scholarly journals Shortening-induced residual force depression in humans

2019 ◽  
Vol 126 (4) ◽  
pp. 1066-1073 ◽  
Author(s):  
Jackey Chen ◽  
Daniel Hahn ◽  
Geoffrey A. Power

When an isometric muscle contraction is immediately preceded by an active shortening contraction, a reduction in steady-state isometric force is observed relative to an isometric reference contraction at the same muscle length and level of activation. This shortening-induced reduction in isometric force, termed “residual force depression” (rFD), has been under investigation for over a half century. Various experimental models have revealed the positive relationship between rFD and the force and displacement performed during shortening, with rFD values ranging from 5 to 39% across various muscle groups, which appears to be due to a stress-induced inhibition of cross-bridge attachments. The current review will discuss the findings of rFD in humans during maximal and submaximal contractions.

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.


Author(s):  
Ryan A. Koppes ◽  
Douglas M. Swank ◽  
David T. Corr

The depression of isometric force after active shortening, termed force depression (FD), is a well-accepted characteristic of skeletal muscle that has been demonstrated in both whole muscle [1,3] and single-fiber preparations [1,2]. Although this history-dependent behavior has been observed experimentally for over 70 years, its underlying mechanism(s) remain unknown. Drosophila melangastor, commonly known as the fruit fly, is a well established, comprehensively understood, and genetically manipulable animal model. Furthermore, Drosophila have proved to be an accurate model species for studying muscle mechanics, and the Tergal Depressor of the Trochanter (TDT), or jump muscle, has most precisely resembled the mechanics of mammalian skeletal muscle [4]. Due to the structural and phenomenological similarities of the TDT muscle to skeletal muscle, in addition to the potential use of genetic mutations in fly models, it is extremely advantageous to investigate the presence of history dependent phenomenon in the TDT. If such phenomena are present, further investigation utilizing different myosin and actin isoforms to study the underlying mechanism(s) could produce new insight into this history-dependent phenomenon, otherwise impossible to elucidate using current experimental models. Thus, it is the goal of this study to determine the presence and degree of FD in the TDT muscle of wild type Drosophila.


2020 ◽  
Vol 45 (6) ◽  
pp. 601-605 ◽  
Author(s):  
Caleb T. Sypkes ◽  
Brian H. Dalton ◽  
Joanna Stuart ◽  
Geoffrey A. Power

Residual torque depression (rTD) is the reduction in steady-state isometric torque following an active shortening contraction when compared with an isometric contraction at the same muscle length and activation level. We have shown that spinal excitability increases in the rTD state, yet the mechanisms remains unknown. Percutaneous electrical tendon stimulation was used to induce tendon-evoked inhibitory reflexes. We demonstrated that in the rTD state, reduced torque contributes to a reduction in inhibitory afferent feedback, which indicates that the history-dependent properties of muscle can alter spinal excitability and the voluntary control of submaximal contractions through changes in peripheral afferent feedback. Novelty Residual force depression is a basic property of skeletal muscle, which can influence spinal and supraspinal excitability via inhibitory reflex activity. Residual force depression alters the voluntary control of force.


2013 ◽  
Vol 115 (8) ◽  
pp. 1191-1195 ◽  
Author(s):  
Gintare Dargeviciute ◽  
Nerijus Masiulis ◽  
Sigitas Kamandulis ◽  
Albertas Skurvydas ◽  
Håkan Westerblad

We studied the relation between two common force modifications in skeletal muscle: the prolonged force depression induced by unaccustomed eccentric contractions, and the residual force depression (rFD) observed immediately after active shortening. We hypothesized that rFD originates from distortion within the sarcomeres and the extent of rFD: 1) correlates to the force and work performed during the shortening steps, which depend on sarcomeric integrity; and 2) is increased by sarcomeric disorganization induced by eccentric contractions. Nine healthy untrained men (mean age 26 yr) participated in the study. rFD was studied in electrically stimulated knee extensor muscles. rFD was defined as the reduction in isometric torque after active shortening compared with the torque in a purely isometric contraction. Eccentric contractions were performed as 50 repeated drop jumps with active deceleration to 90° knee angle, immediately followed by a maximal upward jump. rFD was assessed before and 5 min to 72 h after drop jumps. The series of drop jumps caused a prolonged force depression, which was about two times larger at 20-Hz than at 50-Hz stimulation. There was a significant correlation between increasing rFD and increasing mechanical work performed during active shortening both before and after drop jumps. In addition, a given rFD was obtained at a markedly lower mechanical work after drop jumps. In conclusion, the extent of rFD correlates to the mechanical work performed during active shortening. A series of eccentric contractions causes a prolonged reduction of isometric force. In addition, eccentric contractions exaggerate rFD, which further decreases muscle performance during dynamic contractions.


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.


1991 ◽  
Vol 66 (2) ◽  
pp. 602-612 ◽  
Author(s):  
J. E. Gregory ◽  
D. L. Morgan ◽  
U. Proske

1. The behavior of primary endings of cat soleus muscle spindles was studied during shortening steps carried out at different muscle lengths. 2. Spindles were of two kinds: one, silent spindles, whose afferents fell silent after the shortening, at least over part of the range of lengths tested. The second, spontaneous spindles, resumed firing at all lengths. 3. For silent spindles, the duration of the silent period, measured at lengths where they did recover a resting rate, depended directly on muscle length and became shorter at longer lengths. This is what would be expected if the slack introduced in the spindle by the shortening step was removed more rapidly at longer lengths by the higher passive tension. For spontaneous spindles, on the other hand, the duration of the silent period after the shortening was largely independent of muscle length and depended on the spindle's rate of firing immediately before the shortening. 4. At intermediate lengths the discharge of slack spontaneous spindles remained unaffected by an isometric muscle contraction. It was therefore not possible to produce a pause in the discharge, behavior normally taken as typical of spindles. The discharge could be interrupted by the contraction if this was combined with a large shortening movement. 5. It is proposed that when intrafusal fibers are slackened by a shortening step, the resting discharge in spontaneous spindles is generated by a maintained depolarization of the annulospiral ending resulting from extension of the terminal coils by forces from within the receptor. A shortening contraction compresses the spirals to interrupt the discharge. The sensory endings of silent spindles remain below threshold until the spirals have been opened out sufficiently by external stretch.


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