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Biomedical subjects

J H Mitchell

Publications and source records attributed to J H Mitchell.

At least 91 records · Page 5Linked to original sources
PubMed1993

The effect of epidural anaesthesia with 1% lidocaine on the pressor response to dynamic exercise in man.

1. In order to examine the sensitivity to local anaesthetics of afferent neural feedback from working muscle during dynamic exercise, sixteen subjects cycled for 12 min before and after epidural anaesthesia using 1% lidocaine. The presence of afferent neural blockade was verified by elimination of the blood pressure response to a cold pressor test, laser-induced evoked potentials and increases in pain detection and tolerance thresholds of the foot. Conversely, epidural anaesthesia had no effect on these variables in the unblocked skin areas or on electrically evoked potentials in blocked or unblocked skin. 2. During dynamic exercise, heart rate increased as did mean arterial pressure and cardiac output. Mean arterial pressure remained at the exercise level during post-exercise ischaemia, but heart rate and cardiac output decreased while total peripheral resistance increased. Epidural anaesthesia did not significantly affect these variables during rest, dynamic exercise, post-exercise ischaemia or recovery. 3. The results of this study show that, in order to affect blood pressure during dynamic exercise, epidural anaesthesia must block the pressor response to post-exercise ischaemia. The implication of these data is that complete or almost complete block of group III and/or group IV muscle afferents is necessary to inhibit the pressor response to dynamic exercise in man.

Adult↗
PubMed1993

Neural control of cardiovascular responses and of ventilation during dynamic exercise in man.

1. Nine subjects performed dynamic knee extension by voluntary muscle contractions and by evoked contractions with and without epidural anaesthesia. Four exercise bouts of 10 min each were performed: three of one-legged knee extension (10, 20 and 30 W) and one of two-legged knee extension at 2 x 20 W. Epidural anaesthesia was induced with 0.5% bupivacaine or 2% lidocaine. Presence of neural blockade was verified by cutaneous sensory anaesthesia below T8-T10 and complete paralysis of both legs. 2. Compared to voluntary exercise, control electrically induced exercise resulted in normal or enhanced cardiovascular, metabolic and ventilatory responses. However, during epidural anaesthesia the increase in blood pressure with exercise was abolished. Furthermore, the increases in heart rate, cardiac output and leg blood flow were reduced. In contrast, plasma catecholamines, leg glucose uptake and leg lactate release, arterial carbon dioxide tension and pulmonary ventilation were not affected. Arterial and venous plasma potassium concentrations became elevated but leg potassium release was not increased. 3. The results conform to the idea that a reflex originating in contracting muscle is essential for the normal blood pressure response to dynamic exercise, and that other neural, humoral and haemodynamic mechanisms cannot govern this response. However, control mechanisms other than central command and the exercise pressor reflex can influence heart rate, cardiac output, muscle blood flow and ventilation during dynamic exercise in man.

Adult↗
PubMed1993

Effects of graded muscle contractions on spinal cord substance P release, arterial blood pressure, and heart rate.

The release of substance P (SP)-like immunoreactivity (SP-LI) in the dorsal horn of the spinal cord and the cardiovascular changes to both high-tension (HT) and low-tension (LT) contractions were determined using alpha-chloralose-anesthetized cats. Over a 10-minute period, seven contractions (HT or LT) were induced. Each contraction was 20 seconds in duration and was followed by an 80-second quiescent period. The tension-time index (TTI) for the HT contractions was 2751 +/- 348 kg.s (mean +/- SD), which was greater than the TTI of 813 +/- 167 kg.s for the LT contractions. The HT contractions caused a greater release of SP-LI than the LT contractions: SP-LI increased from 0.18 +/- 0.02 to 0.32 +/- 0.03 fmol/100 microL and from 0.18 +/- 0.02 to 0.25 +/- 0.04 fmol/100 microL for the two types of contractions, respectively. Concomitant with this greater SP-LI release, HT contractions caused larger increases in mean arterial pressure (34 +/- 16 versus 11 +/- 4 mm Hg) and heart rate (18 +/- 7 versus 8 +/- 4 beats per minute) than did the LT contractions. These changes in SP-LI, mean arterial pressure, and heart rate were virtually abolished when the contractions were repeated after sectioning the L-5-S-2 dorsal and ventral roots or when the electrical stimulation of the ventral roots was repeated after muscle paralysis with gallamine triethiodide. These results demonstrate that contraction-evoked SP-LI release in the dorsal horn is related to the developed tension. Furthermore, these data provide additional support for the hypothesis that the release of SP from the central terminations of muscle afferents plays a role in mediating the cardiovascular responses to static contraction of skeletal muscle.

Animals↗
PubMed1993

Determinants of VO2peak in patients with end-stage renal disease: on and off dialysis.

Peak oxygen uptake (VO2peak) of patients on maintenance hemodialysis is very low. Exercise training performed during, or "on" dialysis, and at other times, "off" dialysis, both improve VO2peak. Equivalence of these approaches has not been shown, nor have the physiologic factors limiting VO2peak been clarified in these patients. We hypothesized that hemodialysis does not acutely alter the cardiovascular response to peak exercise, and further that anemia and a low peak heart rate limit VO2peak. Ten patients with end-stage renal disease (ESRD) performed cycle ergometry to peak exercise. Peak oxygen uptake measured immediately prior to dialysis was compared with predicted values, and with measurements obtained during the second 30 min of dialysis. The determinants of VO2peak were compared with previously reported norms. "Off" dialysis, VO2peak for nine of 10 patients was below the 95% confidence limit for normals. Their cardiovascular response to peak exercise was unchanged by 30-60 min of hemodialysis. Stroke volume was similar to that of normals; however, peak heart rate was 77% of predicted, and hematocrit was 27% (at rest). Peak exercise mixed-venous oxygen content was 3.6 ml O2 ml.dl-1 blood, similar to values reported for athletes. These findings show that up to 1 h of dialysis minimally effects VO2peak, and imply that low oxygen delivery limited VO2peak in these patients.

Adult↗
PubMed1992

Left ventricular dimensions and mass using magnetic resonance imaging in female endurance athletes.

Few published studies of left ventricular (LV) mass in female endurance athletes have been performed with M-mode echocardiography, which involves assumptions of LV geometry. Therefore, magnetic resonance imaging, a 3-dimensional technique, was used to examine LV mass, LV end-diastolic volume and mean wall thickness in female long distance runners (n = 13; mean age 29 years), cyclists (n = 12; mean age 26 years) and cross-country skiers (n = 11; mean age 24 years), and the findings were compared with sedentary control subjects (n = 10; mean age 27 years) matched for height and body weight. The physical characteristics for all subjects included height (mean 166 cm, and body weight (mean 56 kg). The percent body fat (mean 11.7) and maximal oxygen uptake (VO2max, mean 63 ml.kg-1.min-1) were similar (p greater than 0.05) among all athletic groups, but significantly different from the control group (body fat, mean 22.5%; VO2max, mean 35 ml.kg-1.min-1). LV mass (mean 159 kg), LV end-diastolic volume (mean 122 ml), and mean wall thickness (mean 11.5 mm) were also similar among the athletic groups and significantly larger than the following control values: LV mass (mean 115 g), LV end-diastolic volume (mean 93 ml) and mean wall thickness (mean 9.8 mm). Ratios of LV mass to lean body weight were similar among all athletic groups, although athletic groups had larger ratios (p less than 0.05) than the sedentary control subjects. LV mass/LV end-diastolic volume ratio was similar (p greater than 0.05) among all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Neurally mediated renal vasoconstriction during isometric muscle contraction in cats.

The aim of this study was to determine if the reflex increase in renal sympathetic nerve activity (RSNA) during static (isometric) muscle contraction evokes renal vasoconstriction and decreases renal blood flow. RSNA, renal blood flow velocity, and arterial pressure were measured simultaneously during isometric contraction of the hindlimb triceps surae muscle in eight chloralose-anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. RSNA and mean arterial pressure (MAP) increased 41 +/- 14% (SE) and 50 +/- 10 mmHg during static contraction, whereas mean renal blood flow velocity (MRBV) decreased 14 +/- 5%. Calculated renal vascular resistance increased 73 +/- 20% during the contraction. The increase in RSNA preceded the decrease in MRBV by 20 s. Passive mechanical stretch of the muscle increased RSNA 21 +/- 12% but did not alter MRBV. Renal denervation abolished the decrease in MRBV during isometric contraction but only attenuated the rise in MAP. Cutting the L4-S1 dorsal roots or muscle paralysis abolished the MRBV and MAP responses. Thus reflex stimulation of RSNA from the contracting muscle can induce renal vasoconstriction and decrease renal blood flow.

Animals↗
PubMed1992

Left ventricular dimensions during hemorrhagic shock measured by biplane cinefluorography.

The effects of hemorrhagic shock on left ventricular dimensions and volume were studied in 15 splenectomized dogs. A 42 +/- 1% decrease in total blood volume caused arterial blood pressure to fall 60% (from 120 +/- 5 to 48 +/- 3 mmHg); the first derivative of left ventricular pressure at a developed pressure of 40 mmHg fell 54% (from 1,930 +/- 94 to 905 +/- 93 mmHg/s, P < 0.05). Cardiac output fell 76% due to a 73% decrease in stroke volume; heart rate was unchanged at the end of hemorrhage but increased 50% during 3 h of sustained shock (from 110 +/- 6 to 166 +/- 8 beats/min, P < 0.05). During hemorrhage the septal-lateral and the anterior-posterior end-diastolic dimensions fell to a greater extent (7.8 mm, -21% and 7.0 mm, -18%, respectively) than the apex-base dimension (2.3 mm, -3.3%, P < 0.05). As a result of these dimensional changes, left ventricular end-diastolic volume fell 39% (from 48 +/- 2 to 28 +/- 1 cm3, P < 0.01). End-systolic dimensions fell in the same proportion during hemorrhage, resulting in a 30% decrease in end-systolic volume (from 30 +/- 2 to 21 +/- 1 cm3, P < 0.05). After 120 min of sustained shock, all end-diastolic dimensions remained unchanged, but end-systolic dimensions and volume increased significantly from values measured at end hemorrhage (P < 0.05), causing ejection fraction and stroke volume to fall to a greater extent. This study confirms a pronounced reduction in the minor axes of the left ventricle during hemorrhagic shock with subsequent reduction in ventricular function.

Animals↗
PubMed1992

Cardiovascular responses to voluntary and nonvoluntary static exercise in humans.

We have measured the cardiovascular responses during voluntary and nonvoluntary (electrically induced) one-leg static exercise in humans. Eight normal subjects were studied at rest and during 5 min of static leg extension at 20% of maximal voluntary contraction performed voluntarily and nonvoluntarily in random order. Heart rate (HR), mean arterial pressure (MAP), and cardiac output (CO) were determined, and peripheral vascular resistance (PVR) and stroke volume (SV) were calculated. HR increased from approximately 65 +/- 3 beats/min at rest to 80 +/- 4 and 78 +/- 6 beats/min (P < 0.05), and MAP increased from 83 +/- 6 to 103 +/- 6 and 105 +/- 6 mmHg (P < 0.05) during voluntary and nonvoluntary contractions, respectively. CO increased from 5.1 +/- 0.7 to 6.0 +/- 0.8 and 6.2 +/- 0.8 l/min (P < 0.05) during voluntary and nonvoluntary contractions, respectively. PVR and SV did not change significantly during voluntary or nonvoluntary contractions. Thus the cardiovascular responses were not different between voluntary and electrically induced contractions. These results suggest that the increases in CO, HR, SV, MAP, and PVR during 5 min of static contractions can be elicited without any contribution from a central neural mechanism (central command). However, central command could still have an important role during voluntary static exercise.

Adult↗
PubMed1992

Effects of axillary blockade on regional cerebral blood flow during dynamic hand contractions.

Regional cerebral blood flow (rCBF) was measured at orbitomeatal (OM) plane +5.0 and +9.0 cm in 10 subjects at rest and during dynamic hand contractions before and after axillary blockade. Handgrip strength was significantly reduced, and rating of perceived exertion increased after blockade. During hand contractions before blockade, contralateral hemispheric cerebral blood flow (CBF) at OM +9.0 increased from a resting value of 58 (49-75) to 63 (52-82) ml.100 g-1.min-1; contralateral motor sensory rCBF at OM +9 from 58 (50-77) to 71 (64-84); motor sensory rCBF at OM +5 from 67 (54-76) to 77 (64-87) and 70 (62-84) contralaterally and ipsilaterally, respectively; and supplementary motor area (SM) rCBF from 64 (53-69) to 75 (67-88) ml.100 g-1.min-1. During dynamic hand contractions after axillary blockade, CBF did not increase at OM +5 or in the SM. Furthermore, contralateral motor sensory rCBF at OM +9 increased much less. Axillary blockade had no effect on resting CBF, rCBF, or increases in the two during hand contractions of the opposite hand. Thus neural feedback from the contracting muscle is necessary for the increases in SM bilateral OM +5 motor sensory rCBF and the maximal increase in contralateral OM +9 motor sensory rCBF during dynamic hand contractions.

Adult↗
PubMed1992

Effect of spinal microinjections of an antagonist to substance P or somatostatin on the exercise pressor reflex.

The purpose of this study was to determine the heart rate and arterial blood pressure changes to isometric skeletal muscle contraction and muscle stretch before and after microinjecting an antagonist to substance P (SP) or somatostatin (SOM) into the L-7 dorsal horn region of the spinal cord of anesthetized cats. Anesthesia was induced by administering an anesthetic gas mixture and was subsequently maintained with alpha-chloralose. Triceps surae contraction was induced by electrically stimulating the L-7 ventral root. Three muscle manipulations (all 1 minute in duration) were performed: 1) continuous tetanic contraction, 2) intermittent tetanic contractions (1 second of contraction, 1 second of relaxation), and 3) passive muscle stretch. Saline microinjections had no effect on the cardiovascular responses to these muscle manipulations. However, both peptide antagonists blunted the pressor response to a continuous tetanic contraction as mean arterial pressure increased 47 +/- 4 and 44 +/- 4 mm Hg before and 28 +/- 3 and 28 +/- 4 mm Hg after microinjecting the SP or SOM antagonist, respectively. In contrast, neither antagonist influenced the increase in mean arterial pressure produced by passive stretch; values were 43 +/- 6 versus 41 +/- 6 mm Hg (SP antagonist) and 39 +/- 7 versus 42 +/- 7 mm Hg (SOM antagonist) before and after injections, respectively. Microinjecting the SOM antagonist attenuated the pressor response to intermittent tetanic contractions (44 +/- 4 mm Hg before SOM antagonist versus 26 +/- 4 mm Hg after SOM antagonist), whereas the SP antagonist had no effect (35 +/- 3 mm Hg before SP antagonist versus 32 +/- 4 mm Hg after SP antagonist).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Multiplicity of the afferent pathways mediating the exercise pressor reflex.

The cardiovascular responses to isometric contraction of the triceps surae muscle of one leg were determined before and after transecting the ipsilateral L7 or L6 and S1 spinal roots. Sectioning only the L7 spinal root slightly attenuated the pressor, but not the heart rate response induced by skeletal muscle contraction, while cutting the L6 and S1 spinal roots (L7 intact) had no effect on the cardiovascular changes. This indicates that there is multiplicity in neural afferent pathways that mediate the exercise pressor reflex.

Animals↗
PubMed1991

The effect of static exercise on renal sympathetic nerve activity in conscious cats.

1. Renal sympathetic nerve activity (RNA), heart rate (HR), arterial blood pressure (AP), and force development were measured simultaneously during voluntary static (isometric) exercise performed by conscious cats. The cats were operantly trained to press a bar with one forelimb. When the force applied to the bar exceeded a predetermined value (threshold), a sound was emitted by a buzzer for audio-feedback. If the cat continued to produce the appropriate force for a period of 26-55 s, food was given as a reward. 2. A total of eighty-nine exercise trials were performed by seven cats. The peak force applied to the bar was 468 +/- 28 g (mean +/- S.E.M.). RNA, HR, and AP increased significantly from the control value during static exercise by 102 +/- 14%, 23 +/- 2 beats/min, and 11 +/- 1 mmHg, respectively. 3. The increase in RNA had both an initial and a late component. The initial component occurred at or immediately before the onset of force development and lasted for 10 s, while the late component gradually increased 14 s after the onset of static exercise and was sustained until the exercise was terminated. 4. HR also increased at the beginning of static exercise with a similar time course as RNA. Then, HR returned to the control value and remained at that level during the remainder of exercise. The increase in AP was delayed by 10 s from the initial increase in RNA and then continued to rise throughout the period of exercise. 5. The sound of the buzzer was emitted during rest to determine any influence of anticipation or conditioning on the response. RNA and AP increased slightly, but HR did not change. The increases in RNA and AP were much smaller than the increases obtained during static exercise. Thus, the increases in RNA, HR and AP during static exercise appeared to be associated with the exercise itself and not due to anticipation and/or conditioning. 6. When AP was elevated by a bolus injection of noradrenaline, RNA during rest was almost abolished and the increase of RNA during static exercise was markedly inhibited. Thus the arterial baroreflex significantly influences RNA both during rest and during static exercise. 7. This study suggests that the initial increases in RNA and HR at the beginning of static exercise in conscious cats are caused by descending input from higher brain centres and not by afferent feedback signals from muscle receptors or by arterial baroreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Hormonal, metabolic, and cardiovascular responses to static exercise in humans: influence of epidural anesthesia.

To determine the role of reflex neural mechanisms for hormonal, metabolic, heart rate (HR), and blood pressure (MABP) changes during static exercise, seven health young males performed 10-min periods of two-legged static knee extension both during control and during epidural anesthesia. Comparisons were made at identical absolute (29 Nm) and relative [15% maximal voluntary contraction (MVC)] force. Afferent nerve blockade was verified by hypesthesia below T10-T12 and attenuated postexercise ischemic pressor response. Leg strength was reduced to 67 +/- 5% of control. At same relative force, increases in MABP and HR occurred more rapidly without than with epidural anesthesia (P less than 0.05). This difference was diminished during identical absolute force. Changes in plasma concentrations of catecholamines followed the pattern of HR and MABP responses, with differences between epidural and control experiments being most pronounced early in the work period. Plasma beta-endorphin was elevated only after control exercise. No response at 15% MVC was found for growth hormone, adrenocorticotropic hormone, insulin, glucagon, cortisol, glycerol, free fatty acids, or glucose (P greater than 0.05). In conclusion, during static exercise with large muscle groups and moderate relative force, modest changes in plasma hormones and metabolites take place. Furthermore, afferent nervous feedback from contracting muscles is important in regulation of blood pressure, heart rate, and catecholamine responses during static exercise in humans.

Adult↗
PubMed1991

Static muscle contraction reflexly increases adrenal sympathetic nerve activity in rats.

Little is known about the mechanisms responsible for activation of sympathoadrenal function during exercise. We hypothesized that sympathoadrenal discharge is activated at the onset of exercise by a reflex arising in the contracting muscle. Adrenal sympathetic nerve activity (SNA) was recorded during 1 min stimulation of the tibial nerve at two times motor threshold, before and during neuromuscular blockade, in 12 alpha-chloralose-anesthetized rats. Static muscle contractions, induced by stimulation before neuromuscular blockade, were repeated during ganglionic blockade (n = 6) to specifically test reflex activation of preganglionic activity to the adrenal gland. During static contraction, adrenal SNA rapidly increased (P less than 0.05) to a maximum of 89 +/- 12% above basal and then declined, reaching basal levels after 30 s of muscle contraction. Tibial nerve stimulation during neuromuscular blockade had no effect on adrenal SNA. In most rats, adrenal SNA decreased with ganglionic blockade, indicating postganglionic as well as preganglionic innervation of the adrenal gland. During ganglionic blockade, static muscle contractions elicited a 140 +/- 21% increase in adrenal preganglionic SNA. In conclusion, static muscle contraction reflexly increases SNA to the adrenal gland, providing a mechanism for sympathoadrenal activation at the onset of exercise.

Adrenal Glands↗
PubMed1991

Effect of axillary blockade on regional cerebral blood flow during static handgrip.

Regional cerebral blood flow (rCBF) was determined at rest and during static handgrip before and after regional blockade with lidocaine. A fast rotating single photon emission computer tomograph system with 133Xe inhalation was used at orbitomeatal plane (OM) +2.5 and +6.5 cm in eight subjects. Median handgrip force during the control study was 41 (range 24-68) N, which represented 10% of the initial maximal voluntary contraction (MVC) and was 24 (18-36) N after axillary blockade (P less than 0.05), which represented 21% of the new MVC. During static handgrip, the rating of perceived exertion was 14 (10-16) exertion units before and 18 (15-20) after blockade (P less than 0.05). Hemispheric mean CBF did not change during handgrip. However, premotor rCBF increased from 55 (44-63) to 60 (50-69) ml.100 g-1.min-1 (P less than 0.05) and motor sensory rCBF from 57 (46-65) to 63 (55-71) ml.100 g-1.min-1 (P less than 0.05) to both the ipsilateral and contralateral sides during handgrip before, but not after, axillary blockade. There was no change in rCBF to other regions of the brain. Regional anesthesia with lidocaine did not alter resting rCBF. However, despite a greater sense of effort during static handgrip, there was no increase in rCBF after partial sensory and motor blockade. Thus bilateral activation occurs in the premotor and motor sensory cortex during static handgrip, and this activation requires neural feedback from the contracting muscles.

Adult↗
PubMed1991

Neural control of the forearm cutaneous vasoconstrictor response to dynamic exercise.

This study was designed to evaluate the relative importance of intended effort ("central command") and of the absolute intensity of dynamic exercise to the cutaneous vasoconstrictor response to the onset of exercise in humans. Skin blood flow (laser-Doppler flowmetry) was measured from the forearm in six healthy individuals during 3-min periods of high- and low-intensity exercise with and without partial neuromuscular blockade. Cutaneous vascular conductance (CVC) was calculated from the ratio of skin blood flow to mean arterial pressure and expressed as a percent change from rest. A rating of perceived exertion (RPE) was expressed as a subjective measure of intended effort. Under control conditions, CVC decreased by 22% (median; range 7-42%, P less than 0.05) during high-intensity exercise [218 (186-268) W; RPE 16 (14-19) exertion units]. In contrast, during control low-intensity exercise [106 (88-128) W; RPE 10 (9-14) exertion units], during low-level exercise with curare [77 (54-98) W; RPE 13 (11-16) exertion units], and during maximal exercise with curare [106 (88-124) W; RPE 19 (18-20) exertion units], CVC did not change significantly. These results suggest that factors related to the activity of the exercising muscle and its metabolism rather than intended effort determine the cutaneous vasoconstrictor response to the initiation of intense dynamic exercise in humans.

Adult↗