Acute and chronic varied exercise intensity effects on total antioxidant capacity and protein carbonylation.

Exercise is known to have positive physiological adaptations to increase various aspects of health. However, during the course of exercise a significant amount of reactive oxygen species (ROS) are produced via increased metabolism. If not counteracted, ROS can oxidize proteins, lipids, and DNA, potentially leading to a disease state. Oxidized proteins may result in protein carbonyls, a marker of damage, particularly in plasma, and can be the result of increased ROS production during exercise metabolism. This could also initiate a cellular signal cascade up‐regulating the expression of antioxidants. Antioxidants are any substance that can delay or prevent oxidation of substrates and are classified as enzymatic (low molecular weight proteins that act by detoxifying free‐radicals in cells) or nonenzymatic (small molecules that directly scavenge ROS). Recently, total antioxidant capacity (TAC) has been utilized to illustrate general antioxidant defenses. Methods Eighteen of a 36 cohort of healthy, overweight (body mass: 87.64 kg; height: 1.68 m) middle‐aged women (age 43.89 years) randomized into two groups, exercised at HIGH (80% VO 2peak ) and LOW (40% VO 2peak ) aerobic intensity, along with identical resistance and flexibility training, were measured. Subjects exercised five days/week for 20 weeks with at least 85% adherence. Subjects were tested pre‐training, 10‐, and 20‐weeks in the laboratory where they underwent a maximal graded exercise (max GXT) test to assess fitness changes and other parameters. Venous blood samples were collected before and after the max GXT. TAC was assessed via spectrophotometry. Plasma samples were depleted of Albumin and IgG to remove the highly abundant proteins. Carbonlyated proteins were marked via 2,4‐Dinitrophenylhyrazine followed by one‐dimensional polyacrylamide gel electrophoresis and western blotting to determine the amount of carbonylation that occurred over the 20‐week period. Results TAC was significantly increased pre‐training following the max GXT in the LOW group and remained consistent over the 20‐week period, whereas the HIGH group was consistent but had a significant increase following the max GXT at 10‐weeks. Protein carbonylation had a significant decline from pre‐training to 10‐weeks in the HIGH group. The LOW group had significant increases in content between pre‐training and 20‐weeks and 10‐ to 20‐weeks. Discussion The highest record levels of TAC occurred (post‐exercise in the LOW group pre‐training), was where the lowest total protein carbonylation was seen. The highest TAC levels in the HIGH group occurred at 10‐weeks post‐exercise which is also where the lowest protein carbonyls in the HIGH group occurred. There was a steady increase in the protein carbonyls in the LOW group with significant differences seen between pre‐training and 20‐weeks and 10‐ to 20‐weeks. It is plausible that when TAC increased over what was a very similar response during the 20‐weeks of training, the consequence was a decrease in protein carbonyls at those times, indicating a protective effect. Support or Funding Information Research reported in this (publication, project, release) was supported by an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under grant number P20GM103449. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of NIGMS or NIH.