156
D. J. RANDALL
1968) and adrenergic receptors in the gills and elsewhere in the circulation (Randall and Stevens, 1967). The effect of epinephrine is to decrease
the resistance to 00w in the gill circulation. Thus the changes in cardiac
output occurring during exercise may be caused, at least in part,
by the action of catecholamines on / 3 receptors in the heart and on other
adrenergic receptors in the peripheral circulation. One would suspect,
from data on the mammalian circulatory system, that other factors, such
as the production of metabolites, play a role in decreasing peripheral
resistance during exercise in fish.
Exercise in the lingcod, Ophiodon elongatus, is accompanied by
stroke volume and cardiac output increases only when the fish is atropinized (Stevens et aZ., 19f39). Exercise in the nonatropinized fish is
accompanied by an increase in vagal tone and a bradycardia, which
decreases cardiac output. Possibly this is a response to the stimulus
which provokes exercise rather than to exercise itself. Lingcod usually remain motionless at the bottom of the tank and must be prodded
or startled to produce short bursts of swimming. An increase in vagal
tone may not be a physiological response to spontaneous swimming
in this animal. Hanson (1967) found that spontaneous activity in a
number of Chondrichthyes was accompanied by an increase in cardiac
output; if, however, the animal was disturbed and then swam away an
initial bradycardia was observed,
An increase in temperature acts directly on the heart, increasing the
intrinsic rate of the pacemaker cells. In the intact lingcod, Ophiodon
ebngatus, stroke volume remains constant over a wide range of temperatures, and a rise in temperature causes an increase in cardiac output
owing to an increase in heart rate (Fig. 9). The in vitro heart of the
trout behaves in a different way (see p. 153); a rise in temperature increases heart rate but decreases stroke volume, and cardiac output remains constant over a wide range of temperatures. In the intact animal,
temperature changes affect the whole animal, whereas in the in vitro
preparation only the response of the heart is recorded. Many factors,
including the magnitude of the peripheral resistance to blood flow, can
affect stroke volume. There are some indications that the peripheral
resistance to blood flow decreases as temperature increases (Davis,
1968), and this would tend to maintain stroke volume in the face of a
negative inotropic effect on the heart caused by a temperature increase.
The balance of evidence indicates that changes in cardiac output in
fish are associated with changes in stroke volume with some adjustment
of heart rate (Randall, 1968). The rate changes are mediated via cholinergic nerve innervating the heart, changes in temperature, and changes
in the level catecholamines. Stroke volume changes occur in response
D. J. RANDALL
1968) and adrenergic receptors in the gills and elsewhere in the circulation (Randall and Stevens, 1967). The effect of epinephrine is to decrease
the resistance to 00w in the gill circulation. Thus the changes in cardiac
output occurring during exercise may be caused, at least in part,
by the action of catecholamines on / 3 receptors in the heart and on other
adrenergic receptors in the peripheral circulation. One would suspect,
from data on the mammalian circulatory system, that other factors, such
as the production of metabolites, play a role in decreasing peripheral
resistance during exercise in fish.
Exercise in the lingcod, Ophiodon elongatus, is accompanied by
stroke volume and cardiac output increases only when the fish is atropinized (Stevens et aZ., 19f39). Exercise in the nonatropinized fish is
accompanied by an increase in vagal tone and a bradycardia, which
decreases cardiac output. Possibly this is a response to the stimulus
which provokes exercise rather than to exercise itself. Lingcod usually remain motionless at the bottom of the tank and must be prodded
or startled to produce short bursts of swimming. An increase in vagal
tone may not be a physiological response to spontaneous swimming
in this animal. Hanson (1967) found that spontaneous activity in a
number of Chondrichthyes was accompanied by an increase in cardiac
output; if, however, the animal was disturbed and then swam away an
initial bradycardia was observed,
An increase in temperature acts directly on the heart, increasing the
intrinsic rate of the pacemaker cells. In the intact lingcod, Ophiodon
ebngatus, stroke volume remains constant over a wide range of temperatures, and a rise in temperature causes an increase in cardiac output
owing to an increase in heart rate (Fig. 9). The in vitro heart of the
trout behaves in a different way (see p. 153); a rise in temperature increases heart rate but decreases stroke volume, and cardiac output remains constant over a wide range of temperatures. In the intact animal,
temperature changes affect the whole animal, whereas in the in vitro
preparation only the response of the heart is recorded. Many factors,
including the magnitude of the peripheral resistance to blood flow, can
affect stroke volume. There are some indications that the peripheral
resistance to blood flow decreases as temperature increases (Davis,
1968), and this would tend to maintain stroke volume in the face of a
negative inotropic effect on the heart caused by a temperature increase.
The balance of evidence indicates that changes in cardiac output in
fish are associated with changes in stroke volume with some adjustment
of heart rate (Randall, 1968). The rate changes are mediated via cholinergic nerve innervating the heart, changes in temperature, and changes
in the level catecholamines. Stroke volume changes occur in response