Early dynamics of O2 uptake and heart rate as affected by exercise work rate

1989 ◽  
Vol 67 (6) ◽  
pp. 2535-2541 ◽  
Author(s):  
K. E. Sietsema ◽  
J. A. Daly ◽  
K. Wasserman
Keyword(s):  
Heart Rate ◽  
Steady State ◽  
Phase I ◽  
Response Times ◽  
Normal Subjects ◽  
Work Rate ◽  
O2 Uptake ◽  
Constant Work Rate ◽  
Two Phases ◽  
Few Data

The kinetics of O2 uptake (Vo2) and heart rate (HR) in response to constant work rate exercise have been characterized as two phases, an immediate response as the result largely of abrupt hemodynamic changes and a slower response as the result of increases in both blood flow and arteriovenous O2 difference (avDo2). There are few data reported concerning Vo2 and HR during phase I or the relationship between their kinetics and work rate or intensity. Because phase I responses depend on abrupt cardiovascular adjustments, it was hypothesized that phase I increases in Vo2 and HR would be greater the more “fit” the subject and would be relatively independent of work rate. To test this, 10 normal subjects exercised from rest to each of five work rates ranging from unloaded cycling to 150 W. The phase I increases of Vo2, HR, and Vo2/HR had small but significant correlations with work rate but not with fitness. At very low work rates (unloaded cycling and 25 W), Vo2 and HR often exceeded their steady-state levels in phase I. There was therefore no phase II increase for Vo2 or HR at these work rates, the entire O2 requirement having been met by phase I circulatory adjustments. For all other work rates, mean response times for Vo2 and HR were related to fitness and were slower than those for Vo2/HR, suggesting that avDo2 reached a steady state before cardiac output did.

scholarly journals Kinetics of oxygen uptake and heart rate at onset of exercise in children

1985 ◽  
Vol 59 (1) ◽  
pp. 211-217 ◽  
Author(s):  
D. M. Cooper ◽  
C. Berry ◽  
N. Lamarra ◽  
K. Wasserman
Keyword(s):  
Heart Rate ◽  
Steady State ◽  
Phase I ◽  
Phase Ii ◽  
Anaerobic Threshold ◽  
Mean Value ◽  
Phase Iii ◽  
Constant Work Rate ◽  
Temporal Coupling ◽  
Kinetics Of

Requirements for cellular homeostasis appear to be unchanged between childhood and maturity. We hypothesized, therefore, that the kinetics of O2 uptake (VO2) in the transition from rest to exercise would be the same in young children as in teenagers. To test this, VO2 and heart rate kinetics from rest to constant work rate (75% of the subject's anaerobic threshold) in 10 children (5 boys and 5 girls) aged 7–10 yr were compared with values found in 10 teenagers (5 boys and 5 girls) aged 15–18 yr. Gas exchange was measured breath to breath, and phases I and II of the transition and phase III (steady-state exercise) were evaluated from multiple transitions in each child. Phase I (the VO2 at 20 s of exercise expressed as percent rest-to-steady-state exercise VO2) was not significantly correlated with age or weight [mean value 42.5 +/- 8.9% (SD)] nor was the phase II time constant for VO2 [mean 27.3 +/- 4.7 (SD) s]. The older girls had significantly slower kinetics than the other children but were also found to be less fit. When the teenagers exercised at work rates well below 75% of their anaerobic threshold, phase I VO2 represented a higher proportion of the overall response, but the phase II kinetics were unchanged. The temporal coupling between the cellular production of mechanical work at the onset of exercise and the uptake of environmental O2 appears to be controlled throughout growth in children.

Effects of separate rib cage and abdominal restriction on exercise performance in normal humans

1985 ◽  
Vol 58 (6) ◽  
pp. 2020-2026 ◽  
Author(s):  
S. N. Hussain ◽  
B. Rabinovitch ◽  
P. T. Macklem ◽  
R. L. Pardy
Keyword(s):  
Minute Ventilation ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Abdominal Muscle ◽  
Work Rate ◽  
Abdominal Pressure ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Constant Work Rate ◽  
And Control

We assessed the effects of selective restriction of movements of the rib cage (Res,rc) and abdomen (Res,ab) on ventilatory pattern, transdiaphragmatic pressure (Pdi), and electrical activity of the diaphragm (Edi) in five normal subjects exercising at a constant work rate (80% of maximum power output) on a cycle ergometer till exhaustion. Restriction of movements was achieved by an inelastic corset applied tightly around the rib cage or abdomen. Edi was recorded by an esophageal electrode, rectified, and then integrated, and peak values during inspiration were measured. Each subject exercised at the same work rate on 3 days: with Res,rc, with Res,ab, and without restriction (control). Res,rc but not Res,ab reduced exercise time (tlim). Up to tlim, minute ventilation (VE) was similar in all three conditions. At any level of VE, however, Res,rc decreased tidal volume and inspiratory and expiratory time, whereas Res,ab had no effect on the pattern of breathing. Res,ab was associated with higher inspiratory Pdi swings at any level of VE, whereas peak Edi was similar to control. Inspiratory Pdi swings were the same with Res,rc as control, but the peak Edi for a given Pdi was greater with Res,rc (P less than 0.05). During Res,rc the abdominal pressure swings in expiration were greater than with Res,ab and control. We conclude that Res,rc altered the pattern of breathing in normal subjects in high-intensity exercise, decreased diaphragmatic contractility, increased abdominal muscle recruitment in expiration, and reduced tlim. On the other hand, Res,ab had no effect on breathing pattern or tlim but was associated with increased diaphragmatic contractility.

The relationship between oxygen uptake reserve and heart rate reserve is affected by intensity and duration during aerobic exercise at constant work rate

2011 ◽  
Vol 36 (6) ◽  
pp. 839-847 ◽  
Author(s):  
Felipe A. Cunha ◽  
Adrian W. Midgley ◽  
Walace D. Monteiro ◽  
Felipe K. Campos ◽  
Paulo T.V. Farinatti
Keyword(s):  
Heart Rate ◽  
Oxygen Uptake ◽  
Exercise Testing ◽  
Exercise Intensity ◽  
Maximal Exercise ◽  
Work Rate ◽  
Heart Rate Reserve ◽  
Constant Work Rate ◽  
The Stability ◽  
The Relationship

The relationship between the percentage of heart rate reserve (%HRR) and percentage of oxygen uptake reserve (%VO2R) has been recommended for prescribing aerobic exercise intensity. However, this relationship was derived from progressive maximal exercise testing data, and the stability of the relationship during prolonged exercise at a constant work rate has not been established. The main aim of this study was to investigate the stability of the %VO2R–%HRR relationship during prolonged treadmill exercise bouts performed at 3 different constant work rates. Twenty-eight men performed 4 exercise tests: (i) a ramp-incremental maximal exercise test to determine maximal heart rate (HRmax) and maximal oxygen uptake (VO2max) and (ii) three 40-min exercise bouts at 60%, 70%, and 80% VO2R. HR and VO2 significantly increased over time and were influenced by exercise intensity (p < 0.001 and p = 0.004, respectively). A 1:1 relationship between %HRR and %VO2R, and between %HRR and %VO2max, was not observed, with mean differences of 8% (t = 5.2, p < 0.001) and 6% (t = 4.8, p < 0.001), respectively. The VO2 values predicted from the ACSM running equation were all significantly higher than the observed VO2 values (p < 0.001 for all comparisons), whereas a difference for HR was observed only for the tenth min of exercise at 80% VO2R (p = 0.041). In conclusion, the main finding of this study was that the %HRR–%VO2R relationship determined by linear regression, obtained from progressive maximal exercise testing, did not apply to prolonged treadmill running performed at 3 work rates.

The Astrand-Ryhming nomogram revisited

1986 ◽  
Vol 61 (3) ◽  
pp. 1203-1209 ◽  
Author(s):  
B. J. Legge ◽  
E. W. Banister
Keyword(s):  
Heart Rate ◽  
Aerobic Power ◽  
Constant Load ◽  
Cycle Ergometry ◽  
Gas Analysis ◽  
Work Rate ◽  
Exercise Heart Rate ◽  
Validation Group ◽  
O2 Uptake ◽  
Maximum Aerobic Power

Relationships among O2 uptake (VO2), heart rate, and work rate during constant-load submaximal cycle ergometry and ramp-forced exercise to exhaustion have been studied in core groups of trained (n = 15) and untrained (n = 10), 20- to 29-yr-old males. A signal aim was to improve on the accuracy of the 1954 Astrand-Ryhming (A-R) nomogram predicting maximum aerobic power from heart rate elevation at submaximum work rates. A new nomogram has been developed based on a linear relationship, established in experimental groups, between VO2 and delta HR, the latter being defined as the elevation of exercise heart rate above that reached during zero-load pedaling at 90 rpm. The delta HR variable used in a nomogram linking it and submaximum VO2 (either derived by calculation from the concomitant steady-state work rate or measured directly from respiratory gas analysis) successfully differentiated maximum aerobic power of trained from untrained subjects in core groups whose different abilities could not otherwise be distinguished by the A-R nomogram itself. In a validation group of trained (n = 5), untrained (n = 5), and moderately trained (n = 4) 20- to 29-yr-old males, the correlation measured between VO2max values and those predicted from the new nomogram was significantly better (r = 0.98) (P less than 0.05) than predictions made from the A-R nomogram (r = 0.80).

Assessment of rebreathing O2 consumption in humans with normal and diseased lungs

1990 ◽  
Vol 68 (4) ◽  
pp. 1443-1452 ◽  
Author(s):  
M. C. Kallay ◽  
R. W. Hyde ◽  
R. J. Smith
Keyword(s):  
Steady State ◽  
Pulmonary Function ◽  
Lung Disease ◽  
Pulse Rate ◽  
Obstructive Lung Disease ◽  
Pulmonary Function Tests ◽  
Normal Subjects ◽  
O2 Consumption ◽  
O2 Uptake ◽  
End Tidal

We investigated sources of error in estimating steady-state O2 consumption (VO2ss) by calculating O2 uptake from an anesthesia bag containing O2, He, and N2 during 10-20 s of rebreathing (VO2rb). In 11 normal resting subjects, VO2rb calculated with end-tidal sampling overestimated VO2ss by 16 +/- 15% (SD) (P less than 0.003). This error was proportional to the increase in pulse rate during rebreathing, so that pulse-corrected VO2rb slightly underestimated VO2ss by 2.1 +/- 12.2% (P = 0.66) in the six subjects who rebreathed 28% O2 in the rebreathing bag but significantly underestimated VO2ss by 7.5 +/- 6.7% (P less than 0.04) in the six subjects who rebreathed 21% O2 in the rebreathing bag. During exercise, VO2rb underestimated VO2ss by 4 +/- 12% (P less than 0.001) and by 7 +/- 6% at O2 consumptions greater than 2,000 ml/min if O2 in the rebreathing bag was kept above 20% throughout rebreathing. We found that VO2rb calculated with end-tidal gas concentrations underestimated VO2ss by 1-43% in patients with moderate-to-severe obstructive lung disease, with even greater errors when mixed expired samples were used. The magnitude of the discrepancy correlated poorly with abnormalities in standard pulmonary function tests. Based on these data, VO2rb closely approximates VO2ss in normal subjects, provided hypoxia during rebreathing is avoided and cardiac acceleration from rebreathing is taken into account during resting measurement.

Effects of beta-adrenergic blockade on ventilation and gas exchange during exercise in humans

1983 ◽  
Vol 54 (5) ◽  
pp. 1306-1313 ◽  
Author(s):  
E. S. Petersen ◽  
B. J. Whipp ◽  
J. A. Davis ◽  
D. J. Huntsman ◽  
H. V. Brown ◽  
...  
Keyword(s):  
Heart Rate ◽  
Gas Exchange ◽  
Time Constant ◽  
Minute Ventilation ◽  
Work Rate ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
O2 Uptake ◽  
Beta Adrenergic ◽  
Co2 Partial Pressure

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.

O2 uptake kinetics above and below the lactic acidosis threshold during sinusoidal exercise

1993 ◽  
Vol 75 (4) ◽  
pp. 1683-1690 ◽  
Author(s):  
P. Haouzi ◽  
Y. Fukuba ◽  
R. Casaburi ◽  
W. Stringer ◽  
K. Wasserman
Keyword(s):  
Heart Rate ◽  
Lactic Acidosis ◽  
State Level ◽  
Sine Wave ◽  
Work Rate ◽  
Phase Lag ◽  
O2 Uptake ◽  
O2 Transport ◽  
Vo2 Kinetics ◽  
Lactic Acidosis Threshold

O2 uptake (VO2) kinetics at the onset of a constant work rate exercise are difficult to describe for work rates above the lactic acidosis threshold (LAT), because the steady-state level of VO2 response can usually not be identified. To describe the ability of the O2 transport system to deliver and the cells to utilize O2 above the LAT relative to that below the LAT, we applied a fluctuating (sinusoidal) variation of work rate. After 4 min of constant work at the midpoint of the sinusoidal work rate, a fluctuating work rate, at a period of 4 min, was applied below the LAT for the next 16 min. This was repeated in a range of work rates above the LAT with the same sine-wave amplitude. VO2 response appeared to follow a sinusoidal pattern similar to that of work rate for below- and above-LAT exercise. However, the amplitude of the VO2 response was significantly reduced (5.4 +/- 2.6 vs. 7.6 +/- 1.9 ml.min-1 x W-1, P < 0.01), and the phase lag increased above- compared with below-LAT work rate. VO2/heart rate fluctuations were dramatically reduced, whereas heart rate amplitude decreased and phase lag increased, for above-LAT sinusoidal work rate changes. These results suggest that VO2 kinetics are slowed in the work rate domain above the LAT relative to that below the LAT and that VO2 kinetics could be limited by the O2 transport mechanisms to the exercising muscle.

Effect of beta-adrenergic blockade during exercise on ventilation and gas exchange

1976 ◽  
Vol 41 (6) ◽  
pp. 886-892 ◽  
Author(s):  
H. V. Brown ◽  
K. Wasserman ◽  
B. J. Whipp
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Steady State ◽  
Minute Ventilation ◽  
Co2 Flux ◽  
Normal Subjects ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Co2 Output ◽  
Ventilatory Effects

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.

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