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  • 1
    Online Resource
    Online Resource
    Contraction–relaxation coupling is unaltered by exercise training and infarction in isolated canine myocardium
    Rockefeller University Press ; 2021
    In:  Journal of General Physiology Vol. 153, No. 7 ( 2021-07-05)
    Details
    In: Journal of General Physiology, Rockefeller University Press, Vol. 153, No. 7 ( 2021-07-05)
    Abstract: The two main phases of the mammalian cardiac cycle are contraction and relaxation; however, whether there is a connection between them in humans is not well understood. Routine exercise has been shown to improve cardiac function, morphology, and molecular signatures. Likewise, the acute and chronic changes that occur in the heart in response to injury, disease, and stress are well characterized, albeit not fully understood. In this study, we investigated how exercise and myocardial injury affect contraction–relaxation coupling. We retrospectively analyzed the correlation between the maximal speed of contraction and the maximal speed of relaxation of canine myocardium after receiving surgically induced myocardial infarction, followed by either sedentary recovery or exercise training for 10–12 wk. We used isolated right ventricular trabeculae, which were electrically paced at different lengths, frequencies, and with increasing β-adrenoceptor stimulation. In all conditions, contraction and relaxation were linearly correlated, irrespective of injury or training history. Based on these results and the available literature, we posit that contraction–relaxation coupling is a fundamental myocardial property that resides in the structural arrangement of proteins at the level of the sarcomere and that this may be regulated by the actions of cardiac myosin binding protein C (cMyBP-C) on actin and myosin.
    Type of Medium: Online Resource
    ISSN: 0022-1295 , 1540-7748
    URL: Article
    DOI: 10.1085/jgp.202012829
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2021
    detail.hit.zdb_id: 1477246-2
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Effect of muscle length on cross-bridge kinetics in intact cardiac trabeculae at body temperature
    Rockefeller University Press ; 2013
    In:  Journal of General Physiology Vol. 141, No. 1 ( 2013-01-01), p. 133-139
    Details
    In: Journal of General Physiology, Rockefeller University Press, Vol. 141, No. 1 ( 2013-01-01), p. 133-139
    Abstract: Dynamic force generation in cardiac muscle, which determines cardiac pumping activity, depends on both the number of sarcomeric cross-bridges and on their cycling kinetics. The Frank–Starling mechanism dictates that cardiac force development increases with increasing cardiac muscle length (corresponding to increased ventricular volume). It is, however, unclear to what extent this increase in cardiac muscle length affects the rate of cross-bridge cycling. Previous studies using permeabilized cardiac preparations, sub-physiological temperatures, or both have obtained conflicting results. Here, we developed a protocol that allowed us to reliably and reproducibly measure the rate of tension redevelopment (ktr; which depends on the rate of cross-bridge cycling) in intact trabeculae at body temperature. Using K+ contractures to induce a tonic level of force, we showed the ktr was slower in rabbit muscle (which contains predominantly β myosin) than in rat muscle (which contains predominantly α myosin). Analyses of ktr in rat muscle at optimal length (Lopt) and 90% of optimal length (L90) revealed that ktr was significantly slower at Lopt (27.7 ± 3.3 and 27.8 ± 3.0 s−1 in duplicate analyses) than at L90 (45.1 ± 7.6 and 47.5 ± 9.2 s−1). We therefore show that ktr can be measured in intact rat and rabbit cardiac trabeculae, and that the ktr decreases when muscles are stretched to their optimal length under near-physiological conditions, indicating that the Frank–Starling mechanism not only increases force but also affects cross-bridge cycling kinetics.
    Type of Medium: Online Resource
    ISSN: 1540-7748 , 0022-1295
    URL: Article
    DOI: 10.1085/jgp.201210894
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2013
    detail.hit.zdb_id: 1477246-2
    SSG: 12
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    IKKα and alternative NF-κB regulate PGC-1β to promote oxidative muscle metabolism
    Rockefeller University Press ; 2012
    In:  Journal of Cell Biology Vol. 196, No. 4 ( 2012-02-20), p. 497-511
    Details
    In: Journal of Cell Biology, Rockefeller University Press, Vol. 196, No. 4 ( 2012-02-20), p. 497-511
    Abstract: Although the physiological basis of canonical or classical IκB kinase β (IKKβ)–nuclear factor κB (NF-κB) signaling pathway is well established, how alternative NF-κB signaling functions beyond its role in lymphoid development remains unclear. In particular, alternative NF-κB signaling has been linked with cellular metabolism, but this relationship is poorly understood. In this study, we show that mice deleted for the alternative NF-κB components IKKα or RelB have reduced mitochondrial content and function. Conversely, expressing alternative, but not classical, NF-κB pathway components in skeletal muscle stimulates mitochondrial biogenesis and specifies slow twitch fibers, suggesting that oxidative metabolism in muscle is selectively controlled by the alternative pathway. The alternative NF-κB pathway mediates this specificity by direct transcriptional activation of the mitochondrial regulator PPAR-γ coactivator 1β (PGC-1β) but not PGC-1α. Regulation of PGC-1β by IKKα/RelB also is mammalian target of rapamycin (mTOR) dependent, highlighting a cross talk between mTOR and NF-κB in muscle metabolism. Together, these data provide insight on PGC-1β regulation during skeletal myogenesis and reveal a unique function of alternative NF-κB signaling in promoting an oxidative metabolic phenotype.
    Type of Medium: Online Resource
    ISSN: 1540-8140 , 0021-9525
    URL: Article
    DOI: 10.1083/jcb.201108118
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2012
    detail.hit.zdb_id: 1421310-2
    SSG: 12
    Location Call Number Limitation Availability
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