Exercise and glycogen depletion: effects on ability to activate muscle phosphorylase

1986 ◽  
Vol 60 (5) ◽  
pp. 1518-1523 ◽  
Author(s):  
S. H. Constable ◽  
R. J. Favier ◽  
J. O. Holloszy
Keyword(s):  
Muscle Contraction ◽  
Muscle Glycogen ◽  
Contractile Activity ◽  
Strenuous Exercise ◽  
Glycogen Depletion ◽  
Significant Difference ◽  
Muscle Phosphorylase ◽  
Glycogen Repletion ◽  
Stimulation Of

Phosphorylase activation reverses during prolonged contractile activity. Our first experiment was designed to determine whether this loss of ability to activate phosphorylase by stimulation of muscle contraction persists following exercise. Phosphorylase activation by stimulation of muscle contraction was markedly inhibited in rats 25 min after exhausting exercise. To evaluate the role of glycogen depletion, we accelerated glycogen utilization by nicotinic acid administration. A large difference in muscle glycogen depletion during exercise of the same duration did not influence the blunting of phosphorylase activation. Phosphorylase activation by stimulation of contraction was more severely inhibited following prolonged exercise than after a shorter bout of exercise under conditions that resulted in the same degree of glycogen depletion. A large difference in muscle glycogen repletion during 90 min of recovery was not associated with a significant difference in the ability of muscle stimulation to activate phosphorylase, which was still significantly blunted. Phosphorylase activation by epinephrine was also markedly inhibited in muscle 25 min after strenuous exercise but had recovered completely in glycogen-repleted muscle 90 min after exercise. These results provide evidence that an effect of exercise other than glycogen depletion is involved in causing the inhibition of phosphorylase activation; however, they do not rule out the possibility that glycogen depletion also plays a role in this process.

scholarly journals The metabolic role of IL-6 produced during exercise: is IL-6 an exercise factor?

2004 ◽  
Vol 63 (2) ◽  
pp. 263-267 ◽  
Author(s):  
B. K. Pedersen ◽  
A. Steensberg ◽  
C. Fischer ◽  
C. Keller ◽  
P. Keller ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Muscle Contraction ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Carbohydrate Supplementation ◽  
Work Factor ◽  
Contracting Muscle ◽  
Metabolic Role ◽  
Stimulation Of

For most of the last century, researchers have searched for a muscle contraction-induced factor that mediates some of the exercise effects in other tissues such as the liver and the adipose tissue. It has been called the ‘work stimulus’, the ‘work factor’ or the ‘exercise factor’. In the search for such a factor, a cytokine, IL-6, was found to be produced by contracting muscles and released into the blood. It has been demonstrated that IL-6 has many biological roles such as: (1) induction of lipolysis; (2) suppression of TNF production; (3) stimulation of cortisol production. The IL-6 gene is rapidly activated during exercise, and the activation of this gene is further enhanced when muscle glycogen content is low. In addition, carbohydrate supplementation during exercise has been shown to inhibit the release of IL-6 from contracting muscle. Thus, it is suggested that muscle-derived IL-6 fulfils the criteria of an exercise factor and that such classes of cytokines could be termed ‘myokines’.

scholarly journals Effects of Nutrient Intake Timing on Post-Exercise Glycogen Accumulation and its Related Signaling Pathways in Mouse Skeletal Muscle

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2555 ◽  
Author(s):  
Takahashi ◽  
Matsunaga ◽  
Banjo ◽  
Takahashi ◽  
Sato ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Nutrient Intake ◽  
Matched Control ◽  
Control Group ◽  
Glycogen Depletion ◽  
Post Exercise ◽  
Glycogen Accumulation ◽  
Matched Control Group ◽  
Significant Difference

We investigated the effects of nutrient intake timing on glycogen accumulation and its related signals in skeletal muscle after an exercise that did not induce large glycogen depletion. Male ICR mice ran on a treadmill at 25 m/min for 60 min under a fed condition. Mice were orally administered a solution containing 1.2 mg/g carbohydrate and 0.4 mg/g protein or water either immediately (early nutrient, EN) or 180 min (late nutrient, LN) after the exercise. Tissues were harvested at 30 min after the oral administration. No significant difference in blood glucose or plasma insulin concentrations was found between the EN and LN groups. The plantaris muscle glycogen concentration was significantly (p < 0.05) higher in the EN group—but not in the LN group—compared to the respective time-matched control group. Akt Ser473 phosphorylation was significantly higher in the EN group than in the time-matched control group (p < 0.01), while LN had no effect. Positive main effects of time were found for the phosphorylations in Akt substrate of 160 kDa (AS160) Thr642 (p < 0.05), 5'-AMP-activated protein kinase (AMPK) Thr172 (p < 0.01), and acetyl-CoA carboxylase Ser79 (p < 0.01); however, no effect of nutrient intake was found for these. We showed that delayed nutrient intake could not increase muscle glycogen after endurance exercise which did not induce large glycogen depletion. The results also suggest that post-exercise muscle glycogen accumulation after nutrient intake might be partly influenced by Akt activation. Meanwhile, increased AS160 and AMPK activation by post-exercise fasting might not lead to glycogen accumulation.

scholarly journals Muscle glycogen and metabolic regulation

2004 ◽  
Vol 63 (2) ◽  
pp. 217-220 ◽  
Author(s):  
Mark Hargreaves
Keyword(s):  
Muscle Glycogen ◽  
Insulin Action ◽  
Metabolic Regulation ◽  
Strenuous Exercise ◽  
Glycogen Depletion ◽  
Excitation Contraction Coupling ◽  
Glycogen Resynthesis ◽  
Contraction Coupling ◽  
Cellular Processes ◽  
Exercise Induced

Muscle glycogen is an important fuel for contracting skeletal muscle during prolonged strenuous exercise, and glycogen depletion has been implicated in muscle fatigue. It is also apparent that glycogen availability can exert important effects on a range of metabolic and cellular processes. These processes include carbohydrate, fat and protein metabolism during exercise, post-exercise glycogen resynthesis, excitation–contraction coupling, insulin action and gene transcription. For example, low muscle glycogen is associated with reduced muscle glycogenolysis, increased glucose and NEFA uptake and protein degradation, accelerated glycogen resynthesis, impaired excitation–contraction coupling, enhanced insulin action and potentiation of the exercise-induced increases in transcription of metabolic genes. Future studies should identify the mechanisms underlying, and the functional importance of, the association between glycogen availability and these processes.

scholarly journals Esophagus: serotoninerdgic regulation

2020 ◽  
pp. 137-142
Author(s):  
A. M. Puzikov
Keyword(s):  
Serotonin Receptors ◽  
Contractile Activity ◽  
Smooth Muscles ◽  
Emg Activity ◽  
Enhancing Effect ◽  
Adventitial Layer ◽  
Important Player ◽  
Ganglion Neurons ◽  
Stimulation Of

Introduction: Serotonin (5-hydroxytryptamine, 5-HT) is a regulatory neurotransmitter and a hormone in the CNS and hole organs, the esophagus including. It is known that serotonin, activating its own receptors, stimulates contractile activity of the esophageal muscles. However, role of different type receptors in the 5-HT induced contractile activity of the esophagus is insufficiently known.The aim: — to determine which type of 5-HT receptors mediate serotonin dependent contractile activity of the esophagus.Material and methods: This is a electromyography study of rat esophagus contractile activity under serotonin stimulation of 5-HT3,4 and 5-HT2,1 receptors separately modulated. The role of different serotonin receptors in the 5-HT induced contractile activity of the esophagus was evaluated by measuring the amplitude and frequency of the slow wave electromyogram (EMG) by the noninvasive microelectrodes imposed on the adventitial layer of the esophagus.Results: Administration of the 5-HT3,4 receptors inhibitors excluded caused by serotonin the increment of EMG activity of the contractile activity of the esophagus. Administration of the 5-HT1,2 receptors inhibitors blocked the serotonin enhanced EMG activity of the esophagus.Conclusion: Our results indicate that serotonin is the important player in the regulation of the rat's esophagus contractility; 5-HT enhancing effect on contraction of the esophageal smooth muscles is mediated through the activation of 5-HT1,2 receptors expressed on the smooth muscle cells, and by activation of 5-HT3,4 receptors expressed on the ganglion neurons.

Effects of exercise and glycogen depletion on glyconeogenesis in muscle

1994 ◽  
Vol 76 (4) ◽  
pp. 1753-1758 ◽  
Author(s):  
A. Bonen ◽  
D. A. Homonko
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Extensor Digitorum Longus ◽  
Treadmill Exercise ◽  
Glycogen Depletion ◽  
Epinephrine Injection ◽  
Slow Twitch ◽  
Glycogen Repletion ◽  
Fast Twitch

In the present study, we investigated the hypotheses that 1) skeletal muscle glyconeogenesis will increase after exercise, 2) greater changes in glyconeogenesis will be observed after exercise in fast-twitch muscles than in slow-twitch muscles, and 3) glycogen repletion will reduce the rates of glyconeogenesis. Mouse soleus and extensor digitorum longus (EDL) glycogen depots were reduced to the same levels by treadmill exercise (60 min) or epinephrine injection (75 micrograms/100 g body wt ip). Untreated animals were used as controls. We were able to prevent glycogen repletion by incubating muscles in vitro with sorbitol (75 mM) and to increase glycogen concentrations in vitro by incubating muscles with glucose (75 mM). The experimental results showed that glyconeogenesis was increased by exercise (EDL, +51%; soleus, +82%) when glycogen levels were kept low. When glycogen depots were increased, the rate of glyconeogenesis was lowered in the exercised EDL (P < 0.05) but not in the soleus (P > 0.05). Reductions in muscle glycogen by epinephrine did not change the rate of glyconeogenesis in EDL, either when glycogen depots were kept low or were repleted (P > 0.05). In contrast, in the soleus, epinephrine-induced reductions in glycogen did stimulate glyconeogenesis (P < 0.05). Analyses in EDL showed that in nonexercised muscles glycogen concentrations were minimally effective in altering the rates of glyconeogenesis. A 30% decrement in glycogen increased glyconeogenesis by 5% in resting muscles, whereas the same decrement increased glyconeogenesis by 51% in exercised muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Postexercise muscle and liver glycogen metabolism in male and female rats

1987 ◽  
Vol 62 (3) ◽  
pp. 1250-1254 ◽  
Author(s):  
P. A. Ivey ◽  
G. A. Gaesser
Keyword(s):  
Sex Difference ◽  
Muscle Glycogen ◽  
Exercise Bout ◽  
Glycogen Metabolism ◽  
Liver Glycogen ◽  
Female Rats ◽  
Glycogen Depletion ◽  
Male And Female ◽  
Glycogen Repletion ◽  
Fast Twitch

Male and female Wistar rats were run for 5 min at 1.7 mph at a 17% grade to determine whether a sex difference exists in the rate of glycogen resynthesis during recovery in fast-twitch red muscle, fast-twitch white muscle, and liver. Rats were killed at one of three time points: immediately after the exercise bout, and at 1 or 4 h later. Males had significantly higher resting muscle glycogen levels (P less than 0.05). Exercise resulted in significant glycogen depletion in both sexes (P less than 0.01). Males utilized approximately 50% more glycogen during the exercise bout than females (P less than 0.05). During the food-restricted 4-h recovery period, muscle glycogen was repleted significantly during the 1st h (P less than 0.05). Liver glycogen was not depleted as a result of the exercise bout, but fell during the first h of recovery (P less than 0.05) and remained low during the subsequent 3 h. The greater glycogen utilization in red and white fast-twitch muscle during exercise by males could represent a true sex difference but could also be attributable in part to the males having performed more work as a result of 20% greater body mass. We conclude that no sex difference was observed in the rates of muscle glycogen repletion after exercise or in liver glycogen metabolism during and after exercise, and rapid postexercise muscle glycogen repletion occurred at a time of accelerated liver glycogen depletion.

Hypoxia causes glycogenolysis without an increase in percent phosphorylase a in rat skeletal muscle

1992 ◽  
Vol 263 (6) ◽  
pp. E1086-E1091 ◽  
Author(s):  
J. M. Ren ◽  
E. A. Gulve ◽  
G. D. Cartee ◽  
J. O. Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Strenuous Exercise ◽  
Rat Skeletal Muscle ◽  
Glycogen Breakdown ◽  
Stimulation Of

Stimulation of skeletal muscle to contract activates phosphorylase b-to-a conversion and glycogenolysis. Despite reversal of the increase in percentage of phosphorylase a after a few minutes, continued glycogen breakdown can occur during strenuous exercise. Hypoxia causes sustained glycogenolysis in skeletal muscle without an increase in percentage of phosphorylase a. We used this model to obtain insights regarding how glycogenolysis is mediated in the absence of an increase in percentage of phosphorylase a. Hypoxia caused a 70% decrease in glycogen in epitrochlearis muscles during an 80-min incubation despite no increase in percentage of phosphorylase a above the basal level of approximately 10%. Muscle Pi concentration increased from 3.8 to 8.6 mumol/g muscle after 5 min and 15.7 mumol/g after 20 min. AMP concentration doubled, attaining a steady state of 0.23 mumol/g in 5 min. Incubation of oxygenated muscles with 0.1 microM epinephrine induced an approximately sixfold increase in percentage of phosphorylase a but resulted in minimal glycogenolysis. Muscle Pi concentration was not altered by epinephrine. Despite no increase in percentage of phosphorylase a, hypoxia resulted in a fivefold greater depletion of glycogen over 20 min than did epinephrine. To evaluate the role of phosphorylase b, muscles were loaded with 2-deoxyglucose 6-phosphate, which inhibits phosphorylase b. The rate of glycogenolysis during 60 min of hypoxia was reduced by only approximately 14% in 2-deoxyglucose 6-phosphate-loaded muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Phasic and tonic modulation of impulse rates in gamma-motoneurons during locomotion in premammillary cats

1984 ◽  
Vol 52 (2) ◽  
pp. 228-243 ◽  
Author(s):  
P. R. Murphy ◽  
R. B. Stein ◽  
J. Taylor
Keyword(s):  
Ventral Root ◽  
The Body ◽  
Triceps Surae ◽  
Medial Gastrocnemius ◽  
Nerve Branch ◽  
Significant Difference ◽  
Natural Stimulation ◽  
Triceps Surae Muscles ◽  
Stimulation Of

To determine the role of gamma-motoneurons in the control of locomotion, we isolated single units from nerves to triceps surae muscles in the premammillary cat. The limb used for recording was largely denervated, except for the muscles of interest, and fixed in place, while the other three limbs walked on a treadmill. One type of gamma-motoneuron (13 units) had a high impulse rate at rest, which changed little on average during walking, but was deeply modulated with each step (phasically modulated gamma-motoneuron or gamma p). Another type (19 units) had a low impulse rate at rest, which increased greatly on average during walking, but was not highly modulated with each step (tonically modulated gamma-motoneuron or gamma t). Peak gamma p rates generally occurred after peak EMG, often near the peak of tension. In contrast, peak gamma t activity generally preceded peak electromyograms (EMG). No significant difference was observed in conduction velocities for the two types of units. At rest all gamma t units were excited by natural stimulation of the fur over a large part of the body surface, whereas 3 of 11 gamma p units were inhibited. During locomotion the same natural stimuli had no observable effect on either type of unit. By recording in continuity from fine branches of the lateral and medial gastrocnemius nerves and stimulating ventral root filaments in continuity, we identified dynamic and static gamma-motoneurons in terms of their effects on muscle spindle afferents. After cutting the nerve branch distally and other ventral root filaments supplying the muscle, the resting discharge of dynamic and static gamma-motoneurons was recorded and found to correspond to that of the gamma p and gamma t units, respectively. Other evidence is presented for a correspondence between phasically and tonically modulated units and dynamic and static gamma-motoneurons, contrary to some suggestions in the literature.

Role of glycogen in control of glycolysis and IMP formation in human muscle during exercise

1991 ◽  
Vol 260 (6) ◽  
pp. E859-E864 ◽  
Author(s):  
M. K. Spencer ◽  
A. Katz
Keyword(s):  
Muscle Glycogen ◽  
Work Load ◽  
Amp Deaminase ◽  
Glycogen Depletion ◽  
Intense Exercise ◽  
O2 Uptake ◽  
Contraction Phase ◽  
Muscle Ph ◽  
Glycogen Stores

The effect of prior glycogen depletion on glycolysis [flux through phosphofructokinase (PFK)] and inosine monophosphate (IMP) formation in human skeletal muscle has been investigated. Eight subjects cycled at a work load calculated to elicit 95% of maximal O2 uptake on two occasions, the first to fatigue [5.5 +/- 0.3 (SE) min] and the second at the same workload and for the same duration as the first. Before the first experiment, muscle glycogen stores were lowered by a combination of exercise and diet. Before the second experiment, muscle glycogen stores were supercompensated. In the low-glycogen (LG) state muscle glycogen decreased from 201 +/- 31 mmol glucosyl units/kg dry wt at rest to 105 +/- 28 after exercise, and in the high-glycogen (HG) state from 583 +/- 40 to 460 +/- 49. The accumulation of fructose 6-phosphate (F-6-P; activator of PFK) during exercise was markedly attenuated in the LG state (P less than 0.01), whereas lactate accumulation in muscle was similar between treatments, suggesting that muscle pH was also similar. Glycolysis (estimated from glycogenolysis minus accumulation of hexose monophosphates) was not measurably different between treatments (LG = 88 +/- 17, HG = 106 +/- 43 mmol/kg dry wt; P greater than 0.05). IMP was significantly greater in the LG state after exercise (3.63 +/- 0.85 vs. 1.97 +/- 0.44 mmol/kg dry wt; P less than 0.05). It is concluded that decreased glycogen availability does not measurably alter the rate of muscle glycolysis during intense exercise. It is hypothesized that the attenuated increase in F-6-P in the LG state, which should theoretically decrease glycolysis, is compensated for by increases in free ADP and AMP (activators of PFK) at the enzymatic site during the contraction phase. The greater increase in IMP in the LG state is consistent with this hypothesis, since ADP and AMP are also activators of AMP deaminase.

Sign in / Sign up

Export Citation Format

Share Document