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- Davids, Charlie J, et al.
(författare)
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Acute cellular and molecular responses and chronic adaptations to low-load blood flow restriction and high-load resistance exercise in trained individuals.
- 2021
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Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 131:6, s. 1731-1749
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Tidskriftsartikel (refereegranskat)abstract
- Blood flow restriction (BFR) with low-load resistance exercise (RE) is often used as a surrogate to traditional high-load RE to stimulate muscular adaptations, such as hypertrophy and strength. However, it is not clear whether such adaptations are achieved through similar cellular and molecular processes. We compared changes in muscle function, morphology and signaling pathways between these differing training protocols. Twenty-one males and females (mean ± SD: 24.3 ± 3.1 years) experienced with resistance training (4.9 ± 2.6 years) performed nine weeks of resistance training (three times per week) with either high-loads (75-80% 1RM; HL-RT), or low-loads with BFR (30-40% 1RM; LL-BFR). Before and after the training intervention, resting muscle biopsies were collected, and quadricep cross-sectional area (CSA), muscular strength and power were measured. Approximately 5 days following the intervention, the same individuals performed an additional 'acute' exercise session under the same conditions, and serial muscle biopsies were collected to assess hypertrophic- and ribosomal-based signaling stimuli. Quadricep CSA increased with both LL-BFR (7.4±4.3%) and HL-RT (4.6±2.9%), with no significant differences between training groups (p=0.37). Muscular strength also increased in both training groups, but with superior gains in squat 1RM occurring with HL-RT (p<0.01). Acute phosphorylation of several key proteins involved in hypertrophy signaling pathways, and expression of ribosomal RNA transcription factors occurred to a similar degree with LL-BFR and HL-RT (all p>0.05 for between-group comparisons). Together, these findings validate low-load resistance training with continuous BFR as an effective alternative to traditional high-load resistance training for increasing muscle hypertrophy in trained individuals.
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| 2. |
- Eftestøl, Einar, et al.
(författare)
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Muscle memory : Are myonuclei ever lost?
- 2020
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Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 128, s. 456-457
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 3. |
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| 4. |
- Psilander, Niklas, et al.
(författare)
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Retention of myonuclei after grave atrophy in human skeletal muscle, a case study
- 2017
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Ingår i: Acta Physiologica Volume 219, Issue S710 February 2017. - : Wiley. ; , s. 14-43
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Konferensbidrag (refereegranskat)abstract
- Introduction: the current textbook model suggests that the myonuclear domain size is constant for muscle fibers in both their atrophic and hypertrophic state. However, recent animal studies show that myonuclear content is maintained after atrophy leading to a decreased myonuclear domain size (Gundersen et al. J Physiol. 2008 Jun 1;586(11):2675-81). This remains to be investigated in human skeletal muscle and the aim of the present study was therefore to study the effect of grave atrophy on myonuclear content and domain size in the vastus medialis muscle.Materials and Methods: biopsies were obtained from vastus medialis on a 22 year old female patient before and 6 weeks after an anterior cruciate ligament reconstructionand meniscus repair surgery. Histochemical analyses were done to analyze fiber cross sectional area (CSA), fiber type composition and number of myonuclei per fiber.Results: the CSA of type II muscle fibers decreased by 35% (from 4297±55 to 2807±64 µm2) whereas the number of myonuclei per fiber remained stable (3.4±0.4 and 3.9±0.5, pre and post respectively). The nuclear domain size was thereby decreased by ~40% (from 1255 to 722 µm2). There were only minor changes in type I muscle fiber CSA, myonuclei content and domain size.Conclusion: in line with previous findings from animal studies, the present case study shows that the number of myonuclei per fiber is maintained and the domain size is reduced in human skeletal muscle after immobilization induced atrophy.
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