No abstract

OBJETIVO: Avaliar, numa situação real de atuação prática, o efeito da prescrição individualizada de caminhada sem supervisão da prática sobre o risco cardiovascular e a aptidão física de usuários de um parque público. MÉTODOS: 186 sujeitos (62 ± 10 anos) foram orientados a caminhar pelo menos 3x/sem, por 30 min, com intensidade de 50 a 80% da frequência cardíaca de reserva e a fazer alongamentos antes e após a caminhada. A aptidão física e os fatores de risco cardiovascular foram avaliados pré e pós-intervenção. A análise dos dados foi dividida em duas fases: 1) análise na amostra total; 2) análise nos indivíduos com fatores de risco alterados. Os dados foram comparados pelo teste t pareado. RESULTADOS: Na amostra total, a aptidão física melhorou nos testes de marcha estacionária (+8,1 ± 14,5 passos, p < 0,05), impulsão vertical (+0,5 ± 2,7 cm, p < 0,05), flexibilidade lombar (+1,1 ± 4,7 cm, p < 0,05) e flexibilidade de ombro (+1,2 ± 2,1 cm, p < 0,05). Não ocorreram alterações nos fatores de risco cardiovascular, com exceção da redução da pressão arterial diastólica (-0,9 ± 6,0 mmHg, p < 0,05). Entretanto, nos subgrupos com fatores alterados, observou-se reduções significantes das pressões arteriais sistólica e diastólica (-13,3 ± 16,9 e -5,8 ± 8,3 mmHg, p < 0,05, respectivamente) nos hipertensos, da colesterolemia total (-19,5 ± 33,5 mg/dl, p < 0,05) nos hipercolesterolêmicos e da circunferência da cintura (-1,0 ± 4,7 cm, p < 0,05) e do índice cintura-quadril (-0,01 ± 0,04, p < 0,05) nos com obesidade central. CONCLUSÃO: Numa situação real de atuação, a prescrição de caminhada sem supervisão da prática foi efetiva em melhorar a aptidão física da amostra geral e em diminuir o risco cardiovascular específico dos indivíduos com fatores de risco.

Blood pressure (BP) and physical activity (PA) levels are inversely associated. Since genetic factors account for the observed variation in each of these traits, it is possible that part of their association may be related to common genetic and/or environmental influences. Thus, this study was designed to estimate the genetic and environmental correlations of BP and PA phenotypes in nuclear families from Muzambinho, Brazil. Families including 236 offspring (6 to 24 years) and their 82 fathers and 122 mothers (24 to 65 years) were evaluated. BP was measured, and total PA (TPA) was assessed by an interview (commuting, occupational, leisure time, and school time PA). Quantitative genetic modeling was used to estimate maximal heritability (h2), and genetic and environmental correlations. Heritability was significant for all phenotypes (systolic BP: h2 = 0.37 ± 0.10, P < 0.05; diastolic BP: h2 = 0.39 ± 0.09, P < 0.05; TPA: h2 = 0.24 ± 0.09, P < 0.05). Significant genetic (rg) and environmental (re) correlations were detected between systolic and diastolic BP (rg = 0.67 ± 0.12 and re = 0.48 ± 0.08, P < 0.05). Genetic correlations between BP and TPA were not significant, while a tendency to an environmental cross-trait correlation was found between diastolic BP and TPA (re = -0.18 ± 0.09, P = 0.057). In conclusion, BP and PA are under genetic influences. Systolic and diastolic BP share common genes and environmental influences. Diastolic BP and TPA are probably under similar environmental influences.

Myocardial infarction (MI) has been associated with increases in reactive oxygen species (ROS). Exercise training (ET) has been shown to exert positive modulations on vascular function and the purpose of the present study was to investigate the effect of moderate ET on the aortic superoxide production index, NAD(P)H oxidase activity, superoxide dismutase activity and vasomotor response in MI rats. Aerobic ET was performed during 11 weeks. Myocardial infarction significantly diminished maximal exercise capacity, and increased vasoconstrictory response to norepinephrine, which was related to the increased activity of NAD(P)H oxidase and basal superoxide production. On the other hand, ET normalized the superoxide production mostly due to decreased NAD(P)H oxidase activity, although a minor SOD effect may also be present. These adaptations were paralleled by normalization in the vasoconstrictory response to norepinephrine. Thus, diminished ROS production seems to be an important mechanism by which ET mediates its beneficial vascular effects in the MI condition.