scholarly journals Cross bridges account for only 20% of total ATP consumption during submaximal isometric contraction in mouse fast-twitch skeletal muscle

2006 ◽  
Vol 291 (1) ◽  
pp. C147-C154 ◽  
Author(s):  
Shi-Jin Zhang ◽  
Daniel C. Andersson ◽  
Marie E. Sandström ◽  
Håkan Westerblad ◽  
Abram Katz
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Force Production ◽  
Physiological Conditions ◽  
Atp Turnover ◽  
Energy Consuming ◽  
Cross Bridges ◽  
Fast Twitch ◽  
Muscle Force Production ◽  
Ion Pumping

It is generally believed that cross bridges account for >50% of the total ATP consumed by skeletal muscle during contraction. We investigated the effect of N-benzyl- p-toluene sulfonamide (BTS), an inhibitor of myosin ATPase, on muscle force production and energy metabolism under near-physiological conditions (50-Hz stimulation frequency at 30°C results in 35% of maximal force). Extensor digitorum longus muscles from mice were isolated and stimulated to perform continuous isometric tetanic contractions. Metabolites of energy metabolism were analyzed with fluorometric techniques. ATP turnover was estimated from the changes in phosphocreatine (PCr), ATP, and lactate (−2ΔATP − ΔPCr + [1.5Δlactate]). During contractions (2–10 s), BTS decreased force production to ∼5% of control. Under these conditions, BTS inhibited ATP turnover by only 18–25%. ATP turnover decreased markedly and similarly with and without BTS as the duration of contraction progressed. In conclusion, cross bridges (i.e., actomyosin ATPase) account for only a small fraction (∼20%) of the ATP consumption during contraction in mouse fast-twitch skeletal muscle under near-physiological conditions, suggesting that ion pumping is the major energy-consuming process.

Dynamics and Consequences of Potassium Shifts in Skeletal Muscle and Heart During Exercise

2000 ◽  
Vol 80 (4) ◽  
pp. 1411-1481 ◽  
Author(s):  
Ole M. Sejersted ◽  
Gisela Sjøgaard
Keyword(s):  
Skeletal Muscle ◽  
Force Production ◽  
Membrane Conductance ◽  
Cell Swelling ◽  
Modifying Factors ◽  
Fast Twitch Muscle ◽  
T Tubules ◽  
Exercise Induced ◽  
Fast Twitch ◽  
Muscle Excitability

Since it became clear that K+shifts with exercise are extensive and can cause more than a doubling of the extracellular [K+] ([K+]s) as reviewed here, it has been suggested that these shifts may cause fatigue through the effect on muscle excitability and action potentials (AP). The cause of the K+shifts is a transient or long-lasting mismatch between outward repolarizing K+currents and K+influx carried by the Na+-K+pump. Several factors modify the effect of raised [K+]sduring exercise on membrane potential ( Em) and force production. 1) Membrane conductance to K+is variable and controlled by various K+channels. Low relative K+conductance will reduce the contribution of [K+]sto the Em. In addition, high Cl−conductance may stabilize the Emduring brief periods of large K+shifts. 2) The Na+-K+pump contributes with a hyperpolarizing current. 3) Cell swelling accompanies muscle contractions especially in fast-twitch muscle, although little in the heart. This will contribute considerably to the lowering of intracellular [K+] ([K+]c) and will attenuate the exercise-induced rise of intracellular [Na+] ([Na+]c). 4) The rise of [Na+]cis sufficient to activate the Na+-K+pump to completely compensate increased K+release in the heart, yet not in skeletal muscle. In skeletal muscle there is strong evidence for control of pump activity not only through hormones, but through a hitherto unidentified mechanism. 5) Ionic shifts within the skeletal muscle t tubules and in the heart in extracellular clefts may markedly affect excitation-contraction coupling. 6) Age and state of training together with nutritional state modify muscle K+content and the abundance of Na+-K+pumps. We conclude that despite modifying factors coming into play during muscle activity, the K+shifts with high-intensity exercise may contribute substantially to fatigue in skeletal muscle, whereas in the heart, except during ischemia, the K+balance is controlled much more effectively.

Beetroot Juice Increases Skeletal Muscle Force Production in Recreationally Active Subjects.

2016 ◽  
Vol 48 ◽  
pp. 897
Author(s):  
Jamie Whitfield ◽  
George J. F. Heigenhauser ◽  
Lawrence L. Spriet ◽  
Graham P. Holloway ◽  
A. Russell Tupling
Keyword(s):  
Skeletal Muscle ◽  
Muscle Force ◽  
Force Production ◽  
Beetroot Juice ◽  
Muscle Force Production

scholarly journals Milrinone inhibits contractility in skinned skeletal muscle fibers

1998 ◽  
Vol 274 (5) ◽  
pp. C1306-C1311 ◽  
Author(s):  
C. Y. Seow ◽  
L. Morishita ◽  
B. H. Bressler
Keyword(s):  
Skeletal Muscle ◽  
Direct Action ◽  
Force Production ◽  
Isometric Tension ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Reduction In Force ◽  
Cross Bridge ◽  
The Cross ◽  
Cross Bridges

Direct action of the cardiotonic bipyridine milrinone on the cross bridges of single fibers of skinned rabbit skeletal muscle was investigated. At 10°C and pH 7.0, milrinone reduced isometric tension in a logarithmically concentration-dependent manner, with a 55% reduction in force at 0.6 mM. Milrinone also reduced Ca2+ sensitivity of skinned fibers in terms of force production; the shift in the force-pCa curve indicated a change in the pCa value at 50% maximal force from 6.10 to 5.94. The unloaded velocity of shortening was reduced by 18% in the presence of 0.6 mM milrinone. Parts of the transient tension response to step change in length were altered by milrinone, so that the test and control transients could not be superimposed. The results indicate that milrinone interferes with the cross-bridge cycle and possibly detains cross bridges in low-force states. The results also suggest that the positive inotropic effect of milrinone on cardiac muscle is probably not due to the drug’s direct action on the muscle cross bridges. The specific and reversible action of the bipyridine on muscle cross bridges makes it a potentially useful tool for probing the chemomechanical cross-bridge cycle.

scholarly journals Transverse tubule remodeling enhances Orai1-dependent Ca2+ entry in skeletal muscle

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Antonio Michelucci ◽  
Simona Boncompagni ◽  
Laura Pietrangelo ◽  
Maricela García-Castañeda ◽  
Takahiro Takano ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Time Course ◽  
Acute Exercise ◽  
Muscle Force ◽  
Contractile Function ◽  
Force Production ◽  
High Frequency Stimulation ◽  
Frequency Stimulation ◽  
Muscle Force Production ◽  
Muscle Contractile

Exercise promotes the formation of intracellular junctions in skeletal muscle between stacks of sarcoplasmic reticulum (SR) cisternae and extensions of transverse-tubules (TT) that increase co-localization of proteins required for store-operated Ca2+ entry (SOCE). Here, we report that SOCE, peak Ca2+ transient amplitude and muscle force production during repetitive stimulation are increased after exercise in parallel with the time course of TT association with SR-stacks. Unexpectedly, exercise also activated constitutive Ca2+ entry coincident with a modest decrease in total releasable Ca2+ store content. Importantly, this decrease in releasable Ca2+ store content observed after exercise was reversed by repetitive high-frequency stimulation, consistent with enhanced SOCE. The functional benefits of exercise on SOCE, constitutive Ca2+ entry and muscle force production were lost in mice with muscle-specific loss of Orai1 function. These results indicate that TT association with SR-stacks enhances Orai1-dependent SOCE to optimize Ca2+ dynamics and muscle contractile function during acute exercise.

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