Resistance training increases lower body negative pressure tolerance.

This study investigated whether whole body resistance training would increase tolerance to lower body negative pressure (LBNP). Twelve males (age = 19.6 +/- 0.4 yr; mean +/- SD) underwent an acute, 12-wk program of upper and lower body resistance training (ART). Pre- and posttraining, the ART group and a control group (CON; N = 8; age = 25.4 +/- 2.4 yr) underwent LBNP tolerance tests and neck pressure-suction testing. Additionally, a group of chronically resistance-trained individuals (CRT group; N = 5; age = 22.4 +/- 0.9 yr) were tested. LBNP tolerance was increased in the ART group after training and the CRT group exhibited a significantly higher LBNP tolerance than the other groups. The ART group exhibited a decreased leg circumference change at the same absolute negative pressure at which tolerance occurred pretraining. This indicated a decreased fluid pooling after ART. The CRT group exhibited a "flattened" hypotensive portion of the carotid sinus-heart rate baroreflex curve, but this appeared to be due to the increased neck muscle mass of the subjects. We conclude that whole body ART increases LBNP tolerance possibly mediated through alterations in vascular compliance. CRT results in even greater LBNP tolerance with the responsible mediating mechanisms unclear.

Persistent hyperdynamic cardiovascular state at rest and during exercise in children after successful repair of coarctation of the aorta.

OBJECTIVES: The purposes of this study were to evaluate left ventricular performance and contractility at rest and during exercise to determine mechanisms and correlates for alterations in performance and blood pressure in pediatric patients after successful repair of coarctation of the aorta. BACKGROUND: Blood pressure and left ventricular function are elevated in children despite successful repair. The mechanisms for these changes are not understood. METHODS: Thirty asymptomatic pediatric patients with successful coarctation repair (mean age [+/- SD] 12.5 +/- 4 years) underwent echocardiographic determination of left ventricular mass, performance (shortening fraction), preload (indexed diastolic dimension), afterload (end-systolic wall stress), contractility (velocity of circumferential fiber shortening/wall stress relation) and Doppler gradient at rest and during exercise. Data were compared with those of 24 control subjects (mean age 21.0 +- 4 years). Because of the age discrepancy between groups, age-dependent echocardiographic data were indexed by body surface area. RESULTS: The mean age at operation was 5 +/- 4 years, and the average follow-up period was 7.5 +/- 3 years. The average blood pressure gradient between upper and lower limbs was 4 mm Hg. Left ventricular mass was higher in the postoperative group than in the control group (1.58 vs. 1.31 g/ht2.7, p = 0.04), as were values at rest for performance (44% vs. 31%, p = 0.0001), preload (3.9 vs. 3.7 cm/body surface area0.5), indexes systolic blood pressure (1.05 vs. 0.91, p = 0.0001) and contractility (0.23 vs. -0.05 circumferences/s, p= 0.001). Afterload was lower at rest (36 vs. 52 g/cm2, p = 0.0004). These differences between groups persisted during and after exercise. Contractility underwent an exaggerated increase after exercise in the postoperative group. CONCLUSIONS: Left ventricular performance in children after coarctation repair is higher at rest and during exercise than in control subjects as a result of higher preload and contractility and lower afterload. These changes may be due to associated hypertrophy. Persistent postoperative hypertension may be due to a hyperdynamic, hypercontractile state caused by residual gradients manifested only during exertion.

Echocardiographic determination of left ventricular preload, afterload, and contractility during and after exercise.

Left ventricular (LV) performance increases during acute exercise, but the mechanisms for this increase are not known. To determine the feasibility of studying echocardiographic indexes of performance and its determinants (preload, afterload, and contractility) during exercise, and to examine changes in these indexes, we tested 24 normal male subjects (aged 21 +/- 5 years) by echocardiography--at rest; at 25%, 50%, 75%, and 100% maximal oxygen consumption; and immediately, 3 minutes, and 5 minutes after cycle ergometry. The LV performance (shortening fraction), preload (LV end-diastolic dimension), afterload (wall stress), contractility, heart rate, and peak systolic blood pressure were measured. Data could be obtained during 98% of the exercise studies. The LV performance, heart rate, blood pressure, and contractility increased significantly with increasing exercise, reaching peak levels at maximal exercise, and decreased toward resting levels in the post-exercise period. The LV afterload and preload decreased significantly with increasing exercise intensity, reaching nadir levels at maximal exercise, and increased toward resting levels in the post-exercise period. We conclude that echocardiographic measurement of LV performance and its determinants is feasible during exercise. Performance of the LV increases with increasing exercise intensity because of an associated increase in contractility and decrease in afterload. These data will serve as a basis for comparison with those from other patient populations.

Transient and steady-state cardiopulmonary responses to combined rhythmic and isometric exercise.

The transient and steady-state cardiopulmonary responses to combined rhythmic (R) and isometric (I) exercise were examined in nine subjects. Isometric exercise at 30% maximal voluntary contraction (MVC) was started 1.5 min prior to either a 50% or 75% maximal oxygen uptake (VO2max) cycle ride and continued for 1.5 min into the 10-min R. Systolic (Pas) and diastolic (P(ad)) blood pressure, heart rate (fc), inspired ventilation volumes (VI), and oxygen uptake (VO2) were recorded every 30 s throughout each experiment. Responses to I effort alone were recorded for comparison with experiments in which the combined exercises were performed during the first 1.5 min when R had not yet begun. Pas responses in the first 1.5 min of I (no R) showed the typical rapid linear increase. Addition of the R effort further increased Pas to levels which remained nearly constant (steady state) throughout R. R alone produced a slower Pas increase to approximately the same steady-state levels as those of the combined R and I exercise. For P(ad), the linear increase which occurred during the first 1.5 min of I was attenuated with the superimposition of R. Following cessation of I, P(ad) fell rapidly during continued R to levels not different from experiments with R alone. The fc during I alone increased slightly. As I continued, the onset of the R induced a further rapid increase in fc to levels not different from R alone. The VI showed a similar response to fc. VO2 during I alone did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Stress reactivity: hemodynamic adjustments in trained and untrained humans.

There is mounting evidence to suggest a relationship between heightened cardiovascular (CV) and sympathetic nervous system (SNS) reactivity to behaviorally stressful situations and cardiovascular pathology. Exercise training has been suggested as a non-pharmacological, therapeutic intervention technique to counter behaviorally induced CV and SNS reactivity. This approach is based on well-documented adaptations in CV and SNS functioning that result from exercise training. However, the theoretical basis for the relationship between physical fitness and stress reactivity has not been fully explored. Additionally, there are methodological and design considerations that inhibit comparison and interpretation of research studies regarding the role of physical fitness or exercise training and cardiovascular and SNS reactivity during behavioral stress. The focus of our laboratory studies has been to more fully described the CV and SNS responses to behaviorally challenging novel and learned tasks in highly fit, exercise trained, and untrained college-age males. The results from these studies suggest that highly fit and untrained males exhibit similar CV and SNS responses to a novel task. However, upon repeated exposure to the task, fit individuals exhibit attenuated mean arterial pressure and cardiac output responses. The data from the longitudinal studies suggest that there is an exercise training induced attenuation in the cardiac output response to behavioral challenge and that this is at least partially the result of an attenuated stroke volume response to the task. Thus, exercise training does appear to alter cardiovascular functioning during familiar, behaviorally challenging situations.

Cardiopulmonary responses to combined rhythmic and isometric exercise in humans.

A rhythmic (R) and an isometric (I) exercise were performed separately and in combination to assess their additive effects on arterial systolic (P(as)) and diastolic (P(ad)) blood pressures, heart rate (fc), and minute ventilation (VI). The isometric effort consisted of a 40% maximal voluntary handgrip contraction (MVC) performed for a duration of 80% of a previously determined 40% MVC fatiguing effort. The R effort consisted of a 13-min cycle effort at 75% maximum oxygen consumption (VO2max). For the combined efforts, I was performed starting simultaneously with or ending simultaneously with R. Data on nine subjects yield statistically significant evidence (P less than 0.05) that the effects of I and R are not additive for the following three cases: (1) P(as) when I and R are ended simultaneously (I alone = 4.9, SEM 0.5 kPa increase; R alone = no significant change from steady state; I + R = 1.2, SEM 0.4 kPa increase), (2) P(ad) when I and R are started simultaneously (I alone = 4.1, SEM 0.4 kPa increase; R alone = 0.7, SEM 0.3 kPa decrease; I + R = 1.9, SEM 0.4 kPa increase), and (3) P(ad) when I and R are ended simultaneously (I alone = 4.1, SEM 0.4 kPa increase; R alone = 0.3, SEM 0.5 kPa decrease; I + R = 0.8, SEM 0.3 kPa increase). For all other variables and cases, there is not sufficient evidence to conclude that the effects of I and R are not additive. We conclude that R and I exercises do not invariably produce strictly additive cardiopulmonary responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Ten weeks of aerobic training do not affect lower body negative pressure responses.

Based mostly on cross-sectional data, it has been suggested that aerobic training may decrease lower body negative pressure (LBNP) tolerance through a hypothesized attenuation in both high- and low-pressure baroreflex gain. An experimental group (EXP) of eight male subjects [22.1 +/- 1.4 (SD) yr] underwent a 10-wk treadmill and cycle ergometer training program, which resulted in a 21% increase in maximal O2 uptake (VO2 max), 45.7 +/- 1.5 vs. 55.2 +/- 1.7 (SE) ml.kg-1.min-1; P less than 0.05]. A control group, (CON; n = 7; 27.3 +/- 5.7 yr), which did not undergo training, had no significant changes in VO2 max (49.4 +/- 3.3 vs. 48.8 +/- 3.2 ml.kg-1.min-1). Before and after training the EXP and CON groups participated in LBNP tolerance tests (terminated at presyncope) and neck pressure-suction testing (to describe the carotid sinus-heart rate baroreflex). LBNP tolerance, as defined by three different indexes, and carotid sinus-heart rate baroreflex gain were not altered in either group after training. Furthermore, there were no changes in LBNP heart rate, blood pressure, leg circumference, forearm blood flow, or forearm vascular resistance responses at any level of LBNP challenge after training. In conclusion, 10 wk of aerobic training did not change LBNP tolerance or alter the reflex cardiovascular compensatory mechanisms activated during LBNP.

Aerobic power and cardiovascular response to stress.

The relationship between aerobic fitness as measured by maximal O2 uptake (VO2max) and the cardiovascular response to laboratory stressors was examined in two experiments. First, 34 male college students were screened on the basis of their heart rate (HR) response to a reaction time-shock avoidance (RT-AV) task. The six individuals showing an average HR increase of 45 beats/min (reactives) and the six subjects showing an average increase of 8 beats/min (nonreactives) did not differ in VO2max (47.7 +/- 2 vs. 48.7 +/- 1 ml.kg-1.min-1, respectively). However, a statistically significant association between a reported family history of hypertension and peak HR response to RT-AV was seen. In the second series of experiments, the plasma catecholamine and cardiovascular responses of eight elite endurance-trained athletes (VO2max 70.6 +/- 1 ml.kg-1.min-1) and eight untrained volunteers (VO2max 45.5 +/- 1 ml.kg-1.min-1) were compared on the following: RT-AV, reaction time for monetary reward (RT-AP), cold pressor, isometric handgrip, and orthostatic challenge (standing). The trained group exhibited a significantly lower mean HR at rest (P less than 0.05), otherwise there were no significant differences between the two groups. The results indicate that although individual differences (e.g., family history of hypertension and high resting HR) can be related to the potential for cardiovascular responses to novel laboratory challenges, the contribution of fitness to this characteristic is much less clear. Further exploration of questions pertaining to fitness and stress should focus on individuals with a predisposition to stress reactivity.