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.

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

A metabolic basis for impaired muscle force production and neuromuscular compensation during sprint cycling

2006 ◽  
Vol 291 (5) ◽  
pp. R1457-R1464 ◽  
Author(s):  
Matthew W. Bundle ◽  
Carrie L. Ernst ◽  
Matthew J. Bellizzi ◽  
Seth Wright ◽  
Peter G. Weyand
Keyword(s):  
External Force ◽  
Time Course ◽  
Muscle Force ◽  
Anaerobic Metabolism ◽  
Maximum Voluntary Contraction ◽  
Force Production ◽  
Neuromuscular Activity ◽  
Sprint Cycling ◽  
Metabolic Basis ◽  
Muscle Force Production

For both different individuals and modes of locomotion, the external forces determining all-out sprinting performances fall predictably with effort duration from the burst maximums attained for 3 s to those that can be supported aerobically as trial durations extend to roughly 300 s. The common time course of this relationship suggests a metabolic basis for the decrements in the force applied to the environment. However, the mechanical and neuromuscular responses to impaired force production (i.e., muscle fatigue) are generally considered in relation to fractions of the maximum force available, or the maximum voluntary contraction (MVC). We hypothesized that these duration-dependent decrements in external force application result from a reliance on anaerobic metabolism for force production rather than the absolute force produced. We tested this idea by examining neuromuscular activity during two modes of sprint cycling with similar external force requirements but differing aerobic and anaerobic contributions to force production: one- and two-legged cycling. In agreement with previous studies, we found greater peak per leg aerobic metabolic rates [59% (±6 SD)] and pedal forces at V̇o2 peak [30% (±9)] during one- vs. two-legged cycling. We also determined downstroke pedal forces and neuromuscular activity by surface electromyography during 15 to 19 all-out constant load sprints lasting from 12 to 400 s for both modes of cycling. In support of our hypothesis, we found that the greater reliance on anaerobic metabolism for force production induced compensatory muscle recruitment at lower pedal forces during two- vs. one-legged sprint cycling. We conclude that impaired muscle force production and compensatory neuromuscular activity during sprinting are triggered by a reliance on anaerobic metabolism for force production.

scholarly journals Taurine supplementation increases skeletal muscle force production and protects muscle function during and after high-frequency in vitro stimulation

2009 ◽  
Vol 107 (1) ◽  
pp. 144-154 ◽  
Author(s):  
Craig A. Goodman ◽  
Deanna Horvath ◽  
Christos Stathis ◽  
Trevor Mori ◽  
Kevin Croft ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Frequency ◽  
Muscle Function ◽  
Muscle Force ◽  
High Frequency Stimulation ◽  
Specific Force ◽  
Tetanic Force ◽  
Control Muscle ◽  
Frequency Stimulation

Recent studies report that depletion and repletion of muscle taurine (Tau) to endogenous levels affects skeletal muscle contractility in vitro. In this study, muscle Tau content was raised above endogenous levels by supplementing male Sprague-Dawley rats with 2.5% (wt/vol) Tau in drinking water for 2 wk, after which extensor digitorum longus (EDL) muscles were examined for in vitro contractile properties, fatigue resistance, and recovery from fatigue after two different high-frequency stimulation bouts. Tau supplementation increased muscle Tau content by ∼40% and isometric twitch force by 19%, shifted the force-frequency relationship upward and to the left, increased specific force by 4.2%, and increased muscle calsequestrin protein content by 49%. Force at the end of a 10-s (100 Hz) continuous tetanic stimulation was 6% greater than controls, while force at the end of the 3-min intermittent high-frequency stimulation bout was significantly higher than controls, with a 12% greater area under the force curve. For 1 h after the 10-s continuous stimulation, tetanic force in Tau-supplemented muscles remained relatively stable while control muscle force gradually deteriorated. After the 3-min intermittent bout, tetanic force continued to slowly recover over the next 1 h, while control muscle force again began to decline. Tau supplementation attenuated F2-isoprostane production (a sensitive indicator of reactive oxygen species-induced lipid peroxidation) during the 3-min intermittent stimulation bout. Finally, Tau transporter protein expression was not altered by the Tau supplementation. Our results demonstrate that raising Tau content above endogenous levels increases twitch and subtetanic and specific force in rat fast-twitch skeletal muscle. Also, we demonstrate that raising Tau protects muscle function during high-frequency in vitro stimulation and the ensuing recovery period and helps reduce oxidative stress during prolonged stimulation.

Cellular mechanisms of fatigue in skeletal muscle

1991 ◽  
Vol 261 (2) ◽  
pp. C195-C209 ◽  
Author(s):  
H. Westerblad ◽  
J. A. Lee ◽  
J. Lannergren ◽  
D. G. Allen
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
High Frequency ◽  
Force Production ◽  
High Frequency Stimulation ◽  
Tetanic Stimulation ◽  
Cellular Mechanisms ◽  
Frequency Stimulation ◽  
T Tubules ◽  
Underlying Mechanisms

Prolonged activation of skeletal muscle leads to a decline of force production known as fatigue. In this review we outline the ionic and metabolic changes that occur in muscle during prolonged activity and focus on how these changes might lead to reduced force. We discuss two distinct types of fatigue: fatigue due to continuous high-frequency stimulation and fatigue due to repeated tetanic stimulation. The causes of force decline are considered under three categories: 1) reduced Ca2+ release from the sarcoplasmic reticulum, 2) reduced myofibrillar Ca2+ sensitivity, and 3) reduced maximum Ca(2+)-activated tension. Reduced Ca2+ release can be due to impaired action potential propagation in the T tubules, and this is a principal cause of the tension decline with continuous tetanic stimulation. Another type of failing Ca2+ release, which is homogeneous across the fibers, is prominent with repeated tetanic stimulation; the underlying mechanisms of this reduction are not fully understood, although several possibilities emerge. Changes in intracellular metabolites, particularly increased concentration of Pi and reduced pH, lead to reduced Ca2+ sensitivity and reduced maximum tension, which make an important contribution to the force decline, especially with repeated tetanic stimulation.

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