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Skeletal Muscle Oxidative Capacity i...

Chung, Susie.

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Skeletal Muscle Oxidative Capacity in the Elderly.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Skeletal Muscle Oxidative Capacity in the Elderly./
Author:	Chung, Susie.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
Description:	109 p.
Notes:	Source: Masters Abstracts International, Volume: 57-06.
Contained By:	Masters Abstracts International57-06(E).
Subject:	Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10903217
ISBN:	9780438129221

Skeletal Muscle Oxidative Capacity in the Elderly.
Chung, Susie.

Skeletal Muscle Oxidative Capacity in the Elderly. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 109 p.

Source: Masters Abstracts International, Volume: 57-06.

Thesis (M.S.E.S.)--The University of Texas at Arlington, 2018.

Age is the greatest risk factor for chronic disease and is associated with a marked decline in functional capacity and quality of life, with loss of skeletal muscle function regarded as a key contributing factor. While the exact mechanism(s) for the loss of skeletal muscle function remains incompletely understood, age-related mitochondrial dysfunction is thought to play a major role. To explore this question further, we studied 15 independently-living seniors (age: 72 +/- 5 yrs; m/f: 4/11; BMI: 27.6 +/- 5.9) and 17 young volunteers (age: 25 +/- 4 years; m/f: 8/9; BMI: 24.0 +/- 3.3). Skeletal muscle oxidative function was measured in non-locomotor forearm muscle as the recovery kinetics of muscle oxygen consumption using near-infrared spectroscopy (NIRS). Aging was associated with a significant prolongation of the time constant of oxidative recovery following handgrip exercise (51.8 +/- 5.4 s vs. 37.1 +/- 2.1 s, p = 0.04, old vs. young, respectively), suggesting an overall reduction in mitochondrial function. To determine whether we could improve this age-related impairment in skeletal muscle oxidative capacity, we performed an exercise training study in eight elderly participants from the local Dallas-Fort Worth community (73 +/- 7 yrs; m/f: 2/6; BMI: 25.9 +/- 3.1 kg). Training was performed five days a week, at 30% of maximal voluntary contraction (MVC), for a total of 600, 900, 1200, and 1500 grips per day, respectively. Skeletal muscle oxidative capacity was assessed using the aforementioned NIRS protocol. In contrast to our hypothesis, neither grip strength (pre-training MVC: 24.5 +/- 12.2 kg; post-training MVC = 26.1 +/- 11.4 kg; p = 0.12) nor skeletal muscle oxidative capacity (pre-exercise training tau: 44.6 +/- 14.1s; post-exercise training tau: 46.9 +/- 11.3 s; p = 1.00) were significantly improved. These data conflict with several prior investigations showing an improvement in skeletal muscle oxidative capacity with exercise training in the elderly. That our participants were on average 10 years older than the majority of participants previously studied, with some history of cardiovascular risk factors, may suggest an upper limit to skeletal muscle adaptation. More work in this area is indeed needed.

ISBN: 9780438129221Subjects--Topical Terms:

518431
Physiology.

Skeletal Muscle Oxidative Capacity in the Elderly.
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520 $a Age is the greatest risk factor for chronic disease and is associated with a marked decline in functional capacity and quality of life, with loss of skeletal muscle function regarded as a key contributing factor. While the exact mechanism(s) for the loss of skeletal muscle function remains incompletely understood, age-related mitochondrial dysfunction is thought to play a major role. To explore this question further, we studied 15 independently-living seniors (age: 72 +/- 5 yrs; m/f: 4/11; BMI: 27.6 +/- 5.9) and 17 young volunteers (age: 25 +/- 4 years; m/f: 8/9; BMI: 24.0 +/- 3.3). Skeletal muscle oxidative function was measured in non-locomotor forearm muscle as the recovery kinetics of muscle oxygen consumption using near-infrared spectroscopy (NIRS). Aging was associated with a significant prolongation of the time constant of oxidative recovery following handgrip exercise (51.8 +/- 5.4 s vs. 37.1 +/- 2.1 s, p = 0.04, old vs. young, respectively), suggesting an overall reduction in mitochondrial function. To determine whether we could improve this age-related impairment in skeletal muscle oxidative capacity, we performed an exercise training study in eight elderly participants from the local Dallas-Fort Worth community (73 +/- 7 yrs; m/f: 2/6; BMI: 25.9 +/- 3.1 kg). Training was performed five days a week, at 30% of maximal voluntary contraction (MVC), for a total of 600, 900, 1200, and 1500 grips per day, respectively. Skeletal muscle oxidative capacity was assessed using the aforementioned NIRS protocol. In contrast to our hypothesis, neither grip strength (pre-training MVC: 24.5 +/- 12.2 kg; post-training MVC = 26.1 +/- 11.4 kg; p = 0.12) nor skeletal muscle oxidative capacity (pre-exercise training tau: 44.6 +/- 14.1s; post-exercise training tau: 46.9 +/- 11.3 s; p = 1.00) were significantly improved. These data conflict with several prior investigations showing an improvement in skeletal muscle oxidative capacity with exercise training in the elderly. That our participants were on average 10 years older than the majority of participants previously studied, with some history of cardiovascular risk factors, may suggest an upper limit to skeletal muscle adaptation. More work in this area is indeed needed.
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