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Biomedical subjects

J P Buckley

Publications and source records attributed to J P Buckley.

At least 19 recordsLinked to original sources
PubMed2004

Reliability and validity of measures taken during the Chester step test to predict aerobic power and to prescribe aerobic exercise.

OBJECTIVES: To evaluate the reliability and validity of measures taken during the Chester step test (CST) used to predict VO(2)max and prescribe subsequent exercise. METHODS: The CST was performed twice on separate days by 7 males and 6 females aged 22.4 (SD 4.6) years. Heart rate (HR), ratings of perceived exertion (RPE), and oxygen uptake (VO(2)) were measured at each stage of the CST. RESULTS: RPE, HR, and actual VO(2) were the same at each stage for both trials but each of these measures was significantly different between CST stages (p<0.0005). Intertrial bias +/-95% limits of agreement (95% LoA) of HR reached acceptable limits at CST stage IV (-2+/-10 beats/min) and for RPE at stages III (0.2+/-1.4) and IV (0.5+/-1.9). Age estimated HRmax significantly overestimated actual HRmax of 5 beats/min (p = 0.016) and the 95% LoA showed that this error could range from an underestimation of 17 beats/min to an overestimation of 7 beats/min. Estimated versus actual VO(2) at each CST stage during both trials showed errors ranging between 11% and 19%. Trial 1 underestimated actual VO(2)max by 2.8 ml/kg/min (p = 0.006) and trial 2 by 1.6 ml/kg/min (not significant). The intertrial agreement in predicted VO(2)max was relatively narrow with a bias +/-95% LoA of -0.8+/-3.7 ml/kg/min. The RPE and %HRmax (actual) correlation improved with a second trial. At all CST stages in trial 2 RPE:%HRmax coefficients were significant with the highest correlations at CST stages III (r = 0.78) and IV (r = 0.84). CONCLUSION: CST VO(2)max prediction validity is questioned but the CST is reliable on a test-retest basis. VO(2)max prediction error is due more to VO(2) estimation error at each CST stage compared with error in age estimated HRmax. The HR/RPE relation at >50% VO(2)max reliably represents the recommended intensity for developing cardiorespiratory fitness, but only when a practice trial of the CST is first performed.

Adult↗
PubMed2000

Ratings of perceived exertion in braille: validity and reliability in production mode.

OBJECTIVES: (a) To assess the validity and reliability of producing and reproducing a given exercise intensity during cycle ergometry using a braille version of Borg's standard 6-20 rating of perceived exertion (RPE) scale, and (b) to determine whether the exercise responses of blind participants, at a given produced RPE, were similar to those reported in recognised guidelines for sighted subjects. METHODS: Ten healthy registered blind volunteer participants (four women, six men; mean (SD) age 23.2 (9.0) years) performed an initial graded exercise cycle test to determine maximal heart rate (HRMAx) and maximal oxygen uptake (VO2MAX). Three trials of three exercise bouts at RPEs 9, 11, and 13 were then performed in random order on three separate days of the same week, with expired air and heart rate measured continuously. Each exercise bout was followed by 10 minutes of rest. The validity of the scale as a means of producing different exercise intensities was assessed using a two factor (RPE x trial) repeated measures analysis of variance. Intertrial reliability was assessed using intraclass correlation coefficients (ICC) and the bias +/-95% limits of agreement (95%LoA) procedure. RESULTS: Participants reported no difficulty in using the braille RPE scale. When asked to produce exercise intensities equating to RPE 9, 11, and 13, they elicited mean %VO2MAX values of 47%, 53%, and 63% respectively. Analysis of variance showed no significant differences in either %HRMAx or %VO2MAX between trials at each of the three RPEs, but there was a significant difference (p<0.001) in both %HRMAx and %VO2MAX between the three RPE levels. All pairwise comparisons of the three different RPEs were significantly different (p<0.016). The ICC between the second and third trial for %HRMAx was significant (p <0.05) for all three RPEs. Similarly for %VO2MAX, the ICC was significant for RPE 9 and 11 but not 13. The 95%LoA decreased for both %HRMAx and %VO2MAX with each successive trial. CONCLUSIONS: Blind participants were successful in using a braille RPE scale to differentiate exercise intensity on a cycle ergometer. In every trial at RPE 13, all participants achieved %HRMAX and %VO2MAX levels, which fell within the recommendedrange for developing cardiorespiratory fitness. Using %HRMAx as a judge of intertrial reliability, the participants were able to repeat similar exercise intensities after two trials at each of the three RPEs (9, 11,13). The same was true for RPE 9 and 11, when %VO2MAX was used as a judge, but further trials were required to achieve similar reliability at RPE 13. A braille RPE scale can be used by healthy blind people during cycle ergometry, with similar effect to the visual analogue scale recommended for use in healthy sighted people.

Adult↗
PubMed1999

Cardio-respiratory responses to rowing ergometry and treadmill exercise soon after myocardial infarction.

PURPOSE: The aim of this study was to compare the cardio-respiratory differences between rowing ergometry and treadmill exercise in beta-blocked men participating in exercise rehabilitation soon after myocardial infarction (postMI). METHODS: Eleven males all receiving beta-blockade medication were measured for oxygen consumption (VO2), respiratory exchange ratio (RER), and rating of perceived exertion (RPE) at individualized submaximal exercise target heart rates (THR) during 6 min of exercise on each of a motorized treadmill and a rowing ergometer 2-6 wk (4.9 +/- 1.4) postMI. RESULTS: The mean THR of the group, predetermined from an exercise ECG stress test, was 107 +/- 16 beats x min(-1). No significant difference was found between rowing versus treadmill VO2 (19.4 +/- 3.2 vs 19.7 +/- 4.2 mL x kg(-1) x min(-1); P = 0.53) or RPE (12.6 +/- 1 vs 12.7 +/- 1; P = 0.72). RER was significantly greater (P = 0.02) during rowing (0.99 +/- 0.07) compared with treadmill exercise (0.94 +/- 0.07). CONCLUSION: Exercising at a specified submaximal THR during rowing versus treadmill exercise in beta-blocked men participating in very early cardiac rehabilitation represents the same VO2 and RPE. A significantly greater RER was, however, apparent during rowing compared with treadmill exercise; thus, agreement was shown with previous studies on healthy individuals where rowing ergometry was less metabolically efficient than treadmill exercise. The results suggest that establishing a THR from a standard treadmill stress test soon after MI is not only suitable for walking/treadmill exercise but also in setting exercise intensity for rowing ergometry.

Adrenergic beta-Antagonists↗
PubMed1992

The ouabain-dependent Na(+)-K+ pump and the brain renin-angiotensin system.

The present study investigated the role of ouabain-dependent inhibition of the Na(+)-K+ pump and stimulation of the brain renin-angiotensin system by looking at 1) the short-term and long-term effects of ouabain on arterial blood pressure, and 2) the acute and chronic effects of angiotensin II (ANG II) intraventricularly (i.c.v.) on the release of an endogenous inhibitor of the Na(+)-K+ pump. Ouabain infused subcutaneously in a dose of 1.5 mg.kg-1. 24 h-1 for 7 days did not affect arterial blood pressure in rats, whereas increases in both blood pressure and weight were observed in rats infused with ouabain at the same dose for a 4-week period. Plasma supernate obtained from pentobarbital-anesthetized dogs acutely treated with ANG II (1 microgram i.c.v. every 30 min for 2 h) induced a 44% decrease in the ouabain-sensitive 86Rb uptake by the rat tail artery which was prevented by pretreatment with saralasin i.c.v. Plasma supernate obtained from dogs that were infused for 4 days with ANG II (20 ng/min i.c.v.) and received saline as the drinking fluid also reduced by 34% the ouabain-sensitive 86Rb uptake by the rat tail artery. The present study provides evidence that chronic inhibition of the Na(+)-K+ pump for 4 weeks leads to the development of hypertension and that the release of an endogenous inhibitor of the Na(+)-K+ pump is implicated in the hypertension resulting from chronic stimulation of the brain angiotensin-system and an increase in sodium chloride intake.

Angiotensin II↗
PubMed1990

Effect of gender in centrally induced angiotensin II hypertension in dogs.

This study was designed to investigate the relation between gender, an endogenous inhibitor of the Na+-K+ pump, and volume-dependent hypertension induced by stimulation of the brain renin-angiotensin system and increased salt intake. Angiotensin II (20 ng/min i.c.v.) was infused for 4 weeks in five dogs of each sex with saline as the drinking fluid. In male dogs, angiotensin II induced parallel pressor (30%) and dipsogenic responses (70%), whereas no hypertension and no increase in fluid intake were observed in females. In contrast, the activity of the Na+-K+ pump as assessed by 86Rb uptake was independent of gender. Our data provide novel evidence that gender plays a determining role in the physiological properties of centrally administered angiotensin II.

Angiotensin II↗
PubMed1988

The central effects of the renin-angiotensin system.

The acute administration of ANG II into the brain of experimental animals produces transient pressor effects, a marked increase in drinking, release of the antidiuretic hormone, increase in total peripheral resistance, a diuretic and natriuretic effect and an increase in sympathetic outflow. The chronic administration of ANG II into a cerebrolateral ventricle produces sustained pressor effects only if 0.9% sodium chloride solution is used as the drinking fluid. The hypertension is due to an increase in total peripheral resistance which appears to be due to an increase in intrinsic tone of vascular smooth muscle. In addition there was enhanced responsiveness of the vasculature to norepinephrine and ANG II and a decrease in reflex vasodilatation of the hind limb of ANG II treated dogs. The chronic elevation of ANG II in the CSF plus an increase in NaCl intake produces a low renin, sodium dependent, expanded volume hypertension. Data are presented suggesting that this model of hypertension is induced by the central release of an inhibitor of the Na+,K+-Pump.

Animals↗
PubMed1988

Regional blood flows and cardiac function changes induced by angiotensin II in conscious dogs.

Hemodynamic properties of angiotensin (ANG) II 1, 5, 10 and 100 ng/kg i.v. and 10, 100 and 1000 ng/kg i.v.t. were assessed in conscious dogs. ANG II i.v. produced a dose-dependent pressor response (59 +/- 5-124 +/- 16 mmHg) and renal vasoconstriction (1.3 +/- 0.4-96 +/- 32 mmHg/ml/min). Ganglionic blockade (chlorisondamine 2 mg/kg i.v.) diminished mean arterial responses without altering peptide effects on renal circulation. At the highest dose, ANG II i.v. induced cardiac stimulation: increased heart rate (75 +/- 4-115 +/- 6 beats/min), cardiac output (2.0 +/- 0.1-2.4 +/- 0.2 l/min), dP/dt (2308 +/- 181-2773 +/- 173 mmHg/sec) and coronary blood flow (49 +/- 10-96 +/- 23 ml/min). Although with chlorisondamine cardiac response was more pronounced, subsequent beta blockade abolished it. Concomitantly, an isolated increase in plasma epinephrine was recorded (63 +/- 8-1505 +/- 354 pg/ml). A pressor response (59 +/- 8-89 +/- 13 mmHg) and renal vasoconstriction (1.1 +/- 0.1-2.2 +/- 0.5 mmHg/ml/min) were also produced by ANG II i.v.t. at the highest dose. These centrally mediated changes were prevented by chlorisondamine. Our study demonstrates 1) i.v. ANG II-mediated pressor responses are dependent on direct and indirect components, the relative contribution of each being dependent on the regional circulation; ANG II i.v. also produced a biphasic cardiac response--an initial centrally mediated depression and a secondary stimulation dependent on epinephrine via cardiac beta receptors and 2) i.v.t. ANG II-mediated pressor effects are essentially indirect. Finally, no evidence was found to support the role of vasopressin in ANG II effects.

Angiotensin II↗
PubMed1987

Acute central effects of L-glutamate in pentobarbital-anesthetized dogs.

Microinjections of L-glutamate (10(-10) to 2 X 10(-8) mol/kg) into the nucleus of tractus solitarii produced a dose-dependent increase in mean arterial pressure and a decrease in heart rate. L-Glutamate-induced hypertension was prevented by spinal transection and pretreatment with atropine (1 mg/kg iv) reversed the bradycardia. L-Glutamate also produced a dose-dependent increase in mean arterial pressure when injected intravenously and into the cisterna magna, but the dose-effect curves were shifted to the right. Finally, pretreatment with hexamethonium (30 mg/kg iv) abolished the hypertension resulting from intravenous injections of L-glutamate. These data demonstrate that the nucleus of tractus solitarii may play a determinant role in the central pressor effects of L-glutamate. In addition, we demonstrated that this hypertension was due to a central sympathetic stimulation and that the autonomic nervous system also mediated the pressor effects of intravenous L-glutamate.

Anesthesia↗
PubMed1985

Hemodynamic effects of the intraventricular administration of angiotensin II and renin in awake dogs.

This study was undertaken to investigate the hemodynamic changes induced by intraventricular injections of angiotensin II (A-II), 1 to 100 ng/kg/min, and renin in doses of 0.025 to 0.3 units (u) in conscious instrumented dogs. Angiotensin II produced a dose-related increase in mean arterial pressure; however, only the highest dose produced a significant increase of 23 +/- 6 mmHg. In contrast, renin did not significantly alter mean arterial pressure in the doses administered but 0.1 and 0.3 u induced a significant increase in systolic arterial blood pressure of 10 +/- 2 and 17 +/- 4 mmHg, respectively. Neither A-II nor renin affected heart rate, dP/dt or carotid, coronary or renal blood flows. These data suggest that in conscious dogs, the threshold level of A-II necessary to induce substantial hemodynamic changes is greater than the amount of A-II that can be acutely generated by activation of angiotensinogen. In addition, the present data suggest that the magnitude of the response is dependent on the availability of the substrate rather than the dose of renin injected centrally into conscious dogs.

Angiotensin II↗
PubMed1984

Effects of brain renin-angiotensin on cardiovascular function and saline intake in awake dogs.

Initial studies were undertaken to investigate the effects of prolonged administration of angiotensin II (AII), 1 micrograms twice daily, via the lateral ventricles to mongrel dogs on arterial blood pressure and to determine if sodium intake was essential for the development of hypertension. Increasing AII levels in the cerebrospinal fluid for a prolonged period of time produced a sustained hypertensive state only in those dogs in which the daily intake of sodium was increased. The hypertension appeared to be due to an increase in total peripheral resistance. Central administration of AII increased both fluid intake and urine output. In order to assess the hemodynamic effects of increasing endogenous brain AII, renin was injected in doses of 0.025, 0.05, 0.1 and 0.3 units (from porcine kidney) into the lateral ventricles of chronically instrumented awake dogs. Hemodynamic variables were recorded prior to and one and 2 h after the central administration of renin. Renin produced a dose-dependent increase in mean arterial pressure with no significant change in heart rate or carotid, coronary and renal blood flow velocities. Chronic intraventricular administration of renin, 0.15 units twice daily to awake instrumented dogs receiving saline as the drinking fluid, markedly increased the daily intake of saline and increased diastolic and systolic blood pressure without increasing heart rate or carotid, coronary or renal blood flow velocities. There appears to be a direct significant relationship between the increase in mean blood pressure due to the intraventricular administration of renin and the volume of saline consumed.

Angiotensin II↗
PubMed1983

Central alpha-adrenergic control of blood pressure. Effects of clonidine withdrawal.

Studies were undertaken to investigate the role of the CNS in withdrawal hypertension caused by abrupt cessation of long-term clonidine treatment. The studies were conducted on male wistar rats receiving clonidine, 100 micrograms/kg subcutaneously twice daily for seven days. Withdrawal hypertension occurred 16 to 18 hours following the last injection of clonidine. Pressor responses to posterior hypothalamic stimulation were significantly potentiated in the rats undergoing clonidine withdrawal, and the depressor response to a single injection of 10 micrograms of clonidine into the lateral cerebral ventricle was significantly attenuated in these animals. Studies on pithed rats demonstrated that destruction of the CNS eliminated the withdrawal hypertension. These data suggest that alpha-adrenoreceptors in the nucleus tractus solitarius play an important role in the normal maintenance of blood pressure, and a decrease in sensitivity of these receptors could result in the development of a hypertensive state.

Animals↗
PubMed1981

Cardiovascular effects of chronic intraventricular administration of angiotensin II in dogs.

Intracerebroventricular administration of angiotensin II (AII), 1 microgram twice a day to mongrel dogs plus saline as the drinking fluid for 4 weeks produced a significant sustained elevation in systolic and diastolic blood pressures. The hypertensive state appeared to be due to an increase in total peripheral resistance. Fluid intake and urine output were elevated and there was a significant increase in body weight at the end of week 2, 3 and 4. Serum Na+ levels were significantly decreased and serum Ca++ levels significantly increased in the hypertensive animals. These studies indicate that increasing AII levels in the cerebrospinal fluid for a prolonged period of time produces a sustained hypertensive state only if the daily intake of sodium is increased and that the alterations in vascular resistance may be due to changes in the Na+ - Ca++ fluxes.

Angiotensin II↗
PubMed1981

Cardiovascular actions of angiotensin in the fowl (Gallus domesticus). II. Angiotensin analog agonists and antagonists.

Like angiotensin II (AII) itself, [SAR1] AII induced a biphasic blood pressure response in the conscious chicken--an initial depressor response followed by a pressor response. Angiotensin III, however, induced only a depressor response in the dose range tested. The response to angiotensin I was similar to that to AII, and appeared to be due to its conversion to AII as it was inhibited by prior infusion of the angiotensin converting enzyme inhibitor SQ 20,881. Two angiotensin analog antagonists [SAR1ALA8] AII and [SAR1ILE8] AII inhibited both components of the response to AII, but the pressor response was inhibited at lower concentrations of antagonist than was the depressor response. These findings give further support to the suggestion that the pressor and depressor component of the response to AII in the conscious chicken are mediated via different AII receptors, and indicate the possibility of selective blockade of these two components.

Angiotensin II↗