/pdf/metabolic-recovery-from-exhaustive-exercise-in-rainbow-trout-381l79eq9i.pdf

Metabolic recovery from exhaustive exercise in rainbow trout

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.

/pdf/tissue-intracellular-acid-base-status-and-the-fate-of-43nu7prntz.pdf

Tissue intracellular acid-base status and the fate of lactate after exhaustive exercise in the rainbow trout.

The literature on the substrates, enzymes, pathway, regulation, and physiological function of gluconeogenesis in teleost fishes is reviewed. The information presently available reveals considerable...

Gluconeogenesis in teleost fishes

Elasmobranchs are of metabolic interest for several reasons, including their primitive evolutionary position, their osmotic strategy and their low incidence of neoplasia. Some aspects of the metabolism of elasmobranch fishes are unique when compared with those of the other vertebrates. Although many features of their metabolism can be attributed to their primitive evolutionary position (e.g., fewer isoforms of enzymes and other proteins), some unique features appear to be related to the unusual solute system (urea and methylamines) used by elasmobranchs. The solute system exerts widespread effects, which has an impact on the metabolism of lipids, ketone bodies and amino acids and the structure of proteins and membranes. Effects of urea on the transport of lipid may influence aspects of lipid metabolism, reducing extrahepatic lipid catabolism via effects on nonesterified fatty acid transport and enhancing a need for reliance on ketone bodies. Amino acid metabolism of elasmobranchs is also heavily influenced by the need for continuous synthesis of urea with glutamine as the nitrogen donor. These effects, in turn, may play a role in their low incidence of cancer. Specifically, the reduced availability of glutamine (an important nutrient for rapidly growing cells) coupled with the low levels of nonesterified fatty acids in the blood reduces the availability of molecules essential for tumor growth. This metabolic design may thus provide marine elasmobranchs with a “systemic” resistance to cancer.

RD Dyson

Papers

The reversibility of skeletal muscle pyruvate kinase and an assessment of its capacity to support glyconeogenesis.