Ventilatory Muscle Training for Early Cardiac Rehabilitation Improved Functional Capacity and Modulated Vascular Function of Individuals Undergoing Coronary Artery Bypass Grafting: Pilot Randomized Clinical Trial.

Background: Cardiac rehabilitation with aerobic exercises is the first strategy for nonpharmacological treatment in the postoperative period of individuals undergoing coronary artery bypass grafting (CABG) to improve functional capacity and vascular health. However, other exercise modalities remain uncertain regarding the same benefits. Objectives: Evaluation of the effect of different modalities of exercise, such as early cardiac rehabilitation on subjects submitted to CABG in the six-minute walk test (6-MWT) and on the percentage of flow-mediated dilatation (FMD) of the brachial artery. Methods: A randomized clinical trial in which 15 patients (62.7 ± 6.7 years) who underwent CABG were randomly assigned to the following groups: isometric (IG, Handgrip Jamar®), ventilatory muscle training (VG, PowerBreathe®) and control (CG, conventional respiratory and motor physiotherapy). All patients were attended to physically twice a day (20 min/session) for a consecutive week after the CABG (hospital admission). Functional capacity was assessed by 6-MWT and endothelial function was assessed through the technique of FMD, before and after (~7 days) admission to CABG. The doppler ultrasound videos were analyzed by Cardiovascular Suite® software (Quipu, Pisa, Italy) to measure %FMD. Statistics: Generalized estimation equation, followed by Bonferroni post hoc (p < 0.05). Results: Systolic, diastolic and mean arterial pressure (SBP/DBP/MAP, respectively) were 133, 76 and 95 mmHg. The groups presented walking meters (m) distance before and after intervention of: IGbasal 357.80 ± 47.15 m vs. IGpost 306.20 ± 61.63 m, p = 0.401 (+51 m); VGbasal 261.50 ± 19.91 m vs. VGpost 300.75 ± 26.29 m, p = 0.052 (+39 m); CG basal 487.83 ± 83.23 m vs. CGpost 318.00 ± 31.08, p = 0.006 (−169 m). %FMD before and after intervention was IGbasal 10.4 ± 4.8% vs. IGpost 2.8 ± 2.5%, p = 0.152; VGbasal 9.8 ± 5.1% vs. VGpost 11.0 ± 6.1%, p = 0.825; CGbasal 9.2 ± 15.8% vs. CGpost 2.7 ± 2.6%, p = 0.710 and resting mean basal blood flow was IGbasal 162.0 ± 55.0 mL/min vs. IGpost 129.9 ± 63.7 mL/min, p = 0.662; VGbasal 83.74 ± 12.4 mL/min vs. VGpost 58.7 ± 17.1 mL/min, p = 0.041; CGbasal 375.6 ± 183.7 mL/min vs. CGpost 192.8 ± 115.0 mL/min, p = 0.459. Conclusions: Ventilatory muscle training for early cardiac rehabilitation improved acute functional capacity and modulated mean flow of individuals undergoing CABG.

Individuals with controlled hypertension show endothelial integrity following a bout of moderate-intensity exercise: randomized clinical trial.

To examine the acute effects of aerobic exercise (AE), resistance exercise (RE) or combined exercise (CE) on flow-mediated dilation (FMD), progenitor cells (PCs), endothelial progenitor cells (EPCs), oxidative stress markers and endothelial-cell derived microvesicles (EMVs) in patients with hypertension. This is a randomized, parallel-group clinical trial involving an intervention of one session of three different modalities of exercise. Thirty-three males (43 ± 2y) were randomly divided into three groups: a session of AE (n = 11, 40 min, cycle ergometer, 60% HRR); a session of RE (n = 11, 40 min, 4 × 12 lower limb repetitions, 60% 1-RM); or a session of CE (n = 11, 20-min RE + 20-min AE). FMD was assessed 10 min before and 10, 40 and 70 min post-intervention. Blood samples were collected at the same time points (except 40 min). FMD were similar in all groups and from baseline (within each group) after a single exercise bout (AE, RE or CE). At 70 min, RE group showed higher levels of PCs compared to the AE (81%) and CE group (60%). PC levels were reduced from baseline in all groups (AE: 32%, p = 0.037; RE: 15%, p = 0.003; CE: 17%, p = 0.048). The levels of EPCs, EMVs and oxidative stress were unchanged. There were no acute effects of moderate-intensity exercise on FMD, EPCs, EMVs and oxidative stress, but PCs decreased regardless of the exercise modality. Individuals with controlled hypertension do not seem to have impaired vascular function in response to a single exercise bout.

Publisher Correction: Different exercise training modalities produce similar endothelial function improvements in individuals with prehypertension or hypertension: a randomized clinical trial.

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Different exercise training modalities produce similar endothelial function improvements in individuals with prehypertension or hypertension: a randomized clinical trial Exercise, endothelium and blood pressure.

Endothelial dysfunction is a characteristic of systemic arterial hypertension (SAH) and an early marker of atherosclerosis. Aerobic exercise training (AT) improves endothelial function. However, the effects of resistance training (RT) and combined training (CT) on endothelial function remain controversial in individuals with SAH. We determined the effects of AT, RT, and CT on endothelial function and systolic (SBP)/diastolic blood pressure (DBP) in individuals with prehypertension or hypertension. Forty-two participants (54 ± 11 y, resting SBP/DBP 137 ± 9/86 ± 6 mmHg) were randomly allocated into AT (n = 14, 40 min of cycling, 50-75% heart rate reserve), RT (n = 14, 6 resistance exercises, 4 × 12 repetitions, 60% maximum strength) and CT (n = 14, 2 × 12 repetitions of RT + 20 min of AT). All participants performed a 40-minute exercise session twice a week for 8 weeks. Endothelial function was evaluated by brachial artery flow-mediated dilation (FMD). Blood pressure was evaluated through ambulatory monitoring for 24 hours. After 8 weeks of exercise training, blood pressure was reduced in all 3 groups: -5.1 mmHg in SBP (95%CI -10.1, 0.0; p = 0.003) in AT; -4.0 mmHg in SBP (95%CI -7.8, -0.5; p = 0.027) in RT; and -3.2 mmHg in DBP (95%CI -7.9, 1.5; p = 0.001) in CT. All 3 exercise training modalities produced similar improvements in FMD: + 3.2% (95%CI 1.7, 4.6) (p < 0.001) in AT; + 4.0% (95%CI 2.1, 5.7) (p < 0.001) in RT; and +6.8% (95%CI 2.6, 11.1) (p = 0.006) in CT. In conclusion, different exercise training modalities were similarly effective in improving endothelial function but impacts on ambulatory blood pressure appear to be variable in individuals with prehypertension or hypertension.

Short-Term Detraining does not Change Insulin Sensitivity and RBP4 in Rodents Previously Submitted to Aerobic Exercise.

Elevated serum retinol binding protein 4 (RBP4) levels were previously described in insulin-resistance states. Exercise training can improve insulin sensitivity and RBP4, but the time-response effect of exercise detraining on RBP4 has not been studied. Thus, we examined the effects of exercise training and short-term detraining on insulin resistance, serum RBP4 levels, and GLUT4 expression in spontaneously hypertensive rats (SHR). Thirty-two male SHR, 4 months old, were submitted to 10-week treadmill training, 5 times/week or kept sedentary, followed by a 2- and 4-day detraining period. Body weight, insulin tolerance test, maximum speed in a maximal exercise test, serum RBP4 (ELISA), and epididymal fat GLUT4 expression (Western blot) were measured. Although all rats gained weight (43%, p=0.004) only the trained group showed a reduction (p<0.001) of epididymal fat weight. Detraining did not change these parameters. Exercise training increased insulin sensitivity (26%, p=0.001) and maximum exercise capacity (80%, p<0.001), benefits not lost after detraining. RBP4 levels were reduced in response to exercise training (45%, p<0.001); detraining did not change these benefits. Trained rats had increased GLUT4 expression (microsomal, ~226%; p<0.001 and plasma membrane, ~55%; p=0.011). A slight reduction in GLUT4 expression in the plasma membrane (~28%, p=0.041), but not in the microsomal fraction, was observed after 4 days of detraining. Exercise training is associated with reduced RBP4 levels, increased insulin sensitivity, and epididymal fat GLUT4 expression. Even short periods of detraining (4 days) were shown to be associated with reversal of higher plasma membrane GLUT4.