ABC | Volume 112, Nº5, May 2019

Original Article Gomes et al Thermoregulation in hypertensive rats Arq Bras Cardiol. 2019; 112(5):534-542 Table 1 – General characteristics of the animals studied; data expressed as mean ± standard deviation Variable C-WIS (n = 8) T-WIS (n = 8) C-SHR (n = 8) T-SHR (n = 8) Initial BM (g) 390.0 ± 16.9 356.6 ± 23.7 # 258.6 ± 14.7 + 271.3 ± 13.5 + Final BM (g) 462.6 ± 15.8 * 421.0 ± 35.9 * # 326.5 ± 20.9 * + 309.1 ± 24.6 * + Initial SBP (mmHg) 132.2 ± 9.8 123.7 ± 7.6 172.5 ± 14.9 + 189.7 ± 9.6 #+ Final SBP (mmHg) 129.6 ± 7.6 127.8 ± 8.7 190.0 ± 8.4 * + 167.3 ± 16.6 * #+ Initial DBP (mmHg) 84.0 ± 13.2 90.0 ± 13.2 135.5 ± 18.1 + 143.3 ± 17.8 + Final DBP (mmHg) 90.3 ± 7.9 98.5 ± 14.1 144.5 ± 18.6 + 117.3 ± 28.0 * #+ Initial MBP (mmHg) 100.3 ± 10.7 100.8 ± 10.7 147.6 ± 16.1 + 157.7 ± 14.9 #+ Final MBP (mmHg) 104.0 ± 7.3 107.2 ± 13.2 158.6 ± 12.1 + 133.1 ± 22.6 * #+ Initial RHR (bpm) 338.7 ± 19.5 340.2 ± 12.1 374.2 ± 11.0 + 370.1 ± 12.4 + Final RHR (bpm) 337.5 ± 10.7 311.7 ± 12.1 * # 374.2 ± 16.4 + 365.7 ± 18.6 + TET (min) 21.9 ± 1.9 34.8 ± 4.2 # 23.4 ± 2.5 28.4 ± 3.6 #+ C-WIS: control Wistar; T-WIS: trained Wistar, C-SHR: control SHR, T-SHR: trained SHR. BM: body mass; SBP: systolic blood pressure; DBP: diastolic blood pressure; MBP: mean blood pressure; RHR: resting heart rate; TET: total exercise time at week 8 of the incremental test. * p < 0.05: initial vs. final. # p < 0.05: trained vs. controls within same lineage; + p < 0.05: WIS vs. SHR at the same training level increased in all groups after 12 weeks of training. Lower body mass and higher SBP, DBP, MBP and RHR were observed in SHRs compared with Wistar rats. After the exercise program, RHR was significantly lower in Wistar rats, which was not observed in SHRs. Besides, the low-intensity physical training significantly reduced SBP (12%), DBP (18%) and MBP (12%) in T-SHR, whereas the SBP increased in C-SHR after 12 weeks. The exercise training increased physical performance in both Wistar and SHR groups. Also, T-SHR showed lower physical capacity compared with T-WIS. The effects of acute exercise (at 60% of RMS) on Tcore, VO 2 and T skin are described in Figure 1. Hypertension and physical training had no effect on Tcore during moderate exercise (Figure 1A). The T-WIS group showed higher VO 2 (from 6 minutes to 16 minutes, and at the point of fatigue; Figure 1B) and T skin (from 14 minutes to 18 minutes, and at the point of fatigue; Figure 1 C) compared with the WIS-C. The C-SHR group showed higher T skin than the C-WIS (from 13 minutes to 17 minutes; Figure 1C). Low-intensity training had no effect on T skin or VO 2 in SHR during moderate exercise. In addition, a lower T skin was found in the T-SHR group at the point of fatigue compared with the T-WIS (Figure 1C). Figure 2 shows the threshold and sensitivity of heat dissipation during acute exercise. These parameters did not change with hypertension or low-intensity physical training. In addition, neither hypertension nor physical training affected W during acute exercise (Figure 3A). Hypertensive animals showed lower ME compared with normotensive animals, both in control and trained groups (Figure 3B). Also, physical training had no effect on ME in both Wistar and SHR (Figure 3B). Results of HA and HA/W ratio are illustrated in Figure 4. The T-WIS group showed higher HA than the C-WIS (Figure 4A), and the T-SHR had lower HA compared with T-WIS (Figure 4A). However, when HA was corrected for W, no difference was found in the effects of SAH and physical training (Figure 4B). Discussion The present study aimed to evaluate the effects of low‑intensity physical training on thermal balance in hypertensive rats subjected to an acute exercise program. We tested the hypothesis that low-intensity training could promote positive adaptations and ultimately reversal of the changes in the thermal balance of SHRs. For this purpose, we evaluated Tcore, heat production and heat dissipation in response to exercise. Altogether, our results showed that low-intensity physical training did not cause significant changes in the variables related to thermal balance, and thus, our hypothesis was rejected. Thermal balance results from the relationship between heat production and dissipation, 18 resulting in the Tcore regulation within satisfactory limits. During acute physical exercise, heat production occurs before heat dissipation, and consequently Tcore increases more rapidly than dissipation. 19 This dynamics was observed in the present study (Figure 1) for the thermal balance variables in all experimental groups, i.e ., for heat production (VO 2 ), heat dissipation (T skin ) and resulting outcome (Tcore). Throughout the exercise session, the Tcore threshold for heat dissipation is achieved and the thermoeffector response of heat dissipation occurs, measured by vasodilation in the tail skin. These adaptations allow achievement of thermal balance and regulation of Tcore within adequate limits, 20 which was also observed in our study. An important adjustment, commonly reported in the literature, that confirms this pattern of response is the absence of vasodilation, and even occurrence of vasoconstriction, in the animals’ tails in the beginning of exercise 19 (Figure 1C). Although recent studies of our group have shown that untrained SHR show disturbances in the regulation of body temperature during acute exercise, findings of the present study do not confirm the hypothesis that these thermal balance changes could be reversed by low-intensity aerobic physical training. In these previous studies, untrained SHR showed higher Tcore during constant-intensity acute exercise (60% 536