RESUMEN
Isometric resistance training (IRT) has been shown to reduce resting and ambulatory blood pressure (BP), as well as BP variability and morning BP surge (MBPS). However, there are no data available regarding how long after cessation of IRT these effects are maintained. Therefore, the purpose of this study was to determine the effects of 8 weeks of detraining on resting BP, ambulatory BP and MBPS following 8 weeks of IRT in a population of young normotensive individuals and to further substantiate previously reported reductions in MBPS following IRT. Twenty-five apparently healthy participants with resting BP within the normal range (16 men, age = 23 ± 6 years; 9 women, age = 22 ± 4 years, resting BP: 123 ± 5/69 ± 7 mmHg) were randomly assigned to a training-detraining (TRA-DT, n = 13) or control (CON, n = 12) group. Resting BP, ambulatory BP and MBPS were measured prior to, after 8 weeks of bilateral leg IRT using an isokinetic dynamometer (4 × 2-min contractions at 20% MVC with 2-min rest periods, 3 days/week) and following an 8-week detraining period. There were significant reductions in 24-h ambulatory systolic BP (SBP) and calculated SBP average real variability (ARV) following IRT that were maintained after detraining (pre-to-post detraining, -6 ± 4 mmHg, p = 0.008, -2 ± 1.5 mmHg, p = 0.001). Similarly, the training-induced decreases in daytime SBP and daytime SBP ARV (pre-to-post detraining, -5 ± 6 mmHg, p = 0.001; -2 ± 1.2 mmHg, p = 0.001, respectively), MBPS (pre-to-post detraining, -6 ± 9 mmHg, p = 0.046) and resting SBP (pre-to-post detraining, -4 ± 6 mmHg, p = 0.044) were preserved. There were no changes in night-time or night-time SBP ARV across all time points (pre-to-post detraining, -1 ± 8 mmHg, p = 1.00, -0.7 ± 2.9 mmHg, p = 1.00). These results confirm that IRT causes significant reductions in resting BP, ambulatory BP, ambulatory ARV and MBPS. Importantly, the changes remained significantly lower than baseline for 8 weeks after cessation of training, suggesting a sustained effect of IRT.
RESUMEN
The authors report a patient with mild mental retardation, autistic features, multiple vertebral malformations, and an unusual facial appearance who carries a de novo submicroscopic deletion of chromosome 2p16.3. The patient's deletion is approximately 320 kb in size and includes only the part of the NRXN1 gene that codes for the neurexin1alpha promoter and initial coding exons. The more downstream neurexin1beta promoter and the region surrounding it are intact. Neurexin1beta has been associated with autism in several recent studies, but this is the first reported patient with loss of only neurexin1alpha and not of neurexin1beta. These findings suggest that neurexin1alpha function in correct dosage is necessary for normal neurological development.
