scholarly journals Contribution of net ion transfer mechanisms to acid-base regulation after exhausting activity in the larger spotted dogfish (Scyliorhinus stellaris)

1983 ◽  
Vol 103 (1) ◽  
pp. 31-46 ◽  
Author(s):  
G. F. Holeton ◽  
N. Heisler
Keyword(s):  
Lactic Acid ◽  
Lactate Concentration ◽  
Distribution Patterns ◽  
Environmental Water ◽  
Anaerobic Exercise ◽  
Acid Base ◽  
Acid Processing ◽  
Acid Base Status ◽  
Time Courses ◽  
Net Transfer

Specimens of the larger spotted dogfish (Scyliorhinus stellaris) were electrically stimulated to exhaustion in a closed seawater recirculation system. The production of large quantities of lactic acid by anaerobic metabolism and the resultant efflux of the dissociation products, H+ and lactate, from the white musculature resulted in severe acid-base disturbances and in increases in plasma lactate concentration, the two effects having extremely different time courses. Plasma pH and bicarbonate were maximally depressed 15–30 min after exercise, whereas peak lactate concentrations of up to 30 mM were not attained before 4–8 h after exercise. The acid-base status were restored to normal 10–14 h after exercise, long before the aerobic processing of surplus lactic acid was complete 22–30 h after exercise. This behaviour can be explained on the basis of an interaction of transfer rates, buffer values and equilibria between intracellular and extracellular compartments with the transient net transfer of surplus H+ ions to the environmental water. About half of the original quantity of H+ was transferred net to the environment via the branchial epithelium during the first 8–10 h, and it was later taken up again at the rate of aerobic lactic acid processing in the metabolism of the fish, whereas a transfer of lactate was not observed at any time during the experiment. As a result, the distribution patterns of H+ and lactate differed from each other and varied with time elapsed after anaerobic exercise, leading to the apparent ‘H+ ion deficit’ which has been observed in the blood of several fish species during lactacidosis. Net transfer of H+ ions to the environment facilitates rapid normalization of the acid-base status long before the original stress, lactic acid, is removed from the organism and thus represents an effective regulatory mechanism for the defence of the internal milieu in fish.

Bone and shell contribution to lactic acid buffering of submerged turtles Chrysemys picta bellii at 3°C

2000 ◽  
Vol 278 (6) ◽  
pp. R1564-R1571 ◽  
Author(s):  
Donald C. Jackson ◽  
Carlos E. Crocker ◽  
Gordon R. Ultsch
Keyword(s):  
Lactic Acid ◽  
Lactate Concentration ◽  
Plasma Lactate ◽  
Acid Base ◽  
Bone Ash ◽  
Chrysemys Picta Bellii ◽  
Bone Water ◽  
Plasma Lactate Concentration ◽  
Plasma Calcium Concentration ◽  
Acid Base Status

To evaluate shell and bone buffering of lactic acid during acidosis at 3°C, turtles were submerged in anoxic or aerated water and tested at intervals for blood acid-base status and plasma ions and for bone and shell percent water, percent ash, and concentrations of lactate, Ca2+, Mg2+, Pi, Na+, and K+. After 125 days, plasma lactate concentration rose from 1.6 ± 0.2 mM (mean ± SE) to 155.2 ± 10.8 mM in the anoxic group but only to 25.2 ± 6.4 mM in the aerated group. The acid-base state of the normoxic animals was stable after 25 days of submergence. Plasma calcium concentration ([Ca2+]) rose during anoxia from 3.2 ± 0.2 to 46.0 ± 0.6 mM and [Mg2+] from 2.7 ± 0.2 to 12.2 ± 0.6 mM. Both shell and bone accumulated lactate to concentrations of 135.6 ± 35.2 and 163.6 ± 5.1 mmol/kg wet wt, respectively, after 125 days anoxia. Shell and bone [Na+] both fell during anoxia but the fate of this Na+ is uncertain because plasma [Na+] also fell. No other shell ions changed significantly in concentration, although the concentrations of both bone calcium and bone potassium changed significantly. Control shell water (27.8 ± 0.6%) was less than bone water (33.6 ± 1.1%), but neither changed during submergence. Shell ash (44.7 ± 0.8%) remained unchanged, but bone ash (41.0 ± 1.0%) fell significantly. We conclude that bone, as well as shell, accumulate lactate when plasma lactate is elevated, and that both export sodium carbonate, as well as calcium and magnesium carbonates, to supplement ECF buffering.

The Effect of Long-Term Aerial Exposure on Heart Rate, Ventilation, Respiratory Gas Exchange and Acid-Base Status in the Crayfish Austropotamobius Pallipes

1981 ◽  
Vol 92 (1) ◽  
pp. 109-124
Author(s):  
E. W. TAYLOR ◽  
MICHÈLE G. WHEATLY
Keyword(s):  
Heart Rate ◽  
Lactic Acid ◽  
O2 Consumption ◽  
Aerial Exposure ◽  
Acid Base ◽  
Bicarbonate Buffer ◽  
Content Difference ◽  
Acid Base Status ◽  
Lactate Levels

1. When first removed into air, crayfish showed transient increases in heart rate (fH) and scaphognathite rate (fR) which rapidly recovered to submerged levels and were unchanged for 24 h. The rate of O2 consumption(Moo2) increased from an initially low level and was then maintained for 24 h in air at the same level as in settled submerged animals. 2. There was an initial acidosis in the haemolymph which was both respiratory and metabolic due to the accumulation of CO2 and lactate. Progressive compensation by elevation of the levels of bicarbonate buffer in the haemolymph and reduction of circulating lactate levels returned pH towards submerged levels after 24 h in air. 3. Exposure to air resulted in a marked internal hypoxia with haemolymph O2, tensions, both postbranchial Pa, oo2 and prebranchial Pv, oo2, remaining low throughout the period of exposure. The oxygen content or the haemolymph was initially reduced, with a - vOO2 content difference close to zero. Within 24 h both Ca, oo2 and Cv, OO2 had returned towards their levels in submerged animals. These changes are explained by the Bohr shift on the haemocyanin consequent upon the measured pH changes. 4. After 48 h in air, MO2 and fH were significantly reduced and ventilation became intermittent. There was a slight secondary acidosis, increase in lactic acid levels and reduction in a - vO2 content difference in the haemolymph. 5. When crayfish were returned to water after 24 h in air, MOO2, fHfR were initially elevated by disturbance and there was a period of hyperventilation. In the haemolymph there was an initial slight alkalosis, and an increase in Ca, OO2 lactic acid. All variables returned to their settled submerged levels within 8 h.

Effect Of Environmental Water Salinity on Acid-Base Regulation During Environmental Hypercapnia in the Rainbow Trout (Oncorhynchus Mykiss)

1991 ◽  
Vol 158 (1) ◽  
pp. 1-18 ◽  
Author(s):  
GEORGE K. IWAMA ◽  
NORBERT HEISLER
Keyword(s):  
Rainbow Trout ◽  
Respiratory Acidosis ◽  
Environmental Water ◽  
Ammonia Concentration ◽  
Acid Base ◽  
Clear Trend ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Exchange Processes ◽  
Total Ammonia ◽  
Time Courses

Acid-base regulation in rainbow trout acclimated to about 3, 100 and 500 mmol l−1 Na+ and Cl−, at constant water [HCO3−], was assessed during 24h of exposure to 1% CO2 and during recovery. The respiratory acidosis induced by a rise in plasma PCOCO2 to about 1.15kPa (8.5mmHg, 3mmol l−1), 1.33kPa (10mmHg, 100 mmol l−1) or 1.5 kPa (11.2 mmHg, 500 mmol l−1) was partially compensated for by accumulation of plasma HCO3−. The degree of pH compensation depended on the salinity of the environmental water, being about 61, 82 and 88% at 3, 100 and 300 mmol l−1 Na+ and Cl−, respectively. [HCO3−] in animals acclimated to 100 and 500 mmol l−1 rose to higher values than that in fish at 3 mmol l−1. Plasma [Cl−] decreased during hypercapnia as compared to control concentrations in all groups of fish. Plasma [Na+] rose during the first 8 h of hypercapnia in fish acclimated to all three salinities, but recovered towards control values during the remainder of hypercapnia. The rise in plasma [HCO3−] was significantly related to the fall in plasma [Cl−], whereas the changes in plasma [Na+] were unaffected by simultaneous changes in plasma [HCO3−]. Time courses of changes in plasma [Na+] and total ammonia concentration, [Tamm], were similar but in opposite directions. The transepithelial potential (TEP) of blood relative to water was negative, close to zero and positive, averaging −21, −5.8 and +6.2 mV for fish acclimated to 3, 100 and 300 mmol l−1 Na+, respectively. After initiation of hypercapnia, which caused a quite heterogeneous response among groups, a clear trend towards depolarization was observed during the remainder of hypercapnia. These results confirm the role of active HCO3−/Cl− exchange processes for the compensation of extracellular pH during respiratory acidoses in fish.

Studies on blood acid-base status and muscle metabolism in working bullocks

1985 ◽  
Vol 40 (1) ◽  
pp. 11-16 ◽  
Author(s):  
R. C. Upadhyay ◽  
M. L. Madan
Keyword(s):  
Heart Rate ◽  
Lactic Acid ◽  
Rectal Temperature ◽  
Muscle Metabolism ◽  
Creatine Phosphate ◽  
Minute Volume ◽  
Acid Base ◽  
Distress Symptoms ◽  
Acid Base Status ◽  
Heavy Loads

ABSTRACTHaryana and crossbred (Holstein × local Haryana) bullocks were subjected to work under heavy loads in summer. During the work, bullocks exhibited distress symptoms. After work, rectal temperature, respiration rate, heart rate and minute volume increased significantly, the average pO2 content increased, muscle lactic acid increased and creatine phosphate level declined. From the results it was evident that oxygen availability in blood improved during work. Despite the enhanced oxygenation of blood, there was accumulation of lactic acid in muscle. This indicated a certain degree of tissue hypoxia, which probably brought about fatigue earlier.

Effect of acid–base status on plasma phosphorus response to lactate

1984 ◽  
Vol 62 (8) ◽  
pp. 939-942 ◽  
Author(s):  
James R. Oster ◽  
Helen C. Alpert ◽  
Carlos A. Vaamonde
Keyword(s):  
Lactic Acid ◽  
Lactic Acidosis ◽  
Sodium Bicarbonate ◽  
Sodium Lactate ◽  
Phosphorus Concentration ◽  
Acid Anion ◽  
Acid Base ◽  
Phosphorus Response ◽  
Acid Base Status ◽  
Plasma Phosphorus

The mechanism(s) underlying the hyperphosphatemia of lactic acidosis is uncertain. We assessed the interacting influence of the acid anion and acid–base status on plasma phosphorus concentration by administering lactic acid alone, lactic acid plus sodium bicarbonate, sodium bicarbonate alone, and sodium lactate alone to four different groups of dogs. The findings of (1) no increase in plasma phosphorus concentration with lactic acid plus sodium bicarbonate versus a marked increment with lactic acid alone, and (2) no difference in the plama phosphorus response to sodium lactate versus sodium bicarbonate indicate that acidemia is necessary for the expression of lactate-induced hyperphosphatemia. The apparent greater propensity for marked hyperphosphatemia in lactic acidosis than in other types of metabolic acidosis remains unexplained, but conceivably might relate to differences in intracellular pH and in the rate of glycolysis.

scholarly journals Single Sodium Pyruvate Ingestion Modifies Blood Acid-Base Status and Post-Exercise Lactate Concentration in Humans

Nutrients ◽  
2014 ◽  
Vol 6 (5) ◽  
pp. 1981-1992 ◽  
Author(s):  
Robert Olek ◽  
Sylwester Kujach ◽  
Damian Wnuk ◽  
Radoslaw Laskowski
Keyword(s):  
Lactate Concentration ◽  
Acid Base ◽  
Sodium Pyruvate ◽  
Post Exercise ◽  
Acid Base Status

The effects of hypercapnia on intracellular and extracellular acid-base status in the toad Bufo marinus

1982 ◽  
Vol 97 (1) ◽  
pp. 79-86
Author(s):  
D. P. Toews ◽  
N. Heisler
Keyword(s):  
Extracellular Space ◽  
Environmental Water ◽  
Bufo Marinus ◽  
Acid Base ◽  
Relative Preference ◽  
Base Parameters ◽  
Initial Drop ◽  
Acid Base Status ◽  
Body Compartments ◽  
Induced Changes

Toads (Bufo marinus) were exposed to environmental hypercapnia of 5% CO2 in air, and extracellular and intracellular acid-base parameters were determined 1 and 24 h after the onset of hypercapnia. The initial drop in pH was compensated by the elevation of extracellular and intracellular bicarbonate. Relating the pH compensation to the pH drop that is expected to occur by increased PCO2 at constant bicarbonate concentration, the pH compensation in the extracellular space was 30% and reached the following values for intracellular body compartments: 65% in skeletal muscle, 77% in heart muscle and 44% in skin. The additional bicarbonate was partly produced by blood and intracellular non-bicarbonate buffers; the major portion of the remainder was related to the excretion of ammonia into the environmental water. The hypercapnia-induced changes of pH were considerably smaller in all tissue cells than in the extracellular space. Thus Bufo marinus exhibits the relative preference of intracellular over extracellular acid-base regulation that has been observed in other vertebrates.

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