Sympathoadrenal system and activation of glycogenolysis during muscular activity

1985 ◽  
Vol 58 (4) ◽  
pp. 1122-1127 ◽  
Author(s):  
L. J. Cartier ◽  
P. D. Gollnick

Comparisons were made of the appearance of phosphorylase (PHOS) a and lactate (LA) during electrical stimulation of the gastrocnemius (GM) and soleus (SM) muscles of normal and sympathectomized (SYMPX) rats. Ten-second stimulation at 3 Hz increased PHOS a approximately fourfold in the GM of normal rats, whereafter it declined during stimulation until at 60 s it was similar to rest. The increase in PHOS a of GM from SYMPX rats after 10 s of stimulation was approximately 50% that of normal rats. Stimulation of the SM produced smaller and slower increases in PHOS a with the peak occurring after 60 s, which remained constant to 90 s. SYMPX did not alter this effect in the SM. LA production and creatine phosphate depletion in the GM were continuous throughout stimulation and uninfluenced by SYMPX. This was true for the SM with the exception of LA production being greater after SYMPX. [ATP] was unchanged by electrical stimulation. The rate and magnitude of the PHOS a appearance was a function of stimulation frequency. Reversion of PHOS to the b form after stimulation was rapid, with approximately 50% of the peak value being attained in 2.5 s, and at 5 s the values were those of rest. These data demonstrate that an intact sympathoadrenal system is not obligatory for the initiation of glycogenolysis in skeletal muscle.

1987 ◽  
Vol 63 (6) ◽  
pp. 2331-2339 ◽  
Author(s):  
M. I. Lindinger ◽  
G. J. Heigenhauser ◽  
L. L. Spriet

The purpose of this study was to compare changes in ions and metabolites in four different rat hindlimb muscles in response to intense swimming exercise in vivo (263 +/- 33 s) (SWUM), and to 5 min (300 s) of tetanic electrical stimulation of artificially perfused rat hindlimbs (STIM). With both swimming and electrical stimulation, soleus (SOL) contents of creatine phosphate (CP), ATP, and glycogen changed the least, whereas the largest decreases in these metabolites occurred in the white gastrocnemius (WG). Lactate (La-) accumulation and glycogen breakdown were significantly greater in SWUM hindlimb muscles compared with STIM. The high arterial La- concentration [( La-] = 20 meq.l-1) in SWUM may have contributed to elevated muscle [La-], whereas one-pass perfusion kept arterial [La-] below 2 meq.l–1 in STIM. In SWUM, intracellular [Na+] increased significantly in the plantaris (PL), red gastrocnemius (RG), and WG, but not in SOL. [Cl-] increased, and [K+], [Ca2+], and [Mg2+] decreased in all muscles. In STIM, intracellular [K+], [Mg2+], and [Ca2+] decreased significantly, whereas [Na+] and [Cl-] increased in all muscles. Differences in the magnitude of ion and fluid fluxes between groups can be explained by the different methods of hindlimb perfusion. In conclusion, STIM is a useful model of in vivo energy metabolism and permits mechanisms of transsarcolemmal ion movements to be studied.


2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.


1978 ◽  
Vol 45 (6) ◽  
pp. 852-857 ◽  
Author(s):  
P. D. Gollnick ◽  
J. Karlsson ◽  
K. Piehl ◽  
B. Saltin

Experiments were conducted to examine the conversions of phosphorylase b to phosphorylase a in human skeletal muscle during bicycle exercise or isometric contractions. Muscle biopsies were obtained from the vastus lateralis with the needle technique at rest and either during or immediately after activity and frozen in liquid nitrogen within 2--4 s. Total phosphorylase and phosphorylase a activities were differentiated by measurement in the presence and absence of AMP, respectively. At rest 8.5% of the total phosphorylase activity existed in the a form. Little or no change in the percent of phosphorylase in the a form occurred during voluntary dynamic or static muscular activity that produced muscle lactate concentrations in excess of 18 mmol.kg-1 wet muscle. Electrical stimulation of the vastus lateralis muscle also failed to produce an increase in the percentage of phosphorylase a. These data suggest that during exercise the conversion of phosphorylase to the a form is of minor importance. An increased activity of phosphorylase b due to changes in muscle concentrations of ATP, AMP, and inorganic phosphate may regulate glycogenolysis during voluntary exercise in man.


1997 ◽  
Vol 272 (5) ◽  
pp. H2369-H2376 ◽  
Author(s):  
R. L. Davisson ◽  
O. S. Possas ◽  
S. P. Murphy ◽  
S. J. Lewis

Skeletal muscle vasculature of the hindlimb is innervated by a sympathetic noncholinergic vasodilator system. The aim of this study was to determine whether this vasodilator system may represent postganglionic lumbar sympathetic neurons that synthesize and release nitric oxide (NO) or related NO-containing factors. We examined whether NO synthase (NOS)-positive postganglionic lumbar nerves innervate the hindlimb vasculature of the rat and whether the hindlimb vasodilation produced by electrical stimulation of the lumbar sympathetic chain of anesthetized rats is reduced after the systemic administration of the specific inhibitor of neuronal NOS 7-nitroindazole (7-NI). Subpopulations of lumbar sympathetic cell bodies stained intensely for NOS. Postganglionic fibers and varicosities within the iliac and femoral arteries also stained for NOS. Double ligation of the lumbar chain demonstrated that NOS was transported from the cell bodies toward the peripheral terminals. Low-intensity electrical stimulation of the lumbar chain produced a pronounced hindlimb vasodilation that was markedly diminished by pretreatment with 7-NI (45 mg/kg i.v.). In contrast, the vasodilator potency of acetylcholine and S-nitrosocysteine were augmented by 7-NI. These results suggest that postganglionic lumbar sympathetic neurons may synthesize and release NO-containing factors.


1999 ◽  
Vol 276 (2) ◽  
pp. R331-R339 ◽  
Author(s):  
H. Gissel ◽  
T. Clausen

In isolated rat extensor digitorum longus (EDL) muscle mounted for isometric contractions, chronic low-frequency electrical stimulation was found to lead to an increased uptake of45Ca (154% above control after 240 min) and a progressive accumulation of Ca2+ (85% above control after 240 min). In soleus, however, this treatment led to a small, but significant, increase in 45Ca uptake (30% above control after 180 min) but no significant accumulation of Ca2+. In muscles mounted for isotonic contractions without any external load, electrical stimulation gave rise to a larger45Ca uptake and accumulation of Ca2+ in both EDL and soleus. These uptakes of Ca2+ coincided with an accumulation of Na+. During isometric or isotonic contractions, stimulation at 40 Hz increased the initial (60 s) rate of 45Ca uptake in soleus muscle 15- and 30-fold, respectively. The stimulation-induced increase in 45Ca uptake was only reduced by 17% by the Ca2+-channel blockers nifedipine and verapamil but was blocked by tetrodotoxin. The initial rate of stimulation-induced 22Na and45Ca uptake was correlated ( r = 0.80; P < 0.003). Stimulation of Na+ channels with veratridine increased 45Ca uptake by 93 and 139% in soleus and EDL, respectively ( P < 0.001), effects that were abolished by tetrodotoxin. The results indicate that in skeletal muscle, excitation induces a considerable influx of Ca2+, mediated by Na+ channels.


2010 ◽  
Vol 108 (2) ◽  
pp. 298-305 ◽  
Author(s):  
G. Nathan Nakken ◽  
Daniel L. Jacobs ◽  
David M. Thomson ◽  
Natasha Fillmore ◽  
William W. Winder

Cushing's syndrome is characterized by marked central obesity and insulin insensitivity, effects opposite those seen with chronic AMP-activated protein kinase (AMPK) activation. This study was designed to determine whether chronic exposure to excess glucocorticoids influences LKB1/AMPK signaling in skeletal muscle. Corticosterone pellets were implanted subcutaneously in rats (hypercorticosteronemia, Hypercort) for 2 wk. Controls were sham operated and fed ad libitum or were sham operated and food restricted (pair-weighted group, Pair) to produce body weights similar to Hypercort rats. At the end of the 2-wk treatment period, rats were anesthetized, and the right gastrocnemius-plantaris (gastroc) and soleus muscles were removed. Left muscles were removed after electrical stimulation for 5 min. No significant differences were noted between treatment groups in ATP, creatine phosphate, or LKB1 activity. The α- and β-subunit isoforms were not significantly influenced in gastroc by corticosterone treatment. Expression of the γ3-subunit decreased, and γ1- and γ2-subunit expression increased. Both α2-AMPK and α1-AMPK activities were increased in the gastroc in response to electrical stimulation, but the magnitude of the increase was less for α2 in the Hypercort rats. Despite elevated plasma insulin and elevated plasma leptin in the Hypercort rats, phosphorylation of TBC1D1 was lower in both resting and stimulated muscle compared with controls. Malonyl-CoA content was elevated in gastroc muscles of resting Hypercort rats. These changes in response to excess glucocorticoids could be responsible, in part, for the decrease in insulin sensitivity and adiposity seen in Cushing's syndrome.


2020 ◽  
Author(s):  
Elahe Ganji ◽  
C. Savio Chan ◽  
Christopher W. Ward ◽  
Megan L. Killian

AbstractOptogenetics is an emerging alternative to traditional electrical stimulation to initiate action potentials in activatable cells both ex vivo and in vivo. Optogenetics has been commonly used in mammalian neurons and more recently, it has been adapted for activation of cardiomyocytes and skeletal muscle. Therefore, the aim of this study was to evaluate the stimulation feasibility and sustain isometric muscle contraction and limit decay for an extended period of time (1s), using non-invasive transdermal light activation of skeletal muscle (triceps surae) in vivo. We used inducible Cre recombination to target expression of Channelrhodopsin-2 (ChR2(H134R)-EYFP) in skeletal muscle (Acta1-Cre) in mice. Fluorescent imaging confirmed that ChR2 expression is localized in skeletal muscle and does not have specific expression in sciatic nerve branch, therefore, allowing for non-nerve mediated optical stimulation of skeletal muscle. We induced muscle contraction using transdermal exposure to blue light and selected 10Hz stimulation after controlled optimization experiments to sustain prolonged muscle contraction. Increasing the stimulation frequency from 10Hz to 40Hz increased the muscle contraction decay during prolonged 1s stimulation, highlighting frequency dependency and importance of membrane repolarization for effective light activation. Finally, we showed that optimized pulsed optogenetic stimulation of 10 Hz resulted in comparable ankle torque and contractile functionality to that of electrical stimulation. Our results demonstrate the feasibility and repeatability of non-invasive optogenetic stimulation of muscle in vivo and highlight optogenetic stimulation as a powerful tool for non-invasive in vivo direct activation of skeletal muscle.


1999 ◽  
Vol 87 (6) ◽  
pp. 2259-2265 ◽  
Author(s):  
D. Paul Thomas ◽  
Olga Hudlická

The purpose of this study was to assess whether electrical stimulation-induced increases in muscular activity could improve capillary supply and correct previously documented abnormal vasodilator and vasoconstrictor responses of arterioles in limb skeletal muscle post-myocardial infarction (MI). Extensor digitorum longus (EDL) muscle from rats with surgically induced MI (∼30% of the left ventricle) was chronically stimulated (Stim) 8 h/day for 6 ± 1 days, at 11 wk post-MI. Third- (3A) and fourth-order (4A) arterioles in EDL from nine MI rats and four MI+Stim rats were compared with those of 11 controls (Con). Compared with Con rats, MI alone caused a reduction in the resting diameter of 3A and 4A arterioles, which was completely reversed by MI+Stim. However, Stim did not correct the attenuated vasodilator response to 10−4M adenosine seen in 4A arterioles from MI rats compared with Con. The constrictor response of both 3A and 4A vessels in MI rats to low doses of acetylcholine (10−9 M, 10−8 M) and norepinephrine (10−9 M) was accentuated in MI+Stim. The proportion of oxidative fibers in EDL was unaffected by MI or MI+Stim combination. However, Stim significantly increased ( P < 0.05) the capillary-to-fiber ratio in this muscle compared with Con. Thus, although the increase in muscle activity induced by chronic electrical stimulation normalized the reduction in resting vessel diameter seen after MI, it failed to correct the abnormalities in vasoreactivity of these same vessels.


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