Accurate assessment of in situ isometric contractile properties of hindlimb plantar and dorsal flexor muscle complex of intact mice

2000 ◽  
Vol 439 (5) ◽  
pp. 665-670 ◽  
Author(s):  
M. Gorselink ◽  
M.R. Drost ◽  
J. de Louw ◽  
P.J.B. Willems ◽  
N. Rosielle ◽  
...  
2000 ◽  
Vol 439 (5) ◽  
pp. 665-670 ◽  
Author(s):  
M. Gorselink ◽  
M.R. Drost ◽  
J. de Louw ◽  
P.J.B. Willems ◽  
N. Rosielle ◽  
...  

2002 ◽  
Vol 282 (2) ◽  
pp. E348-E354 ◽  
Author(s):  
M. Gorselink ◽  
M. R. Drost ◽  
K. F. J. de Brouwer ◽  
G. Schaart ◽  
G. P. J. van Kranenburg ◽  
...  

GLUT-4 plays a predominant role in glucose uptake during muscle contraction. In the present study, we have investigated in mice whether disruption of the GLUT-4 gene affects isometric and shortening contractile performance of the dorsal flexor muscle complex in situ. Moreover, we have explored the hypothesis that lack of GLUT-4 enhances muscle fatigability. Isometric performance normalized to muscle mass during a single tetanic contraction did not differ between wild-type (WT) and GLUT-4-deficient [GLUT-4(−/−)] mice. Shortening contractions, however, revealed a significant 1.4-fold decrease in peak power per unit mass, most likely caused by the fiber-type transition from fast-glycolytic fibers (IIB) to fast-oxidative fibers (IIA) in GLUT-4(−/−) dorsal flexors. In addition, the resting glycogen content was significantly lower (34%) in the dorsal flexor complex of GLUT-4(−/−) mice than in WT mice. Moreover, the muscle complex of GLUT-4(−/−) mice showed enhanced susceptibility to fatigue, which may be related to the decline in the muscle carbohydrate store. The significant decrease in relative work output during the steady-state phase of the fatigue protocol suggests that energy supply via alternative routes is not capable to compensate fully for the lack of GLUT-4.


2010 ◽  
Vol 108 (3) ◽  
pp. 705-712 ◽  
Author(s):  
Andrés Hernández ◽  
Matthew L. Goodwin ◽  
Nicola Lai ◽  
Marco E. Cabrera ◽  
James R. McDonald ◽  
...  

The purpose of this research was to develop new techniques to 1) rapidly sample venous O2 saturation to determine contraction-by-contraction oxygen uptake (V̇o2), and 2) precisely control the rate and pattern of blood flow adjustment from one chosen steady state to another. An indwelling inline oximeter probe connected to an Oximetrix 3 meter was used to sample venous oxygen concentration ([O2]) (via fractional saturation of Hb with O2). Data from the Oximetrix 3 were filtered, deconvolved, and processed by a moving average second by second. Computer software and a program written in-house were used to control blood flow with a peristaltic pump. The isolated canine gastrocnemius muscle complex (GS) in situ was utilized to test these techniques. A step change in metabolic rate was elicited by stimulating GS muscles via their sciatic nerves (supramaximal voltage, 8 V; 50 Hz, 0.2-ms pulse width; train duration 200 ms) at a rate of either 1 contraction/2 s, or 2 contractions/3 s. With arterial [O2] maintained constant, blood flow and calculated venous [O2] were averaged over each contraction cycle and used in the Fick equation to calculate contraction-by-contraction V̇o2. About 5–8 times more data points were obtained with this method compared with traditional manual sampling. Software-controlled pump perfusion enabled the ability to mimic spontaneous blood flow on-kinetics (τ: 14.3 s) as well as dramatically speed (τ: 2.0 s) and slow (τ: 63.3 s) on-kinetics. These new techniques significantly improve on existing methods for mechanistically altering blood flow kinetics as well as accurately measuring muscle oxygen consumption kinetics during transitions between metabolic rates.


1982 ◽  
Vol 52 (2) ◽  
pp. 473-478 ◽  
Author(s):  
R. R. Roy ◽  
I. D. Meadows ◽  
K. M. Baldwin ◽  
V. R. Edgerton

Chronic overload of a skeletal muscle by removing its synergists produces hypertrophy and marked changes in its metabolic and biochemical properties. In this study alterations in the contractile properties of the plantaris 12–14 wk after bilateral removal of the soleus and gastrocnemius were investigated. In situ isometric and isotonic contractile properties of overloaded plantaris (OP), normal plantaris (NP), and normal soleus (NS) were tested at 33 +/- 1 degree C. Op were 97% heavier than NP and produced 43 and 46% higher twitch (Pt) and tetanic (Po) tensions. However, NP produced more tension per cross-sectional area than OP (mean 26.2 vs. 21.6 N/cm2; P less than 0.001). Isometric twitch time to peak tension (TPT) and half-relaxation time (1/2RT) were significantly longer in OP (mean 36.4 vs. 32.5 ms and 23.9 vs. 18.4 ms). Mean maximum shortening velocity (Vmax, mm/s per 1,000 sarcomeres) were 34.1 for NP and 18.1 for OP (P less than 0.001). The degree of conversion toward the Vmax of NS was 74% compared with only 19 and 14% for TPT and 1/2RT. OP produced a higher proportion of Po at a given stimulation frequency than NP and showed less fatigue than NP after repetitive stimulation. Chronic overload of the fast plantaris modified to varying degrees the contractile properties studied toward that resembling a slow muscle. Although the maximum tension of OP was markedly enhanced it was not in proportion to the increase in muscle mass.


Author(s):  
Jiayu Shi ◽  
Daiki Watanabe ◽  
Masanobu Wada

This study was conducted to examine the effects of an acute bout of vigorous isometric contractions on titin stiffness-related contractile properties in rat fast-twitch skeletal muscles. Intact gastrocnemius muscles were electrically stimulated in situ until the force was reduced to ~50% of the initial force. Immediately after cessation of the stimulation, the superficial regions of the muscles were dissected and subjected to biochemical and skinned fiber analyses. The stimulation resulted in a decrease in the titin-based passive force. The amounts of fragmented titin were unchanged by the stimulation. Protein kinase Cα-treatment increased the passive force in stimulated fibers to resting levels. The stimulation had no effect on the maximum Ca2+-activated force (max Ca2+ force) at a sarcomere length (SL) of 2.4 μm and decreased myofibrillar (my)-Ca2+ sensitivity at 2.6-μm SL. Stretching the SL to 3.0 μm led to the augmentation of the max Ca2+ force and my-Ca2+ sensitivity in both rested and stimulated fibers. For the max Ca2+ force, the extent of the increase was smaller in stimulated than in rested fibers, whereas for my-Ca2+ sensitivity, it was higher in stimulated than in rested fibers. These results suggest that vigorous isometric contractions decrease the titin-based passive force, possibly because of a reduction in phosphorylation by protein kinase Cα, and that the decreased titin stiffness may contribute, at least in part, to muscle fatigue.


Author(s):  
Brian R. MacIntosh ◽  
Shane P. Esau ◽  
R. John Holash ◽  
Jared R. Fletcher

2006 ◽  
Vol 101 (1) ◽  
pp. 256-263 ◽  
Author(s):  
Brian C. Clark ◽  
Bo Fernhall ◽  
Lori L. Ploutz-Snyder

Strength loss following disuse may result from alterations in muscle and/or neurological properties. In this paper, we report our findings on human plantar flexor muscle properties following 4 wk of limb suspension (unilateral lower limb suspension), along with the effect of applied ischemia (Isc) on these properties. In the companion paper (Part II), we report our findings on the changes in neurological properties. Measurements of voluntary and evoked forces, the compound muscle fiber action potential (CMAP), and muscle cross-sectional area (CSA) were collected before and after 4 wk of unilateral lower limb suspension in adults ( n = 18; 19–28 yr). A subset of subjects ( n = 6) received applications of Isc 3 days/wk (3 sets; 5-min duration). In the subjects not receiving Isc, the loss in CSA and strength was as expected (∼9 and 14%). We observed a 30% slowing in the duration of the CMAP, a 10% decrease in evoked doublet force, a 12% increase in the twitch-to-doublet force ratio, and an altered postactivation potentiation response (11% increase in the postactivation potentiation-to-doublet ratio). We also detected a 10% slowing in the ability of the plantar flexor to develop force during the initial phase of an evoked contraction, along with a 6% reduction in in vivo specific doublet force. In the Isc subjects, no preservation was observed in strength or the evoked muscle properties. However, the Isc group did maintain CSA of the lateral gastrocnemius, as the control subjects’ lateral gastrocnemius atrophied 10.2%, whereas the subjects receiving Isc atrophied 4.7%. Additionally, Isc abolished the unweighting-induced slowing in the CMAP. These findings suggest that unweighting alters the contractile properties involved in the excitation-contraction coupling processes and that Isc impacts the sarcolemma.


2001 ◽  
Vol 442 (2) ◽  
pp. 304-311 ◽  
Author(s):  
Gorselink M. ◽  
Drost M. ◽  
J. de Louw ◽  
Willems P. ◽  
Hesselink M. ◽  
...  

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