Rationale:

Strenuous exercise in animal studies has been shown to cause acute oxidative stress due to the generation of oxygen-centered free radicals reflected in lower levels of Glutathione (GSH), higher levels of Glutathione Disulfide (GSSG), and a drop in GSH:GSSG ratios, the maintenance of which is crucial for a variety of cell functions. Human studies on this topic are limited, and in subjects with CAD are lacking.

Purpose:

The purpose of this study was to verify the validity of using a maximal treadmill GXT (Modified Bruce Protocol) as a model to induce acute oxidative stress, with full recovery at 60 minutes post exercise in subjects with CAD.

Methodology:

Twenty subjects with CAD (10 males, and 10 females; age = 63.1 +/- 4 y, weight = 89.4 +/- 7 Kg, and height = 174.9 +/- 12 cm, max Vo2 = 26.2 ml*Kg^-1*min^-1) were used as a sample of convenience. Venous blood samples for GSH, and GSSG were collected directly before, immediately after, and 60 minutes post max GXT. A 2 factor mixed model repeated measures ANOVA was used for data analysis.

Results:

As an acute response to maximal exercise, the GSH levels dropped significantly from a resting baseline value of 1002 [mu]M to an immediate post max GXT value of 780 [mu]M. The GSSG levels significantly increased from 2.6 [mu]M to 3.4 [mu]M. The GSH:GSSG ratio levels significantly dropped from baseline 385 to 229 post exercise. The blood GSH, GSSG, and GSH:GSSG ratios levels showed no significant difference at 60 minutes post max GXT when compared to resting values, indicating full recovery.

Conclusion:

The current data indicated that in subjects with CAD a maximal treadmill GXT is a valid model for inducing acute oxidative stress, with full return to resting baseline levels within 60 minutes of recovery. The potential for using this model in assessing oxidative stress responses to cardiac and pulmonary rehabilitation is of clinical interest with a need for further investigation.