Physiological Consequences of Severe Exercise in the Inactive Benthic Flathead Sole (Hippoglossoides Elassodon): A Comparison With The Active Pelagic Rainbow Trout (Salmo Gairdneri)

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.

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.


1976 ◽  
Vol 33 (1) ◽  
pp. 173-176 ◽  
Author(s):  
William R. Driedzic ◽  
Joe W. Kiceniuk

Rainbow trout (Salmo gairdneri) were exercised to fatigue in a series of 60-min stepwise increasing velocity increments. There was no increase in blood lactate concentration, serially sampled during swimming by means of indwelling dorsal and ventral aortic catheters, at velocities as high as 93% of critical velocity of individuals. The data show that under these conditions the rate of production of lactate by white muscle, at less than critical velocities, is minimal or that the rate of elimination of lactate from white muscle is equal to its rate of utilization elsewhere. Immediately following fatigue blood lactate level increases rapidly. During the recovery period there appears to be a net uptake of lactate by the gills.


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.


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.


1979 ◽  
Vol 57 (10) ◽  
pp. 1863-1865 ◽  
Author(s):  
Roger M. Evans

Seawater-adapted teleosts drink to offset water loss by osmosis. A direct method of monitoring drinking by implanting a fistula to drain the stomach indicated that rainbow trout began drinking from about 9 to 12 (range 1 to 22) h after being placed in 15‰ sea water. Unlike the Japanese eel (Anguilla japonica). in which the onset of drinking has been shown to be immediate and reflex-like, the onset of drinking in trout appears to occur only after appreciable water has been lost to the medium. The trout resembles the eel in that the capacity to shallow water in the absence of postingestional negative feedback exceeds the rate of drinking required to maintain normal water balance.


1972 ◽  
Vol 29 (10) ◽  
pp. 1467-1471 ◽  
Author(s):  
E. Bilinski ◽  
R. E. E. Jonas

A comparative study on the ability of various fish tissues to carry out different stages of lactate oxidation was conducted with rainbow trout (Salmo gairdneri). Rate of oxidation of Na-L-lactate-1-14C (5 mM) and Na-L-lactate-3-14C (5 mM) by tissue slices from white muscle, red lateral line muscle, heart, liver, kidney, and gills was determined at 15 C by measuring the formation of 14CO2. In all tissues the liberation of 14CO2 was considerably higher with lactate-1-14C than with lactate-3-14C. Liver was the most active tissue for oxidation of lactate-1-14C (2805 mμmoles/g wet tissue/hr at 15 C) and gills for oxidation of lactate-3-14C (556 mμmoles/g wet tissue/hr at 15 C). With both substrates activity in the white muscle was very limited, whereas other tissues had an intermediate level of activity. The results suggest that, in trout, the catabolism of lactate may take place through oxidative decarboxylation of pyruvate and that liver plays an important role in such a process. It appears also that complete oxidation of lactate may be of significance in supplying energy for the exchange reactions in gills.


1968 ◽  
Vol 25 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Joseph B. Hunn ◽  
Richard A. Schoettger ◽  
Wayne A. Willford

Rainbow trout: (Salmo gairdneri) anesthetized in 100 mg/liter of M.S. 222 at 12 C excreted the drug in free and acetylated forms via the urine during a 24-hr recovery period in freshwater. Of the M.S. 222 excreted, 77–96% was acetylated. Blood levels of free drug in anesthetized trout approximated 75% of the anesthetic concentration, but the amount of acetylated M.S. 222 was relatively insignificant. The blood and urine were cleared of the two fractions of M.S. 222 in 8 and 24 hr respectively. Low levels of aromatic amines of natural origin occurred in blood and urine and were subtracted from measurements of M.S. 222. Intraperitoneal injections of 10–100 mg/kg of M.S. 222 did not induce anesthesia; however, the 24-hr pattern of drug excretion was similar to that observed after anesthesia by immersion. Only 15–21% of the injected dose was found in the urine, suggesting a second route of drug elimination.


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