In fish, exhaustive exercise stress differs from steady-state aerobic exercise in causing (1) a depletion of glycogen, creatine phosphate (CP) and ATP reserves and an accumulation of lactate and metabolic acid (H+m) in white muscle; (2) blood respiratory and metabolic acidoses {PCO2 and H+m elevations, respectively); (3) marked ionic and fluid volume disturbances; and (4) a surge in plasma catecholamines. During recovery, the smaller fast component (20%) of excess postexercise oxygen consumption (EPOC) is explained by CP and ATP resynthesis and aerobic demands, but the larger slow component (80%) is considerably greater than the cost of lactate clearance and glycogen resynthesis. Ionic and H2O shifts may contribute significantly to EPOC; net fluxes are greatest between extracellular (ECF) and intracellular fluid (ICF) compartments, with smaller disturbances at the kidney (increased filtration, reabsorption and excretion) and gills (passive ion losses and H2O uptake). Modulation of branchial Na+ and Cl exchange is important in the temporary storage of H+m in the environment during recovery. Movements of lactate and H+ from ICF to ECF are dissociated processes; the major portions of both are retained in the white muscle and are probably cleared by oxidation and/or glycogen resynthesis in situ. Elevated catecholamine levels are implicated in many of these responses and serve to protect metabolic processes against acid-base disturbances, but do not appear to contribute to EPOC directly. Catecholamines also cause an elevation in blood Pco2 by a mechanism linked to the β-adrenergic activation of red blood cell Na+/H+ exchange that protects O2 transport. The compound blood addosis stimulates ventilation to meet the demands of EPOC.

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