scholarly journals Gas exchange, metabolite status and excess post-exercise oxygen consumption after repetitive bouts of exhaustive exercise in juvenile rainbow trout

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.

1991 ◽  
Vol 69 (10) ◽  
pp. 2562-2568 ◽  
Author(s):  
M. Scarabello ◽  
C. M. Wood ◽  
G. J. F. Heigenhauser

Glycogen depletion was used as an experimental tool to examine the relationship between excess post-exercise oxygen consumption and lactate metabolism in 6-g rainbow trout. A 5-day starvation period reduced whole-body glycogen stores by 50% and slightly lowered resting lactate levels; resting oxygen consumption, glucose, ATP, and creatine phosphate levels were not affected. After a 5-min bout of exhaustive exercise, significantly less glycogen was utilized by the glycogen-depleted fish, 40% less lactate was accumulated, and glucose levels did not rise in comparison with the control group. Creatine phosphate recovered more quickly in the glycogen-depleted fish, whereas ATP was unaffected. Recovery from excess post-exercise oxygen consumption was not significantly different despite the large absolute differences in lactate removed and glycogen resynthesized. This experimental test demonstrates that the classical oxygen debt hypothesis does not completely explain the excess post-exercise oxygen consumption in the 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.


1993 ◽  
Vol 180 (1) ◽  
pp. 175-193 ◽  
Author(s):  
C. L. Milligan ◽  
S. S. Girard

We have investigated the metabolic fate of blood lactate in resting rainbow trout and in fish recovering from a bout of exhaustive exercise. At rest and during recovery from exercise, the majority of blood lactate was oxidized, the proportion increasing with increasing oxygen consumption. It is estimated that, during recovery from exhaustive exercise, lactate released from the muscle has the potential to fuel a significant portion of oxidative metabolism. The bulk of the remaining blood lactate reappeared in the muscle lactate pool, probably via direct uptake by the muscle. There was a significant incorporation of blood lactate into the muscle glycogen pool, providing strong evidence for in situ glycogenesis as the mode for muscle glycogen replenishment. To investigate the role of the liver in blood lactate clearance, trout were functionally hepatectomized by ligation of the hepatic portal circulation. The exercise performance of hepatectomized fish was equal to that of sham- operated fish and controls, indicating that muscle relies primarily on endogenous fuel stores. Furthermore, blood lactate levels immediately after exercise were greater and muscle metabolic recovery was faster in hepatectomized fish than in sham-operated fish and controls. These observations suggest that glycogen resynthesis in trout muscle may be retarded because of a non- recoverable loss of substrate (i.e. lactate) from the muscle, because the lactate released is utilized by the liver. These results are discussed in view of what is known about these processes in other ectothermic vertebrates.


2001 ◽  
Vol 204 (24) ◽  
pp. 4281-4289
Author(s):  
James D. Kieffer ◽  
Andrea M. Wakefield ◽  
Matthew K. Litvak

SUMMARYExperiments were conducted to determine the physiological responses to exercise of Atlantic sturgeon (Acipenser oxyrhynchus) and shortnose sturgeon (A. brevirostrum). We measured the rates of oxygen consumption and ammonia excretion in both species and a variety of physiological parameters in both muscle (e.g. lactate, glycogen, pyruvate, glucose and phosphocreatine concentrations) and blood (e.g. osmolality and lactate concentration) in juvenile shortnose sturgeon following 5 min of exhaustive exercise.In both species, oxygen consumption and ammonia excretion rates increased approximately twofold following exhaustive exercise. Post-exercise oxygen consumption rates decreased to control levels within 30 min in both sturgeon species, but post-exercise ammonia excretion rates remained high in Atlantic sturgeon throughout the 4 h experiment. Resting muscle energy metabolite levels in shortnose sturgeon were similar to those of other fish species, but the levels decreased only slightly following the exercise period and recovery occurred within an hour. Under resting conditions, muscle lactate levels were low (<1 μmol g–1) but they increased to approximately 6 μmol g–1 after exercise, returning to control levels within 6 h. Unlike similarly stressed teleost fish, such as the rainbow trout, plasma lactate levels did not increase substantially and returned to resting levels within 2 h. Plasma osmolality was not significantly affected by exercise in shortnose sturgeon.Taken together, these results suggest that shortnose and Atlantic sturgeon do not exhibit the physiological responses to exhaustive exercise typical of other fish species. They may possess behavioural or endocrinological mechanisms that differ from those of other fishes and that lead to a reduced ability to respond physiologically to exhaustive exercise.


1995 ◽  
Vol 198 (12) ◽  
pp. 2465-2475 ◽  
Author(s):  
D Hastings ◽  
W Burggren

Well-developed larval Xenopus laevis (NF stages 58­66) are oxygen regulators, at least during mild hypoxia. When and how they change from oxygen conformers (the presumed condition of the fertilized egg) to oxygen regulators is unknown. Also unknown is how anaerobic metabolic capabilities change during development, especially in response to acute hypoxia, and to what extent, if any, anaerobiosis is used to supplement aerobic metabolism. Consequently, we have investigated resting rates of oxygen consumption (M.O2) and concentrations of whole-body lactate (lactic acid) during development in normoxia and in response to acute hypoxia in Xenopus laevis. M.O2 increased in an episodic, non-linear fashion during development. Resting, normoxic M.O2 increased about tenfold (to approximately 0.20 µmol g-1 h-1) between NF stages 1­39 and 40­44, and then another tenfold between NF stages 45­48 and 49­51 (to approximately 2.0 µmol g-1 h-1), remaining at about 2 µmol g-1 h-1 for the remainder of larval development. M.O2 reached its highest level in newly metamorphosed frogs (nearly 4 µmol g-1 h-1), before decreasing to about 1.0 µmol g-1 h-1 in large adults. X. laevis embryos and larvae up to NF stage 54­57 were oxygen conformers when exposed to variable levels of acute hypoxia. The only exception was NF stage 45­48 (external gills present yet body mass still very small), which showed some capability of oxygen regulation. All larvae older than stage 54­57 and adults were oxygen regulators and had the lowest values of Pcrit (the oxygen partial pressure at which M.O2 begins to decline). Whole-body lactate concentration in normoxia was about 1 µmol g-1 for all larval groups, rising to about 12 µmol g-1 in adults. Concentrations of lactic acid in NF stages 1­51 were unaffected by even severe ambient hypoxia. However, whole-body lactate levels in NF stages 52­66 increased in response to severe hypoxia, indicating that some anaerobic metabolism was being used to supplement diminishing aerobic metabolism. The largest increases in concentration of lactate occurred in late larvae and adults.


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.


1975 ◽  
Vol 38 (5) ◽  
pp. 763-767 ◽  
Author(s):  
J. Karlsson ◽  
F. Bonde-Petersen ◽  
J. Henriksson ◽  
H. G. Knuttgen

The ability of additional muscles to perform after certain other muscles of the body had been exercised to exhaustion was studied in three male subjects. Exhaustive exercise was performed in two series: series L-A, a bout of leg exercise preceded a bout of arm exercise; series A-L, arm preceded leg (6-min recovery between bouts). Biopsies were taken during the course of each experiment from both the deltoideus and vastus lateralis muscles for determination of ATP, creatine phosphate, lactate, and pyruvate. Exhaustive exercise led to marked elevations in lactate and decreases in ATP and CP in exercised muscle and marked increases in blood lactate concentration. Similar changes, especially in lactate, were observed during and after the first exercise bout in nonexercised muscle. When arm or leg exercise was performed as the second bout, decreases in performance time were observed as compared to performance as the initial bout. It is suggested that the performance potential of muscle is decreased because of internal changes elicited by elevated blood lactate and/or blood H+ concentrations brought about by other muscle groups previously exercised to exhaustion.


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