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Biomedical subjects

M J Joyner

Publications and source records attributed to M J Joyner.

At least 91 records · Page 5Linked to original sources
PubMed1992

Sympathetic modulation of blood flow and O2 uptake in rhythmically contracting human forearm muscles.

This study tested the effects of sympathetically mediated changes in blood flow to active muscles on muscle O2 uptake (VO2) in humans. Four minutes of graded (15-80% of maximum voluntary contraction, MVC) rhythmic handgrip exercise were performed. Forearm blood flow (FBF) (plethysmography) and deep vein O2 saturation were measured each minute. Forearm O2 uptake was calculated using the Fick principle. In protocol 1, exercise was performed while supine and again while upright to augment sympathetic outflow to the active muscles. Standing reduced FBF at rest from 3.6 to 2.2 ml.100 ml-1.min-1 (P < 0.05). During light exercise (15-40% MVC) FBF was unaffected by body position. Standing reduced FBF (P < 0.05) from 36.0 to 25.2 ml.100 ml-1.min-1 and forearm VO2 from 38.2 to 28.1 ml.kg-1.min-1 during the final work load. In protocol 2, exercise was performed while supine before and after local anesthetic block of the sympathetic nerves to the forearm. Sympathetic block increased FBF at rest from 3.1 to 8.9 ml.100 ml-1.min-1 (P < 0.05), and FBF was higher during all work loads At 70-80% of MVC sympathetic block increased FBF from 35.4 to 50.7 ml.100 ml-1.min-1 (P < 0.05), and forearm VO2 from 45.5 to 54.2 ml.kg-1.min-1 (P < 0.05). These results suggest that in humans sympathetic nerves modulate blood flow to active muscles during light and heavy rhythmic exercise and that this restraint of flow can limit O2 uptake in muscles performing heavy rhythmic exercise.

Adolescent↗
PubMed1992

Electrical activation of expiratory muscles increases with time in pentobarbital-anesthetized dogs.

Although the pentobarbital-anesthetized dog is often used as a model in studies of respiratory muscle activity during spontaneous breathing, there is no information regarding the stability of the pattern of breathing of this model over time. The electromyograms of several inspiratory and expiratory muscle groups were measured in six dogs over a 4-h period by use of chronically implanted electrodes. Anesthesia was induced with pentobarbital sodium (25 mg/kg iv), with supplemental doses to maintain constant plasma pentobarbital concentrations. Phasic electrical activity increased over time in the triangularis sterni, transversus abdominis, and external oblique muscles (expiratory muscles). The electrical activity of the costal diaphragm, crural diaphragm, and parasternal intercostal muscles (inspiratory muscles) was unchanged. These changes in electrical activity occurred despite stable plasma levels of pentobarbital and arterial PCO2. They were associated with changes in chest wall motion and an increased tidal volume with unchanged breathing frequency. We conclude that expiratory muscle groups are selectively activated with time in pentobarbital-anesthetized dogs lying supine. Therefore the duration of anesthesia is an important variable in studies using this model.

Anesthesia↗
PubMed1991

Modeling: optimal marathon performance on the basis of physiological factors.

This paper examines current concepts concerning "limiting" factors in human endurance performance by modeling marathon running times on the basis of various combinations of previously reported values of maximal O2 uptake (VO2max), lactate threshold, and running economy in elite distance runners. The current concept is that VO2max sets the upper limit for aerobic metabolism while the blood lactate threshold is related to the fraction of VO2max that can be sustained in competitive events greater than approximately 3,000 m. Running economy then appears to interact with VO2max and blood lactate threshold to determine the actual running speed at lactate threshold, which is generally a speed similar to (or slightly slower than) that sustained by individual runners in the marathon. A variety of combinations of these variables from elite runners results in estimated running times that are significantly faster than the current world record (2:06:50). The fastest time for the marathon predicted by this model is 1:57:58 in a hypothetical subject with a VO2max of 84 ml.kg-1.min-1, a lactate threshold of 85% of VO2max, and exceptional running economy. This analysis suggests that substantial improvements in marathon performance are "physiologically" possible or that current concepts regarding limiting factors in endurance running need additional refinement and empirical testing.

Fatigue↗
PubMed1991

Does the pressor response to ischemic exercise improve blood flow to contracting muscles in humans?

The purpose of this study was to determine in humans 1) the gain for the reflex pressor response that occurs when perfusion pressure to rhythmically contracting muscles is reduced and 2) whether the pressor response improves blood flow to the contracting muscles. Six normal subjects performed light, moderate, and heavy rhythmic forearm contractions (30/min) with the forearm enclosed in a Plexiglas box. Pressure in the box was increased 10 mmHg each minute up to 50 mmHg to reduce transmural pressure in the arterial system of the forearm. Mean arterial pressure (MAP) was measured continuously. During light exercise no reflex increase in MAP occurred until box pressure was 50 mmHg. During moderate and heavy exercise MAP began to increase with only 10- to 20-mmHg increases in box pressure. The slope of this increase was 3.5-3.9 mmHg per 10 mmHg of box pressure (approximately 60% of that in dogs). In a further study on six subjects a deep vein draining the active forearm muscles was cannulated and deep venous O2 saturation measured to assess how a 50-mmHg increase in box pressure and subsequent reflex increase in MAP altered blood flow to the contracting muscles during heavy rhythmic exercise. The increase in box pressure reduced blood flow to contracting forearm muscles by 20-25% and was followed by a 19-mmHg increase in MAP that did not appear to improve perfusion of the active muscles. This finding was unexpected, because studies in dogs suggest that the pressor response to rhythmic exercise with restricted muscle blood flow can improve perfusion of the active muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Sustained increases in sympathetic outflow during prolonged lower body negative pressure in humans.

The purpose of this study was to determine whether prolonged unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP) causes constant increases in sympathetic outflow to skeletal muscles. Eight healthy subjects underwent a 20-min control period followed by 20 min of 15-mmHg LBNP. This pressure was selected because it did not cause any significant change in mean arterial blood pressure (sphygmomanometry) or heart rate, suggesting that the cardiopulmonary baroreceptors were selectively unloaded and the activity of the arterial baroreceptors was unchanged. Muscle sympathetic nerve activity in the peroneal nerve (MSNA, microneurography) increased from an average of 21.8 +/- 1.7 bursts/min over the last 5 min of control to 29.0 +/- 2.9 bursts/min during the 1st min of LBNP (P less than 0.05 LBNP vs. control). The increase in MSNA observed during the 1st min was sustained throughout LBNP. Forelimb blood flow (plethysmography) decreased abruptly at the onset of the LBNP from a control value of 4.3 +/- 0.5 ml.min-1.100 ml-1 to 2.5 +/- 0.2 at the 1st min; the flow then increased and remained significantly above this value, but below the control value, throughout LBNP. Similar blood flow findings were obtained in additional studies, when the hand circulation was excluded during the flow measurements. Forearm skin blood flow (laser Doppler) also decreased abruptly at the onset of LBNP and was followed by partial recovery, but these changes were too small to account for all the increases in limb blood flow over the course of LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Blood flow to contracting human muscles: influence of increased sympathetic activity.

The purpose of this study was to examine the effects of the increased sympathetic activity elicited by the upright posture on blood flow to exercising human forearm muscles. Six subjects performed light and heavy rhythmic forearm exercise. Trials were conducted with the subjects supine and standing. Forearm blood flow (FBF, plethysmography) and skin blood flow (laser Doppler) were measured during brief pauses in the contractions. Arterial blood pressure and heart rate were also measured. During the first 6 min of light exercise, blood flow was similar in the supine and standing positions (approximately 15 ml.min-1.100 ml-1); from minutes 7 to 20 FBF was approximately 3-7 ml.min-1.100 ml-1 less in the standing position (P less than 0.05). When 5 min of heavy exercise immediately followed the light exercise, FBF was approximately 30-35 ml.min-1.100 ml-1 in the supine position. These values were approximately 8-12 ml.min-1.100 ml-1 greater than those observed in the upright position (P less than 0.05). When light exercise did not precede 8 min of heavy exercise, the blood flow at the end of minute 1 was similar in the supine and standing positions but was approximately 6-9 ml.min-1.100 ml-1 lower in the standing position during minutes 2-8. Heart rate was always approximately 10-20 beats higher in the upright position (P less than 0.05). Forearm skin blood flow and mean arterial pressure were similar in the two positions, indicating that the changes in FBF resulted from differences in the caliber of the resistance vessels in the forearm muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Response of upper limb blood flow to handgrip exercise after Blalock-Taussig operation (for tetralogy of Fallot) or subclavian flap operation (for aortic isthmic coarctation).

To evaluate the effects of long-term reductions in perfusion pressure on blood flow responses to increased functional demand, 5 patients (aged 12 to 26 years) without normal aortic to subclavian artery blood flow to 1 arm as a result of surgery to treat congenital heart disease were studied. Five age- and sex-matched healthy (control) subjects were also studied. In the patients, forearm blood flow was not different in the surgical and normal arms at rest (3.6 +/- 0.6 vs 4.0 +/- 0.7 ml/min/100 ml, respectively, mean +/- standard error, difference not significant) despite lower systolic blood pressure in the surgical arm (87 +/- 2 vs 115 +/- 2 mm Hg, p less than 0.05). The increases in heart rate, systolic blood pressure, forearm electromyographic activity (index of muscle fatigue) and postexercise forearm blood flow (index of muscle oxygen deficit) were not different in response to 2.5 minutes of submaximal rhythmic handgrip exercise (50% of maximal force) performed with the surgical versus the normal arms. Peak forearm blood flow elicited by combined ischemia and maximal isometric handgrip exercise was not significantly different in surgical and normal arms in the group as a whole (39 +/- 4 vs 43 +/- 3 ml/min/100 ml, difference not significant), although some bilateral deficit (20 to 38%) was observed in 2 patients. No bilateral differences were observed in the control subjects under any condition. The finding of normal physiologic adjustments to submaximal rhythmic handgrip exercise with the surgical arm suggests that oxygen delivery during exercise was adequate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1989

Differential control of forearm and calf vascular resistance during one-leg exercise.

The purpose of this study was to determine whether blood flow (BF) and vascular resistance (VR) are controlled differently in the nonactive arm and leg during submaximal rhythmic exercise. In eight healthy men we simultaneously measured BF to the forearm and calf (venous occlusion plethysmography) and arterial blood pressure (sphygmomanometry) and calculated whole limb VR before (control) and during 3 min of cycling with the contralateral leg at 38, 56, and 75% of peak one-leg O2 uptake (VO2). During the initial phase of exercise (0-1.5 min) at all work loads, BF increased and VR decreased in the forearm (P less than 0.05), whereas calf BF and VR remained at control levels. Thereafter, BF decreased and VR increased in parallel and progressive fashion in both limbs. At end exercise, forearm BF and VR were not different from control values (P greater than 0.05); however, in the calf, BF tended to be lower (P less than 0.05 at 75% peak VO2 only) and VR was higher (23 +/- 9, 44 +/- 14, and 88 +/- 23% above control at 38, 56, and 75% of peak VO2, respectively, all P less than 0.05). In a second series of studies, forearm and calf skin blood flow (laser-Doppler velocimetry) and arterial pressure were measured during the same levels of exercise in six of the subjects. Compared with control, skin BF was unchanged and VR was increased (P less than 0.05) in the forearm by end exercise at all work loads, whereas calf skin BF increased (P less than 0.05) and VR decreased (P less than 0.05). The present findings indicate that skeletal muscle and skin VR are controlled differently in the nonactive forearm and calf during the initial phase of rhythmic exercise with the contralateral leg. Skeletal muscle vasodilation occurs in the forearm but not in the calf; forearm skin vasoconstricts, whereas calf skin vasodilates. Finally, during exercise a time-dependent vasoconstriction occurs in the skeletal muscle of both limbs.

Adult↗
PubMed1989

Alterations in plasma lipids consequent to endurance training and beta-blockade.

Alterations in plasma lipids consequent to endurance training and beta-blockade. Med. Sci. Sports Exerc., Vol. 21, No. 3, pp. 288-292, 1989. The chronic use of beta adrenergic blockers (BAB) has been associated with reductions in HDL-cholesterol (HDL-C) and increases in triglycerides (TG). This study evaluated the impact of concurrent endurance exercise training and chronic medication with BAB on plasma lipid and lipoprotein profiles in healthy young adult males. Changes in plasma lipids and lipoproteins were investigated while exercise training under the influence of one of two nonselective BAB [sotalol (320 mg.d-1) and propranolol (160 mg.d-1)], one beta 1 selective BAB [atenolol (100 mg.d-1)], or a placebo control. Total cholesterol (TC), HDL-C, LDL-cholesterol (LDL-C), TG, and the ratios of TC/HDL and LDL/HDL were determined before and after endurance training programs of either 14 (N = 27, sotalol) or 15 (N = 47, propranolol/atenolol) wk duration. The subjects exhibited increases in maximal oxygen uptake of 12-20%. Despite increased endurance capacity, the subjects in both BAB and placebo control groups failed to demonstrate the expected increase in HDL-C and decrease in TG. In fact, HDL-C was significantly decreased post-training in the propranolol group. The placebo groups did decrease TC, LDL-C and the TC/HDL and LDL/HDL ratios, improving their CHD risk profile. Similar changes were not observed in the groups on BAB. Thus, with respect to the present population, BAB does appear to interfere with the usual training-induced improvements in the lipid profile. Endurance training may, however, reduce the deterioration in the lipid profile known to occur with BAB.

Adrenergic beta-Antagonists↗
PubMed1988

Fatigue-related changes in neuromuscular excitability of rat hindlimb muscles.

Brief repetitive trains of supramaximal nerve stimulation produce intermittent muscle activation and, in time, a progressive decline in force (i.e., neuromuscular fatigue) and depression of the electromyogram (EMG). These changes may include within-train reductions in EMG due to a failure of neuromuscular propagation. The aim of the present study was to investigate changes in EMG during a 360-second stimulus regimen designed to fatigue soleus and extensor digitorum longus muscles of anesthetized rats by activating the muscle with repetitive trains of 40 Hz stimuli. Measurements included peak force for each tetanus, variation of the within-train EMG (coefficient of variation for area), and magnitude of the first EMG waveform (area) of each train. Fatigue was characterized as the relative decline in force over the course of the test. The responses of the test muscles were categorized, based on an absolute scale of fatigability, into five groups: potentiated, nonfatigable, low fatigability, intermediate fatigability, and high fatigability. Fatigable muscles (low, intermediate, and high fatigability groups) demonstrated a decreased EMG magnitude and an increased EMG-area variation with repetitive activation. This increased variation, however, was nonmonotonically related to fatigability such that the least and most fatigable muscles had the smallest within-train EMG variation. We suggest that these data can be explained by considering the EMG (compound muscle action potential) as a stochastic process that represents a composite of single-fiber events (axonal to sarcolemmal transmission) with variable probabilities.

Animals↗
PubMed1988

Reductions in blood pressure after acute exercise by hypertensive rats.

Postexercise reductions in blood pressure at rest have been reported for hypertensive subjects. To determine whether post-exercise hypotension would occur in spontaneously hypertensive rats and to test the hypothesis that any reductions would result because of decreases in regional vascular resistances, hypertensive rats (n = 19) were instrumented with indwelling arterial catheters and Doppler probes to measure regional blood flows from the iliac, superior mesenteric, and renal arteries. Data were collected from animals who performed a 20- and a 40-min treadmill test at between 60 and 70% of their maximum O2 uptake. When the animals ran for 20 min, there was a pre- to postexercise drop in mean arterial pressure (MAP) from 158 +/- 3.6 to 150 +/- 3.6 mmHg (P less than 0.05), which was recorded 30 min after the exercise had ceased. The pre- to postexercise reduction in MAP after 40 min of treadmill running was from 154 +/- 3.1 to 138 +/- 3.0 mmHg (P less than 0.05) as recorded 30 min postexercise. Postexercise heart rate was significantly lower after the 40-min exercise bout, from a preexercise mean of 351 +/- 3 beats/min to 324 +/- 5 beats/min 30 min after the treadmill had stopped. Surprisingly, marked pre- to postexercise reductions in regional vascular resistance were not observed in either the iliac, superior mesenteric, or renal vascular beds. These data demonstrated the existence of postexercise hypotension in genetic hypertensive rats and suggested that reductions in cardiac output were the primary hemodynamic mechanism for this finding.

Animals↗
PubMed1988

Effect of beta-blockade on the drift in O2 consumption during prolonged exercise.

The effect of beta-adrenergic blockade on the drift in O2 consumption (VO2 drift) typically observed during prolonged constant-rate exercise was studied in 14 healthy males in moderate heat at 40% of maximal O2 consumption (VO2max). After an initial maximum cycle ergometer test to determine the subjects' control VO2max, subjects were administered each of three medications: placebo, atenolol (100 mg once daily), and propranolol (80 mg twice daily), in a randomized double-blind fashion. Each medication period was 5 days in length and was followed by a 4-day washout period. On the 3rd day of each medication period, subjects performed a maximal cycle ergometer test. On the final day of each medication period, subjects exercised at 40% of their control VO2max for 90 min on a cycle ergometer in a warm (31.7 +/- 0.3 degrees C) moderately humid (44.7 +/- 4.7%) environment. beta-Blockade caused significant (P less than 0.05) reductions in VO2max, maximal minute ventilation (VEmax), maximal heart rate (HRmax), and maximal exercise time. Significantly greater decreases in VO2max, VEmax, and HRmax were associated with the propranolol compared with the atenolol treatment. During the 90-min submaximal rides, beta-blockade significantly reduced heart rate. Substantially lower values for O2 consumption (VO2) and minute ventilation (VE) were observed with propranolol compared with atenolol or placebo. Furthermore, VO2 drift and HR drift were observed under atenolol and placebo conditions but not with propranolol. Respiratory exchange ratio decreased significantly over time during the placebo and atenolol trials but did not change during the propranolol trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Maximal exercise responses to acute and chronic beta-adrenergic blockade in healthy male subjects.

Conflicting data on the alterations in the maximal exercise response to beta blockade (BB) may be the result of differences in the length of time the subject has been on medication, i.e., hours vs days. The purpose of this study was to examine maximal exercise responses during acute and chronic administration of BB. Twenty-eight healthy males, 14 untrained (UT) and 14 involved in a personal training regimen (TR), performed maximal treadmill tests after 1 d and 9 d under three double-blind, randomized conditions: a placebo (PLAC), propranolol (PROP) 80 mg b.i.d., and atenolol (ATEN) 100 mg o.d. Maximal heart rate (HR), oxygen consumption (VO2), ventilation (VE), and treadmill time were significantly reduced by PROP and ATEN after an acute and chronic dose when compared to PLAC (P less than 0.05) in both groups of subjects. Maximal HR was decreased more after 1 d of BB than after 9 d of BB with both PROP and ATEN in the UT subjects and with PROP only in the TR group. VO2max, VEmax, and treadmill time were also less attenuated after 9 d of BB; however, this trend did not reach statistical significance. The nonselective beta blocker, PROP, caused greater reductions in VO2max compared to the selective beta blocker, ATEN, in both groups of subjects. These data indicate that, other than a small change in maximal HR, there is no difference in the exercise response to acute and chronic BB in normal and highly conditioned individuals.

Adrenergic beta-Antagonists↗
PubMed1987

Beta-blockade reduces tidal volume during heavy exercise in trained and untrained men.

The effects of beta-blockade on tidal volume (VT), breath cycle timing, and respiratory drive were evaluated in 14 endurance-trained [maximum O2 uptake (VO2max) approximately 65 ml X kg-1 X min-1] and 14 untrained (VO2max approximately 50 ml X kg-1 X min-1) male subjects at 45, 60, and 75% of unblocked VO2max and at VO2max. Propranolol (PROP, 80 mg twice daily), atenolol (ATEN, 100 mg once a day) and placebo (PLAC) were administered in a randomized double-blind design. In both subject groups both drugs attenuated the increases in VT associated with increasing work rate. CO2 production (VCO2) was not changed by either drug during submaximal exercise but was reduced in both subject groups by both drugs during maximal exercise. The relationship between minute ventilation (VE) and VCO2 was unaltered by either drug in both subject groups due to increases in breathing frequency. In trained subjects VT was reduced during maximal exercise from 2.58 l/breath on PLAC to 2.21 l/breath on PROP and to 2.44 l/breath on ATEN. In untrained subjects VT at maximal exercise was reduced from 2.30 l/breath on PLAC to 1.99 on PROP and 2.12 on ATEN. These observations indicate that 1) since VE vs. VCO2 was not altered by beta-adrenergic blockade, the changes in VT and f did not result from a general blunting of the ventilatory response to exercise during beta-adrenergic blockade; and 2) blockade of beta 1- and beta 2-receptors with PROP caused larger reductions in VT compared with blockade of beta 1-receptors only (ATEN), suggesting that beta 2-mediated bronchodilation plays a role in the VT response to heavy exercise.

Adrenergic beta-Antagonists↗
PubMed1987

Thermoregulation during prolonged exercise in heat: alterations with beta-adrenergic blockade.

Thermoregulation and cardiovascular drift were studied under conditions of prolonged exercise in a warm environment (dry bulb temperature 31.7 +/- 0.3 degrees C, rh 44.7 +/- 4.7%) during beta-adrenergic blockade. Fourteen subjects performed 90-min rides on a cycle ergometer at a work rate equivalent to 40% of their control maximal O2 uptake under each of three treatments provided in a randomized double-blind manner: atenolol (100 mg/day), propranolol (160 mg/day), and a placebo. Exercise during the propranolol trial resulted in significantly higher forearm vascular resistance values and significantly lower forearm blood flows (FBF) compared with the placebo trial. However, the significantly lower FBF during propranolol did not significantly alter the rectal temperature (Tre) response to prolonged exercise. In addition, both beta-blockers produced lower FBF for any given Tre, suggesting that beta-adrenergic blockade affects FBF through nonthermal factors. The slight differences in Tre, despite the large differences in FBF between the various treatments, are apparently the result of an enhanced sweat loss and a lower mean skin temperature during exercise with beta-blockade. The uncoupling of FBF and sweat loss provides evidence of independent regulation. The reduction in FBF at any given Tre was concomitant to lower blood pressure values during beta-blockade and suggests that baroreflexes provide significant input to the control of skin blood flow when both pressure and temperature maintenance are simultaneously challenged.

Adult↗
PubMed1986

Effects of beta-blockade on exercise capacity of trained and untrained men: a hemodynamic comparison.

To study the effects of cardiovascular fitness on hemodynamic responses to exercise during beta-adrenergic blockade (BAB), submaximal [60% of maximum O2 uptake (VO2max)] and maximal treadmill exercise data were collected in 11 trained (T, VO2max 63.3 ml X kg-1 X min-1, 26.8 yr) and 11 untrained (UT, VO2max 44.5 ml X kg-1 X min-1, 25.0 yr) male subjects. Subjects completed two maximal control tests followed by a randomized, double-blind series of maximal tests after 1-wk treatments with placebo (PLAC), propranolol (PROP, 160 mg/day, beta 1- and beta 2-blockade), and atenolol (ATEN, 100 mg/day, beta 1-blockade). Treatments were separated by 1-wk washout periods. At 60% of control VO2max T and UT subjects experienced no reductions in O2 uptake (VO2) with either drug. Submaximal heart rate (HR, beats/min) was 134.8 PLAC, 107.0 PROP, 107.9 ATEN (P less than 0.05 both drugs vs. PLAC) in T subjects and 141.1 PLAC, 106.1 PROP, and 105.0 ATEN (P less than 0.05 both drugs vs. PLAC) in UT subjects. Cardiac output (1/min) for T was 17.3 PLAC, 16.9 PROP, 16.5 ATEN (P less than 0.05 ATEN vs. PLAC in T only) and for UT it was 12.2 (PLAC), 11.7 (PROP), 11.5 (ATEN) (P less than 0.05 both drugs vs. PLAC in UT). Stroke volume increased from 129.8 ml (PLAC) to 158.6 (PROP) and 156.2 (ATEN) in T (P less than 0.05 both drugs vs. PLAC) and from 86.8 (PLAC) to 110.0 (PROP) and 109.8 (ATEN) (P less than 0.05 both drugs vs. PLAC) in UT. The increases in stroke volume (SV) were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Acute response to submaximal and maximal exercise consequent to beta-adrenergic blockade: implications for the prescription of exercise.

Forty-seven healthy male subjects, 17 to 34 years old, completed a test to exhaustion on a motor-driven treadmill to determine their maximal oxygen uptake. A second test was administered 2 days later during which the subject walked for 20 to 25 minutes at a steady-state level representing 60% of the maximal oxygen uptake as determined in the first test. The grade was then increased every 2 minutes until the subject reached the state of exhaustion. After the second test, the subjects were randomly assigned, in a double-blind manner, to either placebo, propranolol (160 mg/day), or atenolol (100 mg/day) treatment for 7 days. Exactly 1 week from the time of the second test, and 3 hours after the last medication, the subjects completed the final exercise test using the same treadmill protocol administered in the second test. Heart rate and systolic blood pressure at rest and during submaximal steady-state exercise were significantly reduced by both drugs, whereas diastolic pressure was unaffected. During submaximal steady-state exercise, cardiac output was reduced in both the placebo and atenolol groups, stroke volume was increased in both atenolol and propranolol groups, oxygen uptake was reduced in the atenolol group, pulmonary ventilation was reduced in both propranolol and atenolol groups, and the respiratory exchange ratio remained unchanged. With maximal exercise, treadmill time was significantly reduced with propranolol, pulmonary ventilation and heart rate were reduced significantly with both drugs, but maximal oxygen uptake remained unchanged. Thus, beta blockade does not appear to limit ability to exercise. However, there appears to be a significant advantage to using a cardioselective rather than a nonselective beta-blocking agent.

Adolescent↗