Abstract

Atlantic salmon (Salmo salar) were acclimated and exhaustively exercised at 12, 18, or 23°C to determine how temperature influences the magnitude of postexercise physiological disturbances. At each temperature, exercise led to decreased white muscle ATP and phosphocreatine concentrations. Phosphocreatine was rapidly restored within 1 h at each temperature whereas ATP restoration took 1-4 h at 18 and 23°C, but considerably longer at 12°C. Exercise-induced depletions of white muscle glycogen were accompanied by elevations in muscle lactate, which contributed to 0.6 unit decreases in white muscle intracellular pH (pHi) at each temperature. Compared with rates of recovery in warmer water, glycogen resynthesis, lactate catabolism, and pHicorrection were slower at 12°C. White muscle REDOX state estimates suggested that slower postexercise recovery at 12°C was not due to oxygen delivery limitations. Marked postexercise elevations in plasma osmolality and lactate concentration were also observed and in each case correction of the disturbance took longer at 12°C. Paradoxically, significant mortality (30%) was observed only at 23°C. We conclude that while warmer water facilitates postexercise recovery of white muscle metabolic and acid-base status in Atlantic salmon, extremely high temperatures may make them more vulnerable to delayed postexercise mortality.

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