Cardiorespiratory measurements and indices of oxidative stress in exercising COPD horses

The effect of a COPD crisis on arterial blood gases, heart rate, lactate and indices of oxidative stress were investigated before, during and 1 h after a 'run up to fatigue' in 6 COPD horses. They were investigated twice, randomly: once in acute crisis (C) and once in clinical remission (R). Arterial and mixed venous blood samples were collected and analysed for partial pressures in O2 and CO2. The mixed venous blood was also analysed for plasma lactate (LA) and packed cell volume (PCV), as well as for indices of oxidative stress, i.e. reduced glutathione, glutathione disulphide, glutathione redox ratio (GRR) and lipid hydroperoxides (LPH). The exercise test was an effort of increasing intensity on a treadmill at 0% slope, which was stopped when the horses showed signs of exhaustion. Their performance was evaluated by the number of steps and the running time in the last step. Heart rate was monitored continuously during the test. Blood sampling was performed before, just after and 1 h after the end of the test. The COPD crisis significantly reduced the time to fatigue. However, despite the fact that the exercise intensity and length were lower, peak HR and peak LA were similar in C and R, while arterial hypoxaemia and hypercapnia, and PCV were significantly higher in C, indicating a higher physiological stress in this condition. By contrast, the oxidative stress seemed to be higher in R than in C as suggested by the fact that, 1 h after exercise, GRR and LPH were significantly increased with regards to their pre-exercise values in R and not in C. The fact that exercise did not induce an oxidative stress in C could be partly related to (1) the lower exercise intensity reached by the horses, and (2) to the more severe hypoxaemia experienced in this condition. In conclusion, COPD horses in acute crisis show a significant decrease in performance. The reasons for this exercise intolerance remain unclear, but do not appear to be related to any increase of the oxidative stress in C.