White Muscle Intracellular Acid-Base and Lactate Status Following Exhaustive Exercise: A Comparison between Freshwater- and Sea Water- Adapted Rainbow Trout

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.


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.


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.


1983 ◽  
Vol 104 (1) ◽  
pp. 247-268 ◽  
Author(s):  
JEFFREY D. TURNER ◽  
CHRIS M. WOOD ◽  
DONNA CLARK

Chronically cannulated rainbow trout were subjected to 6 min of severe burst exercise and monitored over a 12 h recovery period. There were short-lived increases in haematocrit, haemoglobin, plasma protein, Na+ and Cl− levels. Plasma [Cl−] later declined below normal as organic anions accumulated. A much larger and more prolonged elevation in plasma [K+] probably resulted from intracellular acidosis. An intense extracellular acidosis was initially of equal respiratory (i.e. Pa,COa,CO2) a nd metabolic (i.e. ΔH+m) origin. However Pa,COa,CO2 was rapidly corrected while the metabolic component persisted. Plasma ammonia increases had negligible influence on acid-base status. Elevations in blood lactate (ΔLa−) were equal to ΔH+m immediately post-exercise but later rose to twice the latter. Simultaneous white muscle biopsies and blood samples demonstrated that muscle to blood gradients of lactate and pyruvate were maximal immediately post-exercise. As blood levels rose and muscle levels declined, an approximate equilibrium was reached after 4 h of recovery. Intra-arterial infusions of lactic acid in resting trout produced a severe but rapidly corrected metabolic acidosis. The rates of disappearance of ΔH+m and ΔLa− from the blood were equal. Infusions of similar amounts of sodium lactate produced a small, prolonged metabolic alkalosis with a much slower ΔLa− disappearance rate. It is suggested that the excess of ΔLa− over ΔH+m in the blood after exercise is associated with differential release rates of the two species from white muscle rather than differential removal rates from the bloodstream, and that the majority of the lactic acid load in muscle is removed by metabolism in situ.


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.


1993 ◽  
Vol 180 (1) ◽  
pp. 195-207 ◽  
Author(s):  
R. A. Ferguson ◽  
J. D. Kieffer ◽  
B. L. Tufts

The effect of body size on the white muscle acid-base and metabolite status was examined in rainbow trout (Oncorhynchus mykiss) ranging in length from 8 to 54 cm. Following 5 min of exhaustive exercise, white muscle lactate concentration was approximately doubled (approximately 32 micromole g-1) in larger fish than in smaller fish (approximately 16 micromole g-1). Associated with this post-exercise increase in lactate was a nearly parallel increase in the number of metabolic protons produced by larger fish. Larger fish did not possess a greater non-bicarbonate buffering capacity or soluble protein concentration, so their mean muscle intracellular pH (pHi) decreased by approximately 0.70 units compared with a change in mean pHi of about 0.40 units in the smallest fish. The relationship between resting pHi and length was independent of size (mean pHi 7.31). Concentrations of muscle energy metabolites were also determined in trout white muscle before and after exercise. Under resting conditions, larger fish possessed a twofold greater concentration of ATP (approximately 7 micromole g-1) than did smaller fish (approximately 3micromole g-1). Similarly, resting values of muscle glycogen range from about 6 micromole g-1 in the smallest fish to as high as 15 micromole g-1 in the largest fish. However, the smaller fish had higher levels (approximately 35 micromole g- 1) of phosphocreatine (PCr) than the larger fish (approximately 25 micromole g-1). Following exercise, however, both ATP and glycogen concentrations remained size-dependent and increased with increases in fish length. Levels of PCr were size-independent following exercise. These results demonstrate that body size has an important influence on the acid- base and metabolic status of fish before and after exercise.


1983 ◽  
Vol 104 (1) ◽  
pp. 269-288 ◽  
Author(s):  
JEFFREY D. Turner ◽  
CHRIS M. WOOD ◽  
HELVE HÖBE

Chronically cannulated flathead sole were subjected to 10 min of either moderate or exhausting burst exercise and monitored over a 12 h recovery period. Acid-base disturbances were more severe after exhausting exercise, but ionic and haematological changes were the same in the two treatments. Most effects were qualitatively similar to those previously described in severely exercised rainbow trout (Turner, Wood & Clark, 1983). Specific differences are discussed and related to the different external environments sea water vs fresh water), exercise capabilities and ecologies of the two species. The most striking divergence occurred in lactate (La−) and metabolic proton dynamics. Post-exercise La− levels in white muscle in sole were less than half those in trout but declined much more slowly. In contrast to the situation in trout, muscle [La−] remained significantly elevated and large muscle to blood La− gradient persisted even after 12 h recovery. Blood [La−] underwent only minimal elevation (<2 mequiv 1−1), and blood metabolic proton load (ΔH+m) greatly exceeded Δ;La− throughout the recovery period, effects directly opposite those in trout. This observed excess of ΔH+m over ΔLa− in the blood of exercised sole is probably not due to a preferential removal mechanism, because ΔH+m and ΔLa− disappeared from the blood at similar rates after an intra-arterial infusion of lactic acid in resting animals. It is therefore argued that the phenomenon reflects a differential release of the two metabolites from the white muscle of the sole, La− being strictly retained in the muscle for gluconeogenesis in situ.


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