The oxygen debt hypothesis in juvenile rainbow trout after exhaustive exercise

Abstract

A 5 min bout of exhaustive exercise in 2–3 g rainbow trout resulted in a 2.0–2.5 fold increase in oxygen consumption (Ṁ O2), a 5-fold increase in whole-body lactate (LAC) levels and a near depletion in whole-body glycogen (GLY), ATP and creatine phosphate (CP) stores; glucose,ADP and AMP did not change. Recovery of Ṁ O2 and LAC was complete by 6 h, by which time GLY had stabilized at about 65% resting levels without further recovery through 24 h. Complete recovery of ATP required 1.0–1.5 h, whereas restoration of CP required only 5 min. The Ṁ O2 recovery curve was resolved into an initial fast component t 1 2 = h and a second slower component t 1 2 = h , comprising approximately 20% and 80% respectively of the excess post-exercise oxygen consumption (EPOC). The fast component was satisfactorily accounted for by the standard components of the ‘alactacid O 2 debt’. However, the slow component could not be completely explained by changes in whole body LAC and GLY during recovery based on scenarios of either oxidation or GLY resynthesis as the primary fate of LAC. The classical ‘O 2 debt hypothesis’ (Hill and Lupton, Quart. J. Med. 16: 135–171, 1923; Margaria et al., Am. J. Physiol. 106: 9–715, 1933) cannot be the complete explanation of EPOC in the trout.