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Mary Boudreau Conover BSNed

Oxidants are a normal product of aerobic metabolism, but under stress they carry an over abundance of oxygen molecules that contain unpaired electrons, called free radicals. Electrons normally come in pairs. When unpaired, they are highly reactive because of their physiological need to  be paired with another electron. In an effort to satisfy this need, they start a chain reaction that can damage or kill the cell under attack. This damage extends to all components and functions of the cell, including proteins, lipids, DNA, and cell signaling. Oxidative stress exists when oxidants are being produced at elevated rates and there are not enough antioxidants to disarm them. This lack of sufficient antioxidants occurs when our cells are exposed to harmful conditions, such as intense endurance exercise, and dietary factors.

Second hand smoke. Several recent studies have also demonstrated that chronic cigarette exposure from second-hand smoke, can result in significant damage to the heart, characterized by the progressive and irreversible deterioration of cardiac function because of myocardial scarring, thickening, and remodeling. At the cellular level studies have shown damage to adenosine triphosphate (ATP), those power house intracellular organeles in charge of energy production, calcium storage, and the electrophysiology of the mitochondria.1-4

Exercise can protect. The authors of these studies emphasized that exercise protocols of moderate intensity increase the body’s antioxidant defenses and tissue resistance to oxidative organ damage.5 6 Key factors in evaluating the response of the heart and other organs to the oxidative stress of exercise are the type, intensity, frequency, and duration of the exercise.7  This is an important consideration for anyone who is engaging in intense endurance exercise, which inactivates vital enzymes present in the cell membranes of the heart8 and elevates lipid markers for oxidative stress in that organ.8


1. Armani C, Landini L Jr, Leone A. Molecular and biochemical changes of the cardiovascular system due to smoking exposure. Curr Pharm Des. 2009;15:1038-1053.

2. Leone A, Landini L Jr, Biadi O, Balbarini A. Smoking and cardiovascular system: Cellular features of the damage. Curr Pharm Des. 2008;14:1771- 1777.

3. Minicucci MF, Azevedo PS, Paiva SA, Zornoff LA. Cardiovascular remodeling induced by passive smoking. Inflamm Allergy Drug Targets. 2009;8:334-339.

4. Knight-Lozano CA, Young CG, Burow DL, Hu ZY, Uyeminani D, Pinkerton KE, et al. Cigarette smoke exposure and hypercholesterolemia increase mitochondrial damage in cardiovascular tissues. Circulation. 2002;105:849.

5. Pinho RA, Andrades ME, Oliveira MR, et al: Imbalance in SOD/CT activities in rat skeletal muscles submitted to treadmill training exercise, Cell Biol Internat, 30:848-853; 2006.
6. Gomez-Cabrera MC, Domenech E, Ji LL, Via J: Exercise as an antioxidant: It upregulates important enzymes for cell adaptations to exercise, J SCI Med Sport, 2006;21:85-89.

7. Pinho RA, Andrades ME, Oliveira MR, et al: Imbalance in SOD/CT activities in rat skeletal muscles submitted to treadmill training exercise, Cell Biol Internat, 30:848-853; 2006.

8. Mastaloudis A, Leonard SW, Traber MG: Oxidative stress in athletes during endurance exercise, Free Radical Bio Med, 2001;31:911-922.

No Equipment Workout:

*Run 400M, do 20 air squats, 4 rounds ~GO!
*please warm up appropriately
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