An explanation for residual increased tension in striated muscle after stretch during contraction

Morgan, Daniel

doi:10.1113/expphysiol.1994.sp003811

Cited by 117 publications

(147 citation statements)

References 17 publications

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“…The absence of tendons in this preparation eliminates the possibility of changes in those structures being responsible for the shift. The theory predicts that stiffness will fall during the progress of a single stretch, even though tension rises, as active sarcomeres are overstretched and converted from a high active stiffness to a lower passive stiffness (Morgan, 1994). The theory also predicts a cumulative fall in isometric stiffness during the sequence of eccentric contractions, as the number of disrupted sarcomeres increases.…”

Section: Discussionmentioning

confidence: 99%

The effects of repeated active stretches on tension generation and myoplasmic calcium in frog single muscle fibres.

Morgan¹,

Claflin²,

Julian³

1996

The Journal of Physiology

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1. A series of contractions with stretches (eccentric contractions) beyond the optimal length for tension generation (optimum) were shown to induce a shift in that optimum in single muscle fibres of frog, as has been previously reported for whole muscles. Shifts averaging 0 129 jum (sarcomere)-' or 6 % were found, without apparent damage to the fibre.2. The stiffness of fibres was found to fall during a stretch, even though tension was rising. In addition, the isometric stiffness fell as a result of a series of eccentric contractions. 3. Calcium-sensitive fluorescent dyes indicated that such contractions did not reduce the amplitude of the intracellular calcium transient, but did increase its duration. A rise in resting [Ca2+] was found to accompany damage, but not necessarily the shift in optimum. 4. The twitch potentiator nitrate was shown to increase myoplasmic [Ca2+] during twitch and tetani, but not to reverse the shift in optimum length due to eccentric contractions. Both eccentric contractions and twitch potentiation reduced the maximum stimulation rate to which a fibre could respond with propagated action potentials. 5. These results exclude reduced myoplasmic [Ca2+] as the cause of the shift in optimum length in this preparation.

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Section: Discussionmentioning

confidence: 99%

The effects of repeated active stretches on tension generation and myoplasmic calcium in frog single muscle fibres.

Morgan¹,

Claflin²,

Julian³

1996

The Journal of Physiology

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“…Broadly, these mechanisms include increased cross-bridge force, non-uniformities in sarcomere (Morgan, 1990(Morgan, , 1994 or halfsarcomere length, and engagement of structural elements upon muscle activation (Edman et al, 1982;Herzog and Leonard, 2002;. To date, none of these explanations has achieved general acceptance, but neither can any of them be entirely ruled out Minozzo and Lira, 2013).…”

Section: Unraveling the Mechanisms Of Residual Force Enhancementmentioning

confidence: 99%

Eccentric contraction: unraveling mechanisms of force enhancement and energy conservation

Nishikawa

2016

Journal of Experimental Biology

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During the past century, physiologists have made steady progress in elucidating the molecular mechanisms of muscle contraction. However, this progress has so far failed to definitively explain the high force and low energy cost of eccentric muscle contraction. Hypotheses that have been proposed to explain increased muscle force during active stretch include cross-bridge mechanisms, sarcomere and half-sarcomere length non-uniformity, and engagement of a structural element upon muscle activation. The available evidence suggests that force enhancement results from an interaction between an elastic element in muscle sarcomeres, which is engaged upon activation, and the cross-bridges, which interact with the elastic elements to regulate their length and stiffness. Similarities between titin-based residual force enhancement in vertebrate muscle and twitchin-based 'catch' in invertebrate muscle suggest evolutionary homology. The winding filament hypothesis suggests plausible molecular mechanisms for effects of both Ca 2+ influx and crossbridge cycling on titin in active muscle. This hypothesis proposes that the N2A region of titin binds to actin upon Ca 2+ influx, and that the PEVK region of titin winds on the thin filaments during force development because the cross-bridges not only translate but also rotate the thin filaments. Simulations demonstrate that a muscle model based on the winding filament hypothesis can predict residual force enhancement on the descending limb of the length-tension curve in muscles during eccentric contraction. A kinematic model of titin winding based on sarcomere geometry makes testable predictions about titin isoforms in different muscles. Ongoing research is aimed at testing these predictions and elucidating the biochemistry of the underlying protein interactions.

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“…This constitutes the force-sarcomere length relationship, which is generally adhered to during isometric contractions (Gordon et al, 1966). However, following eccentric, or lengthening, contractions the isometric steady-state force produced at a given sarcomere length exceeds the predictions of the force-length relationship (Abbott and Aubert, 1952;Edman et al, 1978;Edman et al, 1982;Morgan, 1994;Herzog et al, 2006;. This property, termed residual force enhancement, provides a direct challenge to the sliding filament-based cross-bridge theory.…”

Section: Introductionmentioning

confidence: 99%

Titin force is enhanced in actively stretched skeletal muscle

Powers

Schappacher‐Tilp

Jinha

et al. 2014

Journal of Experimental Biology

134

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The sliding filament theory of muscle contraction is widely accepted as the means by which muscles generate force during activation. Within the constraints of this theory, isometric, steady-state force produced during muscle activation is proportional to the amount of filament overlap. Previous studies from our laboratory demonstrated enhanced titin-based force in myofibrils that were actively stretched to lengths which exceeded filament overlap. This observation cannot be explained by the sliding filament theory. The aim of the present study was to further investigate the enhanced state of titin during active stretch. Specifically, we confirm that this enhanced state of force is observed in a mouse model and quantify the contribution of calcium to this force. Titin-based force was increased by up to four times that of passive force during active stretch of isolated myofibrils. Enhanced titin-based force has now been demonstrated in two distinct animal models, suggesting that modulation of titin-based force during active stretch is an inherent property of skeletal muscle. Our results also demonstrated that 15% of the enhanced state of titin can be attributed to direct calcium effects on the protein, presumably a stiffening of the protein upon calcium binding to the E-rich region of the PEVK segment and selected Ig domain segments. We suggest that the remaining unexplained 85% of this extra force results from titin binding to the thin filament. With this enhanced force confirmed in the mouse model, future studies will aim to elucidate the proposed titin-thin filament interaction in actively stretched sarcomeres.

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An explanation for residual increased tension in striated muscle after stretch during contraction

Cited by 117 publications

References 17 publications

The effects of repeated active stretches on tension generation and myoplasmic calcium in frog single muscle fibres.

The effects of repeated active stretches on tension generation and myoplasmic calcium in frog single muscle fibres.

Eccentric contraction: unraveling mechanisms of force enhancement and energy conservation

Titin force is enhanced in actively stretched skeletal muscle

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