東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

FindBook

Google Book

Amazon

博客來

Molecular and Cellular Mechanisms of Resistance Training-Induced Skeletal Muscle Hypertrophic Response Heterogeneity in Older Adults.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Molecular and Cellular Mechanisms of Resistance Training-Induced Skeletal Muscle Hypertrophic Response Heterogeneity in Older Adults./
作者:	Bell, Margaret.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2022,
面頁冊數:	125 p.
附註:	Source: Dissertations Abstracts International, Volume: 83-12, Section: B.
Contained By:	Dissertations Abstracts International83-12B.
標題:	Cellular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29161158
ISBN:	9798802756980

Molecular and Cellular Mechanisms of Resistance Training-Induced Skeletal Muscle Hypertrophic Response Heterogeneity in Older Adults.
Bell, Margaret.

Molecular and Cellular Mechanisms of Resistance Training-Induced Skeletal Muscle Hypertrophic Response Heterogeneity in Older Adults. - Ann Arbor : ProQuest Dissertations & Theses, 2022 - 125 p.

Source: Dissertations Abstracts International, Volume: 83-12, Section: B.

Thesis (Ph.D.)--The University of Alabama at Birmingham, 2022.

This item must not be sold to any third party vendors.

Sarcopenia is a decrease in skeletal muscle (SKM) mass occurring with age. This disease is natural, so it is important to increase SKM mass to counteract. This need is seen in diseases leading to muscle atrophy (i.e., insulin resistance and diabetes). The most efficient way to promote SKM hypertrophy is resistance exercise training (RT), however there is high response heterogeneity. To investigate SKM heterogeneity and maximizing SKM hypertrophy, we conducted a double-blind two-site placebo controlled clinical trial: "Metformin to Augment Strength Training Effective Response in Seniors (MASTERS)". Here participants ≥ 65 years underwent RT for 14 weeks. Measurements of SKM mass and SKM samples were obtained.For this dissertation, we used placebo participants from MASTERS to investigate molecular and cellular mechanisms of RT-induced SKM hypertrophy heterogeneity in older adults. For study one, we used RNA from baseline SKM to perform transcriptome wide poly-A RNA sequencing (n=31) investigating transcriptional networks linked to RT-induced SKM hypertrophy measured by mid-thigh CSA. Networks were classified as predictive, responsive, or plastic. Prediction analysis confirmed genes related to training adaptions and uncovered novel genes that could be used for research understanding the baseline gene expression profile responsible for SKM hypertrophy. Responsive networks revealed an increase in genes of aerobic metabolism and decrease in spliceosome and type-1 myofiber genes. There were no significant gene groups from the plasticity analysis. This suggests baseline gene expression contributes more to heterogeneity than RT-induced changes.For the second study, we used myoblast from participants of MASTERS (n=10) to investigate if the magnitude of SKM hypertrophy observed in older adults after RT is recapitulated in vitro. Myoblast were differentiated into myotubes and markers of myogenesis, ribosome biogenesis, and protein synthesis were measured after FBS induced hypertrophy. High responders showed better myotube formation than low responders in vivo. However, there were no significant group-by-treatment interactions with markers of interest. This suggest differences between low and high SKM hypertrophy may be more influenced by the in vivo muscle environment than differences in myogenic cells proper. Taken together, these studies provide great insight to cellular and molecular mechanisms responsible for RT-induced SKM response heterogeneity in older adults.

ISBN: 9798802756980Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Cell culture

Molecular and Cellular Mechanisms of Resistance Training-Induced Skeletal Muscle Hypertrophic Response Heterogeneity in Older Adults.
LDR:03742nmm a2200397 4500 001 2351472
005 20221107085653.5
008 241004s2022 ||||||||||||||||| ||eng d
020 $a 9798802756980
035 $a (MiAaPQ)AAI29161158
035 $a AAI29161158
040 $a MiAaPQ $c MiAaPQ
100 1 $a Bell, Margaret. $3 3691045
245 1 0 $a Molecular and Cellular Mechanisms of Resistance Training-Induced Skeletal Muscle Hypertrophic Response Heterogeneity in Older Adults.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2022
300 $a 125 p.
500 $a Source: Dissertations Abstracts International, Volume: 83-12, Section: B.
500 $a Advisor: Bamman, Marcas.
502 $a Thesis (Ph.D.)--The University of Alabama at Birmingham, 2022.
506 $a This item must not be sold to any third party vendors.
520 $a Sarcopenia is a decrease in skeletal muscle (SKM) mass occurring with age. This disease is natural, so it is important to increase SKM mass to counteract. This need is seen in diseases leading to muscle atrophy (i.e., insulin resistance and diabetes). The most efficient way to promote SKM hypertrophy is resistance exercise training (RT), however there is high response heterogeneity. To investigate SKM heterogeneity and maximizing SKM hypertrophy, we conducted a double-blind two-site placebo controlled clinical trial: "Metformin to Augment Strength Training Effective Response in Seniors (MASTERS)". Here participants ≥ 65 years underwent RT for 14 weeks. Measurements of SKM mass and SKM samples were obtained.For this dissertation, we used placebo participants from MASTERS to investigate molecular and cellular mechanisms of RT-induced SKM hypertrophy heterogeneity in older adults. For study one, we used RNA from baseline SKM to perform transcriptome wide poly-A RNA sequencing (n=31) investigating transcriptional networks linked to RT-induced SKM hypertrophy measured by mid-thigh CSA. Networks were classified as predictive, responsive, or plastic. Prediction analysis confirmed genes related to training adaptions and uncovered novel genes that could be used for research understanding the baseline gene expression profile responsible for SKM hypertrophy. Responsive networks revealed an increase in genes of aerobic metabolism and decrease in spliceosome and type-1 myofiber genes. There were no significant gene groups from the plasticity analysis. This suggests baseline gene expression contributes more to heterogeneity than RT-induced changes.For the second study, we used myoblast from participants of MASTERS (n=10) to investigate if the magnitude of SKM hypertrophy observed in older adults after RT is recapitulated in vitro. Myoblast were differentiated into myotubes and markers of myogenesis, ribosome biogenesis, and protein synthesis were measured after FBS induced hypertrophy. High responders showed better myotube formation than low responders in vivo. However, there were no significant group-by-treatment interactions with markers of interest. This suggest differences between low and high SKM hypertrophy may be more influenced by the in vivo muscle environment than differences in myogenic cells proper. Taken together, these studies provide great insight to cellular and molecular mechanisms responsible for RT-induced SKM response heterogeneity in older adults.
590 $a School code: 0005.
650 4 $a Cellular biology. $3 3172791
650 4 $a Molecular biology. $3 517296
650 4 $a Genetics. $3 530508
650 4 $a Aging. $3 543123
650 4 $a Kinesiology. $3 517627
653 $a Cell culture
653 $a Exercise
653 $a Hypertrophy
653 $a Muscle
653 $a RNA-seq
690 $a 0379
690 $a 0307
690 $a 0369
690 $a 0575
690 $a 0493
710 2 $a The University of Alabama at Birmingham. $b Joint Health Sciences. $3 3691046
773 0 $t Dissertations Abstracts International $g 83-12B.
790 $a 0005
791 $a Ph.D.
792 $a 2022
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29161158