ADRENERGIC ANALYSIS OF EXTRACELLULAR AND INTRACELLULAR LACTATE AND H+ DYNAMICS AFTER STRENUOUS EXERCISE IN THE STARRY FLOUNDER PLATICHTHYS-STELLATUS

Adrenergic blockade with a selective .alpha. antagonist (yohimbine) and .beta. antagonist (propranolol) was employed to test whether catecholamine mobilization was involved in lactate and acidic equivalents (H+) dynamics following strenuous exercise in chronicaly cannulated starry flounder. In control fish (not blocked) sampled repetitively for 8 h after exericse, arterial [lactate] remained characteristically low (< 2 mmol/liter), and acid-base, hematological, and glucose changes were similar to those seen in other studies. Neither .alpha. nor .beta. blockade immediately after exercise nor .beta. blockade before exercise had significant influence on most responses, though hyperglycemia was inhibited by .beta. blockade. Blood [lactate] was also marginally elevated, and red blood cell (RBC) swelling was reduced by .beta. antagonism. A second series involving single-terminal sampling of cannulated flounder demonstrated that RBC intracellular pH (pHi), [NTP], and arterial PO2 remained unchanged in the face of severe postexercise acidosis; hemoglobin (Hb)-bound O2 per unit Hb ([O2]/[Hb]) fell by 25% but had recovered by 1 h. White-muscle [lactate] increased to 10-20 times blood levels, and pHi in muscle, brain, and heart fell substantially, changes which were sustained at 1 h. Postexercise .beta. blockade decreased RBC pHi, inhibited RBC swelling, prevented recovery of [O2]/[Hb], elevated blood [lactate], and increased muscle [lactate] at 1 h. The pHi of muscle, heart, and brain were not significantly affected. In contrast to other investigators, we conclude that catecholamines have little influence on postexercise lactate and H+ dynamics in founder but do help to sustain blood O2 transport in the face of extracellular acidosis. Apparent stimulation of lactate release by .beta. blockade can be explained by increased production of lactate by muscle, owing to hypoxemia.