Intracellular and extracellular acid-base status and H+ exchange with the environment after exhaustive exercise in the rainbow trout

1986 ◽  
Vol 123 (1) ◽  
pp. 93-121 ◽  
Author(s):  
C. L. Milligan ◽  
C. M. Wood

Exhaustive exercise induced a severe short-lived (0–1 h) respiratory, and longer-lived (0–4 h) metabolic, acidosis in the extracellular fluid of the rainbow trout. Blood ‘lactate’ load exceeded blood ‘metabolic acid’ load from 1–12 h after exercise. Over-compensation occurred, so that by 8–12 h, metabolic alkalosis prevailed, but by 24 h, resting acid-base status had been restored. Acid-base changes were similar, and lactate levels identical, in arterial and venous blood. However, at rest venous RBC pHi was significantly higher than arterial (7.42 versus 7.31). After exercise, arterial RBC pHi remained constant, whereas venous RBC pHi fell significantly (to 7.18) but was fully restored by 1 h. Resting mean whole-body pHi, measured by DMO distribution, averaged approx. 7.25 at a pHe of approx. 7.82 and fell after exercise to a low of 6.78 at a pHe of approx. 7.30. Whole-body pHi was slower to recover than pHe, requiring up to 12 h, with no subsequent alkalosis. Whole-body ECFV decreased by about 70 ml kg-1 due to a fluid shift into the ICF. Net H+ excretion to the water increased 1 h after exercise accompanied by an elevation in ammonia efflux. At 8–12 h, H+ excretion was reduced to resting levels and at 12–24 h, a net H+ uptake occurred. Lactate excretion amounted to approx. 1% of the net H+ excretion and only approx. 2% of the whole blood load. Only a small amount of the anaerobically produced H+ in the ICF appeared in the ECF and subsequently in the water. By 24 h, all the H+ excreted had been taken back up, thus correcting the extracellular alkalosis. The bulk of the H+ load remained intracellular, to be cleared by aerobic metabolism.

1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER

The intracellular acid-base status of white muscle of freshwater (FW) and seawater (SW) -adapted rainbow trout was examined before and after exhaustive exercise. Exhaustive exercise resulted in a pronounced intracellular acidosis with a greater pH drop in SW (0.82 pH units) than in FW (0.66 pH units) trout; this was accompanied by a marked rise in intracellular lactate levels, with more pronounced increases occurring in SW (54.4 mmoll−1) than in FW (45.7 mmoll−1) trout. Despite the more severe acidosis, recovery was faster in the SW animals, as indicated by a more rapid clearance of metabolic H+ and lactate loads. Compartmental analysis of the distribution of metabolic H+ and lactate loads showed that the more rapid recovery of pH in SW trout could be due to (1) their greater facility for excreting H+ equivalents to the environmental water [e.g. 15.5 % (SW) vs 5.0 % (FW) of the initial H+ load was stored in external water at 250 min post-exercise] and, to a greater extent, (2) the more rapid removal of H+, facilitated via lactate metabolism in situ (white muscle) and/or the Cori cycle (e.g. heart, liver). The slower pH recovery in FW trout may also be due in part to greater production of an ‘unmeasured acid’ [maximum approx. 8.5 mmol kg−1 fish (FW) vs approx. 6 mmol kg−1 fish (SW) at 70–130 min post-exercise] during the recovery period. Furthermore, the analysis revealed that H+-consuming metabolism is quantitatively the most important mechanism for the correction of an endogenously originating acidosis, and that extracellular pH normalization gains priority over intracellular pH regulation during recovery of acid-base status following exhaustive exercise.


1989 ◽  
Vol 147 (1) ◽  
pp. 471-491 ◽  
Author(s):  
D. G. MCDONALD ◽  
Y. TANG ◽  
R. G. BOUTILIER

Rainbow trout, fitted with arterial catheters, were exercised to exhaustion by manual chasing and then injected with either saline (controls), the β-agonist isoproterenol or the β-antagonist propranolol. Blood acid-base status, branchial unidirectional and net fluxes of Na+ and Cl−, and net fluxes of ammonia and acidic equivalents (JHnet) were monitored over the subsequent 4 h of recovery. These same parameters were also monitored in normoxic, resting fish following isoproterenol injection and in exercised fish following acute post-exercise elevation of external NaCl concentration. In addition to confirming an important role for β-adrenoreceptors in the regulation of branchial gas exchange and red cell oxygenation and acid-base status, we find a significant β-adrenergic involvement in the flux of lactic acid from muscle and in JHnet across the gills. Both isoproterenol infusion (into nonexercised fish) and exhaustive exercise were found to cause net acid excretion. The post-exercise JHnet was further augmented by elevating [NaCl] but was not affected, in this instance, either by β-stimulation or blockade, indicating that JHnet was not entirely regulated by a β-adrenergic mechanism. On the basis of a detailed analysis of unidirectional Na+ and Cl− fluxes, we conclude that the increase in JHnet following exercise arose mainly from increased Na+/H+(NH4+) exchange and that the upper limit on JHnet was set by the supply of external counterions and by the increase in branchial ionic permeability that invariably accompanies exhaustive exercise.


1992 ◽  
Vol 167 (1) ◽  
pp. 155-169 ◽  
Author(s):  
M. Scarabello ◽  
G. J. Heigenhauser ◽  
C. M. Wood

Juvenile rainbow trout (approximately 6 g) were exercised to exhaustion in two 5 min bouts given 6 h apart. Resting levels of whole-body lactate and glycogen were restored prior to the second bout. The rate of O2 consumption increased about threefold 5 min after each bout of exercise, while recovery time decreased from 4 h after the first bout to 2–3 h after the second. The excess post-exercise oxygen consumption, i.e. ‘oxygen debt’, was significantly reduced by 40% after the second exercise bout, despite almost identical rates of lactate clearance and glycogen resynthesis. The rates of CO2 and ammonia excretion increased sixfold and threefold, and recovery times decreased from 4–6 h to 3 h and from 3 h to 1.5 h, respectively. After the first bout, whole-body lactate levels peaked at 5 min post-exercise at about 8.5 times pre-exercise levels. After the second bout, lactate levels peaked at 0 min post-exercise and fell more rapidly during recovery. Whole-body glycogen levels decreased by 70% and 80% and ATP levels decreased by 75% and 65% after the first and second bouts, respectively, while glucose levels increased about 1.5-fold immediately after both bouts. Creatine phosphate levels decreased by 70% and 80% after the first and second bouts, respectively. After 6 h of recovery, creatine phosphate levels were higher after the second bout than after the first. These findings suggest that exhaustive exercise may cause a ‘non-specific’ increase in metabolic rate not directly related to the processing of metabolites, which is reduced upon a subsequent exercise bout. This is in contrast with the classical ‘oxygen debt hypothesis’, which states that the oxygen debt and lactate clearance are linked. Furthermore, it appears that two sequential exercise bouts are sufficient to induce a ‘training effect’, i.e. improved rates of metabolic recovery.


2000 ◽  
Vol 203 (5) ◽  
pp. 921-926 ◽  
Author(s):  
C.L. Milligan ◽  
G.B. Hooke ◽  
C. Johnson

Sustained swimming at 0.9 BL s(−)(1), where BL is fork body length, following a bout of exhaustive exercise enhanced recovery of metabolite and acid-base status in rainbow trout compared with fish held in still water. The most striking effect of an active recovery was a total absence of the elevation cortisol concentration typically associated with exhaustive exercise. In fish swimming at 0. 9 BL s(−)(1), plasma cortisol levels averaged 20–25 ng ml(−)(1) throughout the 6 h recovery period. In contrast, plasma cortisol increased to a peak level of 128.4+/−11.2 ng ml(−)(1) (mean +/− s.e. m., N=6) in fish recovering in still water. Muscle glycogen was completely resynthesized and lactate cleared within 2 h of exercise in swimming fish compared with more than 6 h required in the fish held in still water. Similarly, blood lactate level and acid-base status were restored more quickly in the swimming fish. These observations suggest that the prolonged recovery usually associated with exhaustive exercise in rainbow trout is due to elevations in plasma cortisol concentration and that the stimulus for cortisol release is not exercise per se, but rather post-exercise inactivity.


1996 ◽  
Vol 199 (4) ◽  
pp. 933-940
Author(s):  
B Tufts ◽  
S Currie ◽  
J Kieffer

In vivo experiments were carried out to determine the relative effects of carbonic anhydrase (CA) infusion or inhibition on carbon dioxide (CO2) transport and acid-base status in the arterial and venous blood of sea lampreys recovering from exhaustive exercise. Infusion of CA into the extracellular fluid did not significantly affect CO2 transport or acid-base status in exercised lampreys. In contrast, infusion of the CA inhibitor acetazolamide resulted in a respiratory acidosis in the blood of recovering lampreys. In acetazolamide-treated lampreys, the post-exercise extracellular pH (pHe) of arterial blood was significantly lower than that in the saline-infused (control) lampreys. The calculated arterial and venous partial pressure of carbon dioxide (PCO2) and the total CO2 concentration in whole blood (CCO2wb) and red blood cells (CCO2rbc) during recovery in the acetazolamide-infused lampreys were also significantly greater than those values in the saline-infused control lampreys. These results suggest that the CO2 reactions in the extracellular compartment of lampreys may already be in equilibrium and that the access of plasma bicarbonate to CA is probably not the sole factor limiting CO2 transport in these animals. Furthermore, endogenous red blood cell CA clearly has an important role in CO2 transport in exercising lampreys.


2021 ◽  
pp. 2714-2718
Author(s):  
Annika Heitland ◽  
Ute Klein-Richers ◽  
Katrin Hartmann ◽  
René Dörfelt

Background and Aim: Acetate or lactate buffered, balanced isotonic rehydration fluids are commonly used for fluid therapy in dogs and may influence acid-base and electrolyte status. This study aimed to assess acid-base status, electrolyte levels, and lactate levels in dehydrated dogs after receiving acetate or lactate-containing intravenous rehydration fluids. Materials and Methods: In this prospective, randomized study, 90 dehydrated dogs were included and randomized to receive acetate [Sterofundin® ISO B. Braun Vet Care (STERO), Germany) or lactate (Ringer-Lactat-Lösung nach Hartmann B. Braun Vet Care (RL), Germany] containing intravenous fluids for rehydration. The exclusion criteria were as follows: Age <6 months, liver failure, congestive heart failure, and extreme electrolyte deviation. Physical examination, venous blood gas, and lactate levels were analyzed before and after rehydration. The two groups were compared using t-test and Chi-square test. The significance level was set at p≤0.05. Results: Post-rehydration heart rate decreased in the STERO group (p<0.001) but not in the RL group (p=0.090). Lactate levels decreased in both groups STERO (p<0.001) and in group RL (p=0.014). Sodium and chloride levels increased during rehydration in group STERO (p<0.001; p<0.001) and group RL (p=0.002; p<0.001). There was a larger decrease in lactate levels in group STERO compared to group RL (p=0.047). Conclusion: Both solutions led to a mild increase in sodium and chloride levels and decreased lactate levels. The acetate-containing solution had an inferior effect on the decrease in lactate level.


1997 ◽  
Vol 78 (5) ◽  
pp. 683-693 ◽  
Author(s):  
D. Ball ◽  
R. J. Maughan

The effect of long-term differences in diet composition on whole-body acid–base status was examined in thirty-three young healthy females. The volunteers were recruited from two separate groups matched approximately for age, height and weight; one group regularly ate meat (omnivores; n 20) and one group did not (vegetarians; n 13). All subjects completed a 7 d weighed intake of food, and from their dietary records, total energy, carbohydrate (CHO), fat and protein content were estimated using computer-based food composition tables. During this week they reported to the laboratory on two occasions, following an overnight fast and separated by at least 48h. Arterialized venous blood samples were obtained on each visit and these were analysed for blood acid–base status. Haemoglobin and packed cell volume, serum total cholesterol and HDL-cholesterol, serum albumin and total protein were also determined. Two 24 h urine collections were completed; the volume was recorded and samples were analysed for pH, titratable acid and Mg and Ca concentration. Total energy intake of the omnivores was greater (P = 0.0003) than that of the vegetarian group. Dietary intake of CHO (P = 0.024), fat (P = 0.0054) and protein (P = 0.0002) were higher in the omnivorous group than in the vegetarians. There were no differences between the two groups with respect to blood CO2 partial pressure, plasma HCO3- and blood base excess, but blood pH was slightly higher in the omnivores (P = 0.064). Measures of urine acid–base status suggested a lower pH in the omnivore group, but this difference was not statistically significant; a greater titratable acid output was observed with the omnivorous group compared with the vegetarians (48.9 (se 20.3) ν. 35.3 (se 23.3) mEq/24h; P = 0.018). Although the dietary intake of Ca was not different between the two groups, urinary Ca excretion of the omnivores was significantly higher (3.87 (sd 1.34) ν. 3.22 (sd 1.20) mmol/24h) than that of the vegetarians (P = 0.014). It is suggested that the higher protein intake of the omnivores resulted in an increase in urinary total acid excretion, which may explain the higher rate of Ca excretion.


1986 ◽  
Vol 123 (1) ◽  
pp. 123-144 ◽  
Author(s):  
C. L. Milligan ◽  
C. M. Wood

Exhaustive ‘burst-type’ exercise in the rainbow trout resulted in a severe acidosis in the white muscle, with pHi dropping from 7.21 to a low of 6.62, as measured by DMO distribution. An accumulation of lactate and pyruvate, depletions of glycogen, ATP and CP stores, and a fluid shift from the extracellular fluid to the intracellular fluid of white muscle were associated with the acidosis. The proton load was in excess of the lactate load by an amount equivalent to the drop in ATP, suggesting that there was an uncoupling of ATP hydrolysis and glycolysis. Initially, lactate was cleared more quickly than protons from the muscle, a difference that was reflected in the blood. It is suggested that during the early period of recovery (0–4 h), the bulk of the lactate was oxidized in situ, restoring pHi to a point compatible with glyconeogenesis. At that time, lactate and H+ were used as substrates for in situ glyconeogenesis, which was complete by 24 h. During this time, lactate and H+ disappearance could account for about 75% of the glycogen resynthesized. The liver and heart showed an accumulation of lactate, and it is postulated that this occurred as a result of uptake from the blood. Associated with the lactate load in these tissues was a metabolic alkalosis. Except for an apparent acidosis immediately after exercise, the acid-base status of the brain was not appreciably affected. Despite the extracellular acidosis, red cell pHi remained nearly constant.


1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood

Blood gases, acid-base status, plasma ions, respiration, ventilation and cardiovascular function were measured in white suckers, using standard cannulation methods. Basic respiratory parameters under normoxia were compared to those in the active, pelagic rainbow trout and in other benthic teleosts. Sustained environmental hyperoxia (350–550 torr) increased arterial O2 (102–392 torr) and venous O2 (17–80 torr) tensions so that blood O2 transport occurred entirely via physical solution. Dorsal aortic blood pressure and heart rate fell, the latter due to an increase in vagal tone. Ventilation volume declined markedly (by 50%) due to a decrease in ventilatory stroke volume, but absolute O2 extraction rose so that O2 consumption was unaffected. While the preceding effects were stable with time, arterial and venous CO2 tensions approximately doubled within 4 h, and continued to increase gradually thereafter. This CO2 retention caused an acidosis (7.993–7.814) which was gradually compensated by an accumulation of plasma [HCO3−]. However, even after 72 h, arterial pH remained significantly depressed by 0.10 units. The gradual rise in plasma [HCO3−] was accompanied by a progressive fall in both [Na+] and [Cl−]; [K+] and [Ca2+] remained unchanged. The responses of the sucker to hyperoxia are compared to those of the rainbow trout.


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