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Introduction: Cardiovascular risk increase after ovarian deprivation has been extensively demonstrated by our research group through cardiovascular autonomic analysis. Interventions involving different types of exercises, such as resistance exercises or combined exercises (aerobic and resistance) have been widely recommended to prevent or minimize neuromuscular decline in postmenopausal women, which is aggravated by a sedentary lifestyle. Experimentally, the cardiovascular effects of resistance or combined training, as well as comparison between aerobic, resistance, and combined training, in ovariectomized animals are scarce. Purpose: In this study, we hypothesized that the combination of aerobic and resistance training may be more effective in preventing muscle mass loss, as well as improving cardiovascular autonomic modulation and baroreflex sensitivity, than aerobic or resistance training individually in ovariectomized rats. Animals and Methods: Female rats were divided into 5 groups: sedentary (C); ovariectomized (Ovx); trained ovariectomized submitted to aerobic training (OvxAT); resistance training (OvxRT); combined training (OvxCT). Exercise training lasted 8 weeks, with the combined group alternating between aerobic training and resistance training every other day. At the end of the study, glycemia and insulin tolerance were evaluated. Arterial pressure (AP) was directly recorded. Baroreflex sensitivity was assessed by heart rate response to changes in arterial pressure. Cardiovascular autonomic modulation was evaluated by spectral analysis. Results: Combined training was the only training regime that increased baroreflex sensitivity for tachycardic response and reduced all systolic blood pressure variability parameters. Furthermore, all animals submitted to exercise training on a treadmill (OvxAT and OvxCT) presented lower systolic, diastolic, and mean pressure, as well as improvements in the autonomic modulation for the heart. Conclusion: Combined training showed to be more effective than isolated aerobic and resistance training, mixing the isolated benefits of each modality. It was the only modality able to increase baroreflex sensitivity to tachycardic responses, reduce arterial pressure and all parameters of vascular sympathetic modulation.

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BACKGROUND: Fingolimod slows heart rate (HR) due to vagomimetic effects and might cause additional cardiovascular autonomic changes. While the time course of HR changes is well described, the extent and course of cardiovascular autonomic changes upon fingolimod initiation has not yet been evaluated. This study, therefore, intended to assess cardiovascular autonomic changes during the first 6 h after fingolimod initiation. METHODS: In 21 patients with relapsing-remitting multiple sclerosis (RRMS), we recorded respiration (RESP), electrocardiographic RR interval (RRI), systolic and diastolic blood pressure (BPsys, BPdia) at rest, before and 0.5, 1, 2, 3, 4, 5, and 6 h after fingolimod initiation. We calculated parameters of total autonomic modulation [RRI standard deviation (RRI-SD), RRI coefficient of variation (RRI-CV), RRI-total powers], mainly sympathetic cardiac modulation [RRI low frequency (LF) powers], sympathetic BP modulation (BPsys-LF powers), parasympathetic modulation [square root of the mean squared difference of successive RRIs (RMSSD), RRI high frequency (HF) powers], sympatho-vagal cardiac balance (RRI-LF/HF ratios), and baroreflex sensitivity (BRS). We compared parameters between the eight measurements [analysis of variance (ANOVA) or Friedman test with post-hoc analysis; significance: p < 0.05]. RESULTS: After fingolimod initiation, RESP, BPsys, and BPsys-LF powers remained unchanged while RRIs, RRI-CV, RRI-SD, RRI-total powers, RRI-LF powers, RMSSD, RRI-HF powers, and BRS increased after 1 h and rose to peak values occurring after 5, 1, 2, 2, 1, 4, 4, and 4 h, respectively. After 3 h, BPdia had decreased significantly and was lowest after 5 h. RRI-LF/HF ratios decreased to a nadir after 4 h. CONCLUSIONS: The increases in parasympathetic and overall cardiac autonomic modulation and in BRS seen with fingolimod initiation are theoretically beneficial for the MS patient's cardiovascular system. However, long-term studies must show whether these effects persist or are attenuated (e.g. due to S1P1 receptor down-regulation upon continued fingolimod therapy).

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The cardiovascular system plays a direct role in the maintenance of body temperature. Whether passive heating alters cardiovascular autonomic modulation in conscious rats is still unknown. This study investigated the effects of passive heating on systolic blood pressure variability (SBPV) and heart rate variability (HRV) in conscious rats and the involvement of the renin-angiotensin system in the passive heating effects on SBPV and HRV. Fourteen male Wistar rats were randomly assigned to the control group or the losartan treatment group. A catheter was implanted in the left carotid artery to record pulsatile arterial pressure (PAP), and a telemetry sensor was implanted in the abdominal cavity to measure body temperature (Tbody). After recovering from surgery, the animals were subjected to a passive heating protocol (35°C; 30min) in resting conditions, during which Tbody, tail skin temperature and PAP were measured. The mean arterial pressure, systolic and diastolic blood pressure, heart rate, double product (i.e., the product of systolic blood pressure by heart rate), SBPV and HRV were calculated from the PAP. SBPV and HRV were analyzed in terms of both time and frequency domains. Increases in the thermoregulatory and cardiovascular parameters were observed during passive heating in both groups, and those increases were reflected in the higher time and frequency domains of the SBPV. However, passive heating was not effective in altering HRV. Passive heating altered SBPV but not HRV in conscious rats when they were treated with losartan.

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A hipertensão arterial é frequentemente associada à prejudicada sensibilidade do barorreflexo (SBR). Em ratas espontaneamente hipertensas (SHR), a gravidez reduz a pressão sanguínea, e este efeito tem sido associado ao aumento da biodisponibilidade de óxido nítrico (NO). O aumento da biodisponibilidade do NO tem sido associado a uma SBR restaurada em animais hipertensos. Por isso, testamos a hipótese de que a gravidez melhora a SBR em SHR. Foram realizados experimentos em ratas Wistar e SHR não prenhas (NP) e prenhas (P), sendo dez virgens e dez prenhas em cada grupo, para avaliar a modulação autonômica cardíaca e vasomotora, a SBR em condições basais (espontânea) e após a administração de doses de fenilefrina (FE) e nitroprussiato de sódio (NPS). Séries temporais com valores de intervalo de pulso (IP) e de pressão arterial sistólica (PAS) foram geradas e tiveram espectros calculados pela Transformada Rápida de Fourrier. Em seguida, os espectros foram integrados em bandas de baixa (LF) e alta freqüência (HF), e os poderes das bandas foram tomadas como índices de modulação autonômica cardiovascular. Observamos reduzida pressão arterial média em ratas Wistar prenhas (W-P) e SHR prenhas (SHR-P) quando comparado com ratas NP, no entanto, a frequência cardíaca basal não foi alterada. Em SHR-NP, a análise espectral revelou modulação autonômica cardiovascular alterada quando comparado com os outros grupos (banda de alta LF do espectro PAS e banda de alta HF dos espectros IP). No entanto, em SHR-P os parâmetros autonômicos foram encontrados semelhantes aos observados em ratas WistarNP, sugerindo que a prenhez restaurou as alterações na modulação autonômica. A SBR espontânea não foi alterada em SHR-P quando comparado com W-P. A prenhez reduziu a SBR durante situações de hipotensão no grupo Wistar. A SBR avaliada após a administração de FE ou NPS foi menor em SHR-NP em comparação com Wistar-NP, e não se alterou pela prenhez. Em conclusão, a gravidez não melhorou as SBR em SHR, mas normalizou a alterada modulação vasomotora simpática e a modulação parassimpática cardíaca observados em SHR-NP(AU)

Hypertension is frequently associated to impaired baroreflex sensitivity (BRS). In spontaneously hypertensive rats (SHR), pregnancy reduces blood pressure, and this effect has been associated to increased nitric oxide (NO) availability. Increased NO bioavailability has been linked to improved BRS in hypertensive animals. Therefore, we tested the hypothesis that pregnancy improves the BRS in SHR. Experiments were performed to evaluate the vasomotor and cardiac autonomic modulation, and the BRS at baseline conditions (spontaneous) and after phenylephrine (PE) and sodium nitroprusside (SNP) administrations in female non-pregnant (NP) and pregnant (P) Wistar rats and SHR. Time series with pulse interval (PI) and systolic arterial pressure (SAP) values were generated and had spectra calculated by Fast Fourier Transform. Next, spectra were integrated into low (LF) and high frequency (HF) bands, and the powers of the bands were taken as indexes of cardiovascular autonomic modulation. Reduced mean arterial pressure was observed in Wistar pregnant (W-P) and SHR pregnant (SHR-P) when compared to NP matched rats, however the heart rate was not altered. In SHR-NP, spectral analysis revealed altered cardiovascular autonomic modulation when compared to the other groups (high LF band of the SAP spectra and high HF band of the PI spectra). However, in SHR-P the autonomic parameters were found similar to those observed in Wistar-NP, suggesting that pregnancy prevented changes in autonomic modulation. Spontaneous BRS was not altered in SHR-P when compared to W-P. Pregnancy reduced the BRS during hypotension in Wistar group. BRS assessed with PE and SNP administration was found lower in SHRNP as compared to Wistar-NP, and it was not altered by pregnancy. In conclusion, pregnancy did not improve the BRS in SHR but normalized altered sympathetic vasomotor modulation and parasympathetic cardiac modulation in SHR(AU)

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The objective of the present study was to compare cardiovascular and autonomic responses to a mental stress test and to a maximal isometric exercise test between offspring of normotensive (ON, n = 10) and hypertensive parents (OH, n = 10). Subjects underwent a 3-min Stroop Color Word Test and a maximal isometric exercise test performed in an isokinetic dynamometer with continuous RR interval monitoring. At rest, arterial pressure and heart rate were similar between groups, but there was a significant reduction in total RR interval variance (ON: 5933 ± 493 vs. OH: 2967 ± 390 ms(2)) and an increase in low-high frequency components ratio of heart rate variability (ON: 2.3 ± 0.4 vs. OH: 4.6 ± 0.8) in OH group. In the first minute of the mental stress test and after both tests, the OH group presented increased heart rate as compared with the ON group. After both tests, only the ON group presented an increase in sympathetic component, thus reaching resting values similar to those of the OH group. Our data demonstrated increased resting cardiac sympathetic modulation in offspring of hypertensive parents at similar levels to that observed in offspring of normotensive parents after a mental stress test or a maximal isometric exercise test. Additionally, the exacerbated heart rate responses to these physiological tests in OH subjects may be associated with resting autonomic dysfunction, thus reinforcing these evaluations as important tools for detecting early dysfunctions in this genetically predisposed population.

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