Depletion of high energy phosphates implicates post-exercise mortality in carp and trout; an in vivo 31P-NMR study.

Abstract As in vivo 31 P-Nuclear Magnetic Resonance spectroscopy is currently the state of the art method to measure continuously intracellular pH (pH i ) and energy status of muscle tissue, we used this method to study the recovery from exhaustive exercise. The biochemical changes during recovery are not well understood and it was suggested that post-exercise mortality could be caused by low pH i ; other studies however indicate that energy depletion might be more important. To analyse the mechanism of post-exercise recovery pH i , ATP, P i , and PCr must be measured at the same time, which is possible using in vivo 31 P-NMR. Common carp and rainbow trout of about 100 g were exercised to exhaustion in a swim tunnel. After swimming 10 h at 1.5 body lengths (BL)/s (aerobic control), 50% of the fish were forced to swim at 6 BL/s until exhaustion. Recovery of energy rich phosphates was found to be faster in carp (1.2–1.9 h) than in trout (1.5–2.3 h). The same applied for the recovery from acidosis, which took 1.75 h in carp and 5.75 h in trout. In parallel experiments the energy phosphates and lactate levels were measured in liver, red muscle, and white muscle. Exhaustion caused a significant drop in the energy status of red and white muscle tissue of trout and carp (corroborates NMR data), while no change at all was observed in liver tissue. The lactate levels were increased in the muscle but not in liver and blood. While all experimental animals looked healthy after exhaustion, 40–50% of the carp as well as trout died during the recovery phase. The energy status of those individuals measured by 31 P-NMR was much lower than that of the survivors, while in contrast there was no difference in pH i . Thus, it appears that not acidosis but depletion of high energy phosphates disabled muscle function and therefore may have been the cause of death of the non-survivors.