Importance of the Adaptive Properties of Skeletal Muscle in Long-Term Electrophrenic Stimulation of the Diaphragm

1989 ◽  
Vol 53 (4) ◽  
pp. 223-232 ◽  
Author(s):  
S. Salmons
2002 ◽  
Vol 363 (1) ◽  
pp. 167-174 ◽  
Author(s):  
Lee G.D. FRYER ◽  
Fabienne FOUFELLE ◽  
Kay BARNES ◽  
Stephen A. BALDWIN ◽  
Angela WOODS ◽  
...  

Stimulation of AMP-activated protein kinase (AMPK) in skeletal muscle has been correlated with an increase in glucose transport. Here, we demonstrate that adenoviral-mediated expression of a constitutively active mutant of AMPKα leads to activation of glucose transport in a skeletal-muscle cell line, similar to that seen following treatment with 5-amino-imidazolecarboxamide (AICA) riboside, hyperosmotic stress or insulin. In contrast, expression of a dominant-negative form of AMPK blocked the stimulation of glucose transport by both AICA riboside and hyperosmotic stress, but was without effect on either insulin or phorbol-ester-stimulated transport. These results demonstrate that activation of AMPK is sufficient for stimulation of glucose uptake into muscle cells, and is a necessary component of the AICA riboside- and hyperosmotic-stress-induced pathway leading to increased glucose uptake. On the other hand, AMPK is not required in the insulin- or phorbol-ester-mediated pathways. Long-term (5 days) expression of the constitutively active AMPK mutant increased protein expression of GLUT1, GLUT4 and hexokinase II, consistent with previous reports on the chronic treatment of rats with AICA riboside. Expression of constitutively active AMPK had no detectable effect on p38 mitogen-activated protein kinase levels, although interestingly the level of protein kinase B was decreased. These results demonstrate that long-term activation of AMPK is sufficient to cause increased expression of specific proteins in muscle. Our results add further support to the hypothesis that long-term activation of AMPK is involved in the adaptive response of muscle to exercise training.


1995 ◽  
Vol 269 (2) ◽  
pp. H717-H724 ◽  
Author(s):  
T. H. Adair ◽  
J. Hang ◽  
M. L. Wells ◽  
F. D. Magee ◽  
J. P. Montani

We tested whether chronic stimulation of skeletal muscle can increase the growth of paired arteries and veins in rabbit extensor digitorum longus muscle (EDL). The right EDL of female New Zealand White rabbits was stimulated via the common peroneal nerve at 10 Hz using 300 microseconds square waves at 3-4 V. Two-hour periods of stimulation was alternated with 4-h periods of rest, 7 days/wk for approximately 60 days. The left EDL served as control. The hindlimb vascular system was maximally dilated and perfuse-fixed with 3% glutaraldehyde and 2% paraformaldehyde at arterial and venous pressures of 80-100 and 15-20 mmHg, respectively. Muscles were postfixed in OsO4 and embedded in EPOX 812 resin. One millimeter-thick transverse sections were cut at uniform locations through the entire breadth of the muscle and analyzed using videomicroscopy along with computerized morphometric and stereological techniques. All paired arteries and veins on each full muscle section were analyzed. Chronic muscle stimulation caused the wall volume of paired arteries and veins to increase by an average of approximately twofold and the lumen volume to increase by an average of approximately threefold compared with the contralateral muscles. The wall-to-lumen area ratio of the arteries and veins was not affected. Muscle stimulation also caused the numerical density of arteries having a diameter > 100 microns to increase by approximately fourfold and the density of veins having a perimeter > 500 microns to increase by approximately 10-fold.(ABSTRACT TRUNCATED AT 250 WORDS)


Nature ◽  
1973 ◽  
Vol 244 (5413) ◽  
pp. 225-227 ◽  
Author(s):  
W. S. AL-AMOOD ◽  
A. J. BULLER ◽  
R. POPE

2020 ◽  
Vol 133 (3) ◽  
pp. 830-838 ◽  
Author(s):  
Andrea Franzini ◽  
Giuseppe Messina ◽  
Vincenzo Levi ◽  
Antonio D’Ammando ◽  
Roberto Cordella ◽  
...  

OBJECTIVECentral poststroke neuropathic pain is a debilitating syndrome that is often resistant to medical therapies. Surgical measures include motor cortex stimulation and deep brain stimulation (DBS), which have been used to relieve pain. The aim of this study was to retrospectively assess the safety and long-term efficacy of DBS of the posterior limb of the internal capsule for relieving central poststroke neuropathic pain and associated spasticity affecting the lower limb.METHODSClinical and surgical data were retrospectively collected and analyzed in all patients who had undergone DBS of the posterior limb of the internal capsule to address central poststroke neuropathic pain refractory to conservative measures. In addition, long-term pain intensity and level of satisfaction gained from stimulation were assessed. Pain was evaluated using the visual analog scale (VAS). Information on gait improvement was obtained from medical records, neurological examination, and interview.RESULTSFour patients have undergone the procedure since 2001. No mortality or morbidity related to the surgery was recorded. In three patients, stimulation of the posterior limb of the internal capsule resulted in long-term pain relief; in a fourth patient, the procedure failed to produce any long-lasting positive effect. Two patients obtained a reduction in spasticity and improved motor capability. Before surgery, the mean VAS score was 9 (range 8–10). In the immediate postoperative period and within 1 week after the DBS system had been turned on, the mean VAS score was significantly lower at a mean of 3 (range 0–6). After a mean follow-up of 5.88 years, the mean VAS score was still reduced at 5.5 (range 3–8). The mean percentage of long-term pain reduction was 38.13%.CONCLUSIONSThis series suggests that stimulation of the posterior limb of the internal capsule is safe and effective in treating patients with chronic neuropathic pain affecting the lower limb. The procedure may be a more targeted treatment method than motor cortex stimulation or other neuromodulation techniques in the subset of patients whose pain and spasticity are referred to the lower limbs.


2000 ◽  
Vol 278 (3) ◽  
pp. R705-R711 ◽  
Author(s):  
T. A. McAllister ◽  
J. R. Thompson ◽  
S. E. Samuels

The effect of long-term cold exposure on skeletal and cardiac muscle protein turnover was investigated in young growing animals. Two groups of 36 male 28-day-old rats were maintained at either 5°C (cold) or 25°C (control). Rates of protein synthesis and degradation were measured in vivo on days 5, 10, 15, and 20. Protein mass by day 20 was ∼28% lower in skeletal muscle (gastrocnemius and soleus) and ∼24% higher in heart in cold compared with control rats ( P < 0.05). In skeletal muscle, the fractional rates of protein synthesis ( k syn) and degradation ( k deg) were not significantly different between cold and control rats, although k syn was lower (approximately −26%) in cold rats on day 5; consequent to the lower protein mass, the absolute rates of protein synthesis (approximately −21%; P < 0.05) and degradation (approximately −13%; P < 0.1) were lower in cold compared with control rats. In heart, overall, k syn(approximately +12%; P < 0.1) and k deg(approximately +22%; P < 0.05) were higher in cold compared with control rats; consequently, the absolute rates of synthesis (approximately +44%) and degradation (approximately +54%) were higher in cold compared with control rats ( P < 0.05). Plasma triiodothyronine concentration was higher ( P < 0.05) in cold compared with control rats. These data indicate that long-term cold acclimation in skeletal muscle is associated with the establishment of a new homeostasis in protein turnover with decreased protein mass and normal fractional rates of protein turnover. In heart, unlike skeletal muscle, rates of protein turnover did not appear to immediately return to normal as increased rates of protein turnover were observed beyond day 5. These data also indicate that increased rates of protein turnover in skeletal muscle are unlikely to contribute to increased metabolic heat production during cold acclimation.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.


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