Could "cellular exercise" be the missing ingredient in a healthy life? Diets, caloric restriction, and exercise-induced hormesis.

Overnutrition is a poor dietary habit that has been correlated with increased health risks, especially in the developed world. This leads to an imbalance between energy storage and energy breakdown. Many biochemical processes involving hormones are involved in conveying the excess of energy into pathologic states, mainly atherosclerosis, hypertension, cardiovascular diseases, and diabetes. Diverse modalities of regular exercise have been shown to be beneficial, to varying extents, in overcoming the overnutrition comorbidities. Cellular exercises and hormesis are triggered by dietary protocols that could underlie the cellular mechanisms involved in modulating the deleterious effects of overnutrition through activation of specific cellular signal pathways. Of interest are the oxidative stress signaling, nuclear factor erythroid-2, insulin-like growth factor-1, AMP-activated protein kinase as well as sirtuins and nuclear factor-κB. Therefore, the value of intermittent fasting diets as well as different diet regimens inducing hormesis are evaluated in terms of their beneficial effects on health and longevity. In parallel, important effects of diets on the immune system are explored as essential components that can undermine the overall health outcome. Additionally, the subtle but relevant relation between diet and sleep is investigated for its impact on the cardiovascular system and quality of life. The aim of this review is to focus on how calorie restriction triggers multiple molecular pathways that ultimately lead to hormetic effects resulting in cell longevity and resistance to cardiovascular disease, stroke, and cancer.

Acute exercise and postexercise blood pressure in African American women.

BACKGROUND: Limited data suggest that physical activity increases postexercise blood pressure in African-American women. The purpose of this study was to evaluate the postexercise blood pressure response to acute exercise in normotensive young adult African-American women. METHODS: Eight healthy women (age 22.5+/-.9 years) performed a cycle ergometer bout of 30 minutes at 60% of peak ventilatory oxygen uptake (VO2 peak). Control arterial blood pressure, heart rate, lower leg blood flow, cardiac output, spectral analysis of blood pressure, heart rate variability, and baroreceptor sensitivity were measured for 5 minutes before exercise and were compared to postexercise measurements performed at rest intervals of 15-20, 35-40 and 55-60 minutes after exercise. RESULTS: Exercise performed at 60% VO2 peak produced an arterial pressure of 172+/-10/ 70.1+/-4.0 mm Hg. Postexercise recovery values were not significantly different than the baseline control values. CONCLUSION: These results do not support the hypothesis that acute physical activity exerts an adverse effect on postexercise blood pressure in African American women.

Attenuation of exaggerated exercise blood pressure response in African-American women by regular aerobic physical activity.

INTRODUCTION: A hyperreactive blood pressure response to exercise is a predictor of developing hypertension. The present study determined the influence of physical activity on an exaggerated exercise blood pressure response (EEBPR) in normotensive African-American women. METHODS: We screened 36 women 18-26 years of age for EEBPR defined as a > or = 50 mm Hg difference in systolic blood pressure at rest and during exercise at 50% peak oxygen uptake (VO2peak). Seven subjects demonstrated an EEBPR and participated in the study. Study participants trained for eight weeks on a bicycle ergometer at a work intensity of 70% VO2peak. Blood pressure, heart rate, cardiac output (CO), stroke volume (SV), and total peripheral vascular resistance (TPR) were determined at baseline and during submaximal exercise at power outputs of 30 W and 50% VO2peak. Subjects served as their own controls, and data were evaluated by using a paired t test at P<.05. RESULTS: Effectiveness of the intervention was shown by a significantly greater VO2peak associated with significant decrements in systolic and mean arterial pressures at power outputs of 30 W and 50% VO2peak. A significant decrement in heart rate was observed during exercise at 30 W. Significant increments in CO and SV and decrement in TPR were found during exercise at 50% VO2peak. CONCLUSION: The reduction in TPR associated with regular aerobic physical activity may attenuate the EEBPR and decrease the risk for hypertension in normotensive, young-adult, African-American women.

Normal exercise blood pressure response in African-American women with parental history of hypertension.

BACKGROUND: Genetic and environmental hypotheses may explain why normotensive persons at high risk of developing hypertension often exhibit greater cardiovascular reactivity to stressors than those at low risk. METHODS: Pearson's correlation was used to evaluate reproducibility and independent t test to compare the cardiovascular responses to 30 W of exercise of normotensive young adult African-American women with positive and negative parental histories (PH) of hypertension (PH, n = 23; PH, n = 20). RESULTS: Correlations were significant for duplicate measurements. The effects of PH on blood pressure measured at rest and during exercise were not statistically significant (P > 0.1). A nearly significant trend for greater resting (.-)VO(2) (P = 0.08) was detected in the PH than in the PH group (3.67 +/- 0.18 versus 3.26 +/- 0.14 mL/kg/min). CONCLUSION: A hyper-reactive blood pressure response to exercise, characteristic of the evolution of hypertension, may not be present among the normotensive female offspring of hypertensive African Americans. The significance of an 11% intergroup difference in the mean resting (.-)VO(2) observed in this study is unclear.