Key result
Exercise detraining for 6-8 weeks increased resting systolic, diastolic, and mean arterial blood pressure in young normotensive women with parental hypertension.
Why the study?
Does exercise detraining increase resting blood pressure and alter autonomic responses in young normotensive women with a parental history of hypertension?
Does exercise detraining increase resting blood pressure and alter autonomic responses in young normotensive women with a parental history of hypertension?
Exercise detraining for 6-8 weeks significantly increases resting blood pressure in young normotensive women with a parental history of hypertension, highlighting the rapid loss of cardiovascular benefits from exercise.
Answers are grounded in this paper and cite their sources.
Short detraining may raise BP in young women with parental hypertension; hypothesis-generating for maintenance strategies in prevention.
The effects of exercise detraining on resting finger arterial blood pressure (BP), the carotid-cardiac vagal baroreflex, and BP and heart rate (HR) responses to mental arithmetic and forehead cold exposure were studied in young (19 +/- 1.1 years) normotensive women with parental history of hypertension. Following 8 weeks of aerobic exercise for 25 min, 3 days week-1 at an intensity of 60% VO2peak, subjects ceased training for 6-8 weeks. After detraining, VO2peak (mL kg-1 min-1) was reduced by 11.5% (41.1 +/- 6.9 to 36.4 +/- 4.8) coincident with an approximately equal to 10% increase in submaximal exercise heart rate. Responses to the laboratory tasks were then compared. Detraining was accompanied by increases (P < 0.05) in resting systolic (SBP) (113.6 +/- 8.9 to 121.2 +/- 9.0), diastolic (DBP) (63.0 +/- 8.4 to 68.3 +/- 6.8), and mean arterial (MAP) (78.7 +/- 8.4 to 84.2 +/- 7.3) BP (mmHg). None of the above changes occurred in sedentary matched-control subjects. Systolic blood pressure was elevated during forehead cold exposure and MAP was elevated during mental arithmetic after detraining, but the rates of response and recovery for SBP, DBP and MAP were not altered by detraining. Despite higher submaximal exercise HR after detraining, HR responses to autonomic challenges, including the carotid-cardiac vagal baroreflex, were unchanged between training and detraining. Our results indicate that exercise detraining increases resting finger arterial BP in young normotensive women at risk for hypertension with no effects on the rate of response or recovery of heart rate and BP during autonomic tasks known to elicit sympathetic and carotid-cardiac vagal activities in this population. The use of auscultatory brachial artery pressures in a similar study of women diagnosed with hypertension will clarify the clinical meaning of our findings.
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Buckworth et al. (1997) studied Normotension with parental history of hypertension. Exercise detraining vs. Sedentary matched-control subjects was evaluated on Resting finger arterial blood pressure (systolic, diastolic, and mean arterial pressure) (p=<0.05). Exercise detraining for 6-8 weeks increased resting systolic, diastolic, and mean arterial blood pressure in young normotensive women with parental hypertension.
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