In human medicine, exercise testing (ET) is considered as a practical method, which provides to give important informations about the stage of heart failure. It is useful to formulate a accurate prognosis. The test is based on the response to physical effort by the subjective perception of fatigue, electrocardiographic monitoring, and blood pressure measure (Lainchbury and Richards 2002). The feasibility of ET in patients with congestive heart failure has been investigated in dogs by Kittleson et al. (1996), using submaximal test and measurements of lactate threshold and venous oxygen tension. More recently, Boddy et al. (2004) evaluated the suitability of the 6 min walk test in dogs. However, although the 6 min walk test is simple, it is not based on a full objective evaluation. Indeed, several elements may affect the distance walked in 6 min by a dog, such as the pace of the person walking the dog or the presence of distracting stimuli such as people, animals, or noise in the surrounding environment. One of the primary problems encountered by Kittleson and collegues was the unwillingness of approximately 50 % of the dogs to walk on a treadmill. In our study, none of the patients appeared reluctant undergo the test, probably because the owners were allowed to walk on the treadmill with their dogs.

The increased level of lactate above the physiological ranges suggested that all dogs were subjected to a submaximal physical effort. The failure to increase levels of cTn in subjects of the control group is partially in agreement with those reported in humans and in the horse: cTnI does not undergo significant changes during exercise in healthy subjects (Eijsvogels et al. 2010; Nostell and Häggström 2008). Unlike the significant increase of cTnI in patients of group B (asymptomatic subjects with valve disease) occurred at higher speeds where suggested that exercise may induce myocardial suffering, evidenced by the increase of these values. The significant increase of cTnI if not exceeding the references range for the dog may indicate the presence of a myocardial insult mild and of short duration, such as not to exceed the physiological threshold of cTnI. The release of cTnI could be related to the increase in myocardial work and to higher demand of oxygen or as consequence of oxidative stress triggered in patients by with valve dysfunction by various factors, such as wall stress, spasm coronary artery, and ischemia. Although in our case, the increase in cTnI during treadmill exercise in subjects on class I New York Heart Association (NYHA) was not associated with the signs of exercise intolerance. Then, this parameter can be defined a good indicator of exercise tolerability. In human patients, it has been demonstrated that troponin-I reaches the peak plasma concentration approximately 6 h after acute myocardial damage (Schober et al. 2002).

A similar peak was observed with serum troponin-I in rats after a prolonged and intense. Our study has shown that concentrations of cTnI were raised 2 h after the end of exercise test and remained increased in hours later. The lack of variation of cTnT in control group would seem to be connected to a diagnostic sensitivity of cTnI greater than the cTnT, which seems to have a greater prognostic value (Schober et al. 2002). In conclusion, our study suggests that intensity and duration of exercise can lead to myocardial suffering, undetectable except through objective parameters such as the measurement of cTnI.