Effects of Propranolol and Epinephrine Infusion on Glycogenolysis in Dog Skeletal Muscle In Situ

1972 ◽  
Vol 50 (6) ◽  
pp. 471-475 ◽  
Author(s):  
C. K. Chapler
Keyword(s):  
Electrical Stimulation ◽  
Muscle Glycogen ◽  
Muscle Group ◽  
Epinephrine Infusion ◽  
Beta Receptors ◽  
Glycogen Stores ◽  
Resting Muscle ◽  
Prior Administration ◽  
Stimulation Of

The effect of intravenous administration of propranolol and/or epinephrine on glycogen stores in the dog gastrocnemius-plantaris muscle group was assessed at rest and following 30 min of contractions. In resting muscle, glycogen stores were not altered 60 min following propranolol (0.5 mg/kg) nor did a 10 min infusion of epinephrine (1 μg/kg/min) induce glycogenolysis. Following 30 min of contractions at 5 twitches/s, about 30% of the muscle glycogen stores were depleted. This rate of glycogenolysis was unaffected by prior administration of propranolol, suggesting that the breakdown of glycogen during electrical stimulation of the muscle group is not mediated through activation of beta receptors. When epinephrine was infused during the last 10 min of the contraction period, about 50% of the initial glycogen stores was depleted. This epinephrine-induced glycogenolysis was mediated through activation of beta receptors as it was abolished by pretreatment of the animals with propranolol. These data suggest that the relatively small breakdown of glycogen stores in the gastrocnemius-plantaris during electrical stimulation of the muscle group may reflect the lack of an increase in circulating catecholamines.

Blood flow, blood oxygen tension, oxygen uptake, and oxygen transport in skeletal muscle

1964 ◽  
Vol 206 (4) ◽  
pp. 858-866 ◽  
Author(s):  
Wendell N. Stainsby ◽  
Arthur B. Otis
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Oxygen Tension ◽  
Capillary Density ◽  
Muscle Group ◽  
Blood Oxygen ◽  
Histological Techniques ◽  
Contracting Muscle ◽  
Resting Muscle

The effect of changes in blood flow and of blood oxygen tension on oxygen uptake of the in situ gastrocnemius-plantaris muscle group of the dog was examined. Oxygen uptake by resting muscle was not altered by changes in blood flow or blood oxygen tension except when these parameters were reduced below critical values. When the muscle group was contracting once per second, changes in blood oxygen tension were similarly without effect until a critically low value was reached. Although the contracting muscle used eight times as much oxygen per minute as resting muscle, the critical oxygen tension was lower than that for resting muscle. In an attempt to explain this observation the blood-tissue oxygen tension difference was estimated and used in the Krogh equation to calculate capillary density. The capillary density in contracting muscle was found to be much greater than in resting muscle and was about the same as the capillary density measured by others by histological techniques.

Integration of cornea and cardiorespiratory afferents in the nucleus of the solitary tract of the rat

2002 ◽  
Vol 282 (4) ◽  
pp. H1278-H1287 ◽  
Author(s):  
Pedro Boscan ◽  
Julian F. R. Paton
Keyword(s):  
Electrical Stimulation ◽  
Solitary Tract ◽  
Peripheral Chemoreceptor ◽  
Single Unit Recordings ◽  
Degree Of Convergence ◽  
High Degree ◽  
Working Heart ◽  
Stimulation Of ◽  
Nerve Discharge

We determined the activity of neurons within the nucleus of the solitary tract (NTS) after stimulation of the cornea and assessed whether this input affected the processing of baroreceptor and peripheral chemoreceptor inputs. In an in situ, unanesthetized decerebrate working heart-brain stem preparation of the rat, noxious mechanical or electrical stimulation was applied to the cornea, and extracellular single unit recordings were made from NTS neurons. Cornea nociceptor stimulation evoked bradycardia and an increase in the cycle length of the phrenic nerve discharge. Of 90 NTS neurons with ongoing activity, corneal stimulation excited 51 and depressed 39. There was a high degree of convergence to these NTS neurons from either baroreceptors or chemoreceptors. The excitatory synaptic response in 12 of 19 baroreceptive and 10 of 15 chemoreceptive neurons was attenuated significantly during concomitant electrical stimulation of the cornea. This inhibition was GABAA receptor mediated, being blocked by pressure ejection of bicuculline. Thus the NTS integrates information from corneal receptors, some of which converges onto neurons mediating reflexes from baroreceptors and chemoreceptors to inhibit these inputs.

Glucose turnover in 48-hour-fasted running rats

1987 ◽  
Vol 252 (3) ◽  
pp. R587-R593 ◽  
Author(s):  
B. Sonne ◽  
K. J. Mikines ◽  
H. Galbo
Keyword(s):  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Lactate Production ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Glucose Turnover ◽  
Feedback Mechanisms ◽  
Glycogen Stores ◽  
Resting Muscle ◽  
Fasted Rats

In fed rats, hyperglycemia develops during exercise. This contrasts with the view based on studies of fasted human and dog that euglycemia is maintained in exercise and glucose production (Ra) controlled by feedback mechanisms. Forty-eight-hour-fasted rats (F) were compared to fed rats (C) and overnight food-restricted (FR) rats. [3-3H]- and [U-14C] glucose were infused and blood and tissue sampled. During running (21 m/min, 0% grade) Ra increased most in C and least in F and only in F did Ra not significantly exceed glucose disappearance. Plasma glucose increased more in C (3.3 mmol/l) than in FR (1.6 mmol/l) and only modestly (0.6 mmol/l) and transiently in F. Resting liver glycogen and exercise glycogenolysis were highest in C and similar in FR and F. Resting muscle glycogen and exercise glycogenolysis were highest in C and lowest in F. During running, lactate production and gluconeogenesis were higher in FR than in F. At least in rats, responses of production and plasma concentration of glucose to exercise depend on size of liver and muscle glycogen stores; glucose production matches increase in clearance better in fasted than in fed states. Probably glucose production is stimulated by “feedforward” mechanisms and “feedback” mechanisms are added if plasma glucose decreases.

In vivo modulation by α2-adrenoceptors of adrenal catecholamine release in the anaesthetized dog

1988 ◽  
Vol 66 (3) ◽  
pp. 380-384 ◽  
Author(s):  
Sylvain Foucart ◽  
Jacques de Champlain ◽  
Reginald Nadeau
Keyword(s):  
Electrical Stimulation ◽  
Splanchnic Nerve ◽  
Catecholamine Release ◽  
Agonist Stimulation ◽  
Control Stimulation ◽  
Anaesthetized Dog ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

In this study, the reversal of the potentiating effect of idazoxan, a selective α2-antagonist, on adrenal catecholamine release elicited by splanchnic nerve stimulation in anaesthetized and vagotomized dogs, was investigated with the use of oxymetazoline, a selective α2-agonist. Stimulation of the left splanchnic nerve (5.0-V pulses of 2 ms duration for 3 min at a frequency of 2 Hz) was applied before and 20 min after the i. v. injection of each drug. Blood samples were collected in the adrenal vein before and at the end of each stimulation. The results show that the release of catecholamines induced by electrical stimulation was potentiated by 50% after idazoxan injection (0.1 mg/kg). This enhanced response was significantly antagonized by the subsequent injection of oxymetazoline (2 μg/kg). The α2-modulating effect appears to be related to the amount of catecholamines released during the stimulation, since by subgrouping of the data on the basis of the degree of potentiation by idazoxan, it was observed that this drug was more efficient when catecholamine release was higher during control stimulation. In contrast, the reversing effect of oxymetazoline was found to be more pronounced when catecholamine release was lower. These results thus suggest that the sensitivity of the α2-adrenoceptor mechanism may depend upon the in situ concentration of adrenal catecholamine release during electrical stimulation and that the potentiating effect of α2-blockade can be reversed by activation of those receptors by a selective α2-agonist.

Effect of electrical stimulation of locus coeruleus on the activity of neurons in the cat visual cortex

1989 ◽  
Vol 62 (4) ◽  
pp. 946-958 ◽  
Author(s):  
H. Sato ◽  
K. Fox ◽  
N. W. Daw
Keyword(s):  
Electrical Stimulation ◽  
Visual Cortex ◽  
Adrenergic Receptor ◽  
Suppressive Effect ◽  
Cortical Layer ◽  
Facilitatory Effect ◽  
Receptor Antagonists ◽  
Complex Cells ◽  
Beta Receptors ◽  
Stimulation Of

1. We studied the effect of electrically stimulating the locus coeruleus (LC) and iontophoresing noradrenergic antagonists on visual responses and spontaneous activity of individual cells in the cat primary visual cortex. 2. A bilateral projection from LC to visual cortex was demonstrated anatomically, by retrograde labeling using horseradish peroxidase. Where electrical stimulation of both ipsilateral and contralateral LC affected a cortical neuron, the effect induced by stimulating each side was similar. 3. One hundred and two cells were recorded in area 17: 52% of them had their activity suppressed and 36% had their activity facilitated by LC stimulation. The suppressive effect was predominant in cortical layers II + III and IV, whereas most cells in layer V and one-half of the cells in layer VI were facilitated by LC stimulation. This suggests that LC neurons innervate each cortical layer in a different manner. 4. Simple and complex cells were equally sensitive to LC stimulation. For simple cells, the suppressive effect of LC stimulation was dominant throughout all layers. For complex cells, the suppressive effect was dominant in layers II + III and IV, whereas the facilitatory effect was dominant in layers V and VI. 5. The suppressive effect of LC stimulation was blocked by iontophoretic application of beta-adrenergic receptor antagonists and the facilitatory effect was blocked by either alpha- or beta-adrenergic receptor antagonists. 6. Nonselective alpha-, and selective alpha 1- and alpha 2-receptor antagonists suppressed visual and spontaneous activity in almost all neurons tested, suggesting that these receptors are either facilitatory at a postsynaptic site or inhibitory at a site presynaptic to an inhibitory synapse in the visual cortex. 7. beta-Receptor antagonists facilitated activity in 45% and suppressed activity in 36% of the cells tested, suggesting there are both suppressive and facilitatory types of beta-receptors. 8. The effectiveness of alpha- and beta-antagonists on the activity of neurons without LC stimulation also suggested that spontaneously released noradrenaline activated noradrenergic receptors in the visual cortex even in the anesthetized and paralyzed cat. 9. In most cells tested, both alpha- and beta-receptor antagonists exerted effects on single neurons suggesting that endogenous noradrenaline acts on both alpha- and beta-receptors on the same cell. 10. The activation of LC did not improve the signal- (visual response)to-noise (spontaneous discharge) ratio of neurons in the visual cortex. 11. LC seemed to control the activity of each cortical layer differently, by activating different kinds of noradrenergic receptors in different layers.

Effects of 24-hour fast on cycling endurance time at two different intensities

1986 ◽  
Vol 61 (2) ◽  
pp. 654-659 ◽  
Author(s):  
S. F. Loy ◽  
R. K. Conlee ◽  
W. W. Winder ◽  
A. G. Nelson ◽  
D. A. Arnall ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Plasma Free Fatty Acid ◽  
Normal Diet ◽  
Glycogen Depletion ◽  
Endurance Time ◽  
Competitive Cyclists ◽  
Pedal Frequency ◽  
Glycogen Stores ◽  
Resting Muscle ◽  
Initial Intensity

Ten competitive cyclists were exercised to exhaustion to test the potential of a 24-h fast for increasing endurance. One group (n = 4) was tested at an initial intensity of 86% maximum O2 uptake (VO2max) (HI) and a second group (n = 6) at 79% VO2max (MI). Both groups repeated test rides in fasted and normal-diet conditions. Time to fatigue was designated at two points: fatigue 1 occurred when pedal frequency could not be maintained at the initial percent VO2max; fatigue 2 occurred when pedal frequency could not be maintained at a workload of approximately 65% VO2max. In both HI and MI the 24-h fast had no effect on resting muscle glycogen stores but significantly increased plasma free fatty acid (FFA) levels. Despite the increased FFA availability, time to fatigue was reduced in the fasted groups. Fatigue 1 and 2 times (mean +/- SE) for HI-fasted were 42.0 +/- 6.2 and 170.0 +/- 20.4 min, respectively, compared with those of the HI-normal diet of 115.3 +/- 25.6 and 201.0 +/- 14.8 min. Fatigue 1 and 2 times for MI-fasted were 142.0 +/- 19.6 and 167.5 +/- 10.5 min compared with those of the MI-normal diet of 191.3 +/- 25.0 and 214.3 +/- 18.9 min. The cause of fatigue at fatigue 1 was not readily apparent. Fatigue 2 in all groups seemed to be related to hypoglycemia as well as muscle glycogen depletion.

An Electrophysiological Study of the Photo-Excitative Neurones of Onchidium Verruculatum in Situ

1972 ◽  
Vol 57 (3) ◽  
pp. 661-671
Author(s):  
NOZOMU HISANO ◽  
HIDEKI TATEDA ◽  
MASUTARO KUWABARA
Keyword(s):  
Electrical Stimulation ◽  
Electrophysiological Study ◽  
Spontaneous Discharge ◽  
Light Stimulation ◽  
Direct Response ◽  
Intracellular Stimulation ◽  
The Right ◽  
Animal Preparation ◽  
Stimulation Of

1. The distribution of the axons of the photo-excitative neurones in Onchidium verruculatum has been traced by intracellular stimulation of the soma and extracellular stimulation of the axon. They send axon branches mainly into the pleuroparietal and abdominal nerves in both sides. 2. In the whole-animal preparation, photo-excitative spikes could be recorded from neither the soma nor the nerves of inherently photo-excitative neurones during light stimulation. ‘On’ and ‘off’ spikes were initiated only immediately after the beginning and the cessation of illumination of a whole animal. 3. ‘Off’ spikes originated from dorsal eyes and stalk eyes to which shadow stimuli were applied. Those spikes were not the direct response of photo-excitative neurones to light. 4. The excitation of the inherently photo-excitative neurones in situ was suppressed by inhibitory inputs coming through the right and left pleuro-parietal nerves. Cutting one (or some) of the pleuro-parietal nerves was the only condition that diminished the inhibitory inputs to the photo-excitative neurones in the present work. Adequate electrical stimulation of the pleuro-parietal nerves inhibited spikes of photo-excitative neurones due to photo-excitator or spontaneous discharge.

Nerve stimulation decreases malonyl-CoA in skeletal muscle

1992 ◽  
Vol 72 (3) ◽  
pp. 901-904 ◽  
Author(s):  
C. Duan ◽  
W. W. Winder
Keyword(s):  
Sciatic Nerve ◽  
Creatine Phosphate ◽  
Muscle Group ◽  
Carnitine Palmitoyl Transferase ◽  
Plantaris Muscle ◽  
Malonyl Coa ◽  
Left And Right ◽  
Muscle Groups ◽  
Stimulation Of

This study was designed to determine the effect of in situ electrical stimulation of the sciatic nerve on malonyl-CoA, an inhibitor of carnitine palmitoyl transferase, in the gastrocnemius/plantaris muscle group of rats. The left sciatic nerve was stimulated at a frequency of 5 Hz with 100-ms trains of impulses (50 Hz) for 1, 3, or 5 min. At the end of stimulation, the left and right (nonstimulated) gastrocnemius/plantaris muscle groups were clamp-frozen and later analyzed for malonyl-CoA and other metabolites. No change was observed in the noncontracting contralateral muscles in malonyl-CoA, ATP, creatine phosphate (CP), or citrate. In the stimulated muscles, malonyl-CoA decreased from 1.7 +/- 0.1 to 1.0 +/- 0.1 nmol/g (P less than 0.05), and CP decreased from 15.8 +/- 0.9 to 12.2 +/- 1.0 mumol/g (P less than 0.05) after 3 min of stimulation. After 5 min of stimulation, malonyl-CoA was 1.0 +/- 0.1 nmol/g and CP was 10.3 +/- 1.3 mumol/g. When muscles were stimulated for 5 min with single impulses (5 Hz), malonyl-CoA was decreased from 1.8 +/- 0.3 to 1.0 +/- 0.1 nmol/g, with no change in CP, ATP, or adenosine 3′,5′-cyclic monophosphate. Thus a decline in malonyl-CoA can be induced by muscle contraction independently of humoral influence.

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