Circulating cell free DNA response to exhaustive exercise in average trained men with type I diabetes mellitus

Abstract

It is believed that neutrophils extracellular traps (NETs) formation is responsible for the increase in cf DNA after exercise. Since T1DM is accompanied by enhanced NETs generation, we compared exercise-induced increase in cf DNA in 14 men with T1DM and 11 healthy controls and analyzed its association with exercise load. Subjects performed a treadmill run to exhaustion at speed corresponding to 70% of their personal VO2max. Blood was collected before and just after exercise for determination of plasma cf nuclear and mitochondrial DNA (cf n-DNA, cf mt-DNA) by real-time PCR, blood cell count and metabolic markers. Exercise resulted in the increase in median cf n-DNA from 3.9 ng/mL to 21.0 ng/mL in T1DM group and from 3.3 ng/mL to 28.9 ng/mL in controls. Median exercise-induced increment (∆) in cf n-DNA did not differ significantly in both groups (17.8 ng/mL vs. 22.1 ng/mL, p = 0.23), but this variable correlated with run distance (r = 0.66), Δ neutrophils (r = 0.86), Δ creatinine (r = 0.65) and Δ creatine kinase (r = 0.77) only in controls. Pre- and post-exercise cf mt-DNA were not significantly different within and between groups. These suggest low usefulness of Δ cf n-DNA as a marker of exercise intensity in T1DM men.

Mitochondrial DNA and Exercise: Implications for Health and Injuries in Sports

“…Oxygen uptake and its mitochondrial utilization influence exercise capacity-the maximum individual tolerance to physical effort. In response to acute exercise, in skeletal muscle, the transcription cofactor PGC-1α can be activated by silent mating type information regulation 2 homolog 1 (SIRT1), calcineurin A, Ca 2+ /calmodulindependent protein kinase IV, AMP-activated protein kinase (AMPK), and ROS [10]. PGC-1α then induces the activation of nuclear respiratory factor-1 (NRF1) and -2 (NRF2).…”

“…NRF1 and NRF2 stimulate mitochondrial transcription factor A (TFAM), which translocates into the mitochondria and initiates the replication and transcription of mtDNA [11]. This process promotes the proper formation of electron transport chain multisubunit complexes and an increment of mitochondrial metabolic capacity [10]. In addition, PGC-1α can control ROS levels, which increase during exercise, thanks to the binding between NRF2 and antioxidant response elements (ARE) [12].…”

Exhaustive Exercise Increases Spontaneous but Not fMLP-Induced Production of Reactive Oxygen Species by Circulating Phagocytes in Amateur Sportsmen

“…In our previous studies, an exhaustive treadmill run executed according to the same protocol caused an increase in plasma cf n-DNA and citrullinated H3 histone in healthy average trained men and in those with type 1 diabetes [ 7 , 34 , 43 ]. These two biomolecules belong to the markers of neutrophil extracellular traps (NETs) formation [ 44 , 45 ], and it is believed that NETs formation is involved in the immune-metabolic response to strenuous exercise [ 6 , 46 ].…”

The effects of HIIT/MICT on the inhibition of fat accumulation during training and detraining

“…More detraining duration may stimulate the adipocyte proliferation. [44] What's more, exhaustive exercise caused damaged to cellular DNA which accelerated the process of apoptosis and decreased the mature adipocyte numbers, thus, it may contribute to the reduction of adipose tissue mass and maintained it after training cessation [41,45].…”