Effect of beta-adrenergic blockade on response to exercise in sedentary and active subjects

1989 ◽  
Vol 67 (1) ◽  
pp. 103-109 ◽  
Author(s):  
V. Brusasco ◽  
B. Violante ◽  
G. Buccheri

The response to incremental work after placebo and propranolol (80 mg, orally) was studied in 11 sedentary (S) and 11 physically active (PA) healthy subjects. O2 uptake, CO2 output, and minute ventilation were significantly reduced at all or most work rates after propranolol in S subjects, whereas in PA subjects only O2 uptake was occasionally significantly reduced. Maximum work capacity during the propranolol trial was significantly increased by 17% in the S group but was unaltered in the PA group. A subanaerobic threshold constant work test in five sedentary subjects demonstrated that propranolol had no effect on the respiratory response both early and late in exercise. In addition, propranolol did not impair the ability of the respiratory control system to maintain alveolar PCO2 at new set points when external dead space was added during constant load work. We conclude that alterations of gas exchange during incremental work after propranolol administration are related to both physical fitness and type of exercise.

1996 ◽  
Vol 81 (2) ◽  
pp. 738-742 ◽  
Author(s):  
W. E. Spinnewijn ◽  
H. C. Wallenburg ◽  
P. C. Struijk ◽  
F. K. Lotgering

This study was designed to determine whether pregnancy affects peak O2 uptake (VO2peak) during swimming compared with cycling. We studied 11 women at 30–34 wk gestation and 8–12 wk postpartum. We measured heart rate (HR), O2 uptake (VO2), CO2 output (VCO2), minute ventilation (VE), and lactic acid concentration. Peak HR was not significantly affected by the type of exercise or by pregnancy. VO2peak was 9% lower during swimming than during cycling but was not affected by pregnancy, with values for pregnancy cycling, pregnancy swimming, postpartum cycling, and postpartum swimming of 2.36 +/- 0.12, 2.11 +/- 0.11, 2.29 +/- 0.10, and 2.12 +/- 0.07 l/min, respectively. Peak VCO2 (VCO2peak) and peak VE were significantly lower during swimming than during cycling by 18–25%, but only VCO2peak during swimming was affected by pregnancy (-10%). Lactic acid concentrations were 12–17% lower after swimming than after cycling and 17–31% lower during pregnancy than postpartum. We conclude that perceived maximal exertion is reached at a lower percent maximal VO2 in swimming than in cycling and that the reduced energy expenditure is reflected by lower VO2peak, VCO2peak, and peak VE. Pregnancy, however, does not affect VO2peak in cycling or swimming.


1986 ◽  
Vol 61 (2) ◽  
pp. 523-529 ◽  
Author(s):  
R. P. Adams ◽  
P. A. Cashman ◽  
J. C. Young

Six trained males [mean maximal O2 uptake (VO2max) = 66 ml X kg-1 X min-1] performed 30 min of cycling (mean = 76.8% VO2max) during normoxia (21.35 +/- 0.16% O2) and hyperoxia (61.34 +/- 1.0% O2). Values for VO2, CO2 output (VCO2), minute ventilation (VE), respiratory exchange ratio (RER), venous lactate, glycerol, free fatty acids, glucose, and alanine were obtained before, during, and after the exercise bout to investigate the possibility that a substrate shift is responsible for the previously observed enhanced performance and decreased RER during exercise with hyperoxia. VO2, free fatty acids, glucose, and alanine values were not significantly different in hyperoxia compared with normoxia. VCO2, RER, VE, and glycerol and lactate levels were all lower during hyperoxia. These results are interpreted to support the possibility of a substrate shift during hyperoxia.


1983 ◽  
Vol 54 (5) ◽  
pp. 1306-1313 ◽  
Author(s):  
E. S. Petersen ◽  
B. J. Whipp ◽  
J. A. Davis ◽  
D. J. Huntsman ◽  
H. V. Brown ◽  
...  

The effects of beta-adrenergic blockade induced by intravenous propranolol hydrochloride (0.2 mg/kg) on ventilatory and gas exchange responses to exercise were studied during tests in which the work rate was either increased progressively or maintained at a constant load in six healthy young male subjects. Heart rate during exercise decreased by about 20% and cardiac output, as estimated by a modification of the method of Kim et al. (J. Appl. Physiol. 21: 1338–1344, 1966), by about 15%. The relation between work rate and O2 uptake (VO2) was unaffected by propranolol, whereas maximal O2 uptake (VO2max) decreased by 5% and the anaerobic threshold, estimated noninvasively, was lowered by 23%. The relations between CO2 output (VCO2) and end-tidal CO2 partial pressure (PCO2) and between VCO2 and minute ventilation (VE) were both unaffected. The time constants for changes of VO2, VCO2, and VE during on-transients from unloaded pedaling to either a moderate (ca. 50% VO2max) or a heavy (ca. 67% VO2max) work rate in the control studies were in agreement with previously reported values, i.e., 42, 60, and 69 s, respectively. beta-Blockade was associated with a significantly increased time constant for VO2 of 61 s but with less consistent and insignificant changes for VCO2 and VE. There was a small but significant increase of the time constant for heart rate from 40 to 45 s. It is concluded that propranolol exerts its primary influence during exercise on the cardiovascular system without any discernible effect on ventilatory control.


1983 ◽  
Vol 54 (2) ◽  
pp. 587-593 ◽  
Author(s):  
D. H. Wasserman ◽  
B. J. Whipp

During steady-state exercise, ventilation increases in proportion to CO2 output (VCO2), regulating arterial PCO2. To characterize the dynamics of ventilatory coupling to VCO2 and O2 uptake (VO2) in the nonsteady-state phase, seven normal subjects performed constant-load cycle ergometry to a series of subanaerobic threshold work rates. Each bout consisted of eight 6-min periods of alternating loaded and unloaded cycling. Ventilation and gas exchange variables were computed breath by breath, with the time-averaged response dynamics being established off-line. Ventilation increased as a linear function of VCO2 in all cases, the relationship being identical in the steady- and the nonsteady-state phases. Ventilation, however, bore a curvilinear relation to VO2, the kinetics of the latter being more rapid. Owing to the kinetic disparity between expired minute ventilation (VE) and VO2, there was an overshoot in the direction of change in VE/VO2 and end-tidal PO2 during the work-rate transition. In contrast, there was no overshoot in the direction of change in VE/VCO2 and end-tidal PCO2 throughout the nonsteady-state period. These data suggest that the exercise hyperpnea is coupled to metabolism in men via a signal proportional to VCO2 in both the nonsteady and steady states of moderate exercise.


1976 ◽  
Vol 41 (6) ◽  
pp. 886-892 ◽  
Author(s):  
H. V. Brown ◽  
K. Wasserman ◽  
B. J. Whipp

The ventilatory effects of beta-adrenergic blockade during steady-state exercise were studied in eight normal subjects using intravenous propranolol hydrochloride (0.2 mg/kg). Heart rate decreased in all subjects by an average of 17%. Coincident with the phase of decreasing heart rate was a significant decrease in both minute ventilation (VE) and CO2 output (VCO2), averaging 9.6 and 9.2%, respectively. Both functions returned to prepropranolollevels after heart rate had reached its reduced steady-state value. The change in VE was significantly correlated with the change in VCO2 (r = 0.85, Pless than 0.005), and was associated with negligible changes in endtidal CO2 tensions and ventilatory equivalents for CO2. We interpret these studies as showing that the transient isocapnic hypopnea concomitant with an acute reduction in cardiac output was secondary to a transient decrease in CO2 flux (cardiac output x mixed venous CO2 content). This decrease in VE appearsto be induced by the acute decrease in cardiac output (“cardiodynamic hypopnea”), in fashion similar to the previously described cardiodynamic hyperpnea.


1991 ◽  
Vol 71 (5) ◽  
pp. 1941-1948 ◽  
Author(s):  
M. Ramonatxo ◽  
J. Mercier ◽  
R. Cohendy ◽  
C. Prefaut

In healthy subjects, we compared the effects of an expiratory (ERL) and an inspiratory (IRL) resistive load (6 cmH2O.l-1.s) with no added resistive load on the pattern of respiratory muscle recruitment during exercise. Fifteen male subjects performed three exercise tests at 40% of maximum O2 uptake: 1) with no-added-resistive load (control), 2) with ERL, and 3) with IRL. In all subjects, we measured breathing pattern and mouth occlusion pressure (P0.1) from the 3rd min of exercise, in 10 subjects O2 uptake (VO2), CO2 output (VCO2), and respiratory exchange ratio (R), and in 5 subjects we measured gastric (Pga), pleural (Ppl), and transdiaphragmatic (Pdi) pressures. Both ERL and IRL induced a high increase of P0.1 and a decrease of minute ventilation. ERL induced a prolongation of expiratory time with a reduction of inspiratory time (TI), mean expiratory flow, and ratio of inspiratory to total time of the respiratory cycle (TI/TT). IRL induced a prolongation of TI with a decrease of mean inspiratory flow and an increase of tidal volume and TI/TT. With ERL, in two subjects, Pga increased and Ppl decreased more during inspiration than during control suggesting that the diaphragm was the most active muscle. In one subject, the increases of Ppl and Pga were weak; thus Pdi increased very little. In the two other subjects, Ppl decreased more during inspiration but Pga also decreased, leading to a decrease of Pdi. This suggests a recruitment of abdominal muscles during expiration and of accessory and intercostal muscles during inspiration. With IRL, in all subjects, Ppl again decreased more, Pga began to decrease until 40% of TI and then increased.(ABSTRACT TRUNCATED AT 250 WORDS)


1986 ◽  
Vol 61 (5) ◽  
pp. 1935-1941 ◽  
Author(s):  
L. G. Moore ◽  
A. Cymerman ◽  
S. Y. Huang ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
...  

Decreased maximal O2 uptake (VO2max) and stimulation of the sympathetic nervous system have been previously shown to occur at high altitude. We hypothesized that tachycardia mediated by beta-adrenergic stimulation acted to defend VO2max at high altitude. Propranolol treatment beginning before high-altitude (4,300 m) ascent reduced heart rate during maximal and submaximal exercise in six healthy men treated with propranolol (80 mg three times daily) compared with five healthy subjects receiving placebo (lactose). Compared with sea-level values, the VO2max fell on day 2 at high altitude, but the magnitude of fall was similar in the placebo and propranolol treatment groups (26 +/- 6 vs. 32 +/- 5%, P = NS) and VO2max remained similar at high altitude in both groups once treatment was discontinued. During 30 min of submaximal (80% of VO2max) exercise, propranolol-treated subjects maintained O2 uptake levels that were as large as those in placebo subjects. The maintenance of maximal or submaximal levels of O2 uptake in propranolol-treated subjects at 4,300 m could not be attributed to increased minute ventilation, arterial O2 saturation, or hemoglobin concentration. Rather, it appeared that propranolol-treated subjects maintained O2 uptake by transporting a greater proportion of the O2 uptake with each heartbeat. Thus, contrary to our hypothesis, beta-adrenergic blockade did not impair maximal or submaximal O2 uptake at high altitude due perhaps to compensatory mechanisms acting to maintain stroke volume and cardiac output.


1983 ◽  
Vol 54 (1) ◽  
pp. 13-17 ◽  
Author(s):  
J. Simon ◽  
J. L. Young ◽  
B. Gutin ◽  
D. K. Blood ◽  
R. B. Case

Anaerobic thresholds of five male subjects were determined invasively (ATi), from a marked increase in plasma lactate above resting levels (delta La), and noninvasively (ATn), from a nonlinear increase in minute ventilation (VE) during incremental work (IW) leg cycling tests; work rate was increased 30 W every 2 min. Each subject also performed four constant-load work (CLW) tasks just above and just below their ATn and respiratory compensation threshold (RCT), i.e., the point expressed as O2 consumption (VO2) or work rate, at which VE increases disproportionally to CO2 output during IW. In four of the five subjects the ATn preceded the ATi during IW. Yet the ATn delineated the CLW in which marked lactate accumulation did or did not occur. During CLW just above the ATn in these same four subjects, VE/VO2 and fractional expired O2 (FEO2) peaked well before delta La plateaued. These findings suggest that exercise hyperventilation is not necessarily proportional to increases in plasma lactate.


1982 ◽  
Vol 52 (6) ◽  
pp. 1506-1513 ◽  
Author(s):  
B. J. Whipp ◽  
S. A. Ward ◽  
N. Lamarra ◽  
J. A. Davis ◽  
K. Wasserman

To determine the precise nonsteady-state characteristics of ventilation (VE), O2 uptake (VO2), and CO2 output (VCO2) during moderate-intensity exercise, six subjects each underwent eight repetitions of 100-W constant-load cycling. The tests were preceded either by rest or unloaded cycling (“0” W). An early component of VE, VO2, and VCO2 responses, which was obscured on any single test by the breath-to-breath fluctuations, became apparent when the several repetitions were averaged. These early responses were abrupt when the work was instituted from rest but were much slower and smaller from the 0-W base line and corresponded to the phase of cardiodynamic gas exchange. Some 20 s after the onset of the work a further monoexponential increase to steady state occurred in all three variables, the time constants of which did not differ between the two types of test. Consequently, the exponential behavior of VE, VO2, and VCO2 in response to moderate exercise is best described by a model that incorporates only the second phase of the response.


2021 ◽  
Vol 7 (3) ◽  
pp. e001051
Author(s):  
Caio Sain Vallio ◽  
Gabriela Martins de Oliveira ◽  
Giovana Araujo Kretli Mota ◽  
Alexandre Dias Lopes ◽  
Luiz Hespanhol

BackgroundRunning is an important type of exercise to keep people physically active. However, running also carries a risk of developing running-related injuries (RRI). Therefore, effective and evidence-based RRI prevention programmes are desirable, but are scarce in practice. An approach to face this problem might be the application of methods to develop RRI prevention programmes based on theories of behaviour change.ObjectiveThe purpose of the study was to develop an RRI prevention programme based on perspectives of behavioural and social science theories, as well as taking a framework development approach.MethodsThis was a qualitative study using the Intervention Mapping (IM) framework held between February and March 2018 in São Paulo, Brazil. The participants were involved in running practice. The data collection was conducted during focus group meetings. The data analysis was based on semantic thematic approach using a content analysis orientation based on inductive reasoning.ResultsThe target population of the RRI prevention programme identified was ‘adult recreational runners’. The objectives of the RRI prevention programme were established in two broad actions: (1) to provide feedback on individual training characteristics and RRI risk; and (2) provide/enhance knowledge, skills and self-efficacy on RRI preventive behaviours. The programme is aimed to be delivered through an online system.ConclusionAn RRI prevention programme was developed using the IM framework and a participatory approach. The programme was named ‘RunIn3’, and it is based on providing feedback on running volume and RRI risk, as well as providing knowledge, skills and self-efficacy on RRI preventive behaviours.


Sign in / Sign up

Export Citation Format

Share Document