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Biomedical subjects

C A Ray

Publications and source records attributed to C A Ray.

At least 55 records · Page 3Linked to original sources

Modulation of sympathetic nerve activity during posthandgrip muscle ischemia in humans.

To evaluate modulation of muscle sympathetic nerve activity (MSNA) during posthandgrip muscle ischemia (PHGMI), subjects performed 2 min of isometric handgrip at 33% of maximal voluntary contraction (MVC) followed by 2 min of PHGMI produced by forearm vascular occlusion. The response to PHGMI was studied in the absence and again during the addition of contralateral rhythmic handgrip (RHG; 40 times/min) at 15% (n = 6) and 30% (n = 10) MVC during the second minute of the PHGMI. Additionally, to isolate the effect of central command, response to PHGMI was studied during attempted RHG after sensory nerve blockade (n = 5). RHG for 2 min at 15 and 30% MVC and attempted RHG for 2 min did not increase MSNA. Isometric handgrip elicited an 130 +/- 48% increase in MSNA (P < 0.05), which was maintained during PHGMI. RHG at 15 and 30% MVC elicited an attenuation of MSNA (-10 +/- 7% and -14 +/- 6%, respectively) when performed during the second minute of PHGMI (P < 0.05). In contrast, attempted RHG did not significantly affect MSNA during PHGMI. The findings demonstrate modulation of MSNA during activation of the muscle metaboreflex. The attenuation of metaboreceptor-mediated increases in MSNA appear to be the result of mechanosensitive muscle afferents and not central command.

Adult↗

Naloxone does not affect the cardiovascular and sympathetic adjustments to static exercise in humans.

Previous studies suggested that endogenous opiates may attenuate the cardiovascular and sympathetic adjustments to static exercise. We tested whether this effect originates from exercising skeletal muscle. Eight men performed 2 min of static handgrip (30% maximum) followed by 2 min of posthandgrip muscle ischemia after three interventions: 1) control, 2) intra-arterial injection of naloxone HCl (60 micrograms) or vehicle (saline) in the exercising arm, and 3) systemic infusion of naloxone (4 mg) or vehicle. Naloxone and vehicle trials were performed double blind on separate days. Preexercise baseline muscle sympathetic nerve activity (burst frequency), heart rate, and blood pressure were similar across interventions on either day. During static handgrip, control, intra-arterial, and systemic administration of vehicle and naloxone elicited similar increases in total muscle sympathetic nerve activity (58 +/- 24 vs. 68 +/- 26, 146 +/- 49 vs. 132 +/- 42, 137 +/- 54 vs. 164 +/- 44%, respectively), heart rate (9 +/- 2 vs. 8 +/- 3, 16 +/- 3 vs. 16 +/- 2, 20 +/- 4 vs. 19 +/- 3 beats/min, respectively), and mean arterial pressure (22 +/- 4 vs. 21 +/- 4, 29 +/- 5 vs. 26 +/- 3, 28 +/- 4 vs. 27 +/- 4 mmHg, respectively). Additionally, there were no differences between vehicle and naloxone trials during posthandgrip muscle ischemia. Thus, contrary to previous reports, we conclude that the endogenous opiate peptide system does not modulate cardiovascular and sympathetic responses to brief periods of static exercise or muscle ischemia in humans.

Adolescent↗

Muscle sympathetic nerve responses to dynamic one-legged exercise: effect of body posture.

Previous studies examining muscle sympathetic nerve activity (MSNA) during dynamic exercise have focused on upper extremity exercise. The present study was undertaken to investigate 1) MSNA responses to dynamic one-legged knee extensions (DLE) and 2) the role of the cardiopulmonary baroreflexes in the modulation of MSNA responses to DLE. MSNA was measured during 4 min of DLE at 20 (n = 10) and 30 W (n = 9) and during 3 min of DLE at 40 W (n = 9). DLE was performed in the upright (sitting) position and MSNA was recorded in the contralateral leg (peroneal nerve). DLE elicited significant increases in mean arterial pressure (MAP) and heart rate (HR; P < 0.05). In contrast to previous studies using dynamic arm exercise, MSNA (bursts/min) decreased by 25% (P < 0.05) during the first minute of DLE from resting control and remained suppressed during the remaining 3 min of DLE at 20 and 30 W. During the first minute of DLE at 40 W, MSNA (bursts/min) decreased by 18% (P < 0.05), but returned to control levels during the last minute of exercise. Because dynamic leg exercise in the upright position increases venous return, we postulated that upright DLE might increase cardiac filling pressures and stimulate the cardiopulmonary baroreceptors resulting in suppression of MSNA. To investigate this possibility, we measured MSNA and central venous pressure (CVP) during 4 min of both supine and upright DLE at 30 W. MAP, HR, and CVP increased and MSNA decreased from 30 +/- 3 to 22 +/- 3 bursts/min (mean exercise value; P < 0.05) during upright DLE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Muscle sympathetic nerve responses to prolonged one-legged exercise.

We previously demonstrated that brief dynamic one-legged knee extensions (DKE) performed in the upright position decreased muscle sympathetic nerve activity (MSNA). The present study was undertaken to investigate MSNA responses to prolonged DKE. DKE was performed for 40 min in the upright (sitting) position, and MSNA was recorded in the peroneal nerve of the contralateral leg by microneurography. DKE elicited a significant increase in mean arterial pressure (MAP) from 83 +/- 3 to 101 +/- 6 (SE) mmHg during the 5th min of exercise. The increase in MAP persisted for the remainder of exercise. In contrast, heart rate (HR) showed a gradual increase throughout the 40 min of exercise (80 +/- 3 to 110 +/- 5 beats/min at 40 min of exercise; P < 0.05). MSNA decreased from 34 +/- 3 to 28 +/- 3 bursts/min (P < 0.05) from control to the 5th min of DKE and then returned to control levels by 20 min (35 +/- 3 bursts/min) and remained unchanged for the remainder of exercise. During recovery, MSNA was significantly increased above control for 10 min postexercise (40 bursts/min) when HR and MAP had returned to control levels. These results confirm our previous finding that MSNA is decreased during the early stage of upright DKE. The two new findings are as follows: 1) prolonged DKE failed to increase MSNA above control levels, and 2) during recovery when HR and MAP are at control levels, MSNA is significantly elevated.

Adult↗

Augmentation of muscle sympathetic nerve activity during fatiguing isometric leg exercise.

Recent studies have shown a lack of an increase in muscle sympathetic nerve activity (MSNA) during leg exercise. Experiments using isometric knee extension (IKE) have shown a biphasic response in MSNA with a decrease during the 1st min and a return of MSNA to control levels during the 2nd min of IKE. Moreover, MSNA was not augmented during postexercise muscle ischemia (PEMI) of the exercising leg, suggesting that the muscle metaboreflex may have not been engaged in these experiments. The purpose of the present study was 1) to examine MSNA during IKE performed to fatigue to determine whether MSNA could be increased with leg exercise and 2) to determine whether increases in MSNA during fatiguing IKE were associated with an augmented MSNA response during PEMI. IKE was initially performed to fatigue at 30% of maximal voluntary contraction in the sitting position (n = 7; trial 1). IKE elicited a marked increase in mean arterial pressure and heart rate (P < 0.01). Total MSNA (burst frequency x mean burst amplitude; units) in the contralateral leg increased 96 +/- 40% (P < 0.01) above control levels during the final 30 s of IKE (207 +/- 23 s). Subjects (n = 8) then performed IKE to fatigue followed by PEMI (trial 2). MSNA in the contralateral leg increased 107 +/- 50% (P < 0.01) above control levels during the final 30 s of IKE (169 +/- 12 s) and remained significantly elevated during PEMI (83 +/- 40% above control), indicating that the muscle metaboreflex was engaged during fatiguing IKE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Site-specific RNA cleavage generates the 3' end of a poxvirus late mRNA.

The cowpox virus late mRNAs encoding the major protein of the A-type inclusions have 3' ends corresponding to a single site in the DNA template. The DNA sequence of the Alu I-Xba I fragment at this position encodes an RNA cis-acting signal, designated the AX element, which directs this RNA 3' end formation. In cells infected with vaccinia virus the AX element functions independently of either the nature of the promoter element or the RNA polymerase responsible for generating the primary RNA. At late times during virus replication, vaccinia virus induces or activates a site-specific endoribonuclease that cleaves primary RNAs within the AX element. The 3' end produced by RNA cleavage is then polyadenylylated to form the 3' end of the mature mRNA. Therefore, the poxviruses employ at least two mechanisms of RNA 3' end formation during the viral replication cycle. One mechanism, which is operative at early times in viral replication, involves the termination of transcription [Rohrmann, G., Yuen, L. & Moss, B. (1986) Cell 46, 1029-1035]. A second mechanism, which is operative at late times during viral replication, involves the site-specific cleavage of primary RNAs.

Base Sequence↗

Viral inhibition of inflammation: cowpox virus encodes an inhibitor of the interleukin-1 beta converting enzyme.

Cowpox virus effectively inhibits inflammatory responses against viral infection in the chick embryo. This study demonstrates that one of the viral genes necessary for this inhibition, the crmA gene (a cytokine response modifier gene), encodes a serpin that is a specific inhibitor of the interleukin-1 beta converting enzyme. This serpin can prevent the proteolytic activation of interleukin-1 beta, thereby suppressing an interleukin-1 beta response to infection. However, the modification of this single cytokine response is not sufficient to inhibit inflammatory responses. This suggests that cowpox virus encodes several cytokine response modifiers that act together to inhibit the release of pro-inflammatory cytokines in response to infection. These viral countermeasures to host defenses against infection may contribute significantly to the pathology associated with poxvirus infections.

Amino Acid Sequence↗

Effects of cholinergic agonists on regional brain energy metabolism in the scopolamine-treated rat.

The effects of scopolamine, physostigmine, RS86 and U-80816B on regional energy metabolism were studied in rodents by means of the 2-deoxyglucose autoradiographic technique. Scopolamine depressed metabolism in an area of cerebral cortex, focused around the parietal region. Rats treated with cholinergic direct agonists (U-80816B, RS86) as well as with the indirect agonist (physostigmine) all showed decreases in cortical energy metabolism, similar to scopolamine. They also induced an increase in thalamic metabolism. When these drugs were given in conjunction with scopolamine, metabolism tended to change in the opposite direction from the values obtained with the drug alone. These results suggest that there are complex interactions between pre- and post-synaptic muscarinic receptors. Additionally, nicotinic receptors could also be involved in some of the effects of physostigmine.

Animals↗

A signal-averaging technique for the analysis of human muscle sympathetic nerve activity.

We present a signal-averaging technique for analysis of human muscle sympathetic nerve activity (SNA). Nerve traffic was averaged by coupling signal acquisition to electrocardiographic R waves. The amplitude of the averaged waveform was multiplied by the number of R waves sampled to provide a measure of SNA in arbitrary units. This was compared with SNA measured by manual digitization of hard-copy records. In nine volunteers, SNA was increased or decreased with stepwise infusions of nitroprusside or phenylephrine: there were 10 5-min periods of data in each subject. Across all subjects, the correlation between manual and signal-averaged measures of SNA was excellent during both nitroprusside (r = 0.98) and phenylephrine infusions (r = 0.91) and the slopes of the regression lines were near unity. In three periods of data collection, electrical artifacts were added randomly at frequencies of 0.5 and 0.07 Hz during playback of the signal into the computer. Signal-averaged estimates of SNA were unaffected by artifacts. This technique provides reliable observer-independent measures of SNA.

Blood Pressure↗

Muscle sympathetic nerve responses to static leg exercise.

Previous studies of muscle sympathetic nerve activity (MSNA) during static exercise have employed predominantly the arms. These studies have revealed striking increases in arm and leg MSNA during static handgrip (SHG) and postexercise circulatory arrest (PECA). The purpose of this study was to examine MSNA during static leg exercise (SLE) at intensities and duration commonly used during SHG followed by PECA. During 2 min of SLE (static knee extension) at 10% of maximal voluntary contraction (MVC; n = 18) in the sitting position, mean arterial pressure and heart rate increased significantly. Surprisingly, MSNA in the contralateral leg did not increase above control levels during SLE but rather decreased (23 +/- 5%; P < 0.05) during the 1st min of SLE at 10% MVC. We compared MSNA responses to SHG and SLE (n = 8) at 30% MVC. SHG and SLE elicited comparable increases (P < 0.05) in arterial pressure and heart rate, but SHG elicited significant increases in MSNA, whereas SLE did not. During PECA after SHG and SLE, mean arterial pressure remained significantly above control. However, MSNA was unchanged during PECA after SLE but was significantly greater than control during PECA after SHG. Because previous studies have indicated differences in MSNA responses to the arm and leg, we measured arm and leg MSNA simultaneously in six subjects during SLE at 20% MVC and PECA. During SLE and PECA, MSNA in the contralateral arm and leg did not differ significantly from each other.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗

Differential effects of dietary carbohydrate on RPE at the lactate and ventilatory thresholds.

This study used manipulation of dietary intake and substrate utilization to dissociate the ventilatory (TVE) and lactate (TLAC) thresholds, and investigated the role of the thresholds in perception of effort as measured by the Borg 15-category rating of perceived exertion (RPE) scale. Thirteen males performed graded exercise tests following: a) glycogen depletion (GD) and 3 d on a high-carbohydrate diet (HC, 93% total daily energy intake as carbohydrate), b) GD and 3 d on a low-carbohydrate diet (LC, 21%), and c) a mixed-carbohydrate diet (NC, 51%). During submaximal exercise at intensities between 30 and 90% of peak oxygen uptake (VO2peak), significant differences among conditions (P less than 0.05) were obtained for carbon dioxide elimination, respiratory exchange ratio, and plasma lactate, with HC greater than NC greater than LC. Mean (+/- SD) TLAC occurred at different (P less than 0.05) percentages of VO2peak, with HC (55.6 +/- 2.9%) less than NC (59.6 +/- 2.9%) less than LC (63.8 +/- 2.8%). Means for TVE were not different. RPE at TLAC were significantly different (P less than 0.01) among conditions, with HC (12.6 +/- 0.6) less than NC (13.8 +/- 0.6) less than LC (14.3 +/- 0.7), but RPE at TVE were not different. It was concluded that the perception of exertion as becoming "somewhat hard" to "hard" is more closely linked to TVE than to TLAC.

Adult↗

Regional cerebral glucose metabolism compared in rodents and humans.

In order to compare regional brain glucose metabolism in rats and humans, this parameter was measured using Sokoloff's deoxyglucose method in rats, and positron emission tomography with magnetic resonance imaging in humans. An atlas of cerebral regions of interest common to both species was developed to facilitate the evaluation of the relationship in regional values. We found among the regions studied a significant positive correlation in their metabolic values (r = 0.72, P less than 0.001) and coefficients of variation (r = 0.59, P less than 0.01) suggesting that regional brain glucose consumption is comparable between rat and human. Results of this study support the view that rat and human brain may be phylogenetically linked functionally as well as anatomically.

Aged↗

Interactive effects of body posture and exercise training on maximal oxygen uptake.

To determine the effect of posture on maximal O2 uptake (VO2 max) and other cardiorespiratory adaptations to exercise training, 16 male subjects were trained using high-intensity interval and prolonged continuous cycling in either the supine or upright posture 40 min/day 4 days/wk for 8 wk and 7 male subjects served as non-training controls. VO2 max measured during upright cycling and supine cycling, respectively, increased significantly (P less than 0.05) by 16.1 +/- 3.4 and 22.9 +/- 3.4% in the supine training group (STG) and by 14.6 +/- 2.0 and 6.0 +/- 2.0% in the upright training group (UTG). The increase in VO2 max measured during supine cycling was significantly greater (P less than 0.05) in the STG than in the UTG. The increase in VO2 max in the UTG was significantly greater (P less than 0.05) when measured during upright exercise than during supine exercise. However, there was no significant difference in posture-specific VO2 max adaptations in the STG. A postural specificity was also evident in other maximal cardiorespiratory variables (ventilation, CO2 production, and respiratory exchange ratio). In the UTG, maximal heart rate decreased significantly (P less than 0.05) only during supine cycling; there was no significant difference in maximal heart rate after training in the STG. We conclude that posture affects maximal cardiorespiratory adaptations to cycle training. Additionally, supine training is more effective than upright training in increasing maximal cardiorespiratory responses measured during supine exercise, and the effects of supine training generalize to the upright posture to a greater extent than the effects of upright training generalize to the supine posture.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

Red blood cell pulmonary capillary transit time during exercise in athletes.

The purpose of this study was to test the hypothesis that the exercise-induced hypoxemia observed in endurance athletes is due to a reduction in the mean red blood cell pulmonary capillary transit time consequent to a plateau in pulmonary capillary blood volume (Vc) as exercise intensity progresses from moderate to heavy levels. Measurements of Vc, mean transit time, arterial O2 tension (PaO2), and end tidal-arterial O2 tension difference (AaDO2) were made in 16 subjects (mean maximal oxygen uptake (VO2max) = 4.90 l.min-1) at rest and during five cycle exercise bouts designed to elicit 55, 65, 75, 85, and 95% VO2max. Mean PaO2 fell from 101 mm Hg at rest to 85 mm Hg during heavy exercise. Mean AaDO2 increased linearly from one stage to the next and at the highest work rate equaled 22.3 mm Hg. Mean Vc failed to plateau with increasing exercise intensity and increased on average by 16 ml from one stage to the next. Mean transit time, on average, dropped from 1.05 s at rest to 0.46 s at the lowest work rate. Mean transit time did not decrease further with increasing exercise intensity (range, 0.42-0.46 s). We conclude that, under the conditions of this study, the AaDO2 increases and PaO2 decreases observed in endurance athletes during exercise of increasing intensity is not caused by a plateau in Vc and a consequent reduction in mean transit time.

Adult↗

Relationship of heart rate to oxygen uptake during weight lifting exercise.

To define the relation of heart rate to oxygen uptake during weight lifting (WL), heart rate (HR) and oxygen uptake (VO2) were determined during bouts of WL at four intensities (40, 50, 60, and 70% of one-repetition maximum (1-RM)) in 15 males. The 11.5-min bouts of WL consisted of three circuits using four exercises (bench press, bent-over row, arm curl, and parallel squat), with each performed for ten repetitions over a 30-s period with a 1:1 work/rest ratio. During lifting at the four intensities, mean (+/- SE) VO2 values were 1.31 +/- 0.04, 1.50 +/- 0.07, 1.72 +/- 0.07, and 1.86 +/- 0.08 l.min-1, or 33-47% of treadmill-determined VO2max. Mean (+/- SE) HR values were 124 +/- 4, 134 +/- 4, 148 +/- 5, and 161 +/- 4 beats.min-1, or 63-82% of maximal HR. The slope of the linear regression equation predicting %VO2max from %HRmax (Y = 0.582X - 1.7911, r = 0.86, SEE = 3.4%) was approximately half that reported for dynamic low-resistance exercise such as running or cycling. At a given %HRmax, %VO2max was consistently lower than predicted for dynamic low-resistance exercise. It was concluded that the HR/VO2 relationship during dynamic high-resistance exercise for intensities between 40 and 70% of 1-RM is linear but is different from that reported for dynamic low-resistance exercise. The data are consistent with the conclusion in previous studies that using HR to prescribe the metabolic intensity of WL exercise results in a substantially lower level of aerobic metabolism than during dynamic low-resistance exercise.

Adult↗

Is the gender difference in peak VO2 greater for arm than leg exercise?

Based on observations that the difference between men and women in estimates of arm musculature is greater than the difference in leg musculature, it was hypothesized that the gender difference in peak oxygen uptake (VO2; l.min-1) would be greater for arm exercise than leg exercise. To test this hypothesis, 19 (10 men, 9 women) highly trained swimmers (HT) and 20 (10 men, 10 women) untrained students (UT) were tested for peak VO2 on cycle and arm-crank ergometers. Arm and leg fat-free volumes (FFV) were measured to provide an estimate of muscle distribution. No gender difference was observed in either the arm-to-leg peak VO2 ratio (0.699 for the men vs 0.696 for the women) or in the arm-to-leg FFV ratio (0.410 for the men vs 0.402 for the women). Although the proportion of musculature in the arms as assessed by the FFV appeared to be the same in men and women, the similarity in muscle distribution was probably not responsible for the identical average arm-to-leg peak VO2 ratios. The variance in the muscle distribution accounted for only 2-4% of the variance in the arm-to-leg peak VO2 differences within individuals. We conclude that factors other than arm and leg muscle dimensions account for the variability in the arm-to-leg peak VO2 ratio and that the gender difference in peak VO2 is the same for arm and leg exercise.

Adult↗

Interactive effect of body posture on exercise-induced atrial natriuretic peptide release.

The purpose of this investigation was to test the hypothesis that supine exercise elicits a greater atrial natriuretic peptide (ANP) response than upright exercise because of higher atrial filling pressure attained in the supine posture. Plasma ANP concentration ([ANP]) was measured during continuous graded supine and upright exercise in eight healthy men at rest after 4 min of cycling exercise at 31, 51, and 79% of posture-specific peak oxygen uptake (VO2 peak), after 2 min of cycling at posture-specific VO2 peak, and 5 and 15 min postexercise. [ANP] was significantly increased (P less than 0.05) above rest by 64, 140, and 228% during supine cycling at 51 and 79% and VO2 peak, respectively. During upright cycling, [ANP] was significantly increased (P less than 0.05) at 79% (60%) and VO2 peak (125%). After 15 min of postexercise rest, [ANP] remained elevated (P less than 0.05) only in the supine subjects. [ANP] was 63, 79, and 75% higher (P less than 0.05) in the supine than in the upright position during cycling at 51 and 79% and VO2 peak. Systolic, diastolic, and mean blood pressures were not significantly (P greater than 0.05) different between positions in all measurement periods. Heart rates were lower (P less than 0.05) in the supine position compared with the upright position. In conclusion, these results suggest that supine exercise elicits greater ANP release independent of blood pressure and heart rate but presumably caused by greater venous return, central blood volume, and concomitant atrial filling pressure and stretch.

Adult↗

Postural specificity of cardiovascular adaptations to exercise training.

The purposes of this study were to determine 1) whether posture affects the magnitude of cardiovascular adaptations to training and 2) whether cardiovascular adaptations resulting from exercise training in the supine posture transfer (generalize) to exercise in the upright posture and vice versa. Sixteen sedentary men, aged 18-33 yr, were trained using high-intensity interval and prolonged continuous cycling in the supine (STG; supine training group) or upright (UTG; upright training group) posture 4 days/wk, 40 min/day, for 8 wk, while seven male subjects served as nontraining controls. After training, maximal O2 uptake measured during supine and upright cycling, respectively, increased significantly (P less than 0.05) by 22.9 and 16.1% in the STG and by 6.0 and 14.6% in the UTG. No significant cardiovascular adaptations were observed at rest. During submaximal supine cycling at 100 W, significant increases in end-diastolic volume (21%) and stroke volume (22%) (radionuclide ventriculography and CO2 rebreathing) and decreases in heart rate, blood pressure, and systemic vascular resistance occurred in the STG, whereas only a significant decrease in blood pressure occurred in the UTG. During upright cycling at 100 W, a significant decrease in blood pressure occurred in the STG, whereas significant increases in end-diastolic volume (17%) and stroke volume (18%) and decreases in blood pressure and systemic vascular resistance occurred in the UTG. Volume of myocardial contractility, ejection fraction, and systolic blood pressure-to-end-systolic volume ratio did not change significantly after training when measured during supine and upright cycling in either training group. Blood volume increased significantly in the UTG but remained unchanged in the STG.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗