The Acute Effects of Exercise and Temperature on Regional mtDNA.

Mark L Mcglynn,Halee Schnitzler,Robert Shute,Brent Ruby,Dustin Slivka

doi:10.3390/ijerph18126382

Abstract

A reduced mitochondrial DNA (mtDNA) copy number, the ratio of mitochondrial DNA to genomic DNA (mtDNA:gDNA), has been linked with dysfunctional mitochondria. Exercise can acutely induce mtDNA damage manifested as a reduced copy number. However, the influence of a paired (exercise and temperature) intervention on regional mtDNA (MINor Arc and MAJor Arc) are unknown. Thus, the purpose of this study was to determine the acute effects of exercise in cold (7 °C), room temperature (20 °C), and hot (33 °C) ambient temperatures, on regional mitochondrial copy number (MINcn and MAJcn). Thirty-four participants (24.4 ± 5.1 yrs, 87.1 ± 22.1 kg, 22.3 ± 8.5 %BF, and 3.20 ± 0.59 L·min−1 VO2peak) cycled for 1 h (261.1 ± 22.1 W) in either 7 °C, 20 °C, or 33 °C ambient conditions. Muscle biopsy samples were collected from the vastus lateralis to determine mtDNA regional copy numbers via RT-qPCR. mtDNA is sensitive to the stressors of exercise post-exercise (MIN fold change, −1.50 ± 0.11; MAJ fold change, −1.70 ± 0.12) and 4-h post-exercise (MIN fold change, −0.82 ± 0.13; MAJ fold change, −1.54 ± 0.11). The MAJ Arc seems to be more sensitive to heat, showing a temperature-trend (p = 0.056) for a reduced regional copy number ratio after exercise in the heat (fold change −2.81 ± 0.11; p = 0.019). These results expand upon our current knowledge of the influence of temperature and exercise on the acute remodeling of regional mtDNA.

Highlights

The ratio of mitochondrial DNA to genomic DNA, i.e., mtDNA copy number, has been widely used to quantify mitochondria found within tissue [1,2,3,4,5,6]
When mtDNA is damaged, unlike genomic DNA, errors are often left unrepaired and can persist within the mitochondria. These persisting mtDNA errors, potentially due to increased reactive oxygen species (ROS), have been associated with mitochondrial dysfunction linked to the aging process and many common diseases, e.g., Alzheimer’s disease, diabetes mellitus, and cancer [1,2,3,4,6]
The Major Arc (MAJ) region has been highly linked with diseases associated with dysfunctional mitochondria presenting as a reduced MAJ copy number (MAJcn)

Summary

Introduction

The ratio of mitochondrial DNA (mtDNA) to genomic DNA (gDNA), i.e., mtDNA copy number (mtDNA/gDNA), has been widely used to quantify mitochondria found within tissue [1,2,3,4,5,6]. When mtDNA is damaged, unlike genomic DNA (gDNA), errors are often left unrepaired and can persist within the mitochondria. These persisting mtDNA errors, potentially due to increased reactive oxygen species (ROS), have been associated with mitochondrial dysfunction linked to the aging process and many common diseases, e.g., Alzheimer’s disease, diabetes mellitus, and cancer [1,2,3,4,6]. The mtDNA plasmid can be broken down into two regions, the Minor Arc (MIN) and the Major Arc (MAJ) The locations of these regions and the unique steps of mtDNA transcription place the MAJ at greater risk for transcriptional errors [9]. The MAJ region has been highly linked with diseases associated with dysfunctional mitochondria presenting as a reduced MAJ copy number (MAJcn)

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