scholarly journals The influence of training-induced sarcomerogenesis on the history dependence of force

2020 ◽  
Vol 223 (15) ◽  
pp. jeb218776 ◽  
Author(s):  
Jackey Chen ◽  
Parastoo Mashouri ◽  
Stephanie Fontyn ◽  
Mikella Valvano ◽  
Shakeap Elliott-Mohamed ◽  
...  

ABSTRACTThe increase or decrease in isometric force following active muscle lengthening or shortening, relative to a reference isometric contraction at the same muscle length and level of activation, are referred to as residual force enhancement (rFE) and residual force depression (rFD), respectively. The purpose of these experiments was to investigate the trainability of rFE and rFD on the basis of serial sarcomere number (SSN) alterations to history-dependent force properties. Maximal rFE/rFD measures from the soleus and extensor digitorum longus (EDL) of rats were compared after 4 weeks of uphill or downhill running with a no-running control. SSN adapted to the training: soleus SSN was greater with downhill compared with uphill running, while EDL demonstrated a trend towards more SSN for downhill compared with no running. In contrast, rFE and rFD did not differ across training groups for either muscle. As such, it appears that training-induced SSN adaptations do not modify rFE or rFD at the whole-muscle level.

2020 ◽  
Author(s):  
Jackey Chen ◽  
Parastoo Mashouri ◽  
Stephanie Fontyn ◽  
Mikella Valvano ◽  
Shakeap Elliott-Mohamed ◽  
...  

AbstractThe increase or decrease in isometric force following active muscle lengthening or shortening, relative to a reference isometric contraction at the same muscle length and level of activation, are referred to as residual force enhancement (rFE) and residual force depression (rFD), respectively. The purpose of these experiments was to gain further mechanistic insight into the trainability of rFE and rFD, on the basis of serial sarcomere number (SSN) alterations to length-dependent properties. Maximal rFE/rFD measures from the soleus and extensor digitorum longus (EDL) of rats were compared after 4 weeks of uphill/downhill running and a no running control. Serial sarcomere numbers adapted to the training: soleus serial sarcomere number was greater with downhill compared to uphill running, while EDL demonstrated a trend towards more serial sarcomeres for downhill compared to no running. In contrast, absolute and normalized rFE/rFD did not differ across training groups for either muscle. As such, it appears that training-induced SSN adaptations do not modify rFE/rFD at the whole-muscle level.Summary StatementThe addition and subtraction of serial sarcomeres induced by downhill and uphill running, respectively, did not influence the magnitude of stretch-induced force enhancement and shortening-induced force depression.


2019 ◽  
Vol 126 (3) ◽  
pp. 647-657 ◽  
Author(s):  
Jackey Chen ◽  
Geoffrey A. Power

The increase and decrease in steady-state isometric force following active muscle lengthening and shortening are referred to as residual force enhancement (RFE) and force depression (FD), respectively. The RFE and FD states are associated with decreased (activation reduction; AR) and increased (activation increase; AI) neuromuscular activity, respectively. Although the mechanisms have been discussed over the last 60 years, no studies have systematically investigated the modifiability of RFE and FD with training. The purpose of the present study was to determine whether RFE and FD could be modulated through eccentric and concentric biased resistance training. Fifteen healthy young adult men (age: 24 ± 2 yr, weight: 77 ± 8 kg, height: 178 ± 5 cm) underwent 4 wk of isokinetic dorsiflexion training, in which one leg was trained eccentrically (−25°/s) and the other concentrically (+25°/s) over a 50° ankle excursion. Maximal and submaximal (40% maximum voluntary contraction) steady-state isometric torque and EMG values following active lengthening and shortening were compared to purely isometric values at the same joint angles and torque levels. Residual torque enhancement (rTE) decreased by ~36% after eccentric training ( P < 0.05) and increased by ~89% after concentric training ( P < 0.05), whereas residual torque depression (rTD), AR, AI, and optimal angles for torque production were not significantly altered by resistance training ( P ≥ 0.05). It appears that rTE, but not rTD, for the human ankle dorsiflexors is differentially modifiable through contraction type-dependent resistance training. NEW & NOTEWORTHY The history dependence of force production is a property of muscle unexplained by current cross bridge and sliding filament theories. Whether a muscle is actively lengthened (residual force enhancement; RFE) or shortened (force depression) to a given length, the isometric force should be equal to a purely isometric contraction—but it is not! In this study we show that eccentric training decreased RFE, whereas concentric training increased RFE and converted all nonresponders (i.e., not exhibiting RFE) into responders.


PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5421 ◽  
Author(s):  
Caleb T. Sypkes ◽  
Benjamin J. Kozlowski ◽  
Jordan Grant ◽  
Leah R. Bent ◽  
Chris J. McNeil ◽  
...  

Background Following active muscle lengthening, there is an increase in steady-state isometric force as compared with a purely isometric contraction at the same muscle length and level of activation. This fundamental property of skeletal muscle is known as residual force enhancement (RFE). While the basic mechanisms contributing to this increase in steady-state isometric force have been well documented, changes in central nervous system (CNS) excitability for submaximal contractions during RFE are unclear. The purpose of this study was to investigate spinal and supraspinal excitability in the RFE isometric steady-state following active lengthening of the ankle dorsiflexor muscles. Methods A total of 11 male participants (20–28 years) performed dorsiflexions at a constant level of electromyographic activity (40% of maximum). Half of the contractions were purely isometric (8 s at an ankle angle of 130°), and the other half were during the RFE isometric steady-state following active lengthening (2 s isometric at 90°, a 1 s lengthening phase at 40°/s, and 5 s at 130°). Motor evoked potentials (MEPs), cervicomedullary motor evoked potentials (CMEPs), and compound muscle action potentials (M-waves) were recorded from the tibialis anterior during the purely isometric contraction and RFE isometric steady-state. Results Compared to the purely isometric condition, following active lengthening, there was 10% RFE (p < 0.05), with a 17% decrease in normalized CMEP amplitude (CMEP/Mmax) (p < 0.05) and no change in normalized MEP amplitude (MEP/CMEP) (p > 0.05). Discussion These results indicate that spinal excitability is reduced during submaximal voluntary contractions in the RFE state with no change in supraspinal excitability. These findings may have further implications to everyday life offering insight into how the CNS optimizes control of skeletal muscle following submaximal active muscle lengthening.


2019 ◽  
Vol 126 (6) ◽  
pp. 1782-1789 ◽  
Author(s):  
Walter Herzog

Passive force enhancement is defined as the increase in passive, steady-state, isometric force of an actively stretched muscle compared with the same muscle stretched passively to that same length. Passive force enhancement is long lasting, increases with increasing muscle length and increasing stretch magnitudes, contributes to the residual force enhancement in skeletal and cardiac muscle, and is typically only observed at muscle lengths at which passive forces occur naturally. Passive force enhancement is typically equal to or smaller than the total residual force enhancement, it persists when a muscle is deactivated and reactivated, but can be abolished instantaneously when a muscle is shortened quickly from its stretched length. There is strong evidence that the passive force enhancement is caused by the filamentous sarcomeric protein titin, although the detailed molecular mechanisms underlying passive force enhancement remain unknown. Here I propose a tentative mechanism based on experimental evidence that associates passive force enhancement with the shortening of titin’s free spring length in the I-band region of sarcomeres. I suggest that this shortening is accomplished by titin binding to actin and that the trigger for titin-actin interactions is associated with the formation of strongly bound cross bridges between actin and myosin that exposes actin attachment sites for titin through movement of the regulatory proteins troponin and tropomyosin.


2019 ◽  
Vol 20 (21) ◽  
pp. 5479 ◽  
Author(s):  
Atsuki Fukutani ◽  
Walter Herzog

Muscle contraction is initiated by the interaction between actin and myosin filaments. The sliding of actin filaments relative to myosin filaments is produced by cross-bridge cycling, which is governed by the theoretical framework of the cross-bridge theory. The cross-bridge theory explains well a number of mechanical responses, such as isometric and concentric contractions. However, some experimental observations cannot be explained with the cross-bridge theory; for example, the increased isometric force after eccentric contractions. The steady-state, isometric force after an eccentric contraction is greater than that attained in a purely isometric contraction at the same muscle length and same activation level. This well-acknowledged and universally observed property is referred to as residual force enhancement (rFE). Since rFE cannot be explained by the cross-bridge theory, alternative mechanisms for explaining this force response have been proposed. In this review, we introduce the basic concepts of sarcomere length non-uniformity and titin elasticity, which are the primary candidates that have been used for explaining rFE, and discuss unresolved problems regarding these mechanisms, and how to proceed with future experiments in this exciting area of research.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ricarda M. Haeger ◽  
Dilson E. Rassier

AbstractWhen a muscle is stretched during a contraction, the resulting steady-state force is higher than the isometric force produced at a comparable sarcomere length. This phenomenon, also referred to as residual force enhancement, cannot be readily explained by the force-sarcomere length relation. One of the most accepted mechanisms for the residual force enhancement is the development of sarcomere length non-uniformities after an active stretch. The aim of this study was to directly investigate the effect of non-uniformities on the force-producing capabilities of isolated myofibrils after they are actively stretched. We evaluated the effect of depleting a single A-band on sarcomere length non-uniformity and residual force enhancement. We observed that sarcomere length non-uniformity was effectively increased following A-band depletion. Furthermore, isometric forces decreased, while the percent residual force enhancement increased compared to intact myofibrils (5% vs. 20%). We conclude that sarcomere length non-uniformities are partially responsible for the enhanced force production after stretch.


2019 ◽  
Vol 91 ◽  
pp. 164-169 ◽  
Author(s):  
Rhiannan A.M. Pinnell ◽  
Parastoo Mashouri ◽  
Nicole Mazara ◽  
Erin Weersink ◽  
Stephen H.M. Brown ◽  
...  

2008 ◽  
Vol 105 (2) ◽  
pp. 457-462 ◽  
Author(s):  
Eun-Jeong Lee ◽  
Walter Herzog

Residual force enhancement (FE) following stretch of an activated muscle is a well accepted property of skeletal muscle contraction. However, the mechanism underlying FE remains unknown. A crucial assumption on which some proposed mechanisms are based is the idea that forces in the enhanced state cannot exceed the steady-state isometric force at a sarcomere length associated with optimal myofilament overlap. Although there are a number of studies in which forces in the enhanced state were compared with the corresponding isometric forces on the plateau of the force-length relationship, these studies either did not show enhanced forces above the plateau or, if they did, they lacked measurements of sarcomere lengths confirming the plateau region. Here, we revisited this question by optimizing stretch conditions and measuring the average sarcomere lengths in isolated fibers, and we found that FE exceeded the maximal isometric reference force obtained at the plateau of the force-length relationship consistently (mean ± SD: 4.8 ± 2.1%) and by up to 10%. When subtracting the passive component of FE from the total FE, the enhanced forces remained greater than the isometric plateau force (mean ± SD: 4.3 ± 2.0%). Calcium-induced increases in passive forces, known to be present in single fibers and myofibrils, are too small to account for the FE observed here. We conclude that FE cannot be explained exclusively with a stretch-induced development of sarcomere length nonuniformities, that FE in single fibers may be associated with the recruitment of additional contractile force, and that isometric steady-state forces in the enhanced state are not uniquely determined by sarcomere lengths.


1982 ◽  
Vol 80 (5) ◽  
pp. 769-784 ◽  
Author(s):  
K A Edman ◽  
G Elzinga ◽  
M I Noble

Single fibers from the tibialis anterior muscle of Rana temporaria at 0.8-3.8 degrees C were subjected to long tetani lasting up to 8 s. Stretch of the fiber early in the tetanus caused an enhancement of force above the isometric control level which decayed only slowly and stayed higher throughout the contraction. This residual enhancement was uninfluenced by velocity of stretch and occurred only on the descending limb of the length-tension curve. The absolute magnitude of the effect increased with sarcomere length to a maximum at approximately 2.9 micrometers and then declined. The phenomenon was further characterized by its dependence on the amplitude of stretch. The final force level reached after stretch was usually higher than the isometric force level corresponding to the starting length of the stretch. The possibility that the phenomenon was caused by nonuniformity of sarcomere length along the fiber was examined by (a) laser diffraction studies that showed sarcomere stretch at all locations and (b) studies of 9-10 segments of approximately 0.6-0.7 mm along the entire fiber, which all elongated during stretch. Length-clamped segments showed residual force enhancement after stretch when compared with the tetanus produced by the same segment held at the short length as well as at the long length. It is concluded that residual force enhancement after stretch is a property shown by all individual segments along the fiber.


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