Skeletal muscle bioenergetics during frequency-dependent fatigue

1991 ◽  
Vol 260 (3) ◽  
pp. C643-C651 ◽  
Author(s):  
C. R. Bridges ◽  
B. J. Clark ◽  
R. L. Hammond ◽  
L. W. Stephenson

The bioenergetic correlates of skeletal muscle fatigue were assessed in vivo with phosphorus-31 nuclear magnetic resonance (31P-NMR) spectroscopy. After surgical construction of latissimus dorsi muscle ventricles, seven beagles underwent 31P-NMR spectroscopy during 12-min exercise protocols at 25- and 85-Hz stimulation frequencies and during both isovolumetric and dynamic contractions. Exercise at 85 Hz was associated with significantly greater fatigue than exercise at 25 Hz. At both frequencies, the onset of exercise was associated with a marked increase in inorganic phosphate (Pi) and a decrease in phosphocreatine (PCr). As the muscle fatigued at 85 Hz but not at 25 Hz, the phosphorus spectra returned to near baseline with a decrease in Pi and increase in PCr. For a given amount of force generated, the Pi-to-PCr ratio was higher for dynamic contractions than for isovolumetric contractions. This study indicates that high-frequency fatigue is unlikely to result from the direct effects of high-energy phosphate metabolism and that contractions producing external work consume more metabolic energy than equally forceful isometric contractions.

1992 ◽  
Vol 20 (2) ◽  
pp. 198S-198S
Author(s):  
JOHN S. BEECH ◽  
STEPHEN C.R. WILLIAMS ◽  
ROBERT D. COHEN ◽  
RICHARD A. ILES

1988 ◽  
Vol 254 (2) ◽  
pp. C258-C266 ◽  
Author(s):  
B. J. Clark ◽  
M. A. Acker ◽  
K. McCully ◽  
H. V. Subramanian ◽  
R. L. Hammond ◽  
...  

Chronic stimulation converts skeletal muscle of mixed fiber type to a uniform muscle made up of type I, fatigue-resistant fibers. Here, the bioenergetic correlates of fatigue resistance in conditioned canine latissimus dorsi are assessed with in vivo phosphorus-31 nuclear magnetic resonance (31P-NMR) spectroscopy. After chronic electrical stimulation, five dogs underwent 31P-NMR spectroscopic and isometric tension measurements on conditioned and contralateral control muscle during stimulation for 200, 300, 500, and 800 ms of an 1,100-ms duty cycle. With stimulation, phosphocreatine (PCr) fell proportional to the degree of stimulation in both conditioned and control muscle but fell significantly less in conditioned muscle at all but the least intense stimulation period (200 ms). Isometric tension, expressed as a tension time index per gram muscle, was significantly greater in the conditioned muscle at the two longest stimulation periods. The overall small change in PCr and the lack of a plateau in tension observed in the conditioned muscle are similar to that seen in cardiac muscle during increased energy demand. This study indicates that the conditioned muscle's markedly enhanced resistance to fatigue is in part the result of its increased capacity for oxidative phosphorylation.


2014 ◽  
Vol 114 (4) ◽  
pp. 847-858 ◽  
Author(s):  
Prithvi K. Shah ◽  
Fan Ye ◽  
Min Liu ◽  
Arun Jayaraman ◽  
Celine Baligand ◽  
...  

1993 ◽  
Vol 34 (4) ◽  
pp. 397-404
Author(s):  
B. Moesgaard ◽  
I. Errebo Larsen ◽  
B. Quistorff ◽  
I. Therkelsen ◽  
V. Grøsfjeld Christensen ◽  
...  

1993 ◽  
Vol 74 (4) ◽  
pp. 1549-1554 ◽  
Author(s):  
Y. Hayashi ◽  
T. Inubushi ◽  
S. Nioka ◽  
R. E. Forster

We obtained 202.5-MHz 31P-nuclear magnetic resonance (NMR) spectra of isolated perfused rat lungs, degassed and inflated, and of lung extract. The spectra included those of ATP, ADP, phosphocreatine (PCr), inorganic phosphate (Pi), phosphomonoesters, phosphodiesters, and a broad component due to the membrane phospholipids. The line width at one-half peak height for beta-ATP was 1.0 ppm for the degassed lung and 1.2 ppm for the inflated lung. This suggests that the air-water interfaces in inflated lung, which produce proton NMR line broadening, do not act prominently in 31P-NMR spectroscopy. In a degassed lung, when perfusion was stopped for up to 30 min, PCr and ATP peaks decreased progressively with time while Pi and phosphomonoester peaks increased. On return of flow, these changes reversed. The intracellular pH values calculated from the difference in magnetic field between PCr and Pi peaks of inflated and degassed lungs were 7.16 +/- 0.10 (SD; n = 4) and 6.99 +/- 0.10 (n = 4), respectively. The change of intracellular pH caused by 30 min of ischemia was -0.2 pH units. Our findings indicate that air-water interfaces should not broaden lung 31P peaks in vivo.


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