Changes in Oxidative and Nitrosative Stress Indicators and Vascular Endothelial Growth Factor After Maximum-Intensity Exercise Assessing Aerobic Capacity in Males With Type 1 Diabetes Mellitus.

Łukasz Tota,Małgorzata Morawska-Tota,Tomasz Klupa,Maciej T Malecki,Bartłomiej Matejko,Tomasz Pałka,Wanda Pilch,Sandra Mrozińska

doi:10.3389/fphys.2021.672403

Abstract

In type 1 diabetes mellitus (T1DM), chronic hyperglycemia causes reactive oxygen and nitrogen species production. Exercise alters the oxidant-antioxidant balance. We evaluated the aerobic capacity and oxidant-antioxidant balance changes after maximum-intensity exercise in T1DM patients. The study involved 30 T1DM participants and 23 controls. The patients’ average age was 23.4 ± 5.1 years, with a body mass index of 24.3 ± 3.1 kg m–2 and with satisfactory glycemic control. Among the controls, the respective values equaled 24.7 ± 2.9 years and 22.9 ± 2.1 kg m–2. Aerobic capacity was assessed with a treadmill test. Peak minute oxygen uptake was significantly lower in T1DM compared with the controls (44.7 ± 5.7 vs. 56.0 ± 7.3 mL kg–1 min–1). The total oxidant capacity measured by total oxidative status/total oxidative capacity (TOS/TOC) equaled 321.5 ± 151 μmol L–1 before and 380.1 ± 153 μmol L–1 after exercise in T1DM, and 164.1 ± 75 and 216.6 ± 75 μmol L–1 in the controls (p < 0.05 for all comparisons). A significant difference in the ratio of total antioxidant status/total antioxidant capacity (TAS/TAC) between the groups after the treadmill test was observed (p < 0.05). Nitrosative stress indicators where significantly higher in the T1DM group both before and after the exercise. In conclusion, diabetic patients demonstrated a lower aerobic capacity. The TOS/TOC and nitrosative stress indicators were significantly higher in T1DM before and after the test.

Highlights

IntroductionThe production of reactive oxygen and nitrogen species (RONS) is intensified by biochemical pathways associated with hyperglycemia, such as through glucose autoxidation, non-enzymatic glycation of proteins, mitochondrial overproduction of RONS, overproduction and activation of kinase C, Aerobic Capacity and Oxidant-Antioxidant Imbalance xanthine oxidation, as well as the intensification of aldol and polyol reductase pathways (Martín-Gallán et al, 2007)
Chronic hyperglycemia is the main cause of diabetic complications
Despite the high toxicity of free radicals, a small amount of reactive oxygen and nitrogen species is necessary for proper cell function; their excessive production or insufficient antioxidant defense of the human body may lead to intracellular damage

Summary

Introduction

The production of reactive oxygen and nitrogen species (RONS) is intensified by biochemical pathways associated with hyperglycemia, such as through glucose autoxidation, non-enzymatic glycation of proteins, mitochondrial overproduction of RONS, overproduction and activation of kinase C, Aerobic Capacity and Oxidant-Antioxidant Imbalance xanthine oxidation, as well as the intensification of aldol and polyol reductase pathways (Martín-Gallán et al, 2007). Free radicals react with the molecules that comprise the basic cell structure, such as proteins, lipids, and nucleic acids, and distort their biological function (Frijhoff et al, 2015). This phenomenon is referred to as oxidative stress (Frijhoff et al, 2015; Ighodaro, 2018). Its occurrence in diabetes results from an increase in the level of free radicals, as well as disturbances in the activity of endogenous enzymatic antioxidants and a decrease in the concentration of low-molecular-weight antioxidants (Brownlee, 2001)

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