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ORCID

https://orcid.org/0000-0001-5768-9708

Access Type

Open Access Thesis

Document Type

thesis

Degree Program

Kinesiology

Degree Type

Master of Science (M.S.)

Year Degree Awarded

2023

Month Degree Awarded

February

Abstract

Stretch activation (FSA) is the delayed increase in fiber specific tension (force per cross-sectional area) following a rapid stretch and can improve muscle performance during repetitive cyclical contractions. Historically considered minimal in skeletal muscle, our recent work showed the ratio ofstretch- to calcium-activated specific tension (FSA/F0) increased from 10 to 40% with greater inorganic phosphate (Pi) levels in soleus muscle fibers (Straight et al., 2019). Given Pi increases with muscle fatigue, we hypothesize that FSA helps maintain force generation during fatigue. To test this, FSA, induced by a stretch of 0.5% fiber length, was examined during Active (pCa 4.5 (pCa = -log([Ca2+]), pH 7.0, Pi 5 mM), High Ca2+ Fatigue (pCa 4.5, pH 6.2, Pi 30 mM) and Low Ca2+ Fatigue (pCa 5.1, pH 6.2, Pi 30 mM) in fibers expressing myosin heavy chain (MHC) I, IIA, IIX and IIB isoforms from soleus and extensor digitorum longus muscles of C57BL/6NJ mice. F0 of all MHC isoforms decreased from Active to High Ca2+ Fatigue to Low Ca2+ Fatigue, as expected. In MHC IIX and IIB fibers, FSA occurred under all conditions and FSA/F0 increased from Active (17-20%) to High Ca2+ Fatigue (32-35%) to Low Ca2+ Fatigue (42-44%). In MHC IIA fibers, FSA/F0 increased similarly to MHC IIX and IIB fibers from Active (14%) to High Ca2+ Fatigue (32%) but stayed elevated under Low Ca2+ Fatigue (35%). For MHC I fibers, no discernable FSA was apparent in either High – or Low Ca2+ Fatigue, leaving an FSA/F0 value in Active only ( 4%). These results show that FSA is a significant modulator of specific tension production under fatiguing conditions in fast-contracting muscle fibers. This mechanism could play an important physiological role during cyclical contractions, when the antagonistic muscle rapidly stretches the agonist muscle, by reducing the effect of fatigue on specific tension production.

DOI

https://doi.org/10.7275/32898994

First Advisor

Mark S. Miller

Second Advisor

Jane A. Kent

Third Advisor

Edward E. Debold

Fourth Advisor

Douglas A. Swank

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

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