Search PubMed⌕ Search

Biomedical subjects

J H Mitchell

Publications and source records attributed to J H Mitchell.

At least 109 records · Page 6Linked to original sources
PubMed1990

Cardiovascular and ventilatory responses to dynamic exercise during epidural anaesthesia in man.

1. In order to evaluate the importance of afferent neural feedback from the working muscles for cardiovascular and ventilatory responses to dynamic exercise, epidural anaesthesia was induced at L3-L4. Six healthy males cycled for 20 min at 57% of maximum oxygen uptake and for 8-12 min at increasing work intensities until exhaustion at 238 +/- 30 W without as well as with epidural anaesthesia. 2. Presence of afferent neural blockade was verified by cutaneous sensory analgesia below T10-T11 and attenuated post-exercise ischaemic pressor response (45 +/- 8-24 +/- 6 mmHg). Efferent sympathetic nerves appear to be intact since basal heart rate and blood pressure as well as the cardiovascular responses to a Valsalva manoeuvre and to a cold pressor test were unchanged. 3. During dynamic exercise with epidural anaesthesia, blood pressure was lower than in control experiments; however, ventilation and heart rate were not affected. 4. The results indicate that afferent neural activity from the working muscles is important for blood pressure regulation during dynamic exercise in man but may not be necessary for eliciting the ventilatory and heart rate responses.

Adult↗
PubMed1990

Heart rate and arterial blood pressure at the onset of static exercise in man with complete neural blockade.

1. We tested the 'muscle-heart reflex' hypothesis for the immediate increases in heart rate and blood pressure at the onset of static exercise in man by performing complete blockade of afferent nerves from the working muscles. Brief (5 s) maximal static hand-grip contractions were performed without performing a Valsalva-like manoeuvre and with no increase in central venous pressure both before and after combined axillary and radial blockade with lidocaine. Muscle strength was reduced to near zero. The effectiveness of the afferent neural blockade was evaluated by recording the heart rate and blood pressure responses and rating the perceived pain during a cold pressor test of the blocked and contralateral unblocked hand. 2. The cold pressor test increased blood pressure but had no effect on heart rate. Afferent neural blockade eliminated the increase in blood pressure and the perceived pain associated with the cold pressor test. Maximal hand-grip contractions resulted in immediate and similar increases in heart rate and blood pressure before and after afferent neural blockade of the arm. 3. The results of this study suggest that the immediate increases in heart rate and blood pressure at the onset of static exercise in man occur when the 'muscle-heart reflex' is inoperable.

Adult↗
PubMed1990

Reflex responses of renal nerve activity during isometric muscle contraction in cats.

Renal sympathetic nerve activity (RSNA), arterial blood pressure (AP), and heart rate (HR) were measured during isometric muscle contraction of a hindlimb in chloralose-anesthetized cats. In 14 cats RSNA, AP, and HR increased during a 1-min contraction by 45%, 39 mmHg, and 11 beats/min, respectively; however, in three cats there was a brief initial decrease in RSNA followed by an increase. In 11 cats isometric contraction was maintained for 5 min by alternate stimulation of the L7 and S1 ventral roots. In the first 1 min of sustained contraction, there was a positive correlation (gamma = 0.58, P less than 0.005) between RSNA and tension development. Thereafter RSNA remained elevated despite a tension decrease, and there was no significant correlation between these changes. The RSNA response to contraction of both hindlimbs was greater than that to contraction of either hindlimb alone. Passive stretch of the hindlimb muscle significantly increased RSNA. Thus the initial increase in RSNA during sustained contraction is likely due to activation of muscle mechanoreceptors, whereas the later increase is probably caused by activation of the muscle metaboreceptors.

Animals↗
PubMed1990

Cerebral blood flow during static exercise in humans.

Cerebral blood flow (CBF) was determined in humans at rest and during four consecutive unilateral static contractions of the knee extensors. Each contraction was maintained for 3 min 15 s with the subjects in a semisupine position. The contractions corresponded to 8, 16, 24, and 32% of the maximal voluntary contraction (MVC) and utilized alternate legs. CBF (measured by the 133Xe clearance technique) was expressed by a noncompartmental flow index (ISI). Heart rate and mean arterial pressure increased from resting values of 73 (55-80) beats/min and 88 (74-104) mmHg to 106 (86-138) beats/min and 124 (102-146) mmHg, respectively (P less than 0.0005), during the contraction at 32% MVC. Arterial PCO2 and central venous pressure did not change. Corrected to the average resting PCO2, CBF during control was 55 (35-73) ml.100 g-1.min-1 and remained constant during contractions. Cerebral vascular resistance increased from 1.5 (1.0-2.2) to 2.4 (1.4-3.0) mmHg. 100 g.min.ml-1 (P less than 0.025) at 32% of MVC. There was no difference in CBF between the two hemispheres at rest or during exercise. In contrast to dynamic leg exercise, static leg exercise is not associated with an increase in global CBF when measured by the 133Xe clearance technique.

Adult↗
PubMed1989

Localization of tyrosine hydroxylase and phenylethanolamine N-methyltransferase immunoreactive cells in the medulla of the dog.

The tyrosine hydroxylase (TH)- and phenylethanolamine N-methyltransferase (PNMT)-immunoreactive cells of the medulla are closely associated with cardiovascular control in both the cat and rat. Although it is often the species of choice for cardiovascular studies, no previous study had characterized these cell groups in the dog. The TH- and PNMT-immunoreactive cells of the dog were distributed much as they are in both cat and rat but with some species variations, which may be indicative of their functional role.

Animals↗
PubMed1989

The nucleus reticularis gigantocellularis modulates the cardiopulmonary responses to central and peripheral drives related to exercise.

It is known that muscle afferents and the hypothalamic locomotor region (HLR) both project to the nucleus reticularis gigantocellularis (NGC) and that the NGC is capable of influencing cardiovascular and respiratory variables. Therefore, the role of NGC in the cardiovascular and respiratory response to exercise-related signals was investigated in anesthetized cats. These signals were generated by stimulation of: (1) spinal ventral roots to induce hindlimb muscle contraction (MC) and (2) the HLR. Bilateral electrolytic lesion of the NGC at the pontomedullary border caused tidal volume, respiratory frequency and heart rate responses to HLR stimulation to be greater than the responses recorded prior to lesioning. Lesioning had no effect on the ventilatory or cardiovascular responses to MC but did decrease phrenic responsiveness; lesion had no effect on any resting values. In this preparation, the pontomedullary NGC acts as an inhibitory influence on tidal volume, breathing frequency and heart rate responses to the central command for exercise. In addition, NGC modulation of ventilation would appear to be selective for certain respiratory muscle groups.

Animals↗
PubMed1989

Occlusion of pressor responses to posterior diencephalic stimulation and muscular contraction.

Although neural occlusion has been suggested to occur between the central and reflex mechanisms increasing arterial pressure, evidence consistent with this phenomenon is lacking. To assess the possibility of neural occlusion we recorded, in chloralose-anesthetized cats, the pressor responses to statically contracting the hindlimb muscles and to electrically stimulating histologically confirmed sites in the posterior hypothalamus and subthalamus. We also recorded the pressor responses to topical application of capsaicin onto the intestine and to stimulation of these diencephalic sites. The pressor responses to simultaneous static contraction and diencephalic stimulation were significantly smaller than the algebraic sum of the pressor responses to contraction and diencephalic stimulation evoked separately. Likewise, the pressor responses to simultaneous capsaicin application and diencephalic stimulation were significantly smaller than the algebraic sum of the responses evoked separately. High intensity stimulation of the L7 dorsal root or the diencephalic sites evoked pressor responses similar in magnitude to the algebraic sum of the two responses evoked separately; thus, the inability of the simultaneous maneuvers to evoke pressor responses that summed algebraically was not due to the fact that they caused a maximal effect. Our findings are consistent with the hypothesis that neural occlusion occurs during stimulation of the posterior diencephalon and static muscular contraction.

Animals↗
PubMed1989

Cardiovascular responses to brief static contractions in man with topical nervous blockade.

1. We tested the hypothesis that afferent nerves from working muscles are important in determining the heart rate and blood pressure responses to brief maximal static exercise. 2. In twenty human subjects, the heart rate and arterial blood pressure responses to a brief maximal voluntary handgrip were studied before and after axillary nerve anaesthesia or to maximal one-leg knee extension before and after epidural anaesthesia at L3-L4. Maximal knee extension could not be accomplished without performing a 'Valsalva-like' manoeuvre, but during handgrip it was possible to avoid the use of muscles other than those directly involved in the contraction. Heart rate and blood pressure were also monitored during a Valsalva manoeuvre of similar duration to the maximal voluntary contractions (4 s). 3. During handgrip with normal breathing, axillary nerve anaesthesia reduced the heart rate response but had no effect on the blood pressure response. 4. During a Valsalva manoeuvre, blood pressure increased but heart rate remained stable as long as expiratory pressure was maintained. During one-leg knee extension, epidural anaesthesia reduced the blood pressure response; however, the reduction in blood pressure was probably due to a reduction in the simultaneously performed 'Valsalva-like' manoeuvre. 5. The results of this study suggest that afferent input from the working muscles is of importance for the heart rate responses to brief static muscle contractions. That such influence may be important for the blood pressure response remains unproven.

Adult↗
PubMed1989

Autonomic blockade and cardiovascular responses to static exercise in partially curarized man.

1. The cardiovascular responses, heart rate and mean arterial pressure, were followed in seventeen human subjects who performed static handgrip contractions for 2 min at the same absolute force (15% of the initial maximal voluntary contraction strength) before and during partial curarization. In control contractions the rate of perceived exertion was 10 exertion units, 16 units in contractions with tubocurarine which could be maintained and 20 units in contractions that could not be maintained. Control contractions increased mean arterial pressure by 6 mmHg from 89 mmHg while heart rate was unchanged from the resting value of 68 beats min-1. With tubocurarine, larger increases in mean arterial pressure of 11 mmHg and for heart rate of 8 beats min-1 were obtained during maintained contractions, and 15 mmHg and 16 beats min-1, respectively, during non-maintained contractions. 2. Atropine increased resting heart rate and blood pressure with tubocurarine to 107 beats min-1 and 98 mmHg, respectively, in seven subjects. The blood pressure response to exercise with tubocurarine was unaffected by atropine, but the heart rate increase was reduced from 15 to 4 beats min-1. 3. Propranolol reduced resting heart rate with tubocurarine to 56 beats min-1 with no effect on blood pressure in seven subjects. The cardiovascular responses to exercise with tubocurarine were unaffected by propranolol. In contrast, phentolamine reduced resting blood pressure with tubocurarine to 80 mmHg without affecting heart rate in seven subjects. Exercise responses with tubocurarine were unaffected by phentolamine. Combinations of atropine and propranolol in fourteen subjects or atropine and phentolamine in five subjects showed similar results during exercise with tubocurarine as with the sole use of the agents used to block autonomic receptors. 4. The results suggest that when partial curarization induces a disproportion between the signal from central command and that from exercising muscles, the larger signal arising from central command determines the magnitude of the cardiovascular responses. The centrally generated heart rate response is in part caused by vagal withdrawal. However, the blood pressure response cannot be attenuated by the sole use of alpha- or beta-receptor adrenergic blockade or combinations of these with atropine. This suggests that there may be greater redundancy in the autonomic control of blood pressure than in the vagal control of heart rate associated with central command during static exercise in man.

Adult↗
PubMed1989

Epidural anaesthesia and cardiovascular responses to static exercise in man.

1. In human subjects, sustained static contractions of the knee extensors were performed in one leg with the same absolute (10% of the initial maximal voluntary contraction) and relative (30% of the maximal voluntary contraction immediately prior to the static exercise) intensities before and during epidural anaesthesia. Epidural anaesthesia reduced strength to 62 +/- 8% of the control value and partially blocked sensory input from the working muscles. During contractions performed with the same relative force, the increases in mean arterial pressure and heart rate were greater during control contractions than during epidural anaesthesia. During contractions at the same absolute force, there was no significant difference in magnitude of cardiovascular responses between control contractions and contractions performed during epidural anaesthesia. 2. The metabolic role in the exercise pressor reflex was assessed by applying an arterial leg cuff 10 s before cessation of exercise and through the following 3 min of recovery. Although mean arterial pressure and heart rate decreased immediately after cessation of exercise, application of the arterial occlusion cuff resulted in higher post-exercise mean arterial pressure and heart rate values. Control and epidural mean arterial pressures during arterial occlusion were not significantly different. 3. The results of this study suggest that the reflex neural mechanism rather than the intended effort (central command) is important in determining the blood pressure and heart rate responses to static exercise in man. That is, when epidural anaesthesia diminishes sensory feedback and produces muscular weakness, central command does not determine the cardiovascular response. This conclusion, however, is opposite to that derived from experiments with partial neuromuscular blockade which demonstrated the importance of central command in determining the cardiovascular response to static exercise (Leonard, Mitchell, Mizuno, Rube, Saltin & Secher, 1985). Taken together, these two studies are complementary and support the concept that both central and reflex neural mechanisms play roles in regulating arterial blood pressure and heart rate during static exercise in man.

Adult↗
PubMed1989

Mobilization of glucoregulatory hormones and glucose by hypothalamic locomotor centers.

Recent studies suggest that, in addition to classical humoral metabolic feedback mechanisms, the mobilization of glucoregulatory hormones and glucose in exercise may be regulated by motor centers in the brain. We, therefore, studied the effect of electrically stimulating the posterior hypothalamic locomotor region (PHLR) for 10 min in decorticated (n = 6) and alpha-chloralose-anesthetized (n = 8) cats. Blood pressure and heart rate were measured, and blood samples were drawn for analysis of hormones and metabolites before, during, and after 10 min of PHLR stimulation. Feedback from contracting muscles was prevented by neuromuscular blockade in decorticated cats and by the anesthesia in anesthetized cats. In decorticated cats, PHLR stimulation elicited increases (2 P less than 0.05) in glucose production (delta 54 +/- 16 mumol.min-1.kg-1), plasma glucose (delta 2.2 +/- 0.7 mmol/l), epinephrine (delta 4.9 +/- 1.8 pmol/l), norepinephrine (delta 2.2 +/- 0.9 pmol/l), glucagon (delta 16 +/- 5 pmol/l), decreases (2 P less than 0.05) in plasma insulin (delta 27 +/- 7 pmol/l), and increases (2 P less than 0.05) in blood pressure (delta 48 +/- 9 mmHg) and heart rate (delta 26 +/- 7 beats/min). In anesthetized cats, PHLR stimulation elicited increases (2 P less than 0.05) in glucose production (delta 12 +/- 4 mumol.min-1.kg-1), plasma glucose (delta 0.4 +/- 0.1 mmol/l), blood pressure (delta 39 +/- 7 mmHg), and heart rate (delta 28 +/- 7 beats/min), whereas changes in catecholamine and insulin concentrations did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Stimulating somatic afferent fibers alters coronary arterial resistance.

We used a constant flow preparation to study the changes in left circumflex coronary arterial (LCCA) pressure and resistance evoked by electrical stimulation of branches of muscle, cutaneous, and mixed nerves in the hindlimb of anesthetized dogs. Stimulation (20 Hz) of all three nerve types at 20, 70, 100, and 200 times the voltage threshold that evoked compound action potentials significantly (P less than 0.05) increased LCCA resistance. Stimulation at three and five times threshold had no effect on this same variable. Cooling the nerve to 2-4 degrees C, temperatures that block myelinated nerve fibers, attenuated but did not abolish the increase in LCCA resistance. Combinations of beta- and alpha-adrenergic and cholinergic blockade established that the biphasic change evoked by nerve stimulation was due to an initial alpha-adrenergic vasoconstriction followed by a metabolite-induced vasodilation. These data demonstrate that stimulation of muscle, cutaneous, or mixed nerve afferent C-fibers increases coronary arterial resistance by alpha-adrenergic vasoconstriction.

Afferent Pathways↗
PubMed1989

Cerebral blood flow during submaximal and maximal dynamic exercise in humans.

Cerebral blood flow (CBF) in humans was measured at rest and during dynamic exercise on a cycle ergometer corresponding to 56% (range 27-85) of maximal O2 uptake (VO2max). Exercise bouts were performed by 16 male and female subjects, lasted 15 min each, and were carried out in a semisupine position. CBF (133Xe clearance) was expressed as the initial slope index (ISI) and as the first compartment flow (F1). CBF at rest [ISI, 58 (range 45-73); F1, 76 (range 55-98) ml.100 g-1.min-1] increased during exercise [ISI to 79 (57-94) and F1 to 118 (75-164) ml.100 g-1.min-1, P less than 0.01]. CBF did not differ significantly between work loads from 32 (24-33) to 86% (74-96) of VO2max (n = 10). During exercise, mean arterial pressure increased from 84 (60-100) to 101 (78-124) Torr (P less than 0.01) and PCO2 remained unchanged [5.1 (4.6-5.6) vs. 5.4 (4.4-6.3) kPa, n = 6]. These results demonstrate a median increase of 31% (0-87) in CBF by ISI and a median increase of 58% (0-133) in CBF by F1 during dynamic exercise in humans.

Adult↗
PubMed1989

Effects of partial neuromuscular blockade on sympathetic nerve responses to static exercise in humans.

We used intraneural recordings of sympathetic nerve activity in conscious humans to determine if central command increases sympathetic discharge to resting skeletal muscle during static exercise. In nine healthy subjects, we measured arterial pressure, heart rate, and muscle sympathetic nerve activity with microelectrodes in the peroneal nerve of the resting leg during 1) static handgrip at 15% and 30% maximal voluntary contraction and 2) attempted handgrip during partial neuromuscular blockade produced by systemic administration of tubocurarine chloride (0.075 mg/kg i.v.). During curare, subjects reported that they used near-maximal motor effort to attempt a sustained handgrip contraction, but they generated almost no force. Without sustained contraction, the intent to exercise alone, that is, central command, caused statistically significant (p less than 0.05) increases in muscle sympathetic nerve activity as well as in arterial pressure and heart rate. However, the increases in muscle sympathetic nerve activity (+ 56 +/- 16% over control) and in mean arterial pressure (+ 12 +/- 2 mm Hg) during attempted handgrip were much smaller (p less than 0.05) than the sympathetic nerve response (+ 217 +/- 37% over control) and pressor response (+ 25 +/- 3 mm Hg) during an actual static handgrip at 30% maximal voluntary contraction. In contrast, heart rate increased as much during the attempted contraction (+ 18 +/- 2 beats/min) as during the actual contraction at 30% maximal voluntary contraction (+ 16 +/- 4 beats/min). In 11 additional subjects, the heart rate responses during curare were greatly attenuated (p less than 0.05) by atropine but were not significantly affected by propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1988

Left ventricular mass as determined by magnetic resonance imaging in male endurance athletes.

Although many studies of the effect of dynamic exercise training on left ventricular (LV) mass have been reported, controversy continues to exist. Previous work has been criticized because of the techniques used for measuring LV mass, the variable level of training of the subjects recruited and the methods used to normalize the data. In an attempt to resolve this controversy, LV mass was determined using the very accurate and reproducible technique of magnetic resonance imaging (MRI). Highly trained competitive athletes including cross-country skiers, endurance cyclists and long distance runners (VO2max = 77 +/- 1, 72 +/- 2 and 75 +/- 2 ml (kg X min)-1, respectively) were examined. The data were normalized for body weight, body surface area and lean body mass. LV mass was significantly greater in skiers (239 +/- 9 g), runners (244 +/- 10 g) and cyclists (258 +/- 11 g) when compared with nonathletic control subjects (189 +/- 6 g) (p less than 0.001), which represents percent differences of 26, 29 and 37%, respectively. LV mass remained greater in the athletes, regardless of the method used to normalize the data. In addition, there was a good correlation between LV mass and VO2max (r = 0.80, p less than 0.001). It was concluded that LV mass is significantly greater in highly trained competitive endurance athletes and that normalizing LV mass with respect to body weight, body surface area or lean body mass does not alter this relation.

Adult↗
PubMed1988

Effect of increasing heart rate on left ventricular performance in patients with normal cardiac function.

The influence of an increase in heart rate on left ventricular (LV) contractile performance was assessed in patients with normal LV function. In 19 patients (3 men, 16 women) ages 55 +/- 9 years (mean +/- standard deviation) with normal global and segmental LV function and normal coronary arteries, LV dP/dt max was measured at baseline heart rate and during atrial pacing at baseline +5, baseline +25 and baseline +45 beats/min. In 10 of the patients, intravascular volume was not altered during pacing and, as a result, echocardiographically measured LV end-diastolic dimension decreased (5.4 +/- 0.4 at baseline vs 4.9 +/- 0.5 cm at baseline +45 beats/min, p less than 0.05). In these patients, LV dP/dt max increased modestly (1,571 +/- 237 at baseline vs 1,760 +/- 199 mm Hg/s at baseline +45 beats/min, p less than 0.05). In the other 9 patients, intravascular volume was expanded rapidly (by saline infusion) during pacing and, as a result, LV end-diastolic dimension was held constant (5.2 +/- 0.6 at baseline vs 5.1 +/- 0.6 cm at baseline +45 beats/min, difference not significant). In these patients, LV dP/dt max increased substantially with pacing (1,505 +/- 228 at baseline vs 2,050 +/- 258 mm Hg/s at baseline +45 beats/min, p less than 0.05). Thus, an increase in heart rate induces a modest increase in LV dP/dt max in patients in whom LV preload (as reflected by end-diastolic dimension) is allowed to decrease; in contrast, it causes a marked increase in LV dP/dt max in those in whom LV preload is maintained constant.

Adult↗