Virend K. Somers

Effects of endurance training on baroreflex sensitivity and blood pressure in borderline hypertension

Physical training offers a potential nonpharmacological strategy for control of mild and borderline hypertension, but its effect on blood pressure is controversial. We investigated the effects of endurance training on waking and sleeping blood pressure and on baroreflex sensitivity in 16 borderline hypertensive patients. First, 8 patients were assessed before and after a 6-month endurance training programme. Then, when it was clear that blood pressures were lower after training, a further 8 patients were studied not only at the end of the training programme but also after 4 months abstention from exercise (detraining). Measurements were taken of baroreflex sensitivity (response to iv phenylephrine), blood pressure, R-R interval, and blood pressure and R-R variability. Ambulatory blood pressures were measured in 13 patients (7 trained, 6 detrained) and sleep blood pressures in 6 patients (3 trained, 3 detrained). Increased fitness was associated with a decline in resting arterial blood pressure of 9.7 (SE 2.0) mm Hg systolic and 6.8 (1.2) mm Hg diastolic, and with a decline in ambulatory blood pressure of 4.8 (1.4) mm Hg and 7.5 (2.1) mm Hg, respectively; both p less than 0.05. Baroreflex sensitivity was 14.0 (1.8) ms/mm Hg in the unfit and 17.5 (2.0) ms/mm Hg in the fit; p less than 0.05. Sleep blood pressures were not lower in the fit despite longer sleep R-R intervals. These findings indicate that, in some subjects with borderline or mild hypertension, a physical training programme is sufficient to bring the blood pressure within normal limits.

Systemic and forearm vascular resistance changes after upright bicycle exercise in man.

1. Blood pressure, cardiac function and forearm blood flow following voluntary maximal upright bicycle exercise were studied in thirteen normal volunteers in a cross‐over design against a control day. 2. After exercise there was a short‐lived (5‐10 min) increase in systolic blood pressure, peak aortic blood velocity and aortic acceleration suggesting a persistence of the positive inotropic influence of exercise. 3. Systemic vasodilation, which was seen immediately exercise stopped, lasted at least 60 min. This was associated with a reduction in diastolic blood pressure for the whole hour. After 30 min systolic blood pressure was also reduced. Heart rate and cardiac output were still significantly elevated and systemic vascular resistance still reduced at 60 min post‐exercise. 4. A non‐exercising limb vascular bed (forearm) showed a marked vasodilation for 1 h after predominately leg exercise indicating the presence of a vasodilatory influence affecting vascular beds other than the exercising muscle groups.

Ambulatory pressure monitoring in the assessment of antihypertensive therapy.

SummaryA low-cost, ambulatory blood-pressure monitor has been calibrated and validated against a random zero sphygmomanometer. The repeatability of ambulatory pressure recordings after a placebo month in 44 mild to moderate untreated hypertensives was assessed. Systolic blood pressure showed a mean difference over 1 month of 2.0 mmHg, with a standard deviation of differences of 9.3 mmHg. The diastolic blood pressure mean difference was 0.1 mmHg (SD=6.3 mmHg). This variability was much less than for clinic readings (SD=17.3 mmHg) or for single home pressure readings (SD=19.7 mmHg). Using ambulatory monitoring to detect a drop in pressure of 8/5 mmHg with a power of 0.9, the number of subjects needed in a parallel group trial is reduced from 360 to 68, and in a crossover study from 88 to 16 subjects. The usefulness of ambulatory pressure monitoring is demon-strated in a placebo-controlled comparisom of atenolol, nifedipine retard, or their combination in random order. Eleven subjects, 21–60 years, with initial average blood pressures of 166.5/104.7 mmHg, showed a reduction in pressure with atenolol 50 mg a day of 15.1/10.0 mmHg, with nifedipine retard 20 mg b.i.d. of 21.0/11.6 mmHg, and with atenolol 50 mg and nifedipine retard 20 mg once a day of 26.2/16.8 mmHg. Ambulatory monitoring of pressure improved the accuracy of the trial and demonstrated a reduction in the alerting response with atenolol.

Dynamic coupling between heart rate and ventricular repolarisation

Abstract A novel model for the coupling between ventricular repolarisation and heart rate (QT/RR) is presented. It is based upon a transfer function (TRF) formalism that describes the static and dynamic properties of this coupling, i.e., the behaviour after a sudden change in heart rate. Different TRF models were analysed by comparing their capability to describe experimental data collected from 19 healthy volunteers using several RR stimulation protocols: (i) rest with deep breathing at 0.1 Hz; (ii) tilt with controlled breathing at 0.1 and 0.33 Hz; and (iii) cycling. A search for the best TRF led to unambiguous identification of a three-parameter model as the most suitable descriptor of QT/RR coupling. Compared with established static models (linear or power-law), our model predictions are substantially closer to the experimental results, with errors ∼50% smaller. The shape of the frequency and step responses of the TRF presented is essentially the same for all subjects and protocols. Moreover, each TRF may be uniquely identified by three parameters obtained from the step response, which are believed to be of physiological relevance: (i) gain for slow RR variability; (ii) gain for fast RR variability; and (iii) time during which QT attains 90% of its steady-state value. The TRF successfully describes the behaviour of the RR control following an abrupt change in RR interval, and its parameters may offer a tool for detecting pharmacologically induced changes, particularly those leading to increased arrhythmogenic risk.

Chapter 117 – Sleep Apnea

Publisher Summary nThis chapter focuses on sleep apnea, acute changes during apneic episodes, and chronic changes with obstructive sleep apnea (OSA). Normal human sleep can be divided into rapid eye movement sleep (REM) characterized by desynchronized EEG signals, muscle atony, and dreaming, and nonrapid eye movement (NREM) sleep characterized by synchronous EEG patterns. OSA constitutes a highly prevalent sleep breathing disorder affecting an estimated 15 million adult Americans. Cardiovascular responses to OSA can be explained in part by the diving reflex, a reflex response to prolonged breath hold, during which simultaneous increase in parasympathetic activity to the heart and sympathetic activity to the periphery lead to concomitant bradycardia as well as increased peripheral arterial resistance. Given the surges of SNA occurring with each apneic episode it is not surprising that patients with OSA manifest higher blood pressure (BP) and heart rate (HR) during sleep compared to the nocturnal dip in HR and BP described in normal subjects.