國立虎尾科技大學 |

Is Exercise-Induced Redox Signaling Affected by Aging?

紀錄類型:	書目-語言資料,手稿 : Monograph/item
正題名/作者:	Is Exercise-Induced Redox Signaling Affected by Aging?/
作者:	Ostrom, Ethan L.
面頁冊數:	1 online resource (219 pages)
附註:	Source: Dissertations Abstracts International, Volume: 82-12, Section: B.
Contained By:	Dissertations Abstracts International82-12B.
標題:	Molecular biology. -
電子資源:	click for full text (PQDT)
ISBN:	9798738646928

Is Exercise-Induced Redox Signaling Affected by Aging?
Ostrom, Ethan L.

Is Exercise-Induced Redox Signaling Affected by Aging? - 1 online resource (219 pages)

Source: Dissertations Abstracts International, Volume: 82-12, Section: B.

Thesis (Ph.D.)--Northern Arizona University, 2021.

Includes bibliographical references

Redox signaling dysfunction is a key characteristic of aging cells and tissues and has wide ranging cellular and physiological effects. Exercise is one of the best tools available to promote healthy aging and reduce disease burden, however some evidence suggests exercise is not as effective in older populations. This is likely driven by redox signaling dysfunction because of the critical involvement of redox signaling mechanisms in exercise adaptations. In this work, I have used several studies in humans and mice with multiple methods to elucidate the mechanisms of Nrf2-mediated redox stress response to exercise and the effects of aging on this response. I demonstrate that exercise induced Nrf2 activation is impaired in older compared to younger adults, and that exercise training only partially reverses these effects. Redox stress responses to a non-exercise stressor, a forearm ischemia-reperfusion challenge, is not different between ages, but exercise training does improve the response compared to controls in humans. Finally, acute contractile stimulation of skeletal muscle increases Nrf2 signaling within the muscle, and high intensity stimulation activates Nrf2 in contralateral unstimulated muscle, but low intensity stimulation does not. These effects appear to occur through inhibiting the negative regulator, Keap1. Taken together, these data indicate that exercise is a powerful inducer of the redox stress response transcription factor, Nrf2, but that aging impairs our ability to respond to an acute exercise bout. Future work should aim to discover and utilize therapeutics that act synergistically with exercise to restore redox homeostasis and redox signaling function.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2024

Mode of access: World Wide Web

ISBN: 9798738646928Subjects--Topical Terms:

583443
Molecular biology.
Subjects--Index Terms:

AgingIndex Terms--Genre/Form:

554714
Electronic books.

Is Exercise-Induced Redox Signaling Affected by Aging?
LDR:02974ntm a22003737 4500 001 1149442
005 20241022112056.5
006 m o d
007 cr bn ---uuuuu
008 250605s2021 xx obm 000 0 eng d
020 $a 9798738646928
035 $a (MiAaPQ)AAI28416731
035 $a AAI28416731
040 $a MiAaPQ $b eng $c MiAaPQ $d NTU
100 1 $a Ostrom, Ethan L. $3 1475680
245 1 0 $a Is Exercise-Induced Redox Signaling Affected by Aging?
264 0 $c 2021
300 $a 1 online resource (219 pages)
336 $a text $b txt $2 rdacontent
337 $a computer $b c $2 rdamedia
338 $a online resource $b cr $2 rdacarrier
500 $a Source: Dissertations Abstracts International, Volume: 82-12, Section: B.
500 $a Advisor: Traustadottir, Tinna.
502 $a Thesis (Ph.D.)--Northern Arizona University, 2021.
504 $a Includes bibliographical references
520 $a Redox signaling dysfunction is a key characteristic of aging cells and tissues and has wide ranging cellular and physiological effects. Exercise is one of the best tools available to promote healthy aging and reduce disease burden, however some evidence suggests exercise is not as effective in older populations. This is likely driven by redox signaling dysfunction because of the critical involvement of redox signaling mechanisms in exercise adaptations. In this work, I have used several studies in humans and mice with multiple methods to elucidate the mechanisms of Nrf2-mediated redox stress response to exercise and the effects of aging on this response. I demonstrate that exercise induced Nrf2 activation is impaired in older compared to younger adults, and that exercise training only partially reverses these effects. Redox stress responses to a non-exercise stressor, a forearm ischemia-reperfusion challenge, is not different between ages, but exercise training does improve the response compared to controls in humans. Finally, acute contractile stimulation of skeletal muscle increases Nrf2 signaling within the muscle, and high intensity stimulation activates Nrf2 in contralateral unstimulated muscle, but low intensity stimulation does not. These effects appear to occur through inhibiting the negative regulator, Keap1. Taken together, these data indicate that exercise is a powerful inducer of the redox stress response transcription factor, Nrf2, but that aging impairs our ability to respond to an acute exercise bout. Future work should aim to discover and utilize therapeutics that act synergistically with exercise to restore redox homeostasis and redox signaling function.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2024
538 $a Mode of access: World Wide Web
650 4 $a Molecular biology. $3 583443
650 4 $a Aging. $3 559847
650 4 $a Biology. $3 599573
653 $a Aging
653 $a Exercise
653 $a Redox biology
655 7 $a Electronic books. $2 local $3 554714
690 $a 0306
690 $a 0493
690 $a 0307
710 2 $a Northern Arizona University. $b Department of Biological Sciences. $3 1475681
710 2 $a ProQuest Information and Learning Co. $3 1178819
773 0 $t Dissertations Abstracts International $g 82-12B.
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28416731 $z click for full text (PQDT)