Genetic factors regulating resting and early exercise hemodynamics fully account for genetic effects during later stages of exercise, whereas environmental effects are workload-specific.
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Does not support genetic screening for exercise capacity; leaves open workload-specific environmental targets for future research.
BACKGROUND: Both resting and exercise levels of blood pressure in individuals have been used as predictors of adult hypertension. One possible mechanism underlying the relation between childhood resting and exercise blood pressure and future blood pressure is a set of genes expressed in childhood that persists to regulate adult blood pressure. METHODS AND RESULTS: To investigate the genetic relation of blood pressure and heart rate during both rest and exercise, we asked: (1) Are the genes that regulate resting hemodynamic variables the same genes that regulate these variables during exercise? (2) How much of the variance in exercise hemodynamic variables is genetic and how much is environmental? (3) Do the genetic and environmental influences on hemodynamic responses change with increasing levels of exercise? To determine how genetic and environmental effects expressed at rest influenced responses during dynamic exercise, a genetic analysis was conducted by fitting a series of models to the covariance matrices with the use of the LISREL VII program. CONCLUSIONS: We found that all the genetic effects expressed at the later stages of exercise can be explained by genetic effects expressed at rest and at the first stage of exercise. The environmental effects appear to be workload specific and include errors of measurement.
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Bree et al. (1996) studied this question.
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