74 +/- 0.30 mM; pH 6.5, 24.87 +/- 6.22 and 0.50 +/- 0.25, respectively. By contrast, rats on a high dietary phosphate intake (180 mg/day) demonstrated a large increase in urinary phosphate excretion (18%) following bicarbonate infusion, which was due to a decrease in tubular phosphate absorption from both alkaline and acidic luminal pH values. Acute metabolic acidosis did not significantly alter tubular transport at either intraluminal pH value. In contrast, rats maintained on an elevated dietary acid intake for 5 days had a phosphaturia (fractional excretion 7.1%) and diminished reabsorptive capacity. Dietary acidosis also decreased tubular phosphate transport in rats previously maintained on phosphate-restricted diets. These data suggest that acid-base balance may modulate tubular phosphate transport independent of intraluminal pH and phosphate concentration. Further, these changes depend on the chronicity of exposure and act independent but integral to the effects of parathyroid hormone and the intrinsic adaptation to dietary phosphate availability.

Absorption↗
PubMed1985

Nephron site of resistance to phosphaturic effect of PTH during respiratory alkalosis.

This study was performed to evaluate the nephron site(s) responsible for the blunted phosphaturic effect of parathyroid hormone during respiratory alkalosis. In normocapnic thyroparathyroidectomized rats, parathyroid hormone administration markedly increased the fractional excretion of phosphate (FEp) from 2.1 +/- 0.5 to 36.6 +/- 5.0%. However, in the respiratory alkalotic rats, parathyroid hormone administration did not significantly increase the FEp (1.4 +/- 0.9 to 5.9 +/- 2.2%). This blunted phosphaturic response to parathyroid hormone was not due to a blunted inhibition of phosphate reabsorption by the superficial proximal tubule, since parathyroid hormone administration significantly increased the fractional delivery of phosphate (FDp) at the superficial late proximal tubule in both normal (25.3 +/- 3.0 to 36.2 +/- 3.8%, delta 10.9 +/- 3.2%) and respiratory alkalotic rats (12.2 +/- 3.1 to 30.3 +/- 4.9%, delta 18.0 +/- 4.7%). Parathyroid hormone administration significantly increased the FDp at the superficial early distal tubule from 9.3 +/- 3.9 to 38.7 +/- 7.4% (delta 29.4 +/- 5.1%) in normal rats and from 4.5 +/- 1.7 to 12.9 +/- 3.4% (delta 8.5 +/- 3.2%) in the respiratory alkalotic rats. We conclude that the blunted phosphaturic response to parathyroid hormone in respiratory alkalotic rats is not due to a blunted inhibition of phosphate reabsorption by the proximal convoluted tubule but is primarily due to enhanced reabsorption by the pars recta segment of the proximal tubule.

Absorption↗
PubMed1986

Importance of the kidney in the correction of chloride-depletion alkalosis in the rat.

Correction of chloride-depletion alkalosis (CDA) may involve renal as well as extrarenal mechanisms. To determine the relative contribution of these mechanisms in a rat model of CDA produced by peritoneal dialysis (PD), we studied six groups of anesthetized Sprague-Dawley rats after PD. Groups II-IV and IIa were subjected to functional bilateral nephrectomy, and groups I and Ia were sham-operated. Groups I, Ia, II, and IIa were infused with isotonic fluid containing 70 mM Cl- and 40 mM HCO3-; the infusate in group III was 140 mM Cl- and in group IV, 70 mM neutral PO4 was substituted for Cl-. Groups I and Ia were infused at 0.5 ml . h-1 X 100 g body wt-1 and groups II, IIa, III, and IV at 0.25 ml . h-1 X 100 g-1. After 3 h of infusion, early partial correction with reciprocal changes in plasma Cl (+6.1 +/- 1.9 mmHg) and total CO2 (-6.0 +/- 0.8 meq/liter) occurred (P less than 0.01) only in group I. Hypokalemia (3.1 +/- 0.1 meq/liter) also occurred only in group I. The responses of groups Ia and IIa studied at 5 h were similar to those of groups I and II. These data suggest that the kidney, and not extrarenal mechanisms, is primarily responsible for the correction of CDA during infusion of chloride.

Alkalosis↗
PubMed1988

Plasma AVP and renal concentrating defect in chloride depletion metabolic alkalosis.

These studies were undertaken to determine the effect of chronic chloride depletion metabolic alkalosis (Cl-DEP-MALK) on water intake, plasma arginine vasopressin (AVP) levels, and renal concentrating ability. Cl-DEP-MALK was induced by feeding a chloride-free diet to rats subjected to gastric drainage and to dogs treated with furosemide. All of the animals developed a urine concentrating defect, polydipsia, and a persistent reduction in plasma osmolality. However, AVP release was not suppressed. The results of osmotic loading experiments in dogs analyzed using either linear or log-linear models have shown that chronic Cl-DEP-MALK significantly alters the relation between plasma osmolality and plasma AVP. In the classic linear analysis the results suggest that Cl-DEP-MALK reduces the plasma osmolality at which plasma AVP can be detected, i.e., reduced "threshold," and increases the slope of the plasma osmolality-to-plasma AVP relation nearly twofold, i.e., increased "sensitivity." Finally, we provide evidence that the concentrating defect is not related to high water turnover or deficient endogenous AVP and is therefore nephrogenic.

Alkalosis↗
PubMed1990

NEM-sensitive ATPase activity in rat nephron: effect of metabolic acidosis and alkalosis.

The present study was designed to quantitate the amount and to map the localization of N-ethylmaleimide (NEM)-sensitive adenosinetriphosphatase (ATPase) activity in microdissected segments of the rat nephron. After complete nephron mapping the effect of chronic metabolic acidosis and alkalosis on enzyme activity was determined. In control animals the highest enzyme activity was found in the early proximal convoluted tubule of juxtamedullary nephrons; superficial early proximal tubule as well as medullary and cortical thick ascending limbs and collecting ducts also contained substantial activity. Enzyme activity in the papillary collecting duct before entry into the ducts of Bellini was 329 +/- 93 pmol.mm-1.h-1 (n = 8); after entry, however, enzyme activity was approximately one-fourth that value (60 +/- 9 pmol.mm-1.h-1, n = 8, P less than 0.01). No NEM-sensitive ATPase activity was found in the thin limbs of the loop of Henle. Enzyme activity increased in both the medullary and cortical thick ascending limbs as well as in the cortical collecting tubule in response to NH4Cl-induced chronic metabolic acidosis; in the cortical collecting duct, metabolic acidosis increased maximum activity (Vmax) but did not change Michaelis-Menten constant (Km). In the proximal convoluted tubule, enzyme activity decreased with metabolic acidosis. Bicarbonate loading had no effect on enzyme activity except in the most distal portion of the collecting duct where it was stimulated. These results show that NEM-sensitive ATPase activity exists throughout much of the rat nephron. These data suggest that both the cortical collecting tubule and thick ascending limb are regulatory sites of distal urinary acidification during acid loading.

Acidosis↗
PubMed1990

Total CO2 transport in rat cortical collecting duct in chloride-depletion alkalosis.

Previous studies in chloride-depletion metabolic alkalosis (CDA) generated by intraperitoneal dialysis have suggested major alterations in chloride and bicarbonate transport beyond the distal convoluted tubule. To investigate the possible role of the cortical collecting duct (CCD) in the pathophysiology of CDA, isolated CCD segments were perfused in vitro from either control (CON) rats dialyzed against Ringer-bicarbonate or those made alkalotic by peritoneal dialysis with 0.15 M NaHCO3. Tubules from CDA animals secreted CO2 for greater than or equal to 3 h after dissection (-22.4 +/- 7.2 pmol.mm-1.min-1) compared with CON tubules that absorbed CO2 (18.3 +/- 4.2 pmol.mm-1.min-1). Replacement of luminal chloride with gluconate in the perfusate abolished net total CO2 (tCO2) secretion in tubules from CDA animals (from -21.5 +/- 4.5 to -2.7 +/- 2.3 pmol.mm-1.min-1) but did not alter net tCO2 absorption in tubules from CON animals. In contrast, removal of bath chloride increased net tCO2 secretion (-12.1 +/- 2.9 to -26.1 +/- 3.6 pmol.mm-1.min-1) in CDA tubules, whereas net tCO2 flux was altered from absorption to secretion in CON tubules (15.5 +/- 4.0 to -13.6 +/- 9.2 pmol.mm-1.min-1). These results demonstrate that 1) CDA generated in vivo within 45 min results in stable net tCO2 secretion in vitro up to 240 min in the CCD; 2) luminal chloride is necessary for tCO2 secretion; 3) the shift of net tCO2 flux from absorption to secretion in CON tubules in vitro was not sustained in contrast to CDA tubules.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗
PubMed1991

Maximal proton secretory rate of rat distal tubules is higher during chronic metabolic alkalosis.

In vivo microperfusion studies show augmented proton secretion in the distal tubule of rats with chronic metabolic alkalosis. The present studies used the same technique to determine whether this augmented proton secretion is due predominantly to an increase in substrate affinity or alternatively to a predominant increase in the maximal proton secretory rate. Surface distal tubules of alkalotic and control rats were microperfused in vivo with solutions containing increasing concentrations of HCO3. Proton secretion was determined as the difference between measured net HCO3 reabsorption and passive HCO3 transport calculated by use of the permeability derived from perfusing with a HCO3-free solution. Proton secretion was expressed as a function of the initial luminal HCO3 concentration and was assumed to follow saturable Michaelis-Menten kinetics. Alkalotic animals had a significantly higher Km (33.9 vs. 21.6 mM, P less than 0.03) and Vmax (223.8 vs. 99.1 pmol.mm-1.min-1, P less than 0.001) compared with control. These data are consistent with the augmented proton secretion in the distal tubule of alkalotic animals as predominantly due to an increased maximal proton secretory rate rather than to increased substrate affinity.

Alkalosis↗
PubMed1992

Response of intercalated cells to chloride depletion metabolic alkalosis.

We examined the effect of Cl- depletion metabolic alkalosis (CDA) on H(+)-ATPase and band 3 protein localization in intercalated cells (IC) of the rat cortical collecting duct (CCD) and the outer medullary collecting duct (OMCD). After 30 min of peritoneal dialysis against 0.15 M NaHCO3 to produce CDA, or Ringer bicarbonate to serve as controls (CON), both groups were infused intravenously with an 80 mM Cl- solution for 90 min. For CDA vs. CON, physiological parameters were as follows: plasma total CO2, 38.0 +/- 1.1 vs. 27.8 +/- 0.6 meq/l (P less than 0.001); urinary total CO2 excretion, 141 +/- 89 vs. 20 +/- 3 neq.min-1.100 g body wt-1; and urinary Cl- excretion, 20 +/- 10 vs. 486 +/- 144 neq.min-1.100 g body wt-1 (P less than 0.001). H(+)-ATPase was localized in thin sections using a rabbit polyclonal antibody against the 70-kDa subunit of bovine brain H(+)-ATPase. Band 3 protein was localized using a polyclonal antibody against the 43-kDa subunit of the cytoplasmic domain of human erythrocyte band 3 protein. In CON rats, H(+)-ATPase localized along the apical plasma membrane and over the apical cytoplasmic vesicles of type A ICs in the CCD and ICs of the OMCD. H(+)-ATPase was observed along the basolateral plasma membrane and over cytoplasmic vesicles throughout type B ICs. In CDA rats, H(+)-ATPase was only observed over apical cytoplasmic vesicles in type A ICs and in the majority of OMCD ICs. In type B ICs, H(+)-ATPase staining was intensified along the basal plasma membrane in CDA. Band 3 protein was consistently localized in the basolateral plasma membrane of all type A cells in the CCD and ICs of the OMCD in both CON and CDA. In summary, stimulation of HCO3- secretion in rats caused withdrawal of H(+)-ATPase from the apical plasma membrane and storage in apical cytoplasmic vesicles of ICs of the OMCD and type A ICs of the CCD. H(+)-ATPase appeared to be inserted into the basal plasma membrane of type B ICs. These findings suggest that, during correction of CDA, proton secretion by type A and OMCD ICs is suppressed and proton transport across the basolateral plasma membrane of type B ICs is stimulated.

Adenosine Triphosphatases↗
PubMed1997

The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo.

We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7-10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux (JHCO3) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([HCO3-]) decreased from 29 to 22 mM. Fractional urinary bicarbonate excretion (FEHCO3) increased threefold, but LOH JHCO3 was unchanged. In ARA, blood pH fell to 7.2, and blood [HCO3-] rose from 28 to 34 mM; FEHCO3 was reduced to < 0.1%, but LOH JHCO3 was unaltered. In CRA, blood pH fell to 7.2, and blood [HCO3-] increased to > 50 mM, whereas FEHCO3 decreased to < 0.1%. JHCO3 was reduced by approximately 30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH JHCO3 increased (by 30%) to normal. These results suggest that LOH JHCO3 is affected by the blood-to-tubule lumen [HCO3-] gradient and HCO3- backflux. When the usual perfusing solution at 20 nl/min was made HCO3- free, mean JHCO3 was -34.5 +/- 4.4 pmol/min compared with 210 +/- 28.1 pmol/min plus HCO3-. When a low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide (2 x 10(-4) M, to abolish H(+)-dependent JHCO3) was used, JHCO3 was -112.8 +/- 5.6 pmol/min. Comparable values for JHCO3 at 10 nl/min were -35.9 +/- 5.8 and -72.5 +/- 8.8 pmol/min, respectively. These data indicate significant backflux of HCO3-along the LOH, which depends on the blood-to-lumen [HCO3-] gradient; in addition to any underlying changes in active acid-base transport mechanisms, HCO3- permeability and backflux are important determinants of LOH JHCO3 in vivo.

Acidosis, Respiratory↗
PubMed1999

Expression of rat kidney anion exchanger 1 in type A intercalated cells in metabolic acidosis and alkalosis.

By enzyme-linked in situ hybridization (ISH), direct evidence is provided that acid-secreting intercalated cells (type A IC) of both the cortical and medullary collecting ducts of the rat kidney selectively express the mRNA of the kidney splice variant of anion exchanger 1 (kAE1) and no detectable levels of the erythrocyte AE1 (eAE1) mRNA. Using single-cell quantification by microphotometry of ISH enzyme reaction, medullary type A IC were found to contain twofold higher kAE1 mRNA levels compared with cortical type A IC. These differences correspond to the higher intensity of immunostaining in medullary versus cortical type A IC. Chronic changes of acid-base status induced by addition of NH(4)Cl (acidosis) or NaHCO3 (alkalosis) to the drinking water resulted in up to 35% changes of kAE1 mRNA levels in both cortical and medullary type A IC. These experiments provide direct evidence at the cellular level of kAE1 expression in type A IC and show moderate capacity of type A IC to respond to changes of acid-base status by modulation of kAE1 mRNA levels.

Acidosis↗
PubMed1976

Uteroplacental blood flow during hyperthermia with and without respiratory alkalosis.

The effect of induced maternal hyperthermia (1.5 degrees C rise over 60 min) on the uterine and umbilical circulations was examined in two groups of chronically instrumented pregnant sheep. Hyperventilation occurred in both groups. In the group in which the resultant respiratory alkalosis was untreated (N = 5), uterine blood flow decreased to 53 +/- 3% (mean +/- SE; P less than 0.01) of control at maximal maternal temperature. Umbilical blood flow also decreased 30 +/- 6% (P less than 0.01) below control levels. In the other group, normocapnia was maintained (N = 4). Uterine blood flow decreased in this group to 75% +/- 2% (P less than 0.01) of control levels, but umbilical blood flow did not significantly change. There was no significant change in maternal or fetal mean arterial pressure during hyperthermia in either group. Thus, maternal hyperthermia per se results in a significant decrease in uterine blood flow primarily through an effect on uterine vascular resistance, but without a concomitant change in umbilical blood flow.

Alkalosis, Respiratory↗
PubMed1986

Effect of respiratory alkalosis during exercise on blood lactate.

A biofeedback model of hyperventilation during exercise was used to assess the independent effects of pH, arterial CO2 partial pressure (PaCO2), and minute ventilation on blood lactate during exercise. Eight normal subjects were studied with progressive upright bicycle exercise (2-min intervals, 25-W increments) under three experimental conditions in random order. Arterialized venous blood was drawn at each work load for measurement of blood lactate, pH, and PaCO2. Results were compared with those from reproducible control tests. Experimental conditions were 1) biofeedback hyperventilation (to increase pH by 0.08-0.10 at each work load); 2) hyperventilation following acetazolamide (which returned pH to control values despite ventilation and PaCO2 identical to condition 1); and 3) metabolic acidosis induced by acetazolamide (with spontaneous ventilation). The results showed an increase in blood lactate during hyperventilation. Blood lactate was similar to control with hyperventilation after acetazolamide, suggesting that the change was due to pH and not to PaCO2 or total ventilation. Exercise during metabolic acidosis (acetazolamide alone) was associated with blood lactate lower than control values. Respiratory alkalosis during exercise increases blood lactate. This is due to the increase in pH and not to the increase in ventilation or the decrease in PaCO2.

Acetazolamide↗
PubMed2005

NaHCO3-induced alkalosis reduces the phosphocreatine slow component during heavy-intensity forearm exercise.

During heavy-intensity exercise, the mechanisms responsible for the continued slow decline in phosphocreatine concentration ([PCr]) (PCr slow component) have not been established. In this study, we tested the hypothesis that a reduced intracellular acidosis would result in a greater oxidative flux and, consequently, a reduced magnitude of the PCr slow component. Subjects (n = 10) performed isotonic wrist flexion in a control trial and in an induced alkalosis (Alk) trial (0.3g/kg oral dose of NaHCO3, 90 min before testing). Wrist flexion, at a contraction rate of 0.5 Hz, was performed for 9 min at moderate- (75% of onset of acidosis; intracellular pH threshold) and heavy-intensity (125% intracellular pH threshold) exercise. 31P-magnetic resonance spectroscopy was used to measure intracellular [H+], [PCr], [Pi], and [ATP]. The initial recovery data were used to estimate the rate of ATP synthesis and oxidative flux at the end of heavy-intensity exercise. In repeated trials, venous blood sampling was used to measure plasma [H+], [HCO3-], and [Lac-]. Throughout rest and exercise, plasma [H+] was lower (P < 0.05) and [HCO3-] was elevated (P < 0.05) in Alk compared with control. During the final 3 min of heavy-intensity exercise, Alk caused a lower (P < 0.05) intracellular [H+] [246 (SD 117) vs. 291 nmol/l (SD 129)], a greater (P < 0.05) [PCr] [12.7 (SD 7.0) vs. 9.9 mmol/l (SD 6.0)], and a reduced accumulation of [ADP] [0.065 (SD 0.031) vs. 0.098 mmol/l (SD 0.059)]. Oxidative flux was similar (P > 0.05) in the conditions at the end of heavy-intensity exercise. In conclusion, our results are consistent with a reduced intracellular acidosis, causing a decrease in the magnitude of the PCr slow component. The decreased PCr slow component in Alk did not appear to be due to an elevated oxidative flux.

Acid-Base Equilibrium↗