| Literature DB >> 29093566 |
Janaina de O Brito-Monzani1, Iris Callado Sanches2, Nathalia Bernardes3, Kátia Ponciano2, Ivana C Moraes-Silva4, Maria-Cláudia Irigoyen4, Susana Llesuy5, Kátia De Angelis3.
Abstract
We tested whether hypertension favors the development of additional cardiometabolic changes in fructose-fed ovariectomized rats and how it affects aerobic exercise training (ET) effects. All rats received fructose in drinking water (10%) beginning at weaning, were ovariectomized at 10 weeks of age and divided into the normotensive sedentary (NFOS) and trained (NFOT) and hypertensive sedentary (HFOS) and trained (HFOT) groups. ET was performed on a treadmill. Arterial pressure (AP) was directly recorded; heart rate and AP variabilities were analyzed. Lipoperoxidation (LPO) and antioxidant enzyme levels were measured in the left ventricle. In addition to increased AP levels, when compared with the NFOS group, the hypertensive groups had resting tachycardia, a reduction of 29% in the pulse interval variance (VAR-PI), 19% in RMSSD (root mean square of successive differences, a cardiac parasympathetic index) and 53% in the α-index (spontaneous baroreflex), while the systolic AP variance (VAR-SAP) and its low-frequency band (LF-SAP) were sharply increased. ET did not alter AP levels. Even in the presence of hypertension, ET induced resting bradycardia, decreases of 33% in VAR-SAP and 49% in LF-SAP, and an increase of more than 60% in VAR-PI and the α-index. However, some of these parameters were still impaired relative to those of normotensive rats. LPO was reduced and catalase was increased in both trained groups, with no difference between the normotensive and hypertensive groups. Negative correlations were obtained between LPO and RMSSD (r=-0.60, P<0.05) and α-index (r=-0.63, P<0.05). In conclusion, hypertension augmented the dysfunctions in fructose-fed ovariectomized rats and attenuated metabolic aerobic ET benefits. These changes may be related to cardiovascular autonomic and oxidative stress alterations.Entities:
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Year: 2017 PMID: 29093566 DOI: 10.1038/hr.2017.94
Source DB: PubMed Journal: Hypertens Res ISSN: 0916-9636 Impact factor: 3.872