Contractile Performance of Striated Muscle

Edman, K. A. P.

doi:10.1007/978-1-4419-6366-6_2

Cited by 23 publications

(18 citation statements)

References 97 publications

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“…With the growing evidence from skeletal muscle for the role of Ca 2+ in the Bmanipulation^of length-tension curves, it was apparent that factors other than the degree of myofilament overlap could explain the striking differences in length-tension curves and the enigmatic length dependence of heart muscle. We noted that later findings from (Edman 2010) showed that the length-tension curve in skeletal muscle exhibits a much smoother shape than proposed by Gordon et al (1966). Specifically, the length-tension relationship does not have a pronounced plateau region at 2.0-2.2 μm sarcomere length, while the descending limb was also non-linear.…”

Section: Rank-starling Relationshipmentioning

confidence: 63%

Historical perspective on heart function: the Frank–Starling Law

Sequeira

Velden

2015

Biophys Rev

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More than a century of research on the FrankStarling Law has significantly advanced our knowledge about the working heart. The Frank-Starling Law mandates that the heart is able to match cardiac ejection to the dynamic changes occurring in ventricular filling and thereby regulates ventricular contraction and ejection. Significant efforts have been attempted to identify a common fundamental basis for the Frank-Starling heart and, although a unifying idea has still to come forth, there is mounting evidence of a direct relationship between length changes in individual constituents (cardiomyocytes) and their sensitivity to Ca 2+ ions. As the Frank-Starling Law is a vital event for the healthy heart, it is of utmost importance to understand its mechanical basis in order to optimize and organize therapeutic strategies to rescue the failing human heart. The present review is a historic perspective on cardiac muscle function. We Brevive^a century of scientific research on the heart's fundamental protein constituents (contractile proteins), to their assemblies in the muscle (the sarcomeres), culminating in a thorough overview of the several synergistically events that compose the Frank-Starling mechanism. It is the authors' personal beliefs that much can be gained by understanding the Frank-Starling relationship at the cellular and whole organ level, so that we can finally, in this century, tackle the pathophysiologic mechanisms underlying heart failure.

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Section: Rank-starling Relationshipmentioning

confidence: 63%

Historical perspective on heart function: the Frank–Starling Law

Sequeira

Velden

2015

Biophys Rev

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“…However, in our single myofiber model, we are generally more focused on the pure hypoxic effect on a single skeletal myofiber, since any myoglobin in our model could potentially cause a buffering effect, which may delay or interfere with the required low oxygen condition. In addition, although the frog fiber used in the current study lacks myoglobin, there is a great level of correlation between the frog and mammalian myocytes (9), and these two share a substantial similarity in typical skeletal muscle physiology, especially concerning mitochondrial and contractile function. Xenopus fibers are frequently used as a representative model for analyzing skeletal muscle function and metabolism (34,47).…”

Section: Discussionmentioning

confidence: 99%

Low Po₂conditions induce reactive oxygen species formation during contractions in single skeletal muscle fibers

Zuo

Shiah

Roberts

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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-Contractions in whole skeletal muscle during hypoxia are known to generate reactive oxygen species (ROS); however, identification of real-time ROS formation within isolated single skeletal muscle fibers has been challenging. Consequently, there is no convincing evidence showing increased ROS production in intact contracting fibers under low PO2 conditions. Therefore, we hypothesized that intracellular ROS generation in single contracting skeletal myofibers increases during low PO2 compared with a value approximating normal resting PO2. Dihydrofluorescein was loaded into single frog (Xenopus) fibers, and fluorescence was used to monitor ROS using confocal microscopy. Myofibers were exposed to two maximal tetanic contractile periods (1 contraction/3 s for 2 min, separated by a 60-min rest period), each consisting of one of the following treatments: high PO2 (30 Torr), low PO2 (3-5 Torr), high PO2 with ebselen (antioxidant), or low PO2 with ebselen. Ebselen (10 M) was administered before the designated contractile period. ROS formation during low PO2 treatment was greater than during high PO2 treatment, and ebselen decreased ROS generation in both low-and high-PO2 conditions (P Ͻ 0.05). ROS accumulated at a faster rate in low vs. high PO2. Force was reduced Ͼ30% for each condition except low PO2 with ebselen, which only decreased ϳ15%. We concluded that single myofibers under low PO2 conditions develop accelerated and more oxidative stress than at PO2 ϭ 30 Torr (normal human resting PO2). Ebselen decreases ROS formation in both low and high PO2, but only mitigates skeletal muscle fatigue during reduced PO2 conditions. hypoxia; confocal; reactive oxygen species; ebselen; myofiber REACTIVE OXYGEN SPECIES (ROS) play important roles in biological systems (1,44,46,47,49,50). ROS have been documented as a general response to ischemia-reperfusion injury (26, 43), muscle stimulation (29), and heat stress (44). Excessive ROS disrupt nearly all physiological systems (1,44,46,47,49,50). However, the underlying mechanism of ROS formation in hypoxic skeletal muscle has not been fully elucidated. Moreover, there has been little investigation of ROS generation within single skeletal muscle fibers under low PO 2 conditions using real-time measurements, which eliminates some of the problems associated with these measurements that have been made in whole animal or whole muscle preparations (46). Previous research suggests that in human skeletal muscle, intracellular PO 2 drops from ϳ30 Torr at rest to 3-5 Torr during exercise (40). Thus, it is of interest to investigate intracellular ROS formation during these conditions of low PO 2 in single contracting myocytes.Hypoxia causes a significant accumulation of reducing agents in the mitochondria, such as NADH and FADH 2 . Abrupt exposure to O 2 can promote immediate formation of superoxide anion (O 2 ·Ϫ ) in the mitochondrial electron transport chain (2, 37), thus initiating oxidative stress. Moreover, substantial data point to intracellular ROS formation in cardiac tissue during hypo...

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“…Within the sarcomere, the interaction between the sarcomeric proteins (e.g., actin and myosin) provides the fundamental unit to generate force production. More specifically, the mechanical properties of diaphragm muscle fibers are characterized by the relationship between cytosolic free calcium, crossbridge attachment/cross-bridge cycling rate, and sarcomere length (25). It follows that any factor that influences one or more of these variables can impact diaphragm muscle force generation.…”

Section: Mechanisms Responsible For Mv-induced Diaphragm Contractile mentioning

confidence: 99%

“…In reference to the specific diaphragm muscle proteins that are degraded during MV-induced sarcomere damage, it is established that both titin and myosin play an essential role in skeletal muscle force production (25,113). It follows that an MV-induced loss of titin or myosin from diaphragm muscle fibers could result in contractile dysfunction.…”

Section: R471mentioning

confidence: 99%

Ventilator-induced diaphragm dysfunction: cause and effect

Powers

Wiggs

Sollanek

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

139

156

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Powers SK, Wiggs MP, Sollanek KJ, Smuder AJ. Ventilator-induced diaphragm dysfunction: cause and effect. Am J Physiol Regul Integr Comp Physiol 305: R464 -R477, 2013. First published July 10, 2013 doi:10.1152/ajpregu.00231.2013 is used clinically to maintain gas exchange in patients that require assistance in maintaining adequate alveolar ventilation. Common indications for MV include respiratory failure, heart failure, drug overdose, and surgery. Although MV can be a life-saving intervention for patients suffering from respiratory failure, prolonged MV can promote diaphragmatic atrophy and contractile dysfunction, which is referred to as ventilator-induced diaphragm dysfunction (VIDD). This is significant because VIDD is thought to contribute to problems in weaning patients from the ventilator. Extended time on the ventilator increases health care costs and greatly increases patient morbidity and mortality. Research reveals that only 18 -24 h of MV is sufficient to develop VIDD in both laboratory animals and humans. Studies using animal models reveal that MV-induced diaphragmatic atrophy occurs due to increased diaphragmatic protein breakdown and decreased protein synthesis. Recent investigations have identified calpain, caspase-3, autophagy, and the ubiquitin-proteasome system as key proteases that participate in MV-induced diaphragmatic proteolysis. The challenge for the future is to define the MV-induced signaling pathways that promote the loss of diaphragm protein and depress diaphragm contractility. Indeed, forthcoming studies that delineate the signaling mechanisms responsible for VIDD will provide the knowledge necessary for the development of a pharmacological approach that can prevent VIDD and reduce the incidence of weaning problems. respiratory muscle; atrophy; mechanical ventilation; weaning; muscle wasting MECHANICAL VENTILATION (MV) is used clinically to achieve sufficient pulmonary gas exchange in patients unable to sustain adequate alveolar ventilation on their own. Common indications for MV include respiratory failure due to chronic obstructive pulmonary disease, status asthmaticus, and/or heart failure. In addition, MV is often an essential intervention in patients suffering from acute drug overdose, neuromuscular diseases, sepsis, and during surgery along with postsurgical recovery.The number of patients receiving prolonged MV in the United States exceeds more than 300,000 each year in the intensive care unit (ICU) (20). Although MV can be a lifesaving measure, prolonged MV results in the rapid development of diaphragmatic weakness due to both atrophy and contractile dysfunction. This detrimental impact of prolonged MV on the diaphragm has been termed ventilator-induced diaphragmatic dysfunction (VIDD) and VIDD is predicted to be a major contributor to problems in weaning patients from the ventilator (26, 114). Although previous reports describing the impact of prolonged MV on the diaphragm have appeared in the literature, advances in our understanding of the mechanisms responsible for VIDD h...

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Contractile Performance of Striated Muscle

Cited by 23 publications

References 97 publications

Historical perspective on heart function: the Frank–Starling Law

Historical perspective on heart function: the Frank–Starling Law

Low Po₂conditions induce reactive oxygen species formation during contractions in single skeletal muscle fibers

Ventilator-induced diaphragm dysfunction: cause and effect

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Contractile Performance of Striated Muscle

Cited by 23 publications

References 97 publications

Historical perspective on heart function: the Frank–Starling Law

Historical perspective on heart function: the Frank–Starling Law

Low Po2conditions induce reactive oxygen species formation during contractions in single skeletal muscle fibers

Ventilator-induced diaphragm dysfunction: cause and effect

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Low Po₂conditions induce reactive oxygen species formation during contractions in single skeletal muscle fibers