FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2017451001> ?p ?o ?g. }

• W2017451001 abstract "Getting buff is hard work and invariably involves lots of repetitive and exhausting resistance exercise. Unfortunately, stop the workouts and those hard fought gains can be lost easily. The only heartening part is that getting back into shape is far easier the second time around, a phenomenon known as ‘muscle memory’ (Staron et al. 1991). For many years the prevailing view was that changes within the central nervous system were responsible for this capability. This view is evolving, and recent data suggest that adaptive mechanisms within the muscle itself are responsible for much of this memory.The muscle fibre is one of the few syncytial cells within the body and can contain many hundreds of nuclei. This makes sense when one appreciates that individual muscle fibres can be enormous, achieving lengths of up to ∼600 mm (23 in) (for example in the sartorius muscle) and volumes that are five orders of magnitude greater than a typical mononucleated cell (Bruusgaard et al. 2003). Muscle is also a very plastic tissue that can add or lose contractile proteins when it undergoes hypertrophy or atrophy, respectively. Many studies have proposed that the number of nuclei change in parallel with muscle mass to ensure that the cytoplasmic-to-nuclear volume is maintained, a phenomenon known as the ‘myonuclear domain hypothesis’. Analysing these data is complicated by the fact that muscle is a heterogeneous tissue composed of many different cell types, and determining that a given nucleus has been added to, or lost from, the myoplasm is imprecise. To help overcome this technical challenge the Gundersen lab built upon the pioneering approaches of Jeff Lichtman (Lichtman et al. 1987), and devised techniques for monitoring nuclei over time within individual living muscles fibres in vivo (Bruusgaard et al. 2003, 2008). In these experiments the extensor digitorum longus (EDL) or soleus muscles of anaesthetized mice were exposed under a microscope and individual fibres were injected with fluorescent dyes that differentially labelled the cytoplasm and the nuclei. The incision was then sutured and the mice manipulated in ways that would induce skeletal muscle atrophy or hypertrophy, such as denervation and overload, respectively. The same muscle fibre could then be observed over a span of days or weeks to determine the number and location of nuclei within a uniquely identified cell. Using this approach they demonstrated unambiguously that muscle nuclei are virtually never lost during atrophy. The massive increase in apoptotic nuclei that accompanies atrophy reflects the fate of non-muscle stromal and satellite cells, not the myonuclei. This makes teleological sense given that all of the nuclei within a muscle fibre share a common cytoplasm. Under these circumstances, it is not clear how some nuclei would be protected while their neighbours would be completely degraded during apoptosis. The persistence of myonuclei in atrophic muscle not only challenged well-accepted dogma, it also suggested a new epigenetic mechanism for muscle memory.In a new study described in this issue of The Journal of Physiology, Egner et al. (2013) extend this analysis to inquire about the fate of new nuclei that are acquired during hypertrophy following exercise and/or anabolic steroid treatment. Female mice received subcutaneous testosterone propionate or placebo pellets, then 2 weeks later their EDL and soleus muscles were excised and examined. In a subset of animals, these muscles were also forced to perform extra work by truncating their primary synergistic muscles. Testosterone and exercise independently led to hypertrophy and the anticipated increases in muscle cross-sectional area (CSA) and myonuclear number. In animals that received both treatments, these effects were additive and the muscles displayed an ∼90% increase in the number of myonuclei. Testosterone levels and muscle CSA both declined rapidly when the hormone pellets were removed. However, consistent with earlier reports, this atrophy was not accompanied by a concomitant loss of myonuclei.These results raise an obvious question: are these ‘surplus’ nuclei beneficial? To test this hypothesis, animals were pre-treated with either steroid or placebo for 2 weeks, deprived of hormone for an additional 3 weeks, and then the muscles were forced to work. Prior steroid exposure conferred a distinct advantage to the muscles, with a 44% increase in CSA rather than the 17% increase observed in controls. These benefits were not transient. When the muscles were induced to hypertrophy 3 months after steroid treatments had ended (the mouse equivalent of 10 years of human lifespan), the steroid-treated group displayed a 31% increase in CSA compared to a modest 6% in placebo controls.Taken together, these data suggest that: (1) once you acquire a myonucleus, it is essentially permanent; and (2) more nuclei translate into greater capacity for regrowth, which presumably translates into enhanced muscle strength and/or speed. These observations have significant public health implications, especially with regards to resistance exercise in the young and the potential to reduce the risk of sarcopenia during ageing. There are also potential ramifications for the sporting community. All athletes acquire their myonuclei through persistent hard work, but some individuals can unfairly supplement their pool by cheating with anabolic steroid use. Since the benefits of steroid administration may persist well after the circulating hormone levels have returned to baseline, it may be very hard to catch violators. Obtaining muscle biopsies from athletes to determine if they have ill-gotten nuclei is invasive, unethical (akin to assault), and likely to be ambiguous. This study reveals a potential new hurdle in the arms race between athletes and ethics, and offers the demoralizing realization that perhaps some cheaters may prosper." @default.
• W2017451001 created "2016-06-24" @default.
• W2017451001 creator A5062771064 @default.
• W2017451001 date "2013-12-15" @default.
• W2017451001 modified "2023-09-23" @default.
• W2017451001 title "Muscle nuclei remember to cheat death" @default.
• W2017451001 cites W1547114701 @default.
• W2017451001 cites W1830095996 @default.
• W2017451001 cites W2088997890 @default.
• W2017451001 cites W2107574257 @default.
• W2017451001 cites W2108233606 @default.
• W2017451001 doi "https://doi.org/10.1113/jphysiol.2013.268243" @default.
• W2017451001 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3892465" @default.
• W2017451001 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24339150" @default.
• W2017451001 hasPublicationYear "2013" @default.
• W2017451001 type Work @default.
• W2017451001 sameAs 2017451001 @default.
• W2017451001 citedByCount "0" @default.
• W2017451001 crossrefType "journal-article" @default.
• W2017451001 hasAuthorship W2017451001A5062771064 @default.
• W2017451001 hasBestOaLocation W20174510012 @default.
• W2017451001 hasConcept C105702510 @default.
• W2017451001 hasConcept C121332964 @default.
• W2017451001 hasConcept C134018914 @default.
• W2017451001 hasConcept C167414201 @default.
• W2017451001 hasConcept C169760540 @default.
• W2017451001 hasConcept C207200792 @default.
• W2017451001 hasConcept C2776263037 @default.
• W2017451001 hasConcept C2779959927 @default.
• W2017451001 hasConcept C2780723820 @default.
• W2017451001 hasConcept C2781172350 @default.
• W2017451001 hasConcept C41008148 @default.
• W2017451001 hasConcept C50335755 @default.
• W2017451001 hasConcept C54355233 @default.
• W2017451001 hasConcept C62520636 @default.
• W2017451001 hasConcept C86803240 @default.
• W2017451001 hasConcept C95444343 @default.
• W2017451001 hasConceptScore W2017451001C105702510 @default.
• W2017451001 hasConceptScore W2017451001C121332964 @default.
• W2017451001 hasConceptScore W2017451001C134018914 @default.
• W2017451001 hasConceptScore W2017451001C167414201 @default.
• W2017451001 hasConceptScore W2017451001C169760540 @default.
• W2017451001 hasConceptScore W2017451001C207200792 @default.
• W2017451001 hasConceptScore W2017451001C2776263037 @default.
• W2017451001 hasConceptScore W2017451001C2779959927 @default.
• W2017451001 hasConceptScore W2017451001C2780723820 @default.
• W2017451001 hasConceptScore W2017451001C2781172350 @default.
• W2017451001 hasConceptScore W2017451001C41008148 @default.
• W2017451001 hasConceptScore W2017451001C50335755 @default.
• W2017451001 hasConceptScore W2017451001C54355233 @default.
• W2017451001 hasConceptScore W2017451001C62520636 @default.
• W2017451001 hasConceptScore W2017451001C86803240 @default.
• W2017451001 hasConceptScore W2017451001C95444343 @default.
• W2017451001 hasLocation W20174510011 @default.
• W2017451001 hasLocation W20174510012 @default.
• W2017451001 hasLocation W20174510013 @default.
• W2017451001 hasOpenAccess W2017451001 @default.
• W2017451001 hasPrimaryLocation W20174510011 @default.
• W2017451001 hasRelatedWork W1853307226 @default.
• W2017451001 hasRelatedWork W1963585940 @default.
• W2017451001 hasRelatedWork W1996475391 @default.
• W2017451001 hasRelatedWork W2001210992 @default.
• W2017451001 hasRelatedWork W2026308700 @default.
• W2017451001 hasRelatedWork W2071090788 @default.
• W2017451001 hasRelatedWork W2072107702 @default.
• W2017451001 hasRelatedWork W2090240044 @default.
• W2017451001 hasRelatedWork W2146421743 @default.
• W2017451001 hasRelatedWork W2320386454 @default.
• W2017451001 hasRelatedWork W2326031400 @default.
• W2017451001 hasRelatedWork W2413238398 @default.
• W2017451001 hasRelatedWork W2439827402 @default.
• W2017451001 hasRelatedWork W285776097 @default.
• W2017451001 hasRelatedWork W3023786334 @default.
• W2017451001 isParatext "false" @default.
• W2017451001 isRetracted "false" @default.
• W2017451001 magId "2017451001" @default.
• W2017451001 workType "article" @default.