Intracellular pH and bicarbonate concentration in human muscle during recovery from exercise

1978 ◽  
Vol 45 (3) ◽  
pp. 474-480 ◽  
Author(s):  
K. Sahlin ◽  
A. Alvestrand ◽  
R. Brandt ◽  
E. Hultman

Eight subjects exercised on an ergometer until exhaustion. Femoral venous blood was analyzed for lactate, pyruvate, protein, electrolytes, and acid-base parameters. Muscle samples taken during the recovery period from m. quadriceps femoris were analyzed for water, electrolytes, lactate, and acid-labile CO2. Water content in the muscle biopsy sample was increased after exercise to 78.7 +/- 0.5% compared with the normal 76.7 +/- 0.8% at rest. The distribution of water between the extra- and intracellular space was calculated by the chloride method. In spite of elevated PCO2 in femoral venous blood the content of acid-labile CO2 was decreased in muscle after exercise. One minute after termination of exercise muscle CO2 was about half of the normal content at rest. During the recovery period muscle CO2 increased but was 20 min after termination of exercise still significantly below the value at rest. Intracellular pH (pHi) and bicarbonate concentration ([HCO3-]i) in muscle have been calculated. The validity of the assumptions underlying the calculations are thoroughly discussed. pHi decreased from the normal value at rest, 7.00 +/- 0.06 (mean +/- SD), to about 6.4 after exercise. [HCO3-] decreased from 10.2 +/- 1.2 mmol/l at rest to about 3 mmol/l after exercise. The changes are the greatest so far reported for an in vivo situation. After 20 min recovery pHi was almost the same as at rest, whereas bicarbonate was still well below.

1992 ◽  
Vol 169 (1) ◽  
pp. 105-119
Author(s):  
B. L. TUFTS ◽  
B. BAGATTO ◽  
B. CAMERON

Exercise in sea lampreys resulted in a significant decrease in the extracellular pH (pHe) in both arterial and venous blood. At rest, the erythrocyte pH (pHi) of venous blood was significantly greater than the pHi of arterial blood. Despite the considerable extracellular acidosis after exercise, both arterial and venous pHi were maintained throughout the recovery period. In the venous blood, there was a reversal of the pH gradient (ΔpH) across the erythrocyte membrane immediately after exercise. Exercise also resulted in significant reductions in the partial pressure of oxygen and hemoglobin oxygen-carriage and a significant increase in the partial pressure of CO2 in arterial and venous blood. Although the total CO2 concentration of the plasma decreased after exercise, erythrocyte total CO2 concentrations (CCOCO2,i) increased. In venous blood, the CCOCO2,i immediately after exercise was double the resting value. At rest, partitioning of the total CO2 content between plasma and erythrocytes indicated that 16 % and 22 % of the total CO2 could be attributed to the erythrocytes in arterial and venous whole blood, respectively. After exercise, these percentages increased to 25% (arterial) and 38% (venous). Changes in CCOCO2,i accounted for 62% of the arteriovenous difference in whole-blood total CO2 at rest. This increased to 78% immediately after exercise. Thus, unlike other vertebrates, CO2 transport in the lamprey in vivo is largely dependent on erythrocyte CO2-carriage.


1982 ◽  
Vol 99 (1) ◽  
pp. 9-28 ◽  
Author(s):  
N. Heisler

In the tropical fresh water fish, Synbranchus marmoratus, transition from water breathing to air breathing, induced by reduction of oxygen partial pressure (PO2) in the environmental water below 16 mmHg, causes a considerable rise in the arterial partial pressure of carbon dioxide (PCO2), from 5.6 to 26 mmHg on the average (half time of the rise between 2 and 6.5 h). The associated fall in arterial plasma pH by about 0.6 units is not compensated by an increase in plasma bicarbonate concentration, whereas the intracellular pH of white skeletal muscle and heart muscle is kept almost constant by elevation of the intracellular bicarbonate concentration. The additional bicarbonate is generated by intracellular non-bicarbonate buffering, and by net transfer into the intracellular space of bicarbonate formed by buffering in blood. Only a relatively small quantity of bicarbonate is taken up from environmental water. This type of acid-base regulation, with almost complete intracellular pH compensation and only minor bicarbonate uptake (equivalent H+ release or OH- uptake) from water, is attributed to several factors. Probably the most important of these is the lack of continuous contact of the gills, which are the main site of ion transfer processes, with the environmental water during air breathing. Regardless of the mechanisms involved, this particular strategy of acid-base regulation provides a constant milieu for the intracellular structures and demonstrates the prevalence of intracellular over extracellular acid-base regulation.


1993 ◽  
Vol 75 (2) ◽  
pp. 955-962 ◽  
Author(s):  
C. Decanniere ◽  
P. Van Hecke ◽  
F. Vanstapel ◽  
H. Ville ◽  
R. Geers

Using in vivo 31P-nuclear magnetic resonance spectroscopy, we studied the skeletal muscle metabolism of 17 anesthetized malignant hyperthermia-susceptible piglets and 25 control piglets during and after a halothane stress test. At rest, the phosphocreatine- (PCr) to-ATP ratio was 12% higher in the anesthetized piglets than in the control piglets, which may reflect a higher proportion of fast glycolytic fibers in the former. About 15 min of halothane administration sufficed to provoke onset of a reaction, which was characterized by a reciprocal drop in PCr and an increase in Pi with commencing intracellular acidosis. Halothane was withdrawn after a 20% drop in PCr. Within the next few minutes, intracellular pH dropped sharply and phosphomonoesters (PME) accumulated excessively. ATP was observed to decrease in 8 of the 17 animals. Halothane inhalation provoked a switch of metabolism toward glycolysis. Accumulation of PME suggests a mismatch between glycogenolysis and glycolysis. Despite severe acidification, glycolysis was not completely halted. Recovery of PCr and Pi started approximately 5 min after halothane withdrawal, with a longer time constant for recovery of the former. PME and intracellular pH aberrations lingered and started to recover later. Lost ATP was never restored within the observed recovery period of approximately 20 min.


1977 ◽  
Vol 53 (6) ◽  
pp. 579-586 ◽  
Author(s):  
S. Pors Nielsen ◽  
T. Falch Christiansen ◽  
O. Hartling ◽  
J. Trap-Jensen

1. Normal subjects showed an average increase in serum ionized calcium (Ca2+) concentration of 0·11 mmol/l in peripheral venous blood 10 min after onset of bicycle exercise at 70% of maximum aerobic capacity. The corresponding mean rise in serum total calcium concentration was 0·21 mmol/l. 2. The change in serum Ca2+ as result of acidification was studied in 20 normal subjects by carbon dioxide equilibration in vitro followed by measurement of serum Ca2+. The log serum Ca2+ was inversely proportional to serum pH. 3. The Δlog serum Ca2+/ΔpH in vitro was similar to the Δlog serum Caa+/ΔpH in vivo during exercise, this ratio, however, being somewhat greater during the first minute of exercise. 4. Serum Ca2+ returned to normal values about 20 min after stopping exercise as the pH returned to normal, but the fall immediately after stopping exercise was more pronounced than that due to the change in pH, as predicted from the studies in vitro. 5. Blood lactate concentration rose from 0·86 to 8·41 mmol/l after 10 min exercise, but the rise in blood lactate during exercise was slower than the rise in serum Ca2+. Also the fall during the recovery period was delayed compared with the fall in serum Ca2+. 6. It is suggested that the rise in serum Ca2+ during severe muscular exercise might be important for the physiological adaptations during work, and for bone metabolism.


1982 ◽  
Vol 60 (5) ◽  
pp. 1123-1130 ◽  
Author(s):  
J. H. Booth ◽  
G. F. Jansz ◽  
G. F. Holeton

A review of pertinent literature is provided. Previous research showed that fish exposed to sublethal environmental acidification have reduced blood pH, plasma [HCO3−], and [Cl−] and increased plasma [K+]. Simultaneous sampling from blood and water was used to characterize changes in Cl−, K+, and acid–base regulation in rainbow trout during a 5-day exposure to pH 4 followed by a 24-h recovery period at pH 7. At pH 4, there was a continuous loss of Cl− (49.8 μmol/kg per hour), and K+ (23.0 μmol/kg per hour) to the water. Blood ion concentrations did not change in a corresponding manner. Blood pH and plasma [HCO3−] decreased continuously owing to a net uptake of acid from the water. Recovery at pH 7 involved uptake of Cl− from, and loss of K+ to, the water. Plasma [K+] returned to normal but there was no significant change in plasma [Cl−] during this 24-h period. Internal acid–base parameters recovered much more quickly owing to a net excretion of acid into the water. The more rapid recovery of acid–base balance suggests that branchial acid–base and ionoregulatory mechanisms may be only loosely linked. The irregular changes in blood ion concentrations indicate that considerable ionic and osmotic exchanges between the plasma, the remainder of the extracellular space, and the intracellular space must result from exposure to pH 4.


1976 ◽  
Vol 50 (4) ◽  
pp. 293-299 ◽  
Author(s):  
G. E. Levin ◽  
P. Collinson ◽  
D. N. Baron

1. Viable human leucocytes were isolated from venous blood and suspended in artificial media. Intracellular pH measurements were made by the dimethyloxazolidinedione technique in conditions simulating ‘respiratory’ or ‘metabolic’ acid-base disturbances. 2. Normal intracellular pH was 7·11 ± 0·02 (mean ± 2 sd) at an extracellular Pco2 of 5·8 kPa and a bicarbonate concentration of 25 mmol/l. 3. ‘Respiratory’ and ‘metabolic’ acidosis caused little change in pH1 although increases in Pco2 led to relatively greater falls in pH1 than did reduction in external bicarbonate concentration. 4. ‘Respiratory’ and ‘metabolic’ alkalosis caused similar and relatively greater increases in the pH1 when compared with the response to an external acidosis.


2021 ◽  
Author(s):  
Omer F. Gungor ◽  
Saleh Salman ◽  
Saurav Ranjitkar ◽  
Delong Zhang ◽  
Xiuchun (Cindy) Tian

Abstract Follicular fluid is the microenvironment that supports oocyte maturation and competence. Using Abbott iSTAT1™ and NanoDrop, we determined the dynamics of acid-base, electrolyte, metabolites, and total protein in venous blood, fluids of the dominant follicle (FF), oviduct (OF), and uterus (UF) during the window of oocyte maturation. Holstein heifers (n=36) were synchronized with PGF2α on Days -11 and 0, CIDR during Days -6 to 1, and GnRH given on Day 2 after 2nd PG. Samples were collected at 24h, 48h, 60h, 72h, and 78h after 2nd PG. Most electrolytes analyzed, Cl-, K+, and Ca2+ were significantly affected in blood and FF (P<0.05) by CIDR removal. Similarly, Cl- and Na+ also significantly changed in OF and UF across time. Glucose, lactate, and creatinine significantly changed across time points in FF compared to blood. Moreover, pO2, pCO2, TCO2, and pH significantly changed across time in FF. Most parameters were not significantly correlated between blood and FF across time points except for glucose, Cl- and creatinine. Furthermore, pO2 in FF was nearly 3X higher than blood, suggesting low O2 during in vitro maturation is inappropriate. In conclusion, components of the follicular fluid undergo major changes during the window of oocyte maturation.


1979 ◽  
Vol 236 (3) ◽  
pp. F240-F245 ◽  
Author(s):  
R. Park ◽  
W. J. Leach ◽  
A. I. Arieff

An in vivo method is presented for the determination of liver intracellular pH (pHi) using [14C]dimethadione (DMO) in dogs. This method differs from those previously published in that hepatic venous and portal venous blood pH were selected as the extracellular reference pH, and liver blood space corrections are applied to whole liver tissue [14C]DMO activity. Using these corrections, a normal liver pHi of 6.99 +/- 0.03 (SE) was obtained. During acute metabolic acidosis and alkalosis, as well as during acute respiratory acidosis and alkalosis, the liver pHi remained normal; metabolic acidosis was 7.04 +/- 0.04; metabolic alkalosis was 6.92 +/- 0.08; respiratory acidosis was 6.98 +/- 0.04; and respiratory alkalosis was 7.00 +/- 0.10. None of these values was significantly different from normal (P greater than 0.05). Changes in intracellular bicarbonate and lactate appeared to account in part for the observed stability of the liver pHi despite acute manipulations resulting in a range of pH values between 7.09 and 7.63 in arterial blood.


1977 ◽  
Vol 53 (5) ◽  
pp. 459-466
Author(s):  
K. Sahlin ◽  
A. Alvestrand ◽  
J. Bergström ◽  
E. Hultman

1. A method for measuring intracellular pH and bicarbonate concentration of human muscle is described. 2. Muscle biopsies from the quadriceps muscle of 13 healthy subjects at rest were analysed for acid-labile carbon dioxide and volume of extra- and intra-cellular water. Extracellular water volume was estimated from the chloride content and intracellular water volume from the potassium content, or alternatively derived from the sample weight. 3. The measured total carbon dioxide content in muscle was 9·84 ± 1·39 mmol/kg. 4. Assuming a normal membrane potential (88 mV) and Pco2 of muscle equal to venous blood, calculated intracellular pH was 7·00 ± 0·06 and intracellular bicarbonate concentration was 10·2 ± 1·2 mmol/l of water.


1992 ◽  
Vol 82 (5) ◽  
pp. 559-564 ◽  
Author(s):  
Campbell H. Thompson ◽  
Paul D. Syme ◽  
E. Mark Williams ◽  
John G. G. Ledingham ◽  
George K. Radda

1. The effect of bicarbonate administration on the intracellular pH of rat skeletal muscle was examined by using 31P n.m.r. 2. Bicarbonate administered intraperitoneally caused a significant intracellular acidosis in rat skeletal muscle in vivo. When the bicarbonate was administered intravenously there was no such change in the pH of the skeletal muscle. 3. Bicarbonate administration by either route resulted in an elevated mixed venous partial pressure of carbon dioxide and an elevated arterial pH, but no significant change in the arterial partial pressure of carbon dioxide. The increase in arterial bicarbonate concentration after intraperitoneal injection of bicarbonate was delayed when compared with that after intravenous injection. 4. The administration of hypertonic solutions intravenously caused a transient 40–50% fall in blood pressure, which had resolved within 1 min. 5. The data suggest that the effect of bicarbonate administration on intracellular pH in vivo is related not only to carbon dioxide loading of the cell but also to the rate of change in the extracellular bicarbonate concentration.


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