RECOVERY DURATION FROM HIGH-INTENSITY EXERCISE AND SUBSEQUENT VENTILATORY AND PULMONARY GAS EXCHANGE TRANSIENTS

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S177
Author(s):  
H B. Rossiter ◽  
R Patel ◽  
B J. Whipp
2019 ◽  
Vol 20 (2) ◽  
pp. 211-218
Author(s):  
Jessica A. Freemas ◽  
Daniel P. Wilhite ◽  
Joel T. Greenshields ◽  
Emily M. Adamic ◽  
Timothy D. Mickleborough

2009 ◽  
Vol 107 (6) ◽  
pp. 1743-1756 ◽  
Author(s):  
Stephen J. Bailey ◽  
Anni Vanhatalo ◽  
Daryl P. Wilkerson ◽  
Fred J. DiMenna ◽  
Andrew M. Jones

It has been suggested that a prior bout of high-intensity exercise has the potential to enhance performance during subsequent high-intensity exercise by accelerating the O2 uptake (V̇o2) on-response. However, the optimal combination of prior exercise intensity and subsequent recovery duration required to elicit this effect is presently unclear. Eight male participants, aged 18–24 yr, completed step cycle ergometer exercise tests to 80% of the difference between the preestablished gas exchange threshold and maximal V̇o2 (i.e., 80%Δ) after no prior exercise (control) and after six different combinations of prior exercise intensity and recovery duration: 40%Δ with 3 min (40-3-80), 9 min (40-9-80), and 20 min (40-20-80) of recovery and 70%Δ with 3 min (70-3-80), 9 min (70-9-80), and 20 min (70-20-80) of recovery. Overall V̇o2 kinetics were accelerated relative to control in all conditions except for 40-9-80 and 40-20-80 conditions as a consequence of a reduction in the V̇o2 slow component amplitude; the phase II time constant was not significantly altered with any prior exercise/recovery combination. Exercise tolerance at 80%Δ was improved by 15% and 30% above control in the 70-9-80 and 70-20-80 conditions, respectively, but was impaired by 16% in the 70-3-80 condition. Prior exercise at 40%Δ did not significantly influence exercise tolerance regardless of the recovery duration. These data demonstrate that prior high-intensity exercise (∼70%Δ) can enhance the tolerance to subsequent high-intensity exercise provided that it is coupled with adequate recovery duration (≥9 min). This combination presumably optimizes the balance between preserving the effects of prior exercise on V̇o2 kinetics and providing sufficient time for muscle homeostasis (e.g., muscle phosphocreatine and H+ concentrations) to be restored.


1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.


Respiration ◽  
1978 ◽  
Vol 35 (3) ◽  
pp. 136-147 ◽  
Author(s):  
P. Jebavý ◽  
J. Fabián ◽  
M. Henzlová ◽  
A. Belán

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