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.
Atlantic salmon Salmo salar, returning to freshwater to spawn, were angled and then terminally sampled to test the hypothesis that angling during warmer summer months (water temperatures of 20 ± 2°C) increases the magnitude of physiological disturbances in the white muscle. Angling immediately reduced white muscle ATP and phosphocreatine stores, but these high-energy phosphates were replenished within 2-4 h. Intramuscular glycogen stores were nearly depleted after angling, but unlike the response by salmon angled in the fall at 6°C, there was no glycogen resynthesis during the 4-h recovery period. Marked increases in white muscle lactate and the postexercise metabolic proton load (AH^) accompanied glycogen depletion. The time course of lactate elimination and AH^ correction, however, was much slower than previously observed in fall-angled salmon. Finally, considerable delayed postangling mortality (40%) was observed in a subgroup of Atlantic salmon that were angled at 22°C. We conclude that angling in warm summer water impairs restorative processes and increases the susceptibility of Atlantic salmon to delayed postangling mortality. We suggest that anglers can mitigate the magnitude of angling-induced physiological disturbances in Atlantic salmon during midsummer by minimizing playing time and postangling air exposure.
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