Combination of Coenzyme Q10 Intake and Moderate Physical Activity Counteracts Mitochondrial Dysfunctions in a SAMP8 Mouse Model

C. Andreani, C. Bartolacci, M. Guescini, M. Battistelli, V. Stocchi, F. Orlando, M. Provinciali, A. Amici, C. Marchini, L. Tiano, P. Orlando, S. Silvestri

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Aging skeletal muscles are characterized by a progressive decline in muscle mass and muscular strength. Such muscular dysfunctions are usually associated with structural and functional alterations of skeletal muscle mitochondria. The senescence-accelerated mouse-prone 8 (SAMP8) model, characterized by premature aging and high degree of oxidative stress, was used to investigate whether a combined intervention with mild physical exercise and ubiquinol supplementation was able to improve mitochondrial function and preserve skeletal muscle health during aging. 5-month-old SAMP8 mice, in a presarcopenia phase, have been randomly divided into 4 groups (n = 10): untreated controls and mice treated for two months with either physical exercise (0.5 km/h, on a 5% inclination, for 30 min, 5/7 days per week), ubiquinol 10 (500 mg/kg/day), or a combination of exercise and ubiquinol. Two months of physical exercise significantly increased mitochondrial damage in the muscles of exercised mice when compared to controls. On the contrary, ubiquinol and physical exercise combination significantly improved the overall status of the skeletal muscle, preserving mitochondrial ultrastructure and limiting mitochondrial depolarization induced by physical exercise alone. Accordingly, combination treatment while promoting mitochondrial biogenesis lowered autophagy and caspase 3-dependent apoptosis. In conclusion, the present study shows that ubiquinol supplementation counteracts the deleterious effects of physical exercise-derived ROS improving mitochondrial functionality in an oxidative stress model, such as SAMP8 in the presarcopenia phase.

Original languageEnglish
Number of pages1
JournalOxidative Medicine and Cellular Longevity
Volume2018
DOIs
Publication statusPublished - Jan 1 2018

Fingerprint

coenzyme Q10
Muscle
Exercise
Skeletal Muscle
Oxidative stress
Aging of materials
Oxidative Stress
Muscle Mitochondrion
Premature Aging
Muscles
Mitochondria
Autophagy
Depolarization
Organelle Biogenesis
Caspase 3

ASJC Scopus subject areas

  • Biochemistry
  • Ageing
  • Cell Biology

Cite this

Combination of Coenzyme Q10 Intake and Moderate Physical Activity Counteracts Mitochondrial Dysfunctions in a SAMP8 Mouse Model. / Andreani, C.; Bartolacci, C.; Guescini, M.; Battistelli, M.; Stocchi, V.; Orlando, F.; Provinciali, M.; Amici, A.; Marchini, C.; Tiano, L.; Orlando, P.; Silvestri, S.

In: Oxidative Medicine and Cellular Longevity, Vol. 2018, 01.01.2018.

Research output: Contribution to journalArticle

Andreani, C. ; Bartolacci, C. ; Guescini, M. ; Battistelli, M. ; Stocchi, V. ; Orlando, F. ; Provinciali, M. ; Amici, A. ; Marchini, C. ; Tiano, L. ; Orlando, P. ; Silvestri, S. / Combination of Coenzyme Q10 Intake and Moderate Physical Activity Counteracts Mitochondrial Dysfunctions in a SAMP8 Mouse Model. In: Oxidative Medicine and Cellular Longevity. 2018 ; Vol. 2018.
@article{a4ce5123a7ff45928dc33c0b1de6d471,
title = "Combination of Coenzyme Q10 Intake and Moderate Physical Activity Counteracts Mitochondrial Dysfunctions in a SAMP8 Mouse Model",
abstract = "Aging skeletal muscles are characterized by a progressive decline in muscle mass and muscular strength. Such muscular dysfunctions are usually associated with structural and functional alterations of skeletal muscle mitochondria. The senescence-accelerated mouse-prone 8 (SAMP8) model, characterized by premature aging and high degree of oxidative stress, was used to investigate whether a combined intervention with mild physical exercise and ubiquinol supplementation was able to improve mitochondrial function and preserve skeletal muscle health during aging. 5-month-old SAMP8 mice, in a presarcopenia phase, have been randomly divided into 4 groups (n = 10): untreated controls and mice treated for two months with either physical exercise (0.5 km/h, on a 5{\%} inclination, for 30 min, 5/7 days per week), ubiquinol 10 (500 mg/kg/day), or a combination of exercise and ubiquinol. Two months of physical exercise significantly increased mitochondrial damage in the muscles of exercised mice when compared to controls. On the contrary, ubiquinol and physical exercise combination significantly improved the overall status of the skeletal muscle, preserving mitochondrial ultrastructure and limiting mitochondrial depolarization induced by physical exercise alone. Accordingly, combination treatment while promoting mitochondrial biogenesis lowered autophagy and caspase 3-dependent apoptosis. In conclusion, the present study shows that ubiquinol supplementation counteracts the deleterious effects of physical exercise-derived ROS improving mitochondrial functionality in an oxidative stress model, such as SAMP8 in the presarcopenia phase.",
author = "C. Andreani and C. Bartolacci and M. Guescini and M. Battistelli and V. Stocchi and F. Orlando and M. Provinciali and A. Amici and C. Marchini and L. Tiano and P. Orlando and S. Silvestri",
year = "2018",
month = "1",
day = "1",
doi = "10.1155/2018/8936251",
language = "English",
volume = "2018",
journal = "Oxidative Medicine and Cellular Longevity",
issn = "1942-0900",
publisher = "Hindawi Limited",

}

TY - JOUR

T1 - Combination of Coenzyme Q10 Intake and Moderate Physical Activity Counteracts Mitochondrial Dysfunctions in a SAMP8 Mouse Model

AU - Andreani, C.

AU - Bartolacci, C.

AU - Guescini, M.

AU - Battistelli, M.

AU - Stocchi, V.

AU - Orlando, F.

AU - Provinciali, M.

AU - Amici, A.

AU - Marchini, C.

AU - Tiano, L.

AU - Orlando, P.

AU - Silvestri, S.

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Aging skeletal muscles are characterized by a progressive decline in muscle mass and muscular strength. Such muscular dysfunctions are usually associated with structural and functional alterations of skeletal muscle mitochondria. The senescence-accelerated mouse-prone 8 (SAMP8) model, characterized by premature aging and high degree of oxidative stress, was used to investigate whether a combined intervention with mild physical exercise and ubiquinol supplementation was able to improve mitochondrial function and preserve skeletal muscle health during aging. 5-month-old SAMP8 mice, in a presarcopenia phase, have been randomly divided into 4 groups (n = 10): untreated controls and mice treated for two months with either physical exercise (0.5 km/h, on a 5% inclination, for 30 min, 5/7 days per week), ubiquinol 10 (500 mg/kg/day), or a combination of exercise and ubiquinol. Two months of physical exercise significantly increased mitochondrial damage in the muscles of exercised mice when compared to controls. On the contrary, ubiquinol and physical exercise combination significantly improved the overall status of the skeletal muscle, preserving mitochondrial ultrastructure and limiting mitochondrial depolarization induced by physical exercise alone. Accordingly, combination treatment while promoting mitochondrial biogenesis lowered autophagy and caspase 3-dependent apoptosis. In conclusion, the present study shows that ubiquinol supplementation counteracts the deleterious effects of physical exercise-derived ROS improving mitochondrial functionality in an oxidative stress model, such as SAMP8 in the presarcopenia phase.

AB - Aging skeletal muscles are characterized by a progressive decline in muscle mass and muscular strength. Such muscular dysfunctions are usually associated with structural and functional alterations of skeletal muscle mitochondria. The senescence-accelerated mouse-prone 8 (SAMP8) model, characterized by premature aging and high degree of oxidative stress, was used to investigate whether a combined intervention with mild physical exercise and ubiquinol supplementation was able to improve mitochondrial function and preserve skeletal muscle health during aging. 5-month-old SAMP8 mice, in a presarcopenia phase, have been randomly divided into 4 groups (n = 10): untreated controls and mice treated for two months with either physical exercise (0.5 km/h, on a 5% inclination, for 30 min, 5/7 days per week), ubiquinol 10 (500 mg/kg/day), or a combination of exercise and ubiquinol. Two months of physical exercise significantly increased mitochondrial damage in the muscles of exercised mice when compared to controls. On the contrary, ubiquinol and physical exercise combination significantly improved the overall status of the skeletal muscle, preserving mitochondrial ultrastructure and limiting mitochondrial depolarization induced by physical exercise alone. Accordingly, combination treatment while promoting mitochondrial biogenesis lowered autophagy and caspase 3-dependent apoptosis. In conclusion, the present study shows that ubiquinol supplementation counteracts the deleterious effects of physical exercise-derived ROS improving mitochondrial functionality in an oxidative stress model, such as SAMP8 in the presarcopenia phase.

UR - http://www.scopus.com/inward/record.url?scp=85057134304&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85057134304&partnerID=8YFLogxK

U2 - 10.1155/2018/8936251

DO - 10.1155/2018/8936251

M3 - Article

C2 - 30473743

AN - SCOPUS:85057134304

VL - 2018

JO - Oxidative Medicine and Cellular Longevity

JF - Oxidative Medicine and Cellular Longevity

SN - 1942-0900

ER -