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Biomedical subjects

R L Hughson

Publications and source records attributed to R L Hughson.

At least 145 records · Page 8Linked to original sources

Failure of impedance plethysmography to follow exercise-induced changes in limb blood flow.

1. The blood flow in the forearm and the calf of six healthy volunteers was measured at rest and after exercise by impedance plethysmography using pulsatile (QZp) and venous occlusion (QZocc) methods, and by venous occlusion strain gauge plethysmography (Qsg). 2. At rest, the impedance QZp method gave values slightly higher than those of Qsg. In the forearm, the ratio QZp to Qsg was 1.26 in the supine position and 1.97 in the upright sitting position. For the calf muscle, the ratios were 1.08 in the supine position and 1.23 in the upright position. 3. Immediately after exercise, Qsg increased from resting values of approximately 2-4 ml min-1 100 ml-1 to mean values of 16-25 ml min-1 100 ml-1 in upright and supine arm or leg exercise. In contrast, the QZp values after exercise increased to only 3.1-4.6 ml min-1 100 ml-1. QZocc likewise failed to show increases in flow except in the supine leg exercise, where flow increased to 8.7 ml min-1 100 ml-1. 4. In an additional subject, it was shown that electrode position had no significant effect on the QZp blood flow measurement after exercise. 5. The failure of QZp to accurately follow the change in Qsg with exercise was probably due in part to pulsatile venous outflow. In addition, changes in microvessel packed cell volume and shear rate may influence the observed QZp. It is concluded that impedance plethysmography is not valid for estimation of limb blood flow during reactive hyperaemia after exercise.

Adult↗

Human tibialis anterior contractile responses following fatiguing exercise with and without beta-adrenoceptor blockade.

The effects of oral propranolol (2 x 80 mg/day) on the contractile responses to twitch and tetanic electrical stimulation were examined in the tibialis anterior (TA) muscle of seven healthy young males. The TA muscle was fatigued by four forms of repeated isometric contractions: (1) maximal voluntary contractions (MVC), (2) MVC with circulation occluded, (3) electrically evoked contractions with 20 Hz supramaximal voltage stimulation and (4) electrically evoked contractions with circulation occluded. Each contraction was sustained for 10 s with 5 s recovery. Duration of exercise was 10 min for intact circulation and 4 min for circulatory occlusion. Pre-exercise, both the twitch contraction time and the 1/2 relaxation time were significantly (P less than 0.05) longer with beta-blockade than placebo. beta-blockade did not affect torque output during tetanic stimulation or MVC. Immediately post-exercise, the peak twitch torque was reduced in all beta-blocked and placebo conditions except electrically induced exercise with intact circulation. The 1/2 relaxation time was significantly lengthened by repeated MVC with circulation intact; beta-blockade caused a greater lengthening than placebo (P less than 0.05). The tetanic torque was reduced immediately post-exercise at each of 10, 20, 50 and 100 Hz for both beta-blockade and placebo for each form of exercise. There were no significant beta-blockade effects. Torque output at 10 Hz was still reduced up to 10 min post-exercise. In contrast, 100 Hz torque output recovered by 5 min post-exercise. The changes in tetanic responses were qualitatively similar with intact circulation and with circulatory occlusion. In the tibialis anterior muscle, the effects of fatiguing exercise are not accentuated by beta-blockade. These data in the TA are notably different from those in the triceps surae, where greater fatigue has been shown with beta-blockade.

Adult↗

Kinetics of VO2 with impulse and step exercise in humans.

The constancy of the time course (i.e., dynamic linearity) of the O2 uptake (VO2) response to exercise was examined by testing the law of superposition on data from impulse and step work rate forcings. Two impulses (10 s at a 235-W increase above a 25-W base line, I-235; and 5 s at a 475-W increase above a 25-W base line, I-475), four steps (ST) (25-65 W, ST1; 65-105 W, ST2; 25-105 W, ST3; and 25-145 W, ST4), and the corresponding off-transient responses were performed six to eight times by each of five subjects. The integrated area (G) of the VO2 response for I-235 was similar to that of ST1 and ST2 (P greater than 0.05); the I-475 G was significantly greater (P less than 0.05). The time constant of VO2 during the step function on-transient response for the second exponential component was significantly faster for ST1 and significantly slower for I-235 and I-475 than for ST2, ST3, and ST4 (P less than 0.05). However, I-235 and I-475 time constants for VO2 were not different from the ST off-transient values. Attempts to superimpose the integral of the impulse on the ST data showed that the early rapid increase in VO2 in the ST was underpredicted by the impulse and that the impulse response lagged behind the ST at all points before steady state. It can be concluded that VO2 kinetics failed the test of superposition and are therefore described by a nonlinear dynamic system.

Adolescent↗

On the modeling and interpretation of oxygen uptake kinetics from ramp work rate tests.

Ramp work rate tests have been used to estimate aerobic parameters in exercise stress testing. Previous studies have suggested an assumption of a linear dynamic system for O2 uptake kinetics. The implication is that model parameters estimated from ramp tests should be similar to those estimated from other dynamic tests. In nine healthy subjects, we found that model parameters used to characterize O2 consumption ramp data were not consistent with those used to characterize step data, when the comparison was made on a subject-to-subject basis. Furthermore the ramp data model parameter values were highly dependent (P less than 0.0001) on the ramp slope. A linear dynamic system interpretation of the ramp data model does not appear to be appropriate, suggesting that caution is needed in the interpretation of ramp data aerobic parameters. The data may be better described by nonlinear or higher order function. Ramp exercise testing is not suitable for assessing dynamic control properties of the cardiorespiratory response to exercise.

Adolescent↗

Effects of bromocriptine on sweat gland function during heat acclimatization.

This study examined the involvement of the hormones aldosterone and prolactin in sweat gland function during heat acclimatization. Two groups of male subjects (n = 8) were tested - one receiving a placebo (control), the other receiving bromocriptine. Both groups performed cycle ergometer exercise at 50% of maximal oxygen uptake over 10 consecutive days in an environmental chamber maintained at 39 degrees C and 30% relative humidity. Duration of exercise was 90 min on days 2-4 and 6-9, and 45 min on test days 1, 5 and 10. Electrolyte concentrations were determined by total body washdown. Prolactin increased (p less than 0.001) during exercise on day 1 in the control group but not on days 5 and 10. In contrast, prolactin was suppressed by bromocriptine and did not rise in response to exercise or heat exposure. Plasma aldosterone increased during exercise in both groups, showing no differences between groups. The sodium concentration in sweat decreased significantly (p less than 0.05) in the control group from day 1 to 10 but was unchanged in the treatment group. These data suggest that acclimatization-related changes in sweat gland function may be attenuated by increases in central dopaminergic activity and implicate prolactin in control of sweat gland function.

Acclimatization↗

Twitch potentiation after fatiguing exercise in man.

Twitch potentiation was studied in the human triceps surae complex before and after intermittent maximal voluntary contractions or electrical stimulation at 20 Hz. Both forms of exercise were conducted with intact circulation for a maximum of 10 min or with circulatory occlusion until force output declined 50%. The relative potentiation was determined when a control twitch was compared to a twitch obtained after 5 s of maximal voluntary plantar flexion. The unpotentiated twitch torque (PT) and potentiated twitch torque (PT*) were reduced most severely after voluntary ischemic exercise (63.2% and 52.5% respectively, (P less than 0.001)). However, the relative potentiation (PT*/PT) immediately after voluntary ischemic exercise increased to 1.65 +/- 0.18 from 1.22 +/- 0.13 at rest. Both PT and PT* recovered quickly after exercise. At rest, twitch contraction time (CT) and one-half relaxation time (1/2 RT) in the unpotentiated twitch were longer than that of contraction (CT*) and one-half relaxation time (1/2 RT*) in the potentiated twitch. Following non-occluded exercise, CT, CT*, 1/2 RT and 1/2 RT* were shortened relative to rest. After ischemic exercise CT and CT* were shortened although 1/2 RT and 1/2 RT* increased relative to rest. Both CT* and 1/2 RT* quickly recovered to pre-exercise values by 5 min post-exercise. Ratios of potentiated/control twitch parameters were not altered after nonoccluded exercise, but were increased after ischemic exercise. These results suggest that the mechanisms of fatigue which depress voluntary torque and twitch and potentiated twitch torques, do not interfere with the extent of potentiation after fatiguing exercise.

Adult↗

The effects of beta-blockade on electrically stimulated contraction in fatigued human triceps surae muscle.

The contractile characteristics of the triceps surae muscle group were examined before and after repeated isometric contractions in two groups of eight healthy young males. Single twitches and trains of stimuli at 10, 20, 50 and 100 Hz were delivered to the muscle using supramaximal voltages. Subjects were treated with beta-blockade (2 X 80 mg oral propranolol, beta-b) or matched placebo in a double-blind crossover design. Four different exercise conditions were studied: (I) maximal voluntary contraction (MVC); (II) MVC during circulatory occlusion; (III) electrical stimulation at 20 Hz using 50% of voltage required for maximal torque production; and (IV) electrical stimulation with occlusion. Each contraction was for 5 s with 5 s recovery. Total duration of exercise was 10 min for non-occluded contractions and to a 50% decline in torque output with occlusion. At rest prior to exercise, maximal voluntary contraction was significantly reduced (5.7%) by beta-b during 40 observations in 16 subjects. Following exercise without occlusion (I and III), the reduction in torque output of the muscle at 10 and 20 Hz stimulation was generally greater during beta-b than placebo. This low frequency fatigue was longer-lasting with beta-b. The shorter lasting reduction in torque at 50 and 100 Hz was generally not different between beta-b placebo. After exercise with occlusion (II and IV), the torque output at all stimulation frequencies was reduced to a similar extent in both placebo and beta-b at most comparison points. Twitch responses after exercise with occlusion showed decreases in peak tension and time to peak tension and a lengthening of one-half relaxation time in both placebo and beta-b. It was concluded that the greater reduction in torque output of the triceps surae muscle group at low frequencies during beta-b was probably a consequence of a reduction in blood flow relative to the placebo treatment. This relative low frequency fatigue could be responsible for the increased perception of effort in patients exercising during beta-blocker therapy.

Adult↗

Contractile properties of the human triceps surae following prolonged exercise and beta-blockade.

Sixteen healthy males volunteered to perform both an incremental maximal and prolonged submaximal treadmill test with beta-blockade (2 X 80 mg oral propranolol per day) or matched placebo in a blind crossover design. Prior to and following the prolonged exercise, electrical stimulation of the triceps surae was performed to examine contractile properties. During the maximal test, the heart rate (HR) was reduced at all times by beta-blockade. The time to exhaustion in this test was significantly reduced by beta-blockade (P less than 0.03), while the maximal oxygen uptake (VO2 max) was not significantly lower (P = 0.06). In response to prolonged treadmill walking at 60% of VO2 max, the HR was reduced but VO2, respiratory quotient and ventilation were not affected by beta-blockade relative to placebo. Plasma concentrations of free fatty acids increased during exercise in the placebo but not beta-blocked treatment (P less than 0.0001). Plasma noradrenalin and adrenalin increased with exercise; the increase in adrenalin with beta-blockade was greater than that with placebo (P less than 0.0001). The RPE obtained at intervals during the prolonged exercise were greater for beta-blockades than placebo. Eight of 16 subjects were unable to complete full 90 min with beta-blockade; but all 16 completed the test with placebo. The electrically evoked twitches in the triceps surae muscle group after exercise did not differ in peak torque or one-half relaxation time compared to pre-exercise. The time to peak twitch torque was significantly shorter after exercise. No differences in twitch were observed due to beta-blockade. The tetanic responses at 10, 20, 50 and 100 Hz were not affected by either exercise or the beta-blockade. In conclusion, an increased subjective estimate of fatigue (RPE) was observed during prolonged exercise with beta-blockade. This subjective fatigue did not relate to altered peripheral muscle force production during electrical stimulation. The results suggest either a central rather than peripheral origin of fatigue, or fatigue in a muscle group not examined by stimulation of the triceps surae.

Adult↗

Cardiac output in exercise by impedance cardiography during breath holding and normal breathing.

Estimation of cardiac output by impedance cardiography (QZ) in exercise during normal breathing (NB) has been limited by motion artifact. Our objective was to obtain readable impedance cardiograms on five subjects during upright cycle exercise at 0, 50, 100, 150, and 200 W to permit comparisons of QZ during NB, expiratory breath hold (EXP) and inspiratory breath hold (INSP). Q was also determined using an equilibration CO2 rebreathing method [Q(RB)]. QZ during NB exceeded EXP QZ at 100, 150, and 200 W, and exceeded INSP QZ at 100 W (P less than 0.05). The low EXP QZ values were due to a significantly lower stroke volume at 100, 150, and 200 W (P less than 0.05). For the INSP QZ at 100 W, heart rate was lower than during EXP (P less than 0.05). Regression of QZ (NB) against Q(RB) resulted in a linear relationship (r = 0.93) over the range of Q = 7-26 1/min. The slope of the regression differed significantly from 1.0 (P less than 0.05). We conclude that QZ values obtained during EXP or INSP should not be assumed to represent QZ during NB, at least at work rates greater than 50 W. A consequence of the linear relationship between QZ(NB) and Q(RB) over the range of 0-200 W is that estimates of CO2 rebreathing cardiac output can be obtained by impedance cardiography if QZ is adjusted using an appropriate empirical factor.

Adult↗

Supramaximal exercise after training-induced hypervolemia. I. Gas exchange and acid-base balance.

The effect of an exercise-induced reduction in blood O2-carrying capacity on ventilatory gas exchange and acid-base balance during supramaximal exercise was studied in six males [peak O2 consumption (VO2peak), 3.98 +/- 0.49 l/min]. Three consecutive days of supramaximal exercise resulted in a preexercise reduction of hemoglobin concentration from 15.8 to 14.0 g/dl (P less than 0.05). During exercise (120% VO2peak) performed intermittently (1 min work to 4 min rest); a small but significant (P less than 0.05) increase was found for both O2 consumption (VO2) (l X min) and heart rate (beats/min) on day 2 of the training. On day 3, VO2 (l/min) was reduced 3.2% (P less than 0.05) over day 1 values. No changes were found in CO2 output and minute ventilation during exercise between training days. Similarly, short-term training failed to significantly alter the changes in arterialized blood PCO2, pH, and [HCO-3] observed during exercise. It is concluded that hypervolemia-induced reductions in O2-carrying capacity in the order of 10-11% cause minimal impairment to gas exchange and acid-base balance during supramaximal non-steady-state exercise.

Acid-Base Equilibrium↗

Blood lactate concentration increases as a continuous function in progressive exercise.

The relationship between arterialized blood lactate concentration [( La-]) and O2 uptake (VO2) was examined during a total of 23 tests by eight subjects. Exercise was on a cycle ergometer with work rate incremented from loadless pedaling to exhaustion as a 50-W/min ramp function. Two different mathematical models were studied. One model employed a log-log transformation of [La-] and VO2 to yield [La-] threshold as proposed by Beaver et al. (J. Appl. Physiol. 59: 1936-1940, 1985). The other model was a continuous exponential plus constant of the form La- = a + b[exp(cVO2)]. In 21 of 23 data sets, the mean square error (MSE) of the continuous model was less than that of the log-log model (P less than 0.001). The MSE was on average 3.5 times greater in the log-log model than in the continuous model. The residuals were randomly distributed about the line of best fit for the continuous model. In contrast, the log-log model showed a nonrandom pattern indicating an inappropriate model. As an index of the position of the [La-]-VO2 continuous model, the VO2 at which the rate of increase of [La-] equaled the rate of increase of VO2 (d[La-]/dVO2 = 1) was determined. This VO2 was 2.241 +/- 0.081 l/min, which averaged 64.6% of maximal VO2. It is proposed that this lactate slope index could be used as a relative indicator of fitness instead of the previously applied threshold concept. The change in [La-] could be better described mathematically by a continuous model rather than the threshold model of Beaver et al.

Adolescent↗

Fiber type specific glycogen utilization in rat diaphragm during treadmill exercise.

To examine the significance of endogenous stores of glycogen in specific fiber types (I, IIa, IIb) of the costal region of the diaphragm, adult male Wistar rats performed continuous running (25 m/min, 8 degrees grade) exercise for either 30 min or until fatigue. At 30 min of exercise, glycogen loss, as measured microphotometrically using the periodic acid-Schiff technique averaged between 73 and 80% (P less than 0.05) in the different fiber types. When exercise was performed to exhaustion, representing an additional 94 min, no further reduction in glycogen was observed in any fiber type. Biochemical determinations of glycogen from the diaphragm confirmed the extensive reduction in glycogen concentration with exercise. Large reductions (P less than 0.05) in glycogen were also noted in the soleus, plantaris, and vastus lateralis red. Although significant depletion (P less than 0.05) occurred in the vastus lateralis white, it was not as pronounced as in these other muscles. Repletion to preexercise glycogen concentration was complete by 4 h of recovery in all muscles except the vastus lateralis white. It is concluded that endogenous glycogen is a significant substrate in all muscles sampled regardless of fiber composition. In the case of the costal region of the diaphragm, the increased work of breathing resulting from heavy exercise leads to the recruitment of all fiber types, and each fiber type depends on glycogen as a substrate at least early in the exercise.

Animals↗

Estimate of mean tissue O2 consumption at onset of exercise in males.

A mathematical model has been developed that permitted the calculation of the flow-weighted mean tissue O2 consumption (VO2T) at the onset of a step increase in work rate. From breath-by-breath measurements of alveolar O2 consumption (VO2A) and cardiac output (Q) by impedance cardiography and assumptions about the site of depletion of O2 stores, the rate of change in O2 stores (VO2s) was determined. The sum of VO2A + VO2s = VO2T. Six very fit males performed six repetitions of each of two step increases in work rate. STlo was a transition from rest to 100-W cycling; SThi was a transition from 100- to 200-W cycling. For each work rate transition, the responses of VO2A and Q were averaged over the six repetitions of each subject and the model was solved to yield VO2T. The responses of VO2A, VO2T, and Q after the increase in work rate were fit with a monoexponential function. This function included a time constant and time delay, the sum of which gave the mean response time (MRT). In the STlo test, the MRT of VO2A (24.9 +/- 1.1 s, mean +/- SE) was longer than that of VO2T (15.3 +/- 1.3 s) and of Q (16.5 +/- 6.5 s) (P less than 0.05). The MRT of VO2T and Q did not differ significantly. Also for SThi, the MRT of VO2A (34.4 +/- 3.3 s) was significantly longer than that of VO2T (30.0 +/- 3.4 s) (P less than 0.05). The MRT of VO2T and Q (30.3 +/- 5.5 s) were not significantly different at this work rate either.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Training-induced hypervolemia: lack of an effect on oxygen utilization during exercise.

To investigate the effect of training-induced increases in plasma volume on maximal aerobic power, 8 male subjects (age 19 to 24 yr) underwent a 4-d training program (2 h X d-1) at an estimated 71% maximal aerobic power. Following training, plasma volume measured using 131I-human serum albumin increased by 20.3% (P less than 0.01) whereas red cell volume remained unchanged and total blood volume increased by 12.3% (P less than 0.01). During progressive sub-maximal cycle exercise, oxygen consumption, carbon dioxide production, ventilation, and blood lactate concentration remained unchanged following the training whereas heart rate was significantly elevated (P less than 0.05). Significant post-training elevations were also noted in carbon dioxide production (P less than 0.05), blood lactate (P less than 0.01), and peak power output (P less than 0.05) during maximal exercise. Maximal aerobic power and ventilation were not altered. It is concluded that hypervolemia induced by short-term exercise training does not affect oxygen consumption either during sub-maximal or maximal exercise.

Adult↗

Effect of exercise on recovery blood pressure in normotensive and hypertensive subjects.

The effects of dynamic exercise on the acute recovery blood pressure (BP) were studied in normotensive and hypertensive subjects. Three groups [eight normotensives, age 19 to 29 yr (N1); eight normotensives, age 35 to 62 yr (N2); and eight hypertensives, age 44 to 57 yr (H)] were tested over three separate sessions. The first two sessions were for familiarization with the protocol and test procedures. Resting systolic BP decreased (P less than 0.01) in all groups from sessions 1 to 3: N1 = 126 to 121 mm Hg; N2 = 127 to 120; H = 155 to 142. Resting diastolic BP decreased (P less than 0.05) in the N1 and H groups from 77 to 73 and 98 to 95 mm Hg, respectively. On the third day, each subject followed the protocol of Wilcox et al. (8) of 15 min of seated rest, five 10-min periods of treadmill walking with a 3-min rest between each period, and 60 min of seated recovery. Exercise was performed at 67% of estimated maximal heart rate. In all three groups, significant (P less than 0.05) reductions in both systolic BP (N1 = -12 +/- 1; N2 = -10 +/- 2; H = -12 +/- 3) and diastolic BP (N1 = -5 +/- 2; N2 = -5 +/- 1; H = -7 +/- 2) occurred from pre-exercise rest to post-exercise rest. Systolic BP remained lower following 60-min recovery (P less than 0.02), while diastolic BP returned to pre-exercise levels in all three groups. No between-group differences were observed in the magnitude of reduction of BP post-exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Computerized estimation of lactate threshold.

Traditional approaches to estimating a lactate threshold during a progressive exercise test have utilized visual inspection of the data. We describe a computerized approach which utilizes a log-log transformation to yield two approximately linear segments. Linear regression lines are fit to these segments and the intersection of the two lines yields an estimate of the lactate threshold. An approximate 95% confidence interval is also generated.

Algorithms↗

Faster kinetics of VO2 during arm exercise with circulatory occlusion of the legs.

Occlusion of the nonworking leg muscles prior to the onset of supine arm exercise was examined for an effect on the kinetics of respiratory gas exchange (VO2 and VCO2), ventilation (VE), and heart rate (HR). Seven subjects performed arm cycling at 40 W (two females) or 50 W (five males) for 8 min following 4 min of "0" W pedaling. Six repetitions of each of uncuffed and cuffed leg conditions were averaged for individual subject analysis. The VO2 kinetics were significantly faster in the cuffed than the uncuffed condition (mean response time 66.0 +/- 26.4 vs 81.2 +/- 37.5 s, P less than 0.04). The kinetics of VCO2, VE, and HR were not affected by occlusion. It is concluded that the faster VO2 kinetics with the prior occlusion of nonworking leg muscles was a consequence of increased availability of oxygen to the working arm muscles at the onset of exercise.

Adult↗