Summary

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 {P_CO2 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.