Adrenergic Regulation of Blood Acid-Base Status following Exhaustive Exercise in Seawater-Adapted Rainbow Trout, Salmo gairdneri

1989 ◽  
Vol 62 (4) ◽  
pp. 950-963 ◽  
Author(s):  
Y. Tang ◽  
D. G. McDonald ◽  
R. G. Boutilier
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 141 (1) ◽  
pp. 407-418 ◽  
Author(s):  
Y. TANG ◽  
D. G. McDONALD ◽  
R. G. BOUTILIER

Blood acid-base regulation following exhaustive exercise was investigated in freshwater- (FW) and seawater- (SW) adapted rainbow trout (Salmo gairdneri) of the same genetic stock. Following exhaustive exercise at 10°C, both FW and SW trout displayed a mixed respiratory and metabolic blood acidosis. However, in FW trout the acidosis was about double that of SW trout and arterial blood pH took twice as long to correct. These SW/FW differences were related to the relative amounts of net H+ equivalent excretion to the environmental water, SW trout excreting five times as much as FW trout. The greater H+ equivalent excretion in SW trout may be secondary to changes in the gills that accompany the adaptation from FW to SW. It may also be related to the higher concentrations of HCO3− as well as other exchangeable counter-ions (Na+ and Cl−) in the external medium in SW compared to FW.


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.


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.


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.


1988 ◽  
Vol 134 (1) ◽  
pp. 297-312 ◽  
Author(s):  
Y. Tang ◽  
S. Nolan ◽  
R. G. Boutilier

A fall in blood pH was induced by intra-arterial infusion of HCl in seawater-adapted rainbow trout (Salmo gairdneri). The acute acidosis resulting from HCl infusion caused a short-lived decrease in plasma bicarbonate concentration ([HCO3-]) and an increase in arterial CO2 tension (PaCO2). Erythrocyte pH and bicarbonate concentrations were not significantly altered by the infusion of acid. Injection of acid did, however, stimulate a branchial net H+ efflux which could be primarily accounted for by a net uptake of bicarbonate equivalent ions from the environmental water. Acid infusion of animals pre-treated with the beta-adrenergic blocking agent, propranolol, induced a similar pattern of change in plasma acid-base status. However, the recovery of plasma pH and restoration of plasma [HCO3-] were slower than in animals infused with acid alone. Red cell pH fell significantly in the face of plasma acidosis in the beta-blocked animals. Erythrocyte [HCO3-] showed a similar pattern of change to that of erythrocyte pH. Branchial net H+ efflux increased to a lesser extent following acid infusion in animals treated with propranolol. We conclude that catecholamines released into the bloodstream during periods of acute acidosis may play an important role in facilitating branchial H+ efflux in seawater-adapted rainbow trout.


1987 ◽  
Vol 128 (1) ◽  
pp. 235-253 ◽  
Author(s):  
S. I. Perry ◽  
M. G. Vermette

Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels of this hormone to those measured during periods of acute extracellular acidosis (approximately 5 X 10(−8) mol l-1). Concomitant effects on selected blood respiratory acid-base and ionic variables were evaluated. Infusion of epinephrine caused a transient respiratory acidosis as a result of hypoventilation and/or inhibition of red blood cell (RBC) bicarbonate dehydration. The acidosis was regulated by gradual accumulation of plasma bicarbonate. Even though whole blood pH (pHe) was depressed by 0.16 units, RBC pH (pHi) remained constant, thereby causing the transmembrane pH gradient (pHe-pHi) to decrease. A similar effect of epinephrine on RBC pH was observed in vitro, although the response required a higher concentration of epinephrine (2.0 X 10(−7) mol l-1). We speculate that the release of epinephrine during periods of depressed blood pH is important for preventing excessive shifts in RBC pH and for initiating a series of responses leading to plasma HCO3- accumulation and eventual restoration of blood acid-base status.


1981 ◽  
Vol 59 (6) ◽  
pp. 1126-1132 ◽  
Author(s):  
S. F. Perry ◽  
T. A. Heming

Effect of pseudobranch denervation on the ability of Salmo gairdneri to regulate blood ionic and acid–base balance was investigated in freshwater and following transfer to seawater. Denervation of the pseudobranch did not affect internal ionic or acid–base equilibrium in freshwater. Plasma [Cl−], [Na+], pH, total [Formula: see text], and partial pressure of [Formula: see text] of trout were affected by transfer from freshwater to seawater, and by transfer back to freshwater. These ionic and acid–base responses were not affected by denervation of the pseudobranch. It is concluded that alone, the pseudobranch plays little or no role in ionic and osmotic regulation during transfer between freshwater and seawater.


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