Effect of aerobic exercise training and deconditioning on oxidative capacity and muscle mitochondrial enzyme machinery in young and elderly individuals

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Standard

Effect of aerobic exercise training and deconditioning on oxidative capacity and muscle mitochondrial enzyme machinery in young and elderly individuals. / Fritzen, Andreas Mæchel; Andersen, Søren Peter; Qadri, Khaled Abdul Nasser; Thøgersen, Frank Dyrehauge; Krag, Thomas; Ørngreen, Mette Cathrine; Vissing, John; Jeppesen, Tina Dysgaard.

I: Journal of Clinical Medicine, Bind 9, Nr. 10, 3113, 2020.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Fritzen, AM, Andersen, SP, Qadri, KAN, Thøgersen, FD, Krag, T, Ørngreen, MC, Vissing, J & Jeppesen, TD 2020, 'Effect of aerobic exercise training and deconditioning on oxidative capacity and muscle mitochondrial enzyme machinery in young and elderly individuals', Journal of Clinical Medicine, bind 9, nr. 10, 3113. https://doi.org/10.3390/jcm9103113

APA

Fritzen, A. M., Andersen, S. P., Qadri, K. A. N., Thøgersen, F. D., Krag, T., Ørngreen, M. C., Vissing, J., & Jeppesen, T. D. (2020). Effect of aerobic exercise training and deconditioning on oxidative capacity and muscle mitochondrial enzyme machinery in young and elderly individuals. Journal of Clinical Medicine, 9(10), [3113]. https://doi.org/10.3390/jcm9103113

Vancouver

Fritzen AM, Andersen SP, Qadri KAN, Thøgersen FD, Krag T, Ørngreen MC o.a. Effect of aerobic exercise training and deconditioning on oxidative capacity and muscle mitochondrial enzyme machinery in young and elderly individuals. Journal of Clinical Medicine. 2020;9(10). 3113. https://doi.org/10.3390/jcm9103113

Author

Fritzen, Andreas Mæchel ; Andersen, Søren Peter ; Qadri, Khaled Abdul Nasser ; Thøgersen, Frank Dyrehauge ; Krag, Thomas ; Ørngreen, Mette Cathrine ; Vissing, John ; Jeppesen, Tina Dysgaard. / Effect of aerobic exercise training and deconditioning on oxidative capacity and muscle mitochondrial enzyme machinery in young and elderly individuals. I: Journal of Clinical Medicine. 2020 ; Bind 9, Nr. 10.

Bibtex

@article{875fcdf11d6a49568719f03e552c9ddc,
title = "Effect of aerobic exercise training and deconditioning on oxidative capacity and muscle mitochondrial enzyme machinery in young and elderly individuals",
abstract = "Mitochondrial dysfunction is thought to be involved in age-related loss of muscle mass and function (sarcopenia). Since the degree of physical activity is vital for skeletal muscle mitochondrial function and content, the aim of this study was to investigate the effect of 6 weeks of aerobic exercise training and 8 weeks of deconditioning on functional parameters of aerobic capacity and markers of muscle mitochondrial function in elderly compared to young individuals. In 11 healthy, elderly (80 ± 4 years old) and 10 healthy, young (24 ± 3 years old) volunteers, aerobic training improved maximal oxygen consumption rate by 13%, maximal workload by 34%, endurance capacity by 2.4-fold and exercise economy by 12% in the elderly to the same extent as in young individuals. This evidence was accompanied by a similar training-induced increase in muscle citrate synthase (CS) (31%) and mitochondrial complex I-IV activities (51-163%) in elderly and young individuals. After 8 weeks of deconditioning, endurance capacity (-20%), and enzyme activity of CS (-18%) and complex I (-40%), III (-25%), and IV (-26%) decreased in the elderly to a larger extent than in young individuals. In conclusion, we found that elderly have a physiological normal ability to improve aerobic capacity and mitochondrial function with aerobic training compared to young individuals, but had a faster decline in endurance performance and muscle mitochondrial enzyme activity after deconditioning, suggesting an age-related issue in maintaining oxidative metabolism.",
keywords = "Faculty of Science, Aerobic exercise training, Mitochondria, Sarcopenia, Endurance, Deconditioning, Skeletal muscle, Elderly",
author = "Fritzen, {Andreas M{\ae}chel} and Andersen, {S{\o}ren Peter} and Qadri, {Khaled Abdul Nasser} and Th{\o}gersen, {Frank Dyrehauge} and Thomas Krag and {\O}rngreen, {Mette Cathrine} and John Vissing and Jeppesen, {Tina Dysgaard}",
note = "CURIS 2020 NEXS 321",
year = "2020",
doi = "10.3390/jcm9103113",
language = "English",
volume = "9",
journal = "Journal of Clinical Medicine",
issn = "2077-0383",
publisher = "M D P I AG",
number = "10",

}

RIS

TY - JOUR

T1 - Effect of aerobic exercise training and deconditioning on oxidative capacity and muscle mitochondrial enzyme machinery in young and elderly individuals

AU - Fritzen, Andreas Mæchel

AU - Andersen, Søren Peter

AU - Qadri, Khaled Abdul Nasser

AU - Thøgersen, Frank Dyrehauge

AU - Krag, Thomas

AU - Ørngreen, Mette Cathrine

AU - Vissing, John

AU - Jeppesen, Tina Dysgaard

N1 - CURIS 2020 NEXS 321

PY - 2020

Y1 - 2020

N2 - Mitochondrial dysfunction is thought to be involved in age-related loss of muscle mass and function (sarcopenia). Since the degree of physical activity is vital for skeletal muscle mitochondrial function and content, the aim of this study was to investigate the effect of 6 weeks of aerobic exercise training and 8 weeks of deconditioning on functional parameters of aerobic capacity and markers of muscle mitochondrial function in elderly compared to young individuals. In 11 healthy, elderly (80 ± 4 years old) and 10 healthy, young (24 ± 3 years old) volunteers, aerobic training improved maximal oxygen consumption rate by 13%, maximal workload by 34%, endurance capacity by 2.4-fold and exercise economy by 12% in the elderly to the same extent as in young individuals. This evidence was accompanied by a similar training-induced increase in muscle citrate synthase (CS) (31%) and mitochondrial complex I-IV activities (51-163%) in elderly and young individuals. After 8 weeks of deconditioning, endurance capacity (-20%), and enzyme activity of CS (-18%) and complex I (-40%), III (-25%), and IV (-26%) decreased in the elderly to a larger extent than in young individuals. In conclusion, we found that elderly have a physiological normal ability to improve aerobic capacity and mitochondrial function with aerobic training compared to young individuals, but had a faster decline in endurance performance and muscle mitochondrial enzyme activity after deconditioning, suggesting an age-related issue in maintaining oxidative metabolism.

AB - Mitochondrial dysfunction is thought to be involved in age-related loss of muscle mass and function (sarcopenia). Since the degree of physical activity is vital for skeletal muscle mitochondrial function and content, the aim of this study was to investigate the effect of 6 weeks of aerobic exercise training and 8 weeks of deconditioning on functional parameters of aerobic capacity and markers of muscle mitochondrial function in elderly compared to young individuals. In 11 healthy, elderly (80 ± 4 years old) and 10 healthy, young (24 ± 3 years old) volunteers, aerobic training improved maximal oxygen consumption rate by 13%, maximal workload by 34%, endurance capacity by 2.4-fold and exercise economy by 12% in the elderly to the same extent as in young individuals. This evidence was accompanied by a similar training-induced increase in muscle citrate synthase (CS) (31%) and mitochondrial complex I-IV activities (51-163%) in elderly and young individuals. After 8 weeks of deconditioning, endurance capacity (-20%), and enzyme activity of CS (-18%) and complex I (-40%), III (-25%), and IV (-26%) decreased in the elderly to a larger extent than in young individuals. In conclusion, we found that elderly have a physiological normal ability to improve aerobic capacity and mitochondrial function with aerobic training compared to young individuals, but had a faster decline in endurance performance and muscle mitochondrial enzyme activity after deconditioning, suggesting an age-related issue in maintaining oxidative metabolism.

KW - Faculty of Science

KW - Aerobic exercise training

KW - Mitochondria

KW - Sarcopenia

KW - Endurance

KW - Deconditioning

KW - Skeletal muscle

KW - Elderly

U2 - 10.3390/jcm9103113

DO - 10.3390/jcm9103113

M3 - Journal article

C2 - 32993104

VL - 9

JO - Journal of Clinical Medicine

JF - Journal of Clinical Medicine

SN - 2077-0383

IS - 10

M1 - 3113

ER -

ID: 249427289