Differential ventilatory control during constant work rate and incremental exercise

1994 ◽  
Vol 97 (2) ◽  
pp. 175-187 ◽  
Author(s):  
N.C. Syabbalo ◽  
B. Krishnan ◽  
T. Zintel ◽  
C.G. Gallagher
2019 ◽  
Vol 127 (6) ◽  
pp. 1519-1527 ◽  
Author(s):  
Danilo Iannetta ◽  
Rafael de Almeida Azevedo ◽  
Daniel A. Keir ◽  
Juan M. Murias

The dissociation between constant work rate of O2 uptake (V̇o2) and ramp V̇o2 at a given work rate might be mitigated during slowly increasing ramp protocols. This study characterized the V̇o2 dynamics in response to five different ramp protocols and constant-work-rate trials at the maximal metabolic steady state (MMSS) to characterize 1) the V̇o2 gain (G) in the moderate, heavy, and severe domains, 2) the mean response time of V̇o2 (MRT), and 3) the work rates at lactate threshold (LT) and respiratory compensation point (RCP). Eleven young individuals performed five ramp tests (5, 10, 15, 25, and 30 W/min), four to five time-to-exhaustions for critical power estimation, and two to three constant-work-rate trials for confirmation of the work rate at MMSS. G was greatest during the slowest ramp and progressively decreased with increasing ramp slopes (from ~12 to ~8 ml·min−1·W−1, P < 0.05). The MRT was smallest during the slowest ramp slopes and progressively increased with faster ramp slopes (1 ± 1, 2 ± 1, 5 ± 3, and 10 ± 4, 15 ± 6 W, P < 0.05). After “left shifting” the ramp V̇o2 by the MRT, the work rate at LT was constant regardless of the ramp slope (~150 W, P > 0.05). The work rate at MMSS was 215 ± 55 W and was similar and highly correlated with the work rate at RCP during the 5 W/min ramp ( P > 0.05, r = 0.99; Lin’s concordance coefficient = 0.99; bias = −3 W; root mean square error = 6 W). Findings showed that the dynamics of V̇o2 (i.e., G) during ramp exercise explain the apparent dichotomy existing with constant-work-rate exercise. When these dynamics are appropriately “resolved”, LT is constant regardless of the ramp slope of choice, and RCP and MMSS display minimal variations between each other. NEW & NOTEWORTHY This study demonstrates that the dynamics of V̇o2 during ramp-incremental exercise are dependent on the characteristics of the increments in work rate, such that during slow-incrementing ramp protocols the magnitude of the dissociation between ramp V̇o2 and constant V̇o2 at a given work rate is reduced. Accurately accounting for these dynamics ensures correct characterizations of the V̇o2 kinetics at ramp onset and allows appropriate comparisons between ramp and constant-work-rate exercise-derived indexes of exercise intensity.


2016 ◽  
Vol 116 (11-12) ◽  
pp. 2415-2422 ◽  
Author(s):  
Matthew I. Black ◽  
Andrew M. Jones ◽  
James A. Kelly ◽  
Stephen J. Bailey ◽  
Anni Vanhatalo

Author(s):  
Markus Hein ◽  
Kristine Chobanyan-Jürgens ◽  
Uwe Tegtbur ◽  
Stefan Engeli ◽  
Jens Jordan ◽  
...  

Abstract Purpose To test the hypothesis that the combination of endurance training and hypoxia leads to greater improvements in resting and exercise blood pressure in old sedentary individuals compared to endurance training only. Methods We randomly assigned 29 old overweight participants (age: 62 ± 6 years, body mass index (BMI): 28.5 ± 0.5 kg/m2, 52% men) to single blind 8-week bicycle exercise in hypoxia (fraction of inspired oxygen (FIO2) = 0.15) or normoxia (FIO2 = 0.21). Brachial blood pressure was measured at rest, during maximal incremental exercise testing, and during a 30 min constant work rate test, at baseline and after the training period. Results Work rate, heart rate and perceived exertion during training were similar in both groups, with lower oxygen saturation for participants exercising under hypoxia (88.7 ± 1.5 vs. 96.2 ± 1.2%, t(27) = − 13.04, p < 0.001, |g|= 4.85). Office blood pressure and blood pressure during incremental exercise tests did not change significantly in either group after the training program. Systolic blood pressure during the constant work rate test was reduced after training in hypoxia (160 ± 18 vs. 151 ± 14 mmHg, t(13) = 2.44 p < 0.05, |d|= 0.55) but not normoxia (154 ± 22 vs. 150 ± 16 mmHg, t(14) = 0.75, p = 0.46, |d|= 0.18) with no difference between groups over time (F = 0.08, p = 0.77, η2 = 0.01). Conclusion In old individuals hypoxia in addition to exercise does not have superior effects on office or exercise blood pressure compared to training in normoxia. Trial registration number ClinicalTrials.gov No. NCT02196623 (registered 22 July 2014).


1989 ◽  
Vol 66 (4) ◽  
pp. 1539-1546 ◽  
Author(s):  
N. Lamarra ◽  
S. A. Ward ◽  
B. J. Whipp

In humans, arterial PCO2 (PaCO2) has been demonstrated to be regulated at or near resting levels in the steady state of moderate exercise (i.e., for work rates not associated with a sustained lactic acidosis). To determine how PaCO2 might be expected to behave under the nonsteady-state conditions of incremental exercise testing, the influence of the dynamic characteristics of the primary variables that determine PaCO2 was explored by means of computer modeling. We constructed a dynamic model that utilized previously reported experimental estimates for the kinetic response parameters of ventilation (VE) and CO2 output (VCO2). In response to incremental work rate forcings, the model yielded an increase in PaCO2, which reflected the disparity between the VE and VCO2 time constants; this hypercapnic condition was maintained despite VE and VCO2 both increasing linearly with respect to the input work rate profile. The degree of hypercapnia increased with the rate of the incremental forcing, reaching 9 Torr for a 50-W/min forcing. In conclusion, therefore, sustained increases in PaCO2 during nonsteady-state incremental exercise should be interpreted with caution, because this is the predicted response even in subjects with normal ventilatory control and lung function.


Pneumologie ◽  
2018 ◽  
Vol 72 (S 01) ◽  
pp. S90-S90
Author(s):  
K Siemon ◽  
F Maltais ◽  
DE O'Donnell ◽  
A Hamilton ◽  
Y Zhao ◽  
...  

2017 ◽  
Vol 57 (1) ◽  
pp. 117-128
Author(s):  
Dalton M. Pessôa Filho ◽  
Leandro O.C. Siqueira ◽  
Astor R. Simionato ◽  
Mário A.C. Espada ◽  
Daniel S. Pestana ◽  
...  

AbstractThe purpose of this study was to investigate whether a tethered-swimming incremental test comprising small increases in resistive force applied every 60 seconds could delineate the isocapnic region during rapidly-incremented exercise. Sixteen competitive swimmers (male, n = 11; female, n = 5) performed: (a) a test to determine highest force during 30 seconds of all-out tethered swimming (Favg) and the ΔF, which represented the difference between Favg and the force required to maintain body alignment (Fbase), and (b) an incremental test beginning with 60 seconds of tethered swimming against a load that exceeded Fbase by 30% of ΔF followed by increments of 5% of ΔF every 60 seconds. This incremental test was continued until the limit of tolerance with pulmonary gas exchange (rates of oxygen uptake and carbon dioxide production) and ventilatory (rate of minute ventilation) data collected breath by breath. These data were subsequently analyzed to determine whether two breakpoints defining the isocapnic region (i.e., gas exchange threshold and respiratory compensation point) were present. We also determined the peak rate of O2 uptake and exercise economy during the incremental test. The gas exchange threshold and respiratory compensation point were observed for each test such that the associated metabolic rates, which bound the heavy-intensity domain during constant-work-rate exercise, could be determined. Significant correlations (Spearman’s) were observed for exercise economy along with (a) peak rate of oxygen uptake (ρ = .562; p < 0.025), and (b) metabolic rate at gas exchange threshold (ρ = −.759; p < 0.005). A rapidly-incremented tethered-swimming test allows for determination of the metabolic rates that define zones for domain-specific constant-work-rate training.


1998 ◽  
Vol 85 (2) ◽  
pp. 627-634 ◽  
Author(s):  
Russell S. Richardson ◽  
Elizabeth A. Noyszewski ◽  
John S. Leigh ◽  
Peter D. Wagner

It remains controversial whether lactate formation during progressive dynamic exercise from submaximal to maximal effort is due to muscle hypoxia. To study this question, we used direct measures of arterial and femoral venous lactate concentration, a thermodilution blood flow technique, phosphorus magnetic resonance spectroscopy (MRS), and myoglobin (Mb) saturation measured by 1H nuclear MRS in six trained subjects performing single-leg quadriceps exercise. We calculated net lactate efflux from the muscle and intracellular[Formula: see text] with subjects breathing room air and 12% O2. Data were obtained at 50, 75, 90, and 100% of quadriceps maximal O2 consumption at each fraction of inspired O2. Mb saturation was significantly lower in hypoxia than in normoxia [40 ± 3 vs. 49 ± 3% (SE)] throughout incremental exercise to maximal work rate. With the assumption of a[Formula: see text] at which 50% of Mb-binding sites are bound with O2 of 3.2 Torr, Mb-associated [Formula: see text] averaged 3.1 ± 0.3 and 2.3 ± 0.2 Torr in normoxia and hypoxia, respectively. Net blood lactate efflux was unrelated to intracellular[Formula: see text] across the range of incremental exercise to maximum ( r = 0.03 and 0.07 in normoxia and hypoxia, respectively) but linearly related to O2 consumption ( r = 0.97 and 0.99 in normoxia and hypoxia, respectively) with a greater slope in 12% O2. Net lactate efflux was also linearly related to intracellular pH ( r = 0.94 and 0.98 in normoxia and hypoxia, respectively). These data suggest that with increasing work rate, at a given fraction of inspired O2, lactate efflux is unrelated to muscle cytoplasmic [Formula: see text], yet the efflux is higher in hypoxia. Catecholamine values from comparable studies are included and indicate that lactate efflux in hypoxia may be due to systemic rather than intracellular hypoxia.


1996 ◽  
Vol 81 (5) ◽  
pp. 1891-1900 ◽  
Author(s):  
Charles S. Fulco ◽  
Steven F. Lewis ◽  
Peter N. Frykman ◽  
Robert Boushel ◽  
Sinclair Smith ◽  
...  

Fulco, Charles S., Steven F. Lewis, Peter N. Frykman, Robert Boushel, Sinclair Smith, Everett A. Harman, Allen Cymerman, and Kent B. Pandolf. Muscle fatigue and exhaustion during dynamic leg exercise in normoxia and hypobaric hypoxia. J. Appl. Physiol. 81(5): 1891–1900, 1996.—Using an exercise device that integrates maximal voluntary static contraction (MVC) of knee extensor muscles with dynamic knee extension, we compared progressive muscle fatigue, i.e., rate of decline in force-generating capacity, in normoxia (758 Torr) and hypobaric hypoxia (464 Torr). Eight healthy men performed exhaustive constant work rate knee extension (21 ± 3 W, 79 ± 2 and 87 ± 2% of 1-leg knee extension O2 peak uptake for normoxia and hypobaria, respectively) from knee angles of 90–150° at a rate of 1 Hz. MVC (90° knee angle) was performed before dynamic exercise and during ≤5-s pauses every 2 min of dynamic exercise. MVC force was 578 ± 29 N in normoxia and 569 ± 29 N in hypobaria before exercise and fell, at exhaustion, to similar levels (265 ± 10 and 284 ± 20 N for normoxia and hypobaria, respectively; P > 0.05) that were higher ( P < 0.01) than peak force of constant work rate knee extension (98 ± 10 N, 18 ± 3% of MVC). Time to exhaustion was 56% shorter for hypobaria than for normoxia (19 ± 5 vs. 43 ± 7 min, respectively; P < 0.01), and rate of right leg MVC fall was nearly twofold greater for hypobaria than for normoxia (mean slope = −22.3 vs. −11.9 N/min, respectively; P < 0.05). With increasing duration of dynamic exercise for normoxia and hypobaria, integrated electromyographic activity during MVC fell progressively with MVC force, implying attenuated maximal muscle excitation. Exhaustion, per se, was postulated to relate more closely to impaired shortening velocity than to failure of force-generating capacity.


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