ABC | Volume 112, Nº5, May 2019

Original Article Gomes et al Thermoregulation in hypertensive rats Arq Bras Cardiol. 2019; 112(5):534-542 Figure 2 – Heat dissipation threshold (ºC) (A) and sensitivity (B) during the acute physical exercise protocol. Data expressed as mean ± SD. C-WIS: control Wistar, T-WIS: trained Wistar, C-SHR: control SHR, T-SHR: trained SHR. 40 39 38 37 36 12 10 8 6 4 2 0 C-WIS T-WIS T-SHR C-SHR C-WIS T-WIS T-SHR C-SHR Heat dissipation threshold (ºC) Sensitivity A B intensity. Although the authors did not observe differences in Tcore between groups of animals with different VO 2max throughout one hour of exercise at 60% of VO 2max , when subjected to exercise at similar absolute intensity, these groups showed different Tcore between them. These data suggest that the magnitude of hyperthermia may be associated with the absolute exercise load, regardless of the training status. In the present study, the T-WIS group showed greater heat production compared with the C-WIS group. This may be due to the higher intensity of exercise, which was counterbalanced by higher heat dissipation, resulting in comparable Tcore values in relation to the C-WIS group. Low-intensity physical exercise increased physical capacity in SHR and reduced blood pressure, without promoting resting bradycardia. The mechanisms responsible for the reduction of blood pressure levels in hypertensive rats following aerobic physical training include structural, vascular and neurohumoral adaptations, such as reduction in sympathetic vasomotor activity, 24,25 lower vascular reactivity, 26 reduction in peripheral vascular resistance, 27,28 reduction of oxidative stress, 29 and changes in the endothelium-derived relaxing and contractile factors. 30 Hypertensive animals showed lower ME compared with normotensive animals, as previously described. 7 This could be explained, at least in part, by the higher proportion of type IIA fibers to type I fibers in the soleus muscle, as type I fibers are inherently more efficient than type IIA fibers. 31 The physiological mechanisms responsible for the change of the muscle fiber profile may be associated with microcirculation rarefaction that precedes microvascular apoptosis, which would result in reduction of type I muscle fibers and augmented muscle anaerobiosis. 31 However, the lower ME did not compromised work performance in the SHR group during acute physical exercise. Low-intensity exercise did not increase ME, neither in normotensive nor in hypertensive rats. The present study has some limitations. It is possible that the difference in body mass between hypertensive and normotensive animals may have influenced the changes in Tcore induced by exercise, since the energy cost of running and heat dissipation from the skin depend on body mass. 32 Nevertheless, this limitation is somewhat expected when both normotensive animals and SHR are studied, especially when they are matched by age. 7,8,10 On the other hand, Drummond et 538