PubMed Health⌕ Search

Biomedical subjects

R L Hughson

Publications and source records attributed to R L Hughson.

At least 73 records · Page 4Linked to original sources
PubMed1997

Time course of brachial artery diameter responses to rhythmic handgrip exercise in humans.

OBJECTIVE: Whether the dimensions of conduit arteries contribute to the time course of change in blood flow during voluntary rhythmic exercise, and the mechanisms governing such a response in humans, are not known. METHODS: The time course of change in the vascular and blood flow dynamics in the brachial artery during the transition between rest and 5 min of rhythmic handgrip exercise was assessed in humans using continuous measures of brachial artery mean blood velocity (MBV; pulsed Doppler), diameter (echo Doppler) and mean arterial pressure (Finapres). The exercise cadence was 1s/1s (Fast) and 1s/2s (Slow) work/rest schedules while supine with the arm positioned above or below the heart. RESULTS: Brachial artery diameter of the active arm was reduced 5% at approximately 10 s following the onset of exercise performed above the heart (P < 0.05), irrespective of work rate, and returned to rest levels by 30 s with no concurrent changes in arterial pressure. By 2 min of the Fast contraction rate exercise, brachial artery diameter of the active arm was greater than rest (P < 0.05) irrespective of arm position. Brachial artery dimensions in the contralateral inactive arm were not altered during exercise (P > 0.05). Compared with rest, MBV and forearm blood flow at 5 s of exercise were increased in the active arm but were reduced transiently in the inactive limb (P < 0.05). CONCLUSIONS: Conduit artery responses to exercise were dependent upon the work rate and arm position. The delayed dilation in the heavier exercise, independent of arm position, suggests that stimuli related to the metabolic activity of the distal active skeletal muscle may influence the dimensions of the conduit artery.

Adult↗
PubMed1997

Orthostatic tests after a 4-day confinement or simulated weightlessness.

Besides microgravity, inactivity is likely to play a role in the cardiovascular deconditioning after space flights and weightlessness simulations. The aim of the study was to compare the effects of a 4-day head-down bed rest (HDBR) (-6 degrees) and a 4-day confinement (C) on cardiovascular responses to orthostatic stress. Eight male subjects underwent head-up tilt (HUT) (+60 degrees) and lower-body negative pressure (LBNP) (-20, -30, -40 and -50 mmHg) before (D-1) and at the end (R1) of each situation. Blood pressure, heart rate variability (HRV) and spontaneous baroreflex slope (SBS) were determined. The HDBR reduced orthostatic tolerance, as five subjects presented orthostatic hypotension during the HUT at R1, compared with two subjects at D-1. These same two subjects presented orthostatic hypotension after confinement. The main findings, after HDBR, included reductions in RR interval and total spectral power and a decrease in the parasympathetic indicator (PNS) in favour of a decrease in vagal tone; the increase in the sympathetic indicator (SNS) was not significant. After confinement, the RR interval was also significantly reduced and PNS decreased, but not significantly. RR interval and PNS were further reduced during HUT and LBNP, reflecting a withdrawal of parasympathetic activity. SBS was reduced after HDBR (P < 0.05) and confinement (P = 0.05), with a further reduction during HUT and LBNP without difference between D-1 and R1. This experiment showed that a 4-day HDBR leads to impaired baroreflex function and changes in autonomic balance, which may contribute to orthostatic intolerance. Although less significant, similar patterns of changes in the autonomic nervous system were observed after confinement, suggesting an influence of the inactivity in cardiovascular deconditioning.

Adult↗
PubMed1997

Contributions of acetylcholine and nitric oxide to forearm blood flow at exercise onset and recovery.

The contributions of acetylcholine and/or nitric oxide (NO) to the rapid changes in human forearm blood flow (FBF) at the onset and recovery from mild exercise were studied in eight subjects. Rhythmic handgrip contractions were performed during brachial artery infusions of saline (2 ml/min; control), atropine (0.2 mg over 3 min), to block acetylcholine binding to muscarinic receptors, or atropine + NG-monomethyl-L-arginine (L-NMMA; 4 mg/min for 4 min), to additionally inhibit NO synthase. Brachial artery mean blood velocity (MBV; pulsed Doppler ultrasound) and diameter (echo Doppler) were measured continuously, and FBF was calculated. Atropine reduced acetylcholine-induced increases in FBF by approximately 71% (P < 0.05). FBF at rest was reduced by atropine and further reduced with atropine + L-NMMA. Both drug conditions reduced FBF during exercise by approximately 10% compared with control, with no difference between drug treatments. Brachial artery diameter was unchanged from rest by exercise, recovery, and drug treatments. Neither drug treatment altered the rate or magnitude of the increase in FBF above rest. Peak FBF after exercise was reduced by atropine and atropine + L-NMMA. Total FBF during 5 min of recovery was reduced with atropine + L-NMMA compared with control and atropine. The results suggest that 1) acetylcholine and NO mechanisms additively contribute to FBF levels at rest, 2) a cholinergic mechanism adjusts the absolute FBF levels during exercise, 3) neither acetylcholine nor NO is essential to observe the normal time course or magnitude of the exercise response, and 4) NO contributes to the FBF response during recovery from exercise.

Acetylcholine↗
PubMed1997

Acceleration of VO2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise.

We examined the hypothesis that O2 uptake (VO2) would change more rapidly at the onset of step work rate transitions in exercise with hyperoxic gas breathing and after prior high-intensity exercise. The kinetics of VO2 were determined from the mean response time (MRT; time to 63% of total change in VO2) and calculations of O2 deficit and slow component during normoxic and hyperoxic gas breathing in one group of seven subjects during exercise below and above ventilatory threshold (VT) and in another group of seven subjects during exercise above VT with and without prior high-intensity exercise. In exercise transitions below VT, hyperoxic gas breathing did not affect the kinetic response of VO2 at the onset or end of exercise. At work rates above VT, hyperoxic gas breathing accelerated both the on- and off-transient MRT, reduced the O2 deficit, and decreased the VO2 slow component from minute 3 to minute 6 of exercise, compared with normoxia. Prior exercise above VT accelerated the on-transient MRT and reduced the VO2 slow component from minute 3 to minute 6 of exercise in a second bout of exercise with both normoxic and hyperoxic gas breathing. However, the summated O2 deficit in the second normoxic and hyperoxic steps was not different from that of the first steps in the same gas condition. Faster on-transient responses in exercise above, but not below, VT with hyperoxia and, to a lesser degree, after prior high-intensity exercise above VT support the theory of an O2 transport limitation at the onset of exercise for workloads >VT.

Adult↗
PubMed1997

Alveolar oxygen uptake and blood flow dynamics in knee extension ergometry.

The relationship was studied between the increase in oxygen uptake (VO2) measured breath-by-breath at the mouth, and the increase in femoral artery blood flow measured continuously with pulsed and echo Doppler methods. Five men exercised at 50 W on a knee extension ergometer in both the supine and the upright posture. The kinetics of the responses were determined by curve fitting to obtain the mean response time (MRT = 63% of the time required to achieve steady state). In the upright position, the increase in blood flow (MRT = 12.4 +/- 9.4 s, mean +/- SD) was faster than the increase in VO2 (29.6 +/- 9.3 s). Likewise in the supine position, blood flow increased more rapidly (25.1 +/- 9.7 s vs. 36.7 +/- 9.6 s). It should be noted that the increase in blood flow appeared to be faster than VO2, yet when blood flow adapted more slowly in the supine posture, it had an impact on the adaptation of VO2. This suggests that blood flow might have important effects on metabolism at the onset of submaximal exercise.

Blood Flow Velocity↗
PubMed1996

Comparison of a 4-day confinement and head-down tilt on endocrine response and cardiovascular variability in humans.

The aim of this study was to determine the effects of a 4-day head-down tilt (HDT; -6 degrees) and 4-day confinement on several indicators that might reflect a state of cardiovascular deconditioning on eight male subjects. Measurements were made of endocrine responses, heart rate variability and spontaneous baroreflex response (SBR) slope before, during and after each intervention. Plasma volume decreased by 10 percent after the 4-day HDT. The concentration of active renin was increased and that of urinary atrial natriuretic peptide decreased during the 4-day experiment in both groups. Plasma arginine vasopressin concentration decreased significantly only after 4-day confinement. After the 4-day HDT, one of the spectrum analysis parameters was statistically changed: the parasympathetic indicator decreased significantly (P <0.05) whereas the sympathetic indicator and the total power spectrum were unaltered. After 4-day confinement spectrum analysis parameters were not statistically altered. A significant decrease of SBR (P <0.05) was noticed only after the 4-day HDT. These data would suggest that exposure to a 4-day HDT was sufficient to induce a cardiovascular deconditioning which may have been induced by confinement and inactivity.

Adult↗
PubMed1996

Forearm blood flow by Doppler ultrasound during test and exercise: tests of day-to-day repeatability.

The between-day repeatability of simultaneous measures of brachial artery diameter (D) (echo Doppler) and mean blood velocity (MBV) (pulsed Doppler) was tested during rest and exercise. On 3 separate days, six volunteers performed one trial of 1-min rest followed by a step increase in dynamic handgrip exercise for 4 min which required the lifting and lowering of a 4.4-kg weight (approximately 8-12% MVC) in a 1s/2s (work/rest) cadence. Measures for MBV and D were collected continuously on a beat-by-beat basis during the transition from rest to end exercise. The mean rest values over one min, and single data points at 30, 60, 120, and 240 s of exercise were extracted from the time series data. At all exercise time points, MBV was greater than rest (P < 0.05), but these levels were not different across test days. Arterial D at all exercise time points ranged from 3.8 +/- 0.1 mm to 4.1 +/- 0.1 mm (mean +/- SEM) and did not differ from rest (3.9 +/- 0.1 mm) (P > 0.05), nor did D differ between days. The mean between-day coefficient of variation for D was 4.08 +/- 0.7% at rest and ranged from 2.90 +/- 0.4% to 3.96 +/- 0.5% during exercise. The coefficient of variation for MBV was 13.2 +/- 2.6% at rest and reached 20.2 +/- 3.1% during the final min of exercise; the exercise variability was reduced to 14.9 +/- 2.4% by averaging MBV over 3 s (the duration of a contraction/relaxation duty cycle) (P < 0.05) with no further advantage of averaging over ten 60-s sample periods. The data indicate that, for the six subjects tested, Doppler ultrasound measures of arterial MBV and diameter during both rest and exercise were reproducible across different test days and can be used as a reliable, noninvasive means of testing hypotheses pertaining to blood flow control.

Adult↗
PubMed1996

Heart rate variability at rest and exercise: influence of age, gender, and physical training.

The adaptive responses of the cardiovascular system to regular physical activity appear to include a reduction in sympathetic (SNS) activity and an increase in parasympathetic (PNS) activity during rest and at different absolute intensities of exercise. In a cross-sectional design, trained individuals who exercised at least 5 days/week for 45 min/day or more were compared with age- and gender-matched untrained controls. There was a relative bradycardia in the trained groups at rest and at the same absolute intensity of exercise in both young and middle-aged subjects. There were no differences in indicators of PNS and SNS activity at rest in young subjects. There was a reduced SNS activity and increased PNS activity in middle-aged trained subjects versus their age-matched controls. Spectral analysis was capable of showing changes in autonomic control of heart rate at rest and across intensities of exercise. These data showed significant shifts to increased PNS and reduced SNS indicators at rest in trained versus untrained middle-aged subjects and in females in both age groups versus males.

Adolescent↗
PubMed1996

Vasodilation and muscle pump contribution to immediate exercise hyperemia.

A rapid (within 0-5 s) increase in skeletal muscle blood flow has been demonstrated following muscle contraction, yet the mechanism remains unresolved. Recently, it was suggested that the entire rapid exercise hyperemia could be attributed to the mechanical muscle pump effect. Other evidence indicates that the muscle pump cannot increase arterial flow. We measured human forearm blood flow with the arm positioned above or below heart level during 1) simulation of rhythmic muscle pump function via repeated inflation/deflation of a forearm cuff to 100 mmHg to achieve mechanical emptying of forearm veins, and 2) 1-s single-cuff inflations, 1-s voluntary forearm contractions, and 1-s contractions performed within a cuff inflation. Rhythmic cuff inflation increased blood flow with the arm below heart level (P < 0.05) but not above. Flow following single contractions was higher than flow following cuff inflation within 2 s (P < 0.05). Peak flow increases due to a single mechanical venous emptying (7.7 +/- 0.7 ml.100 ml(-1) min(-1)) could account for 60% of the peak flow increase due to muscle contraction (12.8 +/- 1.0 ml.100 ml(-1).min(-1)) with the arm below heart level, whereas above heart level mechanical venous emptying accounted for 46% of the flow increase due to contraction (3.0 +/- 0.4 vs. 6.5 +/- 0.6 ml.100 ml(-1).min(-1)). We conclude that a functional muscle pump does exist in the human forearm in vivo, but that a rapid vasodilation detectable within 2 s also contributes to the early exercise hyperemia.

Adult↗
PubMed1996

Cardiorespiratory interactions during fixed-pace resistive breathing.

We tested the hypothesis that the arterial baroreflex was important in the origin of respiratory sinus arrhythmia (RSA) under conditions of normal and resistive breathing. That is, mechanical effects of breathing [indicated by instantaneous lung volume (ILV)] would directly influence left ventricular stroke volume (LVSV), which in turn would influence systolic arterial blood pressure (SABP), causing variation in R-R interval through the baroreflex. Eight healthy young subjects (four men and four women) were monitored in the supine position while breathing with a fixed frequency (0.2 Hz) and tidal volume for 15 min through each of three resistances (R0, R1, and R2) producing inspiratory (-) and expiratory (+) pressures of +/- 1.6, +/- 5.4, and +/- 16.6 cmH2O, respectively. LVSV was estimated by stroke distance [(SDist); by Doppler ultrasound]. There were no differences across R0, R1, and R2 for the mean values of R-R interval, SDist, or SABP. Cross-spectral analysis showed that, at R0, each value of R-R interval, SDist, and SABP lagged ILV by approximately 80 degrees. At R1 and R2, phase was reduced from ILV to SDist and R-R interval, and the transfer magnitude for SDist (R2 only), SABP, and R-R interval increased. The transfer magnitude from SDist to SABP significantly increased as a function of resistance breathing, whereas that from SABP to R-R interval significantly decreased. There were no changes in phase relationships from SDist to SABP to R-R interval. Thus the magnitude of RSA (ILV to R-R interval) was increased, but the transfer through the arterial baroreflex (SABP to R-R interval) was reduced. Although factors other than the arterial baroreflex are probably involved in the genesis of RSA, the constant phase relationship across the levels of breathing resistance among SDist, SABP, and R-R interval suggests an important functional link caused by mechanical effects of breathing.

Adult↗
PubMed1996

Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans.

The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter (D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (gamma = 8.MBV/D), and forearm blood flow (FBF = MBV.pi r2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (approximately 10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and gamma was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 +/- 3 beats/min) compared with placebo (57 +/- 3 beats/min) (P < 0.05) without change to MPP. With placebo, D increased in both arm positions from approximately 4.3 mm at rest to approximately 4.5 mm at 5 min of exercise (P < 0.05). This response was not altered with Ibu (P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow (P > 0.05) in either arm position. The gamma was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise (P < 0.05). Because PG inhibition altered the time course of gamma at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.

Adult↗
PubMed1996

Dependence of muscle VO2 on blood flow dynamics at onset of forearm exercise.

The hypothesis that the rate of increase in muscle O2 uptake (VO2mus) at the onset of exercise is influenced by muscle blood flow was tested during forearm exercise with the arm either above or below heart level to modify perfusion pressure. Ten young men exercised at a power of approximately 2.2 W, and five of these subjects also worked at 1.4 W. Blood flow to the forearm was calculated from the product of blood velocity and cross-sectional area obtained with Doppler techniques. Venous blood was sampled from a deep forearm vein to determine O2 extraction. The rate of increase in VO2mus and blood flow was assessed from the mean response time (MRT), which is the time to achieve approximately 63% increase from baseline to steady state. In the arm below heart position during the 2.2-W exercise, blood flow and VO2mus both increased, with a MRT of approximately 30 s. With the arm above the heart at this power, the MRTs for blood flow [79.8 +/- 15.7 (SE)s] and VO2mus (50.2 +/- 4.0 s) were both significantly slower. Consistent with these findings were the greater increases in venous plasma lactate concentration over resting valued in the above heart position (2.8 +/- 0.4 mmol/l) than in the below heart position (0.9 +/- mmol/l). At the lower power, both blood flow and VO2mus also increased more rapidly with the arm below compared with above the heart. These data support the hypothesis that changes in blood flow at the onset of exercise have a direct effect on oxidative metabolism through alterations in O2 transport.

Adult↗
PubMed1996

Faster femoral artery blood velocity kinetics at the onset of exercise following short-term training.

OBJECTIVE: The hypothesis that the adaptation to endurance exercise training included a faster increase in blood flow at the onset of exercise was tested in 12 healthy young men who endurance-trained (ET) 2 h/day, for 10 days at 65% VO2 peak on a cycle ergometer, and in 11 non-training control (C) subjects. METHODS: Blood flow was estimated from changes in femoral artery mean blood velocity (MBV) by pulsed Doppler. Beat-by-beat changes in cardiac output (CO) and mean arterial pressure (MAP) were obtained by impedance cardiography and a Finapres finger cuff, respectively. MBV, MAP and CO were measured at rest and during 5 min of dynamic knee extension exercise. Both legs worked alternately with 2 s raising and lowering a weight (15% maximal voluntary contraction) followed by 2 s rest while the other leg raised and lowered the weight. RESULTS: In the ET group the time to 63% (T63%) of the approximately exponential increase in MBV following 10 days of training (8.6 +/- 1.2 s, mean +/- s.e.) was significantly faster than the Day 0 response (14.2 +/- 2.1 s, P < 0.05). The T63% of femoral artery vascular conductance (VCfa) was also faster following 10 days of ET (9.4 +/- 0.9 s) versus Day 0 (16.0 +/- 2.5 s) (0.05). There was no change in the T63% of both MBV and VCfa for the C group. The kinetics of CO were not significantly affected by ET, but the amplitude of CO in the adaptive phase, and at steady state, were significantly greater (P < 0.05) at Day 10 compared to Day 0 for the ET group with no change in the C group. CONCLUSIONS: These data supported the hypothesis that endurance training resulted in faster adaptation of blood flow to exercising muscle, and further showed that this response occurred early in the training program.

Adult↗
PubMed1995

Coupling of ventilation and gas exchange during transitions in work rate by humans.

The dynamic responses of expired ventilation (VE) following transitions in work rate were studied during step increases and decreases, and during pseudorandom binary sequence (PRBS) changes in work rate. Six healthy men completed multiple repetitions of each test type under conditions of hypoxia (fractional inspired O2, FIO2 = 0.14), room air and hyperoxia (FIO2 = 0.70). Neither potentiation nor attenuation of the carotid chemoreceptors, with hypoxia or hyperoxia respectively, influenced the magnitude or duration of the phase 1 response at the onset of exercise. However, the off-transient phase 1 was smaller with hypoxia than normoxia or hyperoxia. The time course of phase 2 was faster in hypoxia and slower in hyperoxia, but there was symmetry between on- and off-responses. This was counter to predictions of asymmetry based on the short-term potentiation hypothesis. Tight coupling existed for breath-by-breath VE relative to CO2 output during PRBS exercise, especially in hypoxia (r2 = 0.40 +/- 0.08; 0.64 +/- 0.03; and 0.71 +/- 0.05 for hyperoxia; normoxia; and, hypoxia), but poorer coupling existed to O2 uptake, especially in hyperoxia (r2 = 0.09 +/- 0.04; 0.37 +/- 0.05; and 0.46 +/- 0.07). These data are consistent with neural factors in phase 1, and humoral mediation of phase 2 responses during dynamic exercise in healthy subjects.

Adult↗
PubMed1995

Kinetics of oxygen uptake for submaximal exercise in hyperoxia, normoxia, and hypoxia.

This study evaluated the dynamic response of VO2 in 6 healthy men at the onset and end of submaximal step changes in work rate during a pseudorandom binary sequence (PRBS) exercise test and during ramp incremental exercise to exhaustion while breathing three different gas mixtures. The fractional concentrations of inspired O2 were 0.14, 0.21, and 0.70 for the hypoxic, normoxic, and hyperoxic tests, respectively. Both maximal VO2 and work rate was significantly reduced in hypoxic tests compared to normoxic and hyperoxic tests. Maximal work rate was greater in hyperoxia than in normoxia. Work rate at ventilatory threshold was lower in hypoxia than in normoxia and hyperoxia but above the upper limit of exercise for the submaximal tests. Hypoxia significantly slowed the response of VO2 both at the onset and end of exercise compared to normoxia and hyperoxia. Hypoxia also modified the response to PRBS exercise, and again there was no difference between normoxia and hyperoxia. These data support the concept that VO2 kinetics can be slowed from the normoxic response by a hypoxic gas mixture.

Adaptation, Physiological↗
PubMed1995

Methodology of spontaneous baroreflex relationship assessed by surrogate data analysis.

We tested the hypothesis that the spontaneous beat-by-beat interactions of systolic blood pressure (SBP) and R-R interval reflected true baroreflex events rather than chance interactions. Original data sets of 1,024 heartbeats obtained in seated rest from six healthy subjects [R-R interval = 953 +/- 94 (+/- SE) ms] were compared with isospectral [generated by a windowed (inverse) Fourier transform with phase randomization] and isodistribution (data points randomly shuffled) surrogate data sets. The isospectral data set was used to test for random phase relationships, and the isodistribution data set was used for effects of white noise between SBP and R-R interval. Spontaneous baroreflex sequences were defined as three or more beats in which SBP and the R-R interval of the same (lag 0), next (lag 1), or next following (lag 2) beat changed in the same direction. The total number of baroreflex sequences in the original data was significantly greater than the surrogates (P < 0.001). In the original data, there were significantly (P < 0.001) more lag 0 than lag 1 or lag 2 baroreflex sequences. Therefore, these results indicated that spontaneous baroreflex sequences represented physiological rather than chance interactions and that baroreflex responses can occur within the same beat.

Adult↗