Familial history of hypertension is associated with autonomic dysfunction and increase in blood pressure (BP). However, an active lifestyle has been found to improve a number of health outcomes and reduce all-cause mortality. The aim of the present study was to investigate the effects of an active lifestyle on hemodynamics, heart rate variability (HRV) and oxidative stress markers in offspring of hypertensive parents. One hundred twenty-seven subjects were assigned into four groups: sedentary offspring of normotensives (S-ON) or hypertensives (S-OH); and physically active offspring of normotensives (A-ON) or hypertensives (A-OH). Diastolic BP and heart rate were reduced in the physically active groups when compared to S-OH group. A-ON and A-OH groups presented increased values of RR total variance when compared to the sedentary ones (A-ON: 4,912 ± 538 vs. S-ON: 2,354 ± 159; A-OH: 3,112 ± 236 vs. S-OH: 2,232 ± 241 ms 2 ). Cardiac sympato-vagal balance (LF/HF), systemic hydrogen peroxide and superoxide anion were markedly increased in S-OH group when compared to all other studied groups. Additionally, important correlations were observed between LF/HF with diastolic BP (r = 0.30) and hydrogen peroxide (r = 0.41). Thus, our findings seem to confirm an early autonomic dysfunction in offspring of hypertensive parents, which was associated with a systemic increase in reactive oxygen species and blood pressure. However, our most important finding lies in the attenuation of such disorders in offspring of physically active hypertensives, thus emphasizing the importance of a physically active lifestyle in the prevention of early disorders that may be associated with onset of hypertension.
Familial history of hypertension is associated with autonomic dysfunction and increase in blood pressure (BP). On the other hand, an active lifestyle has been found to improve a number of health outcomes and reduce all‐cause mortality. The aim of the present study was to investigate the effects of an active lifestyle on hemodynamics, heart rate variability (HRV) and oxidative stress markers in offspring of hypertensive parents. One hundred twenty‐seven subjects were assigned into four groups: sedentary offspring of normotensives (S‐ON) or hypertensives (S‐OH); and physically active offspring of normotensives (A‐ON) or hypertensives (A‐OH). The level of physical activity was determined using the International Physical Activity Questionnaire. Heart rate (HR), systolic (SBP) and diastolic BP (DBP) were measured at rest. The assessment of cardiac autonomic modulation was performed by HRV analysis. Oxidant stress was assessed by Hydrogen peroxide concentration, Superoxide anion, Lipid Peroxide levels and Protein Carbonyls measurements in plasma. Diastolic BP and heart rate were reduced in the physically active groups when compared to S‐OH group. A‐ON and A‐OH groups presented increased values of RR total variance when compared to the sedentary ones (A‐ON: 4912±538 vs. S‐ON: 2354±159; A‐OH: 3112±236 vs. S‐OH: 2232±241ms2). Cardiac sympato‐vagal balance (LF/HF), systemic hydrogen peroxide and superoxide anion were markedly increased in S‐OH group when compared to all other studied groups. Systemically, superoxide anion and hydrogen peroxide were increased in S‐OH group when compared to S‐ON group. However, both physically active groups (A‐ON and A‐OH) presented reduced levels of superoxide anion (A‐ON: 41.0±4.1 and A‐OH: 48.3±3.4 vs. S‐OH: 56.7±3.9 nmol/mg of protein) and hydrogen peroxide (A‐ON: 8.95±0.9 and A‐OH: 9.6±1.8 vs. S‐OH: 16.68±2.7 μM) when compared to S‐OH group. Additionally, correlations were observed between LF/HF with diastolic BP (r=0.30, p<0.05) and hydrogen peroxide (r=0.41, p<0.05). Thus, our findings confirm the presence of early autonomic dysfunction in offspring of hypertensive parents, which was associated with a systemic increase in reactive oxygen species and blood pressure. However, our most important finding lies in the attenuation of such disorders in offspring of physically active hypertensives, thus emphasizing the importance of a physically active lifestyle in the prevention of early disorders that may be associated with development of hypertension.Support or Funding InformationFinancial support: UNINOVE, CNPq, CAPES, FAPESP.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The aim this study was to evaluate the effects on hemodynamic, autonomic and inflammatory profile in offspring (from birth to adulthood) of parents submitted to chronic fructose overload. The Fructose genitor group was formed by adult Wistar rats (males and females) that underwent a fructose overload (10%) in drinking water for 60 days. The Control genitor group was formed by adult Wistar rats who were only followed for the same period receiving a standard diet. Mating was carried out and the females continued to receive the same diet (fructose or standard) during all gestation and lactation. On the day of birth, the fructose (F) and control (C) offspring were submitted to an electrocardiogram to analyze heart rate variability (n = 10/group). On the day of weaning two groups were evaluated, the CW group (descendants of the control parents, n = 10) and the FW group (descendants of the fructose parents, n = 10). Another two groups were evaluated 30 days after weaning, group C30 (from control parents, n = 10) and the F30 group (from fructose parents, n = 10). During lifespan, all offspring received a standard diet without fructose. Arterial pressure (AP) were recorded directly. Baroreflex sensitivity was evaluated by increasing dosing of phenylephrine and sodium nitroprusside. Cardiovascular autonomic modulation was evaluated by spectral analysis. Inflammatory profile was measured by ELISA in cardiac tissue. Regarding the autonomic evaluations, the fructose groups presented an impairment from birth to adulthood evidenced by a sympathovagal imbalance (LF/HF) when compared to control groups (F: 0.71 ± 0.08; FW: 0.91 ± 0.08 and F30: 0.72 ± 0.09 vs. C: 0.37 ± 0.04; CW: 0.48 ± 0.07 and C30: 0.38 ± 0.04). Additionally, only the F30 group showed higher vascular sympathetic modulation among groups (4.7 ± 0.6 vs. C30: 2.8 ± 0.4; CW: 1.8 ± 0.4 and FW: 2.9 ± 0.4 mmHg2). Moreover, the fructose groups had a worse tachycardic response when compared to control groups at the same time (FW: −2.8 ± 0.3 and F30: −3.1 ± 0.2 vs. CW: −3.9 ± 0.4 and C30: −4.0 ± 0.1 bpm/mmHg). Finally, group F30 presented worse inflammatory profile compared to group C30, evidenced by the increase of IL‐6 (167.2 ± 9.5 vs C30: 104.9 ± 11.9 pg/ml) and decrease of the IL‐10/TNF alpha ratio (P<0.01). The mean, systolic and diastolic AP was increased only in group F30 when compared to the C30 group (mean AP, F30: 109 ± 1.9 vs. C30: 103 ± 1.3 mmHg). In conclusion, the offspring of parents submitted to fructose overload presented autonomic, hemodynamic and inflammatory cardiovascular dysfunctions. Moreover, the results suggest early autonomic dysfunctions, and these seem to precede hemodynamic and inflammatory changes. These findings suggest cardiovascular autonomic variability as a possible early marker of risk of developing disease in offspring of parents exposed to high fructose consumption. Support or Funding Information FAPESP (2018/17183‐4); CAPES.
In this study we tested the hypothesis that the cardiovascular autonomic dysfunction plays an important role on the management of inflammation and oxidative stress, and that these dysfunctions may in turn be modulated by combined exercise training in an experimental model of hypertension and menopause. Female rats were divided into (n=7/group): control (C) and hypertensive (H), hypertensive ovariectomized (HO) and hypertensive ovariectomized undergoing combined (aerobic+resistance) training (THO). We observed an additional increase in HO group (176±4 mmHg) in relation to H group (165±3 mmHg). However, the THO group (155±3 mmHg) showed a reduction of arterial pressure associated with resting bradycardia. The HO group (50.78±4.61 mmHg2) presented an additional impairment in systolic arterial pressure variability when compared to C and H groups (23.69±0.45 and 34.09±2.37 mmHg2); this dysfunction was not observed in THO group (30.09±2.03 mmHg2). Additionally, an attenuation on vascular sympathetic modulation and an improvement in baroreflex sensitivity were found in the THO when compared to HO group. There was an increase in TNF-α in sedentary hypertensive groups (H and HO vs. C), which was not observed in THO group. Ovariectomy induced an additional increase in cardiac and renal oxidative stress, which were reduced in THO group. The THO group presented an increase in total antioxidant capacity when compared to the other groups. In conclusion, combined exercise training was able to reduce AP associated with improvement on cardiovascular autonomic control, probably reducing cardiac and renal inflammation and oxidative stress, in an experimental model of hypertension and menopause.
Menopause and aging are associated with increased blood pressure. High fructose may modify the development of the pathologies associated with these conditions. The objective was to investigate the effects of exercise training (ET) in aged, oophorectomy mimic of menopause fructose-fed rats. Female Wistar rats (24 months old) were ovariectomized, fed with fructose (100g/L) in drinking water and divided in 5 groups (n=8/group): control (C), ovariectomized (O), ovariectomized trained (OT, n= 8), ovariectomized fructose (OF, n= 8) and ovariectomized fructose trained (OFT, n= 8). The ET was performed on a treadmill (1 h/day; 5 days/wk for 8 wk). The metabolic results showed that ET decreased adipose tissue in both trained groups (OT: 4.3±0.5, OFT: 5.3±0.7), compared with sedentary rats (C: 6.2± 0.6, O: 9.6±1.3, OF: 10.1±0.6, g). The same findings were observed for insulin resistance (OT: 4.6±0.2, OFT: 5.5±0.6 vs C: 3.2± 0.6, O: 3.2±0.3, OF: 4.0±0.5, mg/dl/min). ET increased physical capacity (OT: 20±0.9, OFT: 17.5±0.9 vs C: 11.5± 0.5, O: 10±0.5, OF: 10.3±0.5 Min/h). The hemodynamic results showed that ET attenuated the increase in MBP (C: 109.4± 1.9, OT: 103±1.1, OFT: 107±1.1 vs O: 119.1±1.9, OF: 119.1±2.7, mmHg) and HR (C: 341.4± 8, OT: 302±1, OFT: 306.4±8 vs O: 398.17±19, OF: 378.9±17 Bpm). The sympathetic tonus was decreased in C, OT and OTF (C: 63.6± 4, OT: 62.2±3, OFT: 51.2± 7 beats/ min) when compared with O and OF (O: 102.6±12, OF: 91.9±7 beats/min) while vagal tonus was increased just in OT (OT: 44.8±5) vs (C: 24.9± 6, OFT: 22±3, O: 13±6, OF: 9±2 beats/min). The OT and OTF groups showed an increased bradycardic response to BP changes (C: -1.50±0.06 OT: -1.74±0.12, OFT: -1.77±0.15 vs O: -0.93±0.07, OF: -1.21±0.12 bpm/mmHg). ET increased the Standard deviation of the pulse interval (C: 6.7±1.1 OT: 11.6±0.8, OFT: 13.0±1.5 vs O: 7.05±0.6, OF: 9.57±0.7 ms) and decreased VARR PAS (C: 6.7±1.09 OT: 23.6±0.8, OFT: 30.7±2.6 vs O: 56.4±8.1, OF: 40.5±3.7 mmHg2) as well as representative sympathetic modulation (LF PAS) (C: 6.7±1.1 OT: 3.6±0.5, OFT: 3.7±0.4 vs O: 9.8±1.2, OF: 8.3±0.8 mmHg. In conclusion, ET effectively improved metabolic and cardiovascular parameters altered by aged or excessive fructose consumption in rats submitted to ovarian hormone deprivation.
Purpose: To investigate the mechanoreflex control of respiration and circulation in patients with chronic obstructive pulmonary disease (COPD). Methods: Twenty-eight patients with moderate-to-severe COPD (mean ± SD: 67.0 ± 7.9 yr, 10 women) and 14 age-and sex-matched controls (67.9 ± 2.6 yr, 7 women) participated in the study. Their dominant knee was passively moved to stimulate mechanoreceptors, whereas vastus lateralis surface electrical activity checked active contractions. A differential pressure flowmeter, an electrocardiogram, and a servo-controlled finger photoplethysmograph acquired cardiorespiratory data. To gain insight into the mechanoreflex arc, we further analyzed reduced/oxidized glutathione ratio and mechanoreceptor-related gene expression in a vastus lateralis biopsy of additional nine patients (63.9 ± 8.1 yr, 33% women) and eight controls (62.9 ± 9.1 yr, 38% women). Results: Patients with COPD had a greater peak respiratory frequency response (COPD: Δ = 3.2 ± 2.3 vs Controls: 1.8 ± 1.2 cycles per minute, P = 0.036) and a smaller peak tidal volume response to passive knee movement than controls. Ventilation, heart rate, stroke volume, and cardiac output peak responses, and total peripheral resistance nadir response, were unaltered by COPD. In addition, patients had a diminished glutathione ratio (COPD: 13.3 ± 3.8 vs controls: 20.0 ± 5.5 a.u., P = 0.015) and an augmented brain-derived neurotrophic factor expression (COPD: 2.0 ± 0.7 vs controls: 1.1 ± 0.4 a.u., P = 0.002) than controls. Prostaglandin E receptor 4, cyclooxygenase 2, and Piezo1 expression were similar between groups. Conclusions: Respiratory frequency response to mechanoreceptors activation is increased in patients with COPD. This abnormality is possibly linked to glutathione redox imbalance and augmented brain-derived neurotrophic factor expression within locomotor muscles, which could increase mechanically sensitive afferents' stimulation and sensitivity.
The aim of this study was to verify the effects of three different moderate exercise training protocols (aerobic, resistance and combined (aerobic + resistance)) in a model of metabolic syndrome and menopause on a cardiovascular parameter and oxidative stress. Female SHR rats were divided into (n=8): hypertensive (H), hypertensive ovariectomized submitted to fructose overload (100g/L in drinking water) (HFO), aerobic trained hypertensive ovariectomized submitted to fructose overload (AHOF), resistance trained hypertensive ovariectomized submitted to fructose overload (RHOF) and combined trained hypertensive ovariectomized submitted to fructose overload (CHOF). Arterial pressure (AP) signals were directly recorded. Vascular autonomic modulation was evaluated by spectral analysis. The cardiac oxidative stress was evaluated by lipoperoxidation (LPO) determination. The association of fructose overload and hormone deprivation promoted an increase in AP (HOF: 174±4 vs. H: 146±4 mmHg), heart rate (HOF: 393±10 vs. H: 352±13 bpm), VAR-SAP (HOF: 77.8±11.9 vs H: 31.1±2.6 mmHg2), LF-SAP (HOF: 10.6±2.3 vs H: 5.0±0.9 mmHg2) and LPO, and reduced baroreflex sensitivity (tachycardia response: HOF: 1.06±0.06 vs. H: 1.91±0.17 bpm/mmHg). All exercise training protocols were able to reduce LPO and LF-SAP. It was noted that only the combined exercise training was able in reducing AP (CHOF: 158±4 mm Hg) and heart rate (CHOF: 303±5 bpm). The AP reduction noted only in the CHOF group may be associated with an improve in baroreflex sensitivity, represented by an increase of tachycardic response observed only in the CHOF (1.62±0.1 bpm/mmHg) and in the AHOF (1.54 ±0.07 bpm/mmHg) groups and a reduction of VAR-PAS observed only in the CHOF (30.31±3.85 mmHg 2 ) and in the RHOF (31±2.65 mmHg 2 ) groups. In conclusion, fructose overload induced impairment in hemodynamic, vascular autonomic control and increased oxidative stress in hypertensive rats submitted to ovarian hormones deprivation. However, all exercise training protocols showed a beneficial role. Moreover, the combined exercise training showed additional improvement, suggesting that this could be a better approach than isolated aerobic and resistance training.
Introduction Doxorubicin, has been used as a chemotherapeutic agent, however, it is also associated with significant cardiotoxicity related to an increased oxidative stress (OS). Recent studies have shown that doxorubicin also induces skeletal muscle atrophy in preclinical models. Vitamin C (VC), which presents antioxidant properties, has been used as a pharmacological approach against cardiac toxicity. Nonetheless, the effects of vitamin C on doxorubicin‐induced skeletal muscle atrophy are still unknown. Objective Evaluate the effects of VC on OS parameters in skeletal muscle of rats exposed to doxorubicin. Methods Male Wistar rats divided into 4 groups (C: Control. VC: Vitamin C. D: Doxorubicin and VCD: VC+Dox, n=8‐10/group). Dox was administered in six doses of 2.5 mg/kg, for 3 weeks to obtain a cumulative dose of 15 mg/kg. VC was administered daily (50 mg/kg) orally for six weeks, starting one week before treatment with Dox. The gastrocnemius was weighed and homogenized for OS analysis: antioxidant profile (catalase [CAT], superoxide dismutase [SOD], glutathione peroxidase [GPx] and non‐enzymatic antioxidant capacity [FRAP]), pro‐oxidant (NADPH oxidase, hydrogen peroxide [H2O2], nitrites) and cell damage (protein and lipid oxidation [LPO]). Results Dox reduced the gastrocnemius weight, on the other hand VC prevented it (C: 1.74±0.03; VC: 1.55±0.18; D: 0.99±0.06 and VCD: 1.23±0.06 g). There were no differences in CAT, FRAP, NADPH and nitrites between studied groups. D group showed increased concentration of H2O2 compared to C and VC groups; which was not observed in the VCD group (C: 5.33±0.39; VC: 4.30±1.47; D: 8.72±1.58 and VCD: 3.66±0.73 μM H2O2). SOD was higher in the VCD group compared to the others (C: 8.29±0.61; VC: 8.38±0.48; D: 9.94±0.61 and VCD: 10.38±0.28 USOD/mg protein). GPx was higher in VC and VCD compared to C group and lower in D compared to C and VCD group (C:0.007±0.002; VC: 0.012±0.002; D: 0.009±0.001 and VCD: 0.011±0.001 nmol/mg protein). Protein oxidation was lower in C group compared to the others (C: 3.63± 0.93; VC: 6.98±0.74; D: 5.69±0.49 and VCD: 5.98±0.29 nmol/mg protein). However, LPO was higher in D group compared to C and VC groups, and lower in VCD group compared to D group (C: 342±122; VC:364±153; D: 998±131 and VCD: 389±50 cps/mg protein). Conclusion Vitamin C protects against doxorubicin‐induced skeletal muscle atrophy and oxidative stress, suggesting a potential approach to management cardio functional disorder in patients under doxorubicin treatment.
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