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Biomedical subjects

M J Joyner

Publications and source records attributed to M J Joyner.

At least 37 records · Page 2Linked to original sources
PubMed2000

Sympathetic activity and baroreflex sensitivity in young women taking oral contraceptives.

BACKGROUND: We tested sympathetic and cardiovagal baroreflex sensitivity during the placebo or "low-hormone" phase (LH) and 2 to 3 weeks later during the "high-hormone" phase (HH) of oral contraceptive (OC) use in 9 women. METHODS AND RESULTS: Sympathetic baroreflex sensitivity was assessed by intravenous doses of sodium nitroprusside and phenylephrine and defined as the slope relating muscle sympathetic nerve activity (by microneurography) and diastolic blood pressure. Cardiovagal baroreflex sensitivity was defined as the slope relating R-R interval and systolic blood pressure. No difference was observed for resting muscle sympathetic nerve activity or plasma norepinephrine levels. However, sympathetic baroreflex sensitivity was greater and mean arterial pressure was higher during the LH than in the HH phase. Similarly, cardiovagal baroreflex sensitivity was greater in the LH than in the HH phase. CONCLUSIONS: Sympathetic and cardiovagal baroreflex sensitivities change during the 28-day course of OC use. Furthermore, changes in baroreflex sensitivity with OC differ from changes in baroreflex sensitivity during the normal menstrual cycle.

Adult↗
PubMed2000

Sympathetic vasodilatation in human limbs.

This review focuses on recent developments in our understanding of active vasodilatation in human skin and skeletal muscle. We have attempted to place recent advances in their historical context and review the evolution of thinking on active vasodilatation in these two vascular beds. In human skin, active vasodilatation is well established, but the neurotransmitter responsible for the dilatation is unknown. In human skeletal muscle, older studies provided circumstantial evidence consistent with sympathetically mediated vasodilatation, but the evidence was never unambiguous. By contrast, recent studies on active vasodilatation in human skeletal muscle in conjunction with a reinterpretation of data from previous studies casts doubt on the existence of sympathetic vasodilator fibres in human skeletal muscle.

Animals↗
PubMed2000

Skeletal muscle vasodilatation during sympathoexcitation is not neurally mediated in humans.

Evidence for the existence of sympathetic vasodilator nerves in human skeletal muscle is controversial. Manoeuvres such as contralateral ischaemic handgripping to fatigue that cause vasoconstriction in the resting forearm evoke vasodilatation after local alpha-adrenergic receptor blockade, raising the possibility that both constrictor and dilator fibres are present. The purpose of this study was to determine whether this dilatation is neurally mediated. Ten subjects (3 women, 7 men) performed ischaemic handgripping to fatigue before and after acute local anaesthetic block of the sympathetic nerves (stellate ganglion) innervating the contralateral (resting) upper extremity. Forearm blood flow was measured with venous occlusion plethysmography in the resting forearm. In control studies there was forearm vasoconstriction during contralateral handgripping to fatigue. During contralateral handgripping after stellate block, blood flow in the resting forearm increased from 6.1 +/- 0.7 to 18.7 +/- 2.2 ml dl-1 min-1 (P < 0.05). Mean arterial pressure measured concurrently increased from approximately 90 to 130 mmHg and estimated vascular conductance rose from 6.5 +/- 0.7 to 14.0 +/- 1.5 units, indicating that most of the rise in forearm blood flow was due to vasodilatation. Brachial artery administration of beta-blockers (propranolol) and the nitric oxide (NO) synthase inhibitor N G-monomethyl-L-arginine (L-NMMA) after stellate block virtually eliminated all of the vasodilatation to contralateral handgrip. Since vasodilatation was seen after stellate block, our data suggest that sympathetic dilator nerves are not responsible for limb vasodilatation seen during sympathoexcitation evoked by contralateral ischaemic handgripping to fatigue. The results obtained with propranolol and L-NMMA suggest that beta-adrenergic mechanisms and local NO release contribute to the dilatation.

Adolescent↗
PubMed2000

Influence of the menstrual cycle on sympathetic activity, baroreflex sensitivity, and vascular transduction in young women.

BACKGROUND: Our goal was to test sympathetic and cardiovagal baroreflex sensitivity and the transduction of sympathetic traffic into vascular resistance during the early follicular (EF) and midluteal (ML) phases of the menstrual cycle. METHODS AND RESULTS: Sympathetic baroreflex sensitivity was assessed by lowering and raising blood pressure with intravenous bolus doses of sodium nitroprusside and phenylephrine. It was defined as the slope relating muscle sympathetic nerve activity (MSNA; determined by microneurography) and diastolic blood pressure. Cardiovagal baroreflex sensitivity was defined as the slope relating R-R interval and systolic blood pressure. Vascular transduction was evaluated during ischemic handgrip exercise and postexercise ischemia, and it was defined as the slope relating MSNA and calf vascular resistance (determined by plethysmography). Resting MSNA (EF, 1170+/-151 U/min; ML, 2252+/-251 U/min; P<0.001) and plasma norepinephrine levels (EF, 240+/-21 pg/mL; ML, 294+/-25 pg/mL; P=0. 025) were significantly higher in the ML than in the EF phase. Furthermore, sympathetic baroreflex sensitivity was greater during the ML than the EF phase in every subject (MSNA/diastolic blood pressure slopes: EF, -4.15; FL, -5.42; P=0.005). No significant differences in cardiovagal baroreflex sensitivity or vascular transduction were observed. CONCLUSIONS: The present study suggests that the hormonal fluctuations that occur during the normal menstrual cycle may alter sympathetic outflow but not the transduction of sympathetic activity into vascular resistance.

Adult↗
PubMed2000

Neurogenic vasodilation in human skeletal muscle: possible role in contraction-induced hyperaemia.

Whether or not neurally mediated vasodilation contributes to the rise in skeletal muscle blood flow during exercise in humans remains unknown. Such a mechanism might serve as an important 'feed-forward' regulatory signal causing blood flow to rise prior to the development of a metabolic demand. Research in animal species has identified three neurally mediated vasodilating mechanisms with the potential to increase skeletal muscle blood flow during exercise. These include sympathetic vasodilator nerves, the potential for substances released by motor nerves to evoke vasodilation and the possibility of an 'intrinsic' vasodilator nerve system within the walls of blood vessels. In humans, sympathetic vasodilator nerves are present in several vascular beds (e.g. cutaneous). However, more recent information suggests that the human skeletal muscle is not innervated by this class of nerves. Along these lines, the vasodilator response to exercise is unaffected by sympathectomy or by blockade of the traditional transmitters associated with neurally mediated vasodilation. The possibility that spillover of substances released from motor neurones evokes vasodilation is provocative. For example, acetylcholine could produce both skeletal muscle contraction via nicotinic receptors and vasodilation via endothelial muscarinic receptors. However, in many species including humans, atropine has no effect on exercise hyperaemia. While the concept of an 'intrinsic' vasodilator pathway within the walls of the skeletal muscle vascular bed is fascinating, limited information is available on this mechanism in animals and none is available in humans. Taken together, the current information suggests that neurally mediated vasodilating mechanisms may not exist in human skeletal muscle. Additionally, even if such mechanisms exist, they do not play an obligatory role in governing the rise in muscle blood flow during exercise in humans.

Humans↗
PubMed2000

Effects of atropine and L-NAME on cutaneous blood flow during body heating in humans.

We sought to investigate further the roles of sweating, ACh spillover, and nitric oxide (NO) in the neurally mediated cutaneous vasodilation during body heating in humans. Six subjects were heated with a water-perfused suit while cutaneous blood flow was measured with a laser-Doppler flowmeter. After a rise in core temperature (1. 0 +/- 0.1 degrees C) and the establishment of cutaneous vasodilation, atropine and subsequently the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) were given to the forearm via a brachial artery catheter. After atropine infusion, cutaneous vascular conductance (CVC) remained constant in five of six subjects, whereas L-NAME administration blunted the rise in CVC in three of six subjects. A subsequent set of studies using intradermal microdialysis probes to selectively deliver drugs into forearm skin confirmed that atropine did not affect CVC. However, perfusion of L-NAME resulted in a significant decrease in CVC (37 +/- 4%, P < 0.05). The results indicate that neither sweating nor NO release via muscarinic receptor activation is essential to sustain cutaneous dilation during heating in humans.

Adult↗
PubMed2000

Cardiac output during exercise by the open circuit acetylene washin method: comparison with direct Fick.

An open-circuit (OpCirc) acetylene uptake cardiac output (QT) method was modified for use during exercise. Two computational techniques were used. OpCirc1 was based on the integrated uptake vs. end-tidal change in acetylene, and OpCirc2 was based on an iterative finite difference modeling method. Six subjects [28-44 yr, peak oxygen consumption (VO(2)) = 120% predicted] performed cycle ergometry exercise to compare QT using OpCirc and direct Fick methods. An incremental protocol was repeated twice, separated by a 10-min rest, and subsequently subjects exercised at 85-90% of their peak work rate. Coefficient of variation of the OpCirc methods and Fick were highest at rest (OpCirc1, 7%, OpCirc2, 12%, Fick, 10%) but were lower at moderate to high exercise intensities (OpCirc1, 3%, OpCirc2, 3%, Fick, 5%). OpCirc1 and OpCirc2 QT correlated highly with Fick QT (R(2) = 0.90 and 0.89, respectively). There were minimal differences between OpCirc1 and OpCirc2 compared with Fick up to moderate-intensity exercise (<70% peak VO(2)); however, both techniques tended to underestimate Fick at >70% peak VO(2). These differences became significant for OpCirc1 only. Part of the differences between Fick and OpCirc methods at the higher exercise intensities are likely related to inhomogeneities in ventilation and perfusion matching (R(2) = 0.36 for Fick - OpCirc1 vs. alveolar-to-arterial oxygen tension difference). In conclusion, both OpCirc methods provided reproducible, reliable measurements of QT during mild to moderate exercise. However, only OpCirc2 appeared to approximate Fick QT at the higher work intensities.

Acetylene↗
PubMed2000

Effect of systemic nitric oxide synthase inhibition on postexercise hypotension in humans.

An acute bout of aerobic exercise results in a reduced blood pressure that lasts several hours. Animal studies suggest this response is mediated by increased production of nitric oxide. We tested the extent to which systemic nitric oxide synthase inhibition [N(G)-monomethyl-L-arginine (L-NMMA)] can reverse the drop in blood pressure that occurs after exercise in humans. Eight healthy subjects underwent parallel experiments on 2 separate days. The order of the experiments was randomized between sham (60 min of seated upright rest) and exercise (60 min of upright cycling at 60% peak aerobic capacity). After both sham and exercise, subjects received, in sequence, systemic alpha-adrenergic blockade (phentolamine) and L-NMMA. Phentolamine was given first to isolate the contribution of nitric oxide to postexercise hypotension by preventing reflex changes in sympathetic tone that result from systemic nitric oxide synthase inhibition and to control for alterations in resting sympathetic activity after exercise. During each condition, systemic and regional hemodynamics were measured. Throughout the study, arterial pressure and vascular resistances remained lower postexercise vs. postsham despite nitric oxide synthase inhibition (e.g., mean arterial pressure after L-NMMA was 108.0+/-2.4 mmHg postsham vs. 102.1+/-3.3 mmHg postexercise; P<0.05). Thus it does not appear that postexercise hypotension is dependent on increased production of nitric oxide in humans.

Adult↗
PubMed2000

Over-the-counter supplements and strength training.

The group from the Exercise Science Department at Iowa State University and their colleagues in other departments at Iowa State have conducted two outstanding studies on human responses to resistance training. These have focused on the extent to which products that have been purported to enhance the responses to resistance training in humans (that are available over the counter to the public) actually work. One compound, androstenedione, seemed ineffective under the conditions studied; the other, HMB, seemed to enhance increases in lean body mass and strength in response to resistance training. These studies were well designed and well controlled and should serve as models for those interested in evaluating the impact of various interventions on body composition and strength in humans.

Adaptation, Physiological↗
PubMed1999

Muscle blood flow during exercise: the limits of reductionism.

This paper attempts to integrate some important concepts about the various mechanisms that are thought to cause blood flow to rise during rhythmic exercise. Mechanisms including the muscle pump, substances released by skeletal muscle, substances transported by blood, and factors released by nerves have been postulated to contribute to the rise in muscle blood flow during exercise. Additionally, the factors that initiate the dilation may not be those which sustain it. Although there is normally a close relationship between contractile activity, metabolic rate, and muscle blood flow, this relationship can be disrupted under a variety of circumstances and the active skeletal muscle overperfused. This delinking of flow and metabolism raises important questions about the nature of the vasodilating substances responsible for the rise in blood flow during exercise. We propose that understanding the mechanisms responsible for the "delinking" of flow and metabolism, along with a more synergistic view of current concepts, can provide new insight into the mechanisms which govern exercise hyperemia.

Blood Flow Velocity↗
PubMed1999

Measurement of limb venous compliance in humans: technical considerations and physiological findings.

We conducted a series of studies to develop and test a rapid, noninvasive method to measure limb venous compliance in humans. First, we measured forearm volume (mercury-in-Silastic strain gauges) and antecubital intravenous pressure during inflation of a venous collecting cuff around the upper arm. Intravenous pressure fit the regression line, -0.3 +/- 0.7 + 0.95 +/- 0.02. cuff pressure (r = 0.99 +/- 0.00), indicating cuff pressure is a good index of intravenous pressure. In subsequent studies, we measured forearm and calf venous compliance by inflating the venous collecting cuff to 60 mmHg for 4 min, then decreasing cuff pressure at 1 mmHg/s (over 1 min) to 0 mmHg, using cuff pressure as an estimate of venous pressure. This method produced pressure-volume curves fitting the quadratic regression (Deltalimb volume) = beta(0) + beta(1). (cuff pressure) + beta(2). (cuff pressure)(2), where Delta is change. Curves generated with this method were reproducible from day to day (coefficient of variation: 4.9%). In 11 subjects we measured venous compliance via this method under two conditions: with and without (in random order) superimposed sympathetic activation (ischemic handgrip exercise to fatigue followed by postexercise ischemia). Calf and forearm compliance did not differ between control and sympathetic activation (P > 0.05); however, the data suggest that unstressed volume was reduced by the maneuver. These studies demonstrate that venous pressure-volume curves can be generated both rapidly and noninvasively with this technique. Furthermore, the results suggest that although whole-limb venous compliance is under negligible sympathetic control in humans, unstressed volume can be affected by the sympathetic nervous system.

Blood Pressure↗
PubMed1998

The effect of nitrous oxide on chest wall function in humans and dogs.

UNLABELLED: The purpose of this study was to determine the effects of nitrous oxide (N2O) on the chest wall of anesthetized humans and dogs. Six human subjects and six mongrel dogs were studied during 1 minimum alveolar anesthetic concentration halothane anesthesia before and during the substitution of 70% N2O for 70% N2 in the inspired gas mixture. On a separate occasion, measurements also were made in pentobarbital-anesthetized dogs. Respiratory muscle activity was measured using electromyographic (EMG) electrodes. Chest wall configuration was determined by using fast three-dimensional computed tomography in dogs and by using respiratory impedance plethysmography in humans. N2O consistently decreased inspiratory ribcage displacement, a decrease attributable in dogs to decreased inspiratory activation of parasternal intercostal muscles; parasternal intercostal activity was not present in anesthetized humans. The decrease in ribcage motion decreased the tidal volume in humans, but not in dogs, because displacement of the diaphragm was better preserved in dogs, in association with changes in diaphragm EMG activation. N2O significantly increased phasic expiratory muscle activity in halothane-anesthetized humans and pentobarbital-anesthetized dogs. Thus, as has been demonstrated for other anesthetics, the actions of N2O are caused by alterations in the distribution and timing of neural drive to the respiratory muscles, rather than by a global depression of respiratory motoneuron drive. IMPLICATIONS: In this study, we examined the effects of nitrous oxide on breathing in halothane-anesthetized dogs and humans. Nitrous oxide affected breathing by changing the distribution and timing of neural drive to the respiratory muscles in a species-dependent manner, rather than by causing a global depression of their activity.

Animals↗
PubMed1998

Effect of various lithotomy positions on lower-extremity blood pressure.

BACKGROUND: Compartment syndrome of a lower extremity from hypoperfusion is a rare but potentially devastating complication of the lithotomy position during surgery. The aim of this study is to determine the effects of various lithotomy positions on lower-extremity blood pressures. METHODS: Blood pressure in eight young, healthy people was studied for 10 lithotomy positions. Blood pressure measurements were taken in both the upper arm (brachial artery) and the lower extremity (dorsalis pedis). The heart-to-ankle height gradient in each position was measured, and a predicted lower-extremity systolic pressure was calculated. The measured and predicted lower-extremity systolic blood pressures were compared with repeated measures analysis of variance. RESULTS: As a group, the mean systolic blood pressures in the lower extremities correlated closely with the predicted values. However, the difference between measured and predicted pressures varied among the 10 positions (P < 0.05). CONCLUSIONS: Although lower-extremity systolic blood pressures in the young, healthy volunteers correlated with predicted values, there was an additional reduction in pressure associated with the lithotomy position. This surprising finding suggests that a lengthy procedure necessitating the use of a lithotomy position for only a portion should be planned so the remainder of the procedure can take place before establishing the position or so the position can be changed to an alternative position when it is no longer needed.

Adolescent↗
PubMed1998

Reflex responses to regional venous pooling during lower body negative pressure in humans.

Lower body negative pressure is frequently used to simulate orthostasis. Prior data suggest that venous pooling in abdominal or pelvic regions may have major hemodynamic consequences. Therefore, we developed a simple paradigm for assessing regional contributions to venous pooling during lower body negative pressure. Sixteen healthy men and women underwent graded lower body negative pressure protocols to 60 mmHg while wearing medical anti-shock trousers to prevent venous pooling under three randomized conditions: 1) no trouser inflation (control), 2) only the trouser legs inflated, and 3) the trouser legs and abdominopelvic region inflated. Without trouser inflation, heart rate increased 28 +/- 4 beats/min, mean arterial pressure fell -3 +/- 2 mmHg, and forearm vascular resistance increased 51 +/- 9 units at 60 mmHg lower body negative pressure. With inflation of either the trouser legs or the trouser legs and abdominopelvic region, heart rate and mean arterial pressure did not change during lower body negative pressure. By contrast, although the forearm vasoconstrictor response to lower body negative pressure was attenuated by inflation of the trouser legs (delta forearm vascular resistance 33 +/- 10 units, P < 0.05 vs. control), attenuation was greater with the inflation of the trouser legs and abdominopelvic region (delta forearm vascular resistance 16 +/- 5 units, P < 0.05 vs. control and trouser legs-only inflation). Thus the hemodynamic consequences of pooling in the abdominal and pelvic regions during lower body negative pressure appear to be less than in the legs in healthy individuals.

Abdomen↗
PubMed1998

Influence of age and gender on cardiac output-VO2 relationships during submaximal cycle ergometry.

It is presently unclear how gender, aging, and physical activity status interact to determine the magnitude of the rise in cardiac output (Qc) during dynamic exercise. To clarify this issue, the present study examined the Qc-O2 uptake (Vo2) relationship during graded leg cycle ergometry in 30 chronically endurance-trained subjects from four groups (n = 6-8/group): younger men (20-30 yr), older men (56-72 yr), younger women (24-31 yr), and older women (51-72 yr). Qc (acetylene rebreathing), stroke volume (Qc/heart rate), and whole body Vo2 were measured at rest and during submaximal exercise intensities (40, 70, and approximately 90% of peak Vo2). Baseline resting levels of Qc were 0.6-1.2 l/min less in the older groups. However, the slopes of the Qc-Vo2 relationship across submaximal levels of cycling were similar among all four groups (5.4-5.9 l/l). The absolute Qc associated with a given Vo2 (1.0-2.0 l/min) was also similar among groups. Resting and exercise stroke volumes (ml/beat) were lower in women than in men but did not differ among age groups. However, older men and women showed a reduced ability, relative to their younger counterparts, to maintain stroke volume at exercise intensities above 70% of peak Vo2. This latter effect was most prominent in the oldest women. These findings suggest that neither age nor gender has a significant impact on the Qc-Vo2 relationships during submaximal cycle ergometry among chronically endurance-trained individuals.

Adult↗
PubMed1998

Forearm blood flow responses to handgripping after local neuromuscular blockade.

To test the hypothesis that acetylcholine "spillover" from motor nerves contributes significantly to skeletal muscle vasodilation during exercise, we measured the forearm blood flow responses during attempted handgripping after local paralysis of the forearm with the neuromuscular-blocking drug pipecuronium. This compound blocks postsynaptic nicotinic receptors but has no impact on acetylcholine release from motor nerves. The drug was administered selectively to one forearm by using regional intravenous drug administration techniques in five subjects. Pipecuronium reduced maximum forearm grip strength from 40.0 +/- 3.2 kg before treatment to 0.0 kg after treatment. By contrast, drug administration had no effect on maximum voluntary contraction in the untreated forearm (41.3 +/- 3.3 vs. 41.4 +/- 2.7 kg). During 2 min of attempted maximal contraction of the paralyzed forearm, the forearm blood flow increased from only 3.4 +/- 0.8 to 4.8 +/- 1.2 ml.100 ml-1.min-1 (P < 0.05). Heart rate increased from 63 +/- 3 to 73 +/- 8 beats/min (P > 0.05) during attempted contraction, and only three of five subjects showed obvious increases in heart rate. Mean arterial pressure increased significantly (P < 0.05) from 102 +/- 6 to 109 +/- 9 mmHg during attempted contractions. When these increases in flow are considered in the context of the marked (10-fold or greater) increases in flow seen in contracting forearm skeletal muscle, it appears that acetylcholine spillover from motor nerves has, at most, a minimal impact on the hyperemic responses to contraction in humans.

Adult↗