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Biomedical subjects

R L Hughson

Publications and source records attributed to R L Hughson.

At least 19 recordsLinked to original sources

Heterogeneity of responses to orthostatic stress in homozygous twins.

Early analysis into the role of genetics on cardiovascular regulation has been accomplished by comparing blood pressure and heart rate in homozygous twins during unstressed, resting physiological conditions. However, many variables, including cognitive and environmental factors, contribute to the regulation of cardiovascular hemodynamics. Therefore, the purpose of this study was to determine the hemodynamic response of identical twins to an orthostatic stress, ranging from supine rest to presyncope. Heart rate, arterial blood pressure, middle cerebral artery blood velocity, an index of cerebrovascular resistance, cardiac output, total peripheral resistance, and end-tidal carbon dioxide were measured in 16 healthy monozygotic twin pairs. Five minutes of supine resting baseline data were collected, followed by 5 min of 60 degrees head-up tilt. After 5 min of head-up tilt, lower body negative pressure was applied in increments of 10 mmHg every 3 min until the onset of presyncope, at which time the subject was returned to the supine position for a 5-min recovery period. The data indicate that cardiovascular regulation under orthostatic stress demonstrates a significant degree of variance between identical twins, despite similar orthostatic tolerance. As the level of stress increases, so does the difference in the cardiovascular response within a twin pair. The elevated variance with increasing stress may be due to an increase in the role of environmental factors, as the influential role of genetics nears a functional limit. Therefore, although orthostatic tolerance times were very similar between identical twins, the mechanism involved in sustaining cardiovascular function during increasing stress was different.

Adult↗

The effects of lumbar massage on muscle fatigue, muscle oxygenation, low back discomfort, and driver performance during prolonged driving.

An increasing dependence of society on automobiles for both work and leisure and the corresponding increase in time spent seated in the car has been correlated with a greater risk of low back pain and absence from work (Porter and Gyi 2002). This study examined the effects of three types of lumbar massage units on seating comfort, muscle fatigue, muscle oxygenation, muscle blood flow and driving performance during a 1 h simulated driving task. Electromyographic (EMG) signals were recorded from the right and left thoracic and lumbar erector spinae musculature. Average EMG (AEMG), mean power frequency (MPF), gaps and amplitude probability distribution function (APDF) parameters were analysed from the three massage seats and compared to a control seat. Near infrared spectroscopy (NIRS) and skin temperature from the right thoracic and lumbar erector spinae were used as an indication of muscle oxygenation and blood flow throughout the driving task. Ratings of perceived discomfort were used to assess driver discomfort, and driving performance was assessed by calculating mean lap times for the duration of each driving trial. The results showed statistically significant increases in skin temperature compared with the control seat after 60 min of driving. The NIRS results reflected these trends although the results were not statistically significant. AEMG and MPF measures showed no significant differences between the seats. MPF measures were found to increase over time, effects attributed to increases in muscle temperature. Gaps and APDF analyses revealed greater rest times and lower activation levels, respectively, with the control seat, which could result in increased loading of passive structures. This study demonstrated the beneficial effects of lumbar massage systems in increasing muscle blood flow and oxygenation. Although EMG parameters were not significantly different, the trends support the significant blood flow results. Future research should include longer driving times and adjustments in EMG measures to account for the effects of increasing muscle temperature on AEMG and MPF measures.

Adult↗

Cerebral blood flow during orthostasis: role of arterial CO2.

Reductions in end-tidal Pco(2) (Pet(CO(2))) during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow (CBF). The goal of this study was to determine whether decreases in Pet(CO(2)) reflected decreases in arterial Pco(2) (Pa(CO(2))) and their relation to increases in alveolar ventilation (Va) and decreases in CBF. Fifteen healthy subjects (10 women and 5 men) were subjected to a 10-min head-up tilt (HUT) protocol. Pa(CO(2)), Va, and cerebral flow velocity (CFV) in the middle and anterior cerebral arteries were examined. In 12 subjects who completed the protocol, reductions in Pet(CO(2)) and Pa(CO(2)) (-1.7 +/- 0.5 and -1.1 +/- 0.4 mmHg, P < 0.05) during minute 1 of HUT were associated with a significant increase in Va (+0.7 +/- 0.3 l/min, P < 0.05). However, further decreases in Pa(CO(2)) (-0.5 +/- 0.5 mmHg, P < 0.05), from minute 1 to the last minute of HUT, occurred even though Va did not change significantly (-0.2 +/- 0.3 l/min, P = not significant). Similarly, CFV in the middle and anterior cerebral arteries decreased (-7 +/- 2 and -8 +/- 2%, P < 0.05) from minute 1 to the last minute of HUT, despite minimal changes in Pa(CO(2)). These data suggest that decreases in Pet(CO(2)) and Pa(CO(2)) during upright posture are not solely due to increased Va but could be due to ventilation-perfusion mismatch or a redistribution of CO(2) stores. Furthermore, the reduction in Pa(CO(2)) did not fully explain the decrease in CFV throughout HUT. These data suggest that factors in addition to a reduction in Pa(CO(2)) play a role in the CBF response to orthostatic stress.

Adult↗

Measurements of cardiac output during constant exercises: comparison of two non-invasive techniques.

We compared cardiac output (CO) determined simultaneously by electrical impedance cardiography method (CO (ICG)) and by the CO (2) rebreathing technique (CO (2REB)) during three different steady-state exercises (target heart rate of 120, 140, and 160 min (-1)) in 8 healthy fit young men. The mean difference correlation coefficient obtained between the values of CO (ICG) and CO (2REB) was 0.85 and the mean difference (CO (ICG)-CO (2REB)) was 0.06 l/min (0.12 %). At 120 min (-1), CO (ICG) was lower than CO (2REB) but the tendency was reversed at 140 and 160 min (-1) where CO (ICG) was higher than CO (2REB). This evolution may be explained by the difficulty of using CO (2) rebreathing technique at the highest steady-state exercises and by the progressive acidemia due to exercise. The present results suggest that electrical impedance cardiography method provides acceptable evaluation of CO and may favourably replace the CO (2) rebreathing technique during mild (or moderate) to high steady-state exercises.

Adult↗

Vascular health in space.

Space flight induces many changes within the cardiovascular system that have the potential during long-duration space missions on the International Space Station to result in structural and functional changes in the vascular system. In this paper, we will first briefly review the potential changes in reflex control of the vascular system as observed primarily in short-duration studies of humans. We will then show how the reflex responses might interact with other changes anticipated during long-duration missions based on evidence from animal and human experimentation. This evidence points to the potential for changes in blood vessel structure, metabolism and responses to vasodilator and constrictor substances that might have long-term health consequences paralleling the effects of aging on the cardiovascular system.

Arteries↗

Splanchnic and peripheral vascular resistance during lower body negative pressure (LBNP) and tilt.

We tested the hypothesis that vasoconstriction in response to LBNP or head up tilt would be reflected in a reduction in splanchnic (portal vein) blood flow (PVF) and increases in forearm and total peripheral vascular resistance (TPR). Changes in vascular resistance indicators were obtained from measurement of PVF from portal vein cross-sectional area and blood velocity by Doppler ultrasound, from forearm vascular resistance (FVR, by Doppler) and total peripheral resistance (TPR, by impedance cardiography). 21 subjects were tested during LBNP (0, -10, -20 and -30 mmHg) and 9 subjects during tilt (0, 45 and 70 degrees). During progressive LBNP, PVF decreased approximately linearly with LBNP (-30, -48 and -64% at -10, -20 and -30 mmHg) and with tilt angle (-39 and -58% at 45 and 70 degrees). The increase in FVR approximately mirrored these changes during LBNP (20.1, 44.7 and 55.3%) and tilt (45.6 and 63.6%). However, the changes in TPR during LBNP (12.0, 16.9 and 26.4%) and tilt (25.2 and 29.2%) were markedly less. This observation of different percent changes in forearm versus total peripheral resistance might reflect true physiological differences in the forearm (and splanchnic) circulations compared with the whole body, or the data might suggest that impedance cardiography did not provide a reliable indicator of cardiac output and therefore TPR under these conditions. The primary observation in this study was that Doppler ultrasound measurement of portal vein blood flow provided a non-invasive estimate of splanchnic vascular resistance during postural or LBNP challenge and that using the reduction in portal vein flow as an index of increased vasoconstriction paralleled the change in forearm vascular resistance.

Arm↗

Rapid blunting of sympathetic vasoconstriction in the human forearm at the onset of exercise.

The purpose of this study was to test the hypothesis that sympathetic vasoconstriction is rapidly blunted at the onset of forearm exercise. Nine healthy subjects performed 5 min of moderate dynamic forearm handgrip exercise during -60 mmHg lower body negative pressure (LBNP) vs. without (control). Beat-by-beat forearm blood flow (Doppler ultrasound), arterial blood pressure (finger photoplethysmograph), and heart rate were collected. LBNP elevated resting heart rate by approximately 45%. Mean arterial blood pressure was not significantly changed (P = 0.196), but diastolic blood pressure was elevated by approximately 10% and pulse pressure was reduced by approximately 20%. At rest, there was a 30% reduction in forearm vascular conductance (FVC) during LBNP (P = 0.004). The initial rapid increase in FVC with exercise onset reached a plateau between 10 and 20 s of 126.6 +/- 4.1 ml. min(-1). 100 mmHg(-1) in control vs. only 101.6 +/- 4.1 ml. min(-1). 100 mmHg(-1) in LBNP (main effect of condition, P = 0.003). This difference was quickly abolished during the second, slower phase of adaptation in forearm vascular tone to steady state. These data are consistent with a rapid onset of functional sympatholysis, in which local substances released with the onset of muscle contractions impair sympathetic neural vasoconstrictor effectiveness.

Adult↗

Circulating norepinephrine and cerebrovascular control in conscious humans.

BACKGROUND: Cerebral vasoconstriction without concurrent changes in systemic arterial blood pressure has been observed in both normal individuals and those with idiopathic orthostatic intolerance following several minutes of postural stress when circulating catecholamines are elevated. Therefore, we tested the hypothesis that alpha-adrenergic activation with and without elevated circulating norepinephrine (NE) directly affects cerebrovascular tone in healthy individuals. METHODS: Mean arterial pressure (MAP; tonometry) and cerebral blood flow velocity (MFV) in the middle cerebral artery (transcranial Doppler) were measured in seven healthy individuals during 15 min periods of saline and of 50 (low NE) and 100 (high NE) ng kg(-1) min(-1) infusions of NE. Following this, phentolamine (PHO) was administered to return MAP back to baseline while high NE infusion continued (high NE+PHO). Finally, NE infusion was stopped allowing the persistent effects of PHO to dominate. RESULTS: Circulating NE caused a dose-dependent increase in MAP (P<0.05). During combined high NE+PHO, blood pressure was initially reduced to baseline levels but then increased a second time (P<0.05) during the final approximately 5 min of this phase. MFV remained constant during both low NE and high NE. In contrast, the secondary increase in BP during the late high NE+PHO phase was associated with elevated MFV. Cerebral vascular resistance (CVR) increased during high NE but was reduced to baseline during both early and late portions of the combined high NE+PHO phase (i.e. despite the late-phase increase in blood pressure). CONCLUSIONS: The increase in CVR during NE infusion was explained by an autoregulatory response to the increased blood pressure and not an alpha-mediated constriction. However, PHO appeared to interfere with the normal autoregulatory response to increasing blood pressure.

Adult↗

Oxygen uptake kinetics during two bouts of heavy cycling separated by fatiguing sprint exercise in humans.

We tested the hypothesis that O(2) uptake (Vo(2)) kinetics at the onset of heavy exercise would be altered in a state of muscle fatigue and prior metabolic acidosis. Eight well-trained cyclists completed two identical bouts of 6-min cycling exercise at >85% of peak Vo(2) separated by three successive bouts of 30 s of sprint cycling. Not only was baseline Vo(2) elevated after prior sprint exercises but also the time constant of phase II Vo(2) kinetics was faster (28.9 +/- 2.4 vs. 22.2 +/- 1.7 s; P < 0.05). CO(2) output (Vco(2)) was significantly reduced throughout the second exercise bout. Subsequently Vo(2) was greater at 3 min and increased less after this after prior sprint exercise. Cardiac output, estimated by impedance cardiography, was significantly higher in the first 2 min of the second heavy exercise bout. Normalized integrated surface electromyography of four leg muscles and normalized mean power frequency were not different between exercise bouts. Vo(2) and Vco(2) kinetic responses to heavy exercise were markedly altered by prior multiple sprint exercises.

Adult↗

Gender affects sympathetic neurovascular control during postural stress.

Sympathetic outflow increases during head-up tilt (HUT) to stabilize blood pressure in the presence of decreases in venous return and stroke volume (SV). Otherwise, orthostatic hypotension would develop. Gender differences in orthostatic tolerance have been noted but the mechanisms are still uncertain. More recently, Waters et al. reported in a limited sample, greater susceptibility of women to demonstrate orthostatic intolerance following space flight. Therefore, it is important to understand gender differences in reflex blood pressure regulation. Recently, we reported smaller increments in muscle sympathetic nerve activity (MSNA) in healthy women during graded HUT and a non-baroreflex cold pressor test. The purpose of this report is to examine the hypothesis that gender differences in blood pressure control during HUT are related to important variations in MSNA discharge patterns.

NASA Discipline Neuroscience↗

Modeling heart rate variability in healthy humans: a turbulence analogy.

Many complex systems share similar statistical characteristics. In this Letter, a turbulence analogy is proposed for the long-term heart rate variability of healthy humans. Based on such an analogy, the equivalence of an inertial range is found and a cascade model, which captures the statistical properties of the heart rate data, is given.

Electrocardiography, Ambulatory↗

Effect of prolonged head-down bed rest on complex cardiovascular dynamics.

We postulated that a change in complex dynamics of the cardiovascular system could be involved in the orthostatic intolerance observed after simulated weightlessness. Supine recordings of 1024 consecutive pulse intervals and systolic blood pressures were obtained on 7 subjects adapted to a 42 day head-down bed rest (day 22 and 42) but also before and 6 days after head-down bed rest (-6 degrees). Coarse graining spectral analysis was used to extract the non-harmonic (fractal) component from each time series. The power spectral densities of this fractal component are inversely proportional to their frequency (1/f beta). We fitted an inverse power law estimate to the fractal component to determine the spectral exponent beta. The complex dynamics of blood pressure and heart rate variability were also analyzed by correlation dimension and non-linear prediction. Bed rest induced orthostatic intolerance in 4 subjects. There was a significant increase in the spectral exponent beta of RR-interval variability during and after head-down bed rest (before: 1.039 +/- 0.090; during: 1.552 +/- 0.080 and 1.547 +/- 0.100; after: 1.428 +/- 0.040). Analysis of the blood pressure dynamics indicated lower correlation dimensions during head-down bed rest and higher coefficients of predictability after head-down bed rest. Complexity alterations of RR-interval and blood pressure variability were not linked with one another during head-down bed rest. These alterations seemed to be correlated with the orthostatic intolerance observed after bed rest. These results suggest a change of the integration level of cardiovascular autonomic regulation.

Adult↗

Blood flow in the triceps brachii muscle in humans during sustained submaximal isometric contractions.

The main purpose of this study was to determine the extent to which blood flow through the profunda artery within the triceps brachii muscle may be compromised during maintained low-force isometric fatiguing contractions. Doppler ultrasound techniques were used to record mean blood velocity and arterial diameter of the profunda brachii artery during sustained isometric contractions of 20% maximal voluntary contraction. The arterial diameter did not change throughout the contraction. Thus, blood velocity was considered to be an indicator of blood flow. The mean blood velocity increased initially and then remained constant during the contraction period. When compared to rest [0.06 (SD 0.03) m s-1] mean blood velocity was significantly larger at the start of the contraction [0.13 (SD 0.07) m s-1] and larger yet during recovery following the contraction [0.30 (SD 0.14) m s-1]. Although blood flow through the conduit artery did not drop during the contraction, the post-contraction hyperaemia suggested that circulatory compromise might have occurred at the level of the capillary beds.

Adult↗

Effects of pharmacological adrenergic and vagal modulation on fractal heart rate dynamics.

Breakdown of short-term fractal-like behaviour of HR indicates an increased risk for adverse cardiovascular events and mortality, but the pathophysiological background for altered fractal HR dynamics is not known. Our aim was to study the effects of pharmacological modulation of autonomic function on fractal correlation properties of heart rate (HR) variability in healthy subjects. Short-term fractal scaling exponent (alpha1) along with spectral components of HR variability were analysed during the following pharmacological interventions in healthy subjects: (i) noradrenaline (NE) infusion (n=22), (ii) NE infusion after phentolamine (PHE) (n=8), (iii) combined NE + adrenaline (EPI) infusion (n=12), (iv) vagal blockade with high dose of atropine (n=10), (v) and vagal activation by low dose of atropine (n=10). Then alpha1 decreased progressively during the incremental doses of NE (from 0.85 +/- 0.250 to 0.55 +/- 0.23, P<0.0001). NE also decreased the average HR (P<0.001) and increased the high frequency spectral power (P<0.001). Vagal blockade with atropine increased the alpha1 value (from 0.82 +/- 0.22 to 1.24 +/- 0.41, P<0.05). Combined NE + EPI infusion and vagal activation with a low dose atropine did not result in any changes in alpha1, and alpha-adrenergic blockade by PHE did not completely reverse the effects of NE on alpha1. Increased levels of circulating NE result in reduction of short-term correlation properties of HR dynamics. The results suggest that coactivation of cardiac vagal outflow at the time of high levels of a circulating sympathetic transmitter explains the breakdown of fractal-like behaviour of human HR dynamics.

Adrenergic Fibers↗

Regulation of oxygen consumption at the onset of exercise.

Increased aerobic production of ATP at the onset of exercise could be limited by availability of metabolic substrates independent of O2, or interaction between O2 and metabolic substrates. We point out the importance of feedback control to match O2 supply to demand and discuss metabolic control at the onset of exercise.

Adenosine Triphosphate↗