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Effects of water-based exercises on functioning of postmenopausal women: A systematic review with meta-analysis.
Saquetto, MB, Dos Santos, MR, Alves, IGN, Queiroz, RS, Machado, RM, Neto, MG
Experimental gerontology. 2022;:111875
Abstract
OBJECTIVE The aim of the present study was to compare the efficacy of Water-Based Exercise (WBE) versus Land-Based Exercise (LBE) and of WBE versus Non-Exercise in postmenopausal women on muscle strength, agility, flexibility, bone mineral density and aerobic capacity. METHODS We systematically searched in MEDLINE, PEDro, SciELO and the Cochrane Library RCT published until May 2022. Only randomized controlled trials were included. We analyzed the pooled results using weighted mean differences, standardized mean difference, and 95%CI were calculated. RESULTS Twenty studies met the inclusion criteria; although, sixteen studies were included in the meta-analyses. The studies presented low methodological quality. WBE was more effective than NE for improving muscle strength of knee extension (3.34), knee flexion (2.51), arm curl (6.78 repetitions), VO2Max (4.12 ml/kg), and flexibility (6.38 cm) When comparing WBE with LBE, no significant statistical difference was found regarding muscular strength of lower limbs (1.00), muscular strength of upper limbs (0.47), flexibility (1.95 cm), aerobic capacity (0.82 ml/kg) and lumbar bone mineral density (0.04 g/cm2). CONCLUSIONS WBE promotes significant benefits in muscle strength, aerobic capacity, and flexibility, when compared to no intervention. However, WBE was similar to the LBE for improving muscle strength, aerobic capacity, flexibility, agility, and bone mineral density - lumbar in postmenopausal women.
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Sacubitril/valsartan versus enalapril on exercise capacity in patients with heart failure with reduced ejection fraction: A randomized, double-blind, active-controlled study.
Dos Santos, MR, Alves, MNN, Jordão, CP, Pinto, CEN, Correa, KTS, de Souza, FR, da Fonseca, GWP, Tomaz Filho, J, Costa, M, Pereira, RMR, et al
American heart journal. 2021;:1-10
Abstract
UNLABELLED Sacubitril/valsartan reduces mortality in patients with heart failure with reduced ejection fraction (HFrEF) when compared with enalapril. However, it is unknown the effect of both treatments on exercise capacity. We compared sacubitril/valsartan versus enalapril in patients with HFrEF based on peak oxygen consumption (VO2) and 6-minute walk test (6-MWT). METHODS We included 52 participants with HFrEF with a left ventricular ejection fraction <40% to receive either sacubitril/valsartan (target dose of 400 mg daily) or enalapril (target dose of 40 mg daily). Peak VO2 was measured by using cardiopulmonary exercise testing. Six-minute walk test was also performed. RESULTS At 12 weeks, the sacubitril/valsartan (mean dose 382.6 ± 57.6 mg daily) group had increased peak VO2 of 13.1% (19.35 ± 0.99 to 21.89 ± 1.04 mL/kg/min) and enalapril (mean dose 34.4 ± 9.2 mg daily) 5.6% (18.58 ± 1.19 to 19.62 ± 1.25 mL/kg/min). However, no difference was found between groups (P = .332 interaction). At 24 weeks, peak VO2 increased 13.5% (19.35 ± 0.99 to 21.96 ± 0.98 mL/kg/min) and 12.0% (18.58 ± 1.19 to 20.82 ± 1.18 mL/kg/min) in sacubitril/valsartan (mean dose 400 ± 0 mg daily) and enalapril (mean dose 32.7 ± 11.0 mg daily), respectively. However, no differences were found between groups (P= .332 interaction). At 12 weeks, 6-MWT increased in both groups (sacubitril/valsartan: 459 ± 18 to 488 ± 17 meters [6.3%] and enalapril: 443 ± 22 to 477 ± 21 meters [7.7%]). At 24 weeks, sacubitril/valsartan increased 18.3% from baseline (543 ± 26 meters) and enalapril decreased slightly to 6.8% (473 ± 31 meters), but no differences existed between groups (P= .257 interaction). CONCLUSIONS Compared to enalapril, sacubitril/valsartan did not substantially improve peak VO2 or 6-MWT after 12 or 24 weeks in participants with HFrEF. (NEPRIExTol-HF Trial, ClinicalTrials.gov number, NCT03190304).
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Muscle wasting and cachexia in heart failure: mechanisms and therapies.
von Haehling, S, Ebner, N, Dos Santos, MR, Springer, J, Anker, SD
Nature reviews. Cardiology. 2017;(6):323-341
Abstract
Body wasting is a serious complication that affects a large proportion of patients with heart failure. Muscle wasting, also known as sarcopenia, is the loss of muscle mass and strength, whereas cachexia describes loss of weight. After reaching guideline-recommended doses of heart failure therapies, the most promising approach to treating body wasting seems to be combined therapy that includes exercise, nutritional counselling, and drug treatment. Nutritional considerations include avoiding excessive salt and fluid intake, and replenishment of deficiencies in trace elements. Administration of omega-3 polyunsaturated fatty acids is beneficial in selected patients. High-calorific nutritional supplements can also be useful. The prescription of aerobic exercise training that provokes mild or moderate breathlessness has good scientific support. Drugs with potential benefit in the treatment of body wasting that have been tested in clinical studies in patients with heart failure include testosterone, ghrelin, recombinant human growth hormone, essential amino acids, and β2-adrenergic receptor agonists. In this Review, we summarize the pathophysiological mechanisms of muscle wasting and cachexia in heart failure, and highlight the potential treatment strategies. We aim to provide clinicians with the relevant information on body wasting to understand and treat these conditions in patients with heart failure.
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Glu298Asp eNOS gene polymorphism causes attenuation in nonexercising muscle vasodilatation.
Dias, RG, Alves, MJ, Pereira, AC, Rondon, MU, Dos Santos, MR, Krieger, JE, Krieger, MH, Negrão, CE
Physiological genomics. 2009;(2):99-107
Abstract
The influence of Glu298Asp endothelial nitric oxide synthase (eNOS) polymorphism in exercise-induced reflex muscle vasodilatation is unknown. We hypothesized that nonexercising forearm blood flow (FBF) responses during handgrip isometric exercise would be attenuated in individuals carrying the Asp298 allele. In addition, these responses would be mediated by reduced eNOS function and NO-mediated vasodilatation or sympathetic vasoconstriction. From 287 volunteers previously genotyped, we selected 33 healthy individuals to represent three genotypes: Glu/Glu [n = 15, age 43 +/- 3 yr, body mass index (BMI) 22.9 +/- 0.3 kg/m(2)], Glu/Asp (n = 9, age 41 +/- 3 yr, BMI 23.7 +/- 1.0 kg/m(2)), and Asp/Asp (n = 9, age 40 +/- 4 yr, BMI 23.5 +/- 0.9 kg/m(2)). Heart rate (HR), mean blood pressure (MBP), and FBF (plethysmography) were recorded for 3 min at baseline and 3 min during isometric handgrip exercise. Baseline HR, MBP, FBF, and forearm vascular conductance (FVC) were similar among genotypes. FVC responses to exercise were significantly lower in Asp/Asp when compared with Glu/Asp and Glu/Glu (Delta = 0.07 +/- 0.14 vs. 0.64 +/- 0.20 and 0.57 +/- 0.09 units, respectively; P = 0.002). Further studies showed that intra-arterial infusion of NG-monomethyl-L-arginine (L-NMMA) did not change FVC responses to exercise in Asp/Asp, but significantly reduced FVC in Glu/Glu (Delta = 0.79 +/- 0.14 vs. 0.14 +/- 0.09 units). Thus the differences between Glu/Glu and Asp/Asp were no longer observed (P = 0.62). l-NMMA + phentolamine increased similarly FVC responses to exercise in Glu/Glu and Asp/Asp (P = 0.43). MBP and muscle sympathetic nerve activity increased significant and similarly throughout experimental protocols in Glu/Glu and Asp/Asp. Individuals who are homozygous for the Asp298 allele of the eNOS enzyme have attenuated nonexercising muscle vasodilatation in response to exercise. This genotype difference is due to reduced eNOS function and NO-mediated vasodilatation, but not sympathetic vasoconstriction.