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We have shown that exercise training lowers blood pressure and triglyceride levels, improves physical performance, and improves quality of life in middle-aged and elderly women. Regarding epigenetic data, we noticed that more than 800 sites are differentially methylated in whole blood after physical training. We emphasize that the differentially methylated sites in the promoter region are more hypermethylated after physical training. In addition, this study shows that key members of metabolic pathways, including AMPK signaling, TGF-β signaling, and insulin signaling, are among the genes hypermethylated after physical exercise in older women.

Background: There is little evidence that nutraceuticals from beetroot extract are beneficial with regards to recovery of the cardiovascular parameters and the autonomic nervous system (ANS) after submaximal aerobic exercise, though this formulation is employed widely for this purpose. Objective: To study the effects of beetroot extract supplementation on the recovery of cardiorespiratory and autonomic parameters after a session of submaximal aerobic exercise. Methods: Sixteen healthy male adults commenced a cross-over, randomized, double-blind and placebo-controlled trial. Beetroot extract (600 mg) or placebo (600 mg) were ingested 120 min prior to evaluation on randomized days. We assessed systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), mean arterial pressure (MAP), heart rate (HR) and HR variability (HRV) indexes at Rest and during 60 min of recovery from submaximal aerobic exercise. Results: Beetroot extract ingestion slightly accelerated HR, SBP, DBP and MAP reduction following exercise associated to the placebo protocol (vs. rest). Yet no group effect (p = 0.99) was identified between the beetroot and placebo protocols on HR mean, in addition to interaction (group vs. time) (p = 0.60). No group effect was attained between the SBP (p = 0.90), DBP (p = 0.88), MAP (p = 0.73) and PP (p = 0.99) protocols and no significant differences (group vs. time) were observed between the values of SBP (p = 0.75), DBP (p = 0.79), MAP (p = 0.93) and PP (p = 0.63) between placebo and beetroot protocols. Similarly, the reoccurrence of cardiac vagal modulation after exercise via the HF (ms2) was enhanced, but not with regards to the RMSSD index. No group effect (p = 0.99) was identified for the HF (p = 0.90) and RMSSD (p = 0.67) indices. Likewise, we observed no significant differences (group vs. time) amongst the values of HF (p = 0.69) and RMSSD (p = 0.95) between the placebo and beetroot protocols. Conclusion: Whilst beetroot extract might assist the recovery of the cardiovascular and autonomic systems following submaximal aerobic exercise in healthy males, these results seem insignificant owing to minor differences between interventions and are weak clinically.

Diet and exercise are the main modifiable factors for cardiovascular disease and may be particularly important in older adults. We investigated the effects of fasting during 12 weeks of multicomponent training in the context of the aging process in physically active post-menopausal women. Method: 25 women (60.6 ± 8.9 years) were randomized into two groups: fed (FED, n=12) or fasted (FASTED, n=13) and submitted to multicomponent training. The participants underwent anthropometric, body composition, blood pressure, biochemical blood and physical fitness assessments. Results: There was a reduction in both groups for waist circumference [FED: 100.4±6.8 and 99.1±7.1 cm before and after the intervention, respectively; F = 4.214, p = 0.048; FASTED: 93.1±10.2 and 92.2±8.4 cm before and after the intervention, respectively; p = 0.039]. No significant changes were observed for the other outcomes. Discussion: The current research results, the first in the context of aging, agree with previous studies that analyzed chronic effects of fasting, showing that fasted exercise training did not improve anthropometric measurements, body composition, or blood markers compared to the fed condition after long-term exercise training. Together, these findings suggest that fasting during multicomponent training does not affect health parameters in physically active post-menopausal women.

O aumento da atividade nervosa simpática e a taquicardia em repouso ou durante esforços físicos estão associados ao aumento da morbimortalidade, mesmo na ausência de sinais clínicos de doença cardíaca. Sabendo-se da importância dos receptores α2A/α2C-adrenérgicos na modulação da atividade nervosa e frequência cardíaca (FC), o presente trabalho utiliza um modelo genético de cardiomiopatia induzida por excesso de catecolaminas circulantes baseado na inativação gênica dos receptores α2A/α2C-adrenérgicos em camundongos (α2A/α2CKO) para verificar a resposta da FC ao exercício físico (EF), assim como o controle simpatovagal da FC ao EF. Testou-se a hipótese de que haveria resposta taquicárdica exacerbada durante o EF nos camundongos α2A/α2CKO mesmo quando a função cardíaca ainda estivesse preservada em repouso, sendo o receptor α2A-adrenérgico o principal responsável por essa resposta. Camundongos machos da linhagem C57Bl6J, controle (CO) e com inativação gênica para os receptores α2A (α2AKO), α2C α2CKO) e α2A/α2CKO foram submetidos a um teste de tolerância ao esforço físico. Outros dois grupos de camundongos, CO e α2A/α2CKO, foram submetidos ao bloqueio farmacológico dos receptores muscarínicos e β-adrenérgicos e ao EF progressivo para se avaliar a contribuição simpatovagal para a taquicardia de EF. Observou-se intolerância ao esforço físico (1.220 ± 18 e 1.460 ± 34 vs. 2.630 ± 42m, respectivamente) e maior taquicardia ao EF (765 ± 16 e 792 ± 13 vs. 603 ± 18bpm, respectivamente) nos camundongos α2AKO e α2A/α2CKO vs. CO. Além disso, o balanço autonômico estava alterado nos camundongos α2A/α2CKO pela hiperatividade simpática e menor efeito vagal cardíaco. Esses resultados demonstram a importância dos receptores α2A/α2C-adrenérgicos no controle autonômico não só no repouso, mas também durante o EF, sendo o receptor α2A-adrenérgico o responsável pela hiperatividade simpática e menor efeito vagal observados. Essa resposta taquicárdica exacerbada nos camundongos α2A/α2CKO está presente mesmo quando ainda não se observa disfunção cardíaca.Increase of sympathetic nervous activity and tachycardia at rest or during physical exertions are associated with increase of morbimortality, even in the absence of clinical signs of cardiac disease. Considering the importance of the α2A/α2C-adrenergic receptors in the modulation of the nervous activity and heart rate (HR), the present study uses a genetic model of cardiomyopathy induced by excess of circulating catecholamine in the gene inactivation of the α2A/α2 -adrenergic receptors in mice (α2A/α2CKO) to verify the HR response to physical exercise (PE), as well as the sympathetic-vagal control of the HR to PE. The hypothesis is that there would be exacerbated tachycardic response during PE in α2A/α2CKO mice even when the cardiac function was still preserved at rest, being the α2A-adrenergic receptor the main reason for this response. Male mice of the C57Bl6J lineage, control (CO) and with gene inactivation for the a2A (α2AKO), α2C α2CKO) and α2A/α2CKO receptors were submitted to tolerance to a physical exercise test. Two other groups of mice, CO and α2A/α2CKO, were submitted to pharmacological blocking of the muscarinic and β-adrenergic receptors as well as to progressive PE to assess the sympathetic-vagal contribution to PE tachycardia. Intolerance to physical exercise (1.220 ± 18 and 1.460 ± 34 vs. 2.630 ± 42m, respectively) and higher tachycardia to PE (765 ± 16 e 792 ± 13 vs. 603 ± 18 bpm, respectively) in the α2AKO and α2A/α2CKO vs. CO mice was observed. Moreover, the autonomic balance was altered in the α2A/α2CKO mice by the sympathetic hyperactivity and lower cardiac vagal effect. These outcomes demonstrated the importance of the α2A/α2C-adrenergic receptors in autonomic control not only at rest, but also during PE, being theα2A-adrenergic receptor responsible for the sympathetic hyperactivity and lower vagal effect observed. This exacerbated tachycardic response in α2A/α2CKO mice is present even when cardiac dysfunction is not observed.