ASSESSMENT OF THE RELATIONSHIP BETWEEN CLINICALLY ACCEPTED INDICES OF EXERCISE INTENSITY AND THE VENTILATORY RESPONSE INDEX.

2003 ◽  
Vol 14 (1) ◽  
pp. 18-19
Author(s):  
H S Sadowsky ◽  
D Harrison ◽  
A Hocker ◽  
T Kuznetsova ◽  
N Lillard
Keyword(s):  
Exercise Intensity ◽  
Ventilatory Response ◽  
Response Index ◽  
The Relationship

AN ASSESSMENT OF THE RELIABILITY OF THE VENTILATORY RESPONSE INDEX RELATIVE TO TRADITIONAL INDICES OF EXERCISE INTENSITY IN HEALTHY ADULTS.

2004 ◽  
Vol 18 (4) ◽  
pp. 30
Author(s):  
Colette K. Gallagher ◽  
Taylor Millican ◽  
Lauren Polivka ◽  
Courtney Schrey ◽  
Steven H. Sadowsky
Keyword(s):  
Exercise Intensity ◽  
Ventilatory Response ◽  
Healthy Adults ◽  
Response Index

AN ASSESSMENT OF THE RELIABILITY OF THE VENTILATORY RESPONSE INDEX RELATIVE TO TRADITIONAL INDICES OF EXERCISE INTENSITY IN HEALTHY ADULTS.

2007 ◽  
Vol 18 (4) ◽  
pp. 30
Author(s):  
Colette K. Gallagher ◽  
Taylor Millican ◽  
Lauren Polivka ◽  
Courtney Schrey ◽  
Steven H. Sadowsky
Keyword(s):  
Exercise Intensity ◽  
Ventilatory Response ◽  
Healthy Adults ◽  
Response Index

Relationship of potassium ions and blood lactate to ventilation during exercise

2010 ◽  
Vol 35 (5) ◽  
pp. 691-698
Author(s):  
Robert G. McMurray ◽  
Matthew S. Tenan
Keyword(s):  
Blood Lactate ◽  
Exercise Intensity ◽  
Minute Ventilation ◽  
Potassium Ions ◽  
Ventilatory Control ◽  
Volitional Fatigue ◽  
Relationship Of ◽  
Glycogen Stores ◽  
The Relationship ◽  
Recent Attention

Ventilatory control during exercise is a complex network of neural and humoral signals. One humoral input that has received little recent attention in the exercise literature is potassium ions [K+]. The purpose of this study was to examine the relationship between [K+] and ventilation during an incremental cycle test and to determine if the relationship between [K+] and ventilation differs when blood lactate [lac–] is manipulated. Eight experienced triathletes (4 of each sex) completed 2 incremental, progressive (5-min stages) cycle tests to volitional fatigue: 1 with normal glycogen stores and 1 with reduced glycogen. Minute ventilation was measured during the final minute of each stage, and blood [lac–] and [K+] were measured at the end of each exercise stage. Minute ventilation and [K+] increased with exercise intensity and were similar between trials (p > 0.5), despite lower [lac–] during the reduced-glycogen trial. The concordance correlations (Rc) between [lac–] and minute ventilation were stronger for both trials (Rc = ~0.88–0.96), but the slopes of the relationships were different than the relationships between [K+] and minute ventilation (Rc = ~0.76–0.89). The slope of the relationship between [lac–] and minute ventilation was not as steep during the reduced-glycogen trial, compared with the normal trial (p = 0.002). Conversely, the slope of the relationships between [K+] and minute ventilation did not change between trials (p = 0.454). The consistent relationship of minute ventilation and blood [K+] during exercise suggests a role for this ion in the control of ventilation during exercise. Conversely, the inconsistent relationship between blood lactate and ventilation brings into question the importance of the relationship between lactate and ventilation during exercise.

Plasma free and sulfoconjugated catecholamine responses to varying exercise intensity

1987 ◽  
Vol 63 (2) ◽  
pp. 654-658 ◽  
Author(s):  
M. S. Sothmann ◽  
A. B. Gustafson ◽  
M. Chandler
Keyword(s):  
Oxygen Consumption ◽  
Exercise Intensity ◽  
High Intensity ◽  
Maximal Oxygen Consumption ◽  
High Intensity Exercise ◽  
The Relationship ◽  
Circulating Levels

Plasma free catecholamines rise during exercise, but sulfoconjugated catecholamines reportedly fall. This study examined the relationship between exercise intensity and circulating levels of sulfoconjugated norepinephrine, epinephrine, and dopamine. Seven exercise-trained men biked at approximately 30, 60, and 90% of their individual maximal oxygen consumption (VO2max) for 8 min. The 90% VO2max period resulted in significantly increased plasma free norepinephrine (rest, 219 +/- 85; exercise, 2,738 +/- 1,149 pg/ml; P less than or equal to 0.01) and epinephrine (rest, 49 +/- 49; exercise, 555 +/- 516 pg/ml; P less than or equal to 0.05). These changes were accompanied by consistent increases in sulfoconjugated norepinephrine at both the 60% (rest, 852 +/- 292; exercise, 1,431 +/- 639; P less than or equal to 0.05) and 90% (rest, 859 +/- 311; exercise, 2,223 +/- 1,015; P less than or equal to 0.05) VO2max periods. Plasma sulfoconjugated epinephrine and dopamine displayed erratic changes at the three exercise intensities. These findings suggest that sulfoconjugated norepinephrine rises during high-intensity exercise.

Ventilatory response to moderate and severe hypoxia in adult dogs: role of endorphins

1988 ◽  
Vol 65 (3) ◽  
pp. 1383-1388 ◽  
Author(s):  
J. I. Schaeffer ◽  
G. G. Haddad
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Severe Hypoxia ◽  
Moderate Hypoxia ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Before And After ◽  
The Relationship ◽  
Arterial Po2

To determine the role of opioids in modulating the ventilatory response to moderate or severe hypoxia, we studied ventilation in six chronically instrumented awake adult dogs during hypoxia before and after naloxone administration. Parenteral naloxone (200 micrograms/kg) significantly increased instantaneous minute ventilation (VT/TT) during severe hypoxia, (inspired O2 fraction = 0.07, arterial PO2 = 28-35 Torr); however, consistent effects during moderate hypoxia (inspired O2 fraction = 0.12, arterial PO2 = 40-47 Torr) could not be demonstrated. Parenteral naloxone increased O2 consumption (VO2) in severe hypoxia as well. Despite significant increases in ventilation post-naloxone during severe hypoxia, arterial blood gas tensions remained the same. Control studies revealed that neither saline nor naloxone produced a respiratory effect during normoxia; also the preservative vehicle of naloxone induced no change in ventilation during severe hypoxia. These data suggest that, in adult dogs, endorphins are released and act to restrain ventilation during severe hypoxia; the relationship between endorphin release and moderate hypoxia is less consistent. The observed increase in ventilation post-naloxone during severe hypoxia is accompanied by an increase in metabolic rate, explaining the isocapnic response.

Effect of acute hypoxia on vasopressin release and intravascular fluid during dynamic exercise in humans

2000 ◽  
Vol 279 (1) ◽  
pp. R161-R168 ◽  
Author(s):  
Akira Takamata ◽  
Hiroshi Nose ◽  
Takashi Kinoshita ◽  
Munetaka Hirose ◽  
Toshiyuki Itoh ◽  
...  
Keyword(s):  
Exercise Intensity ◽  
Acute Hypoxia ◽  
Electrolyte Balance ◽  
Vasopressin Release ◽  
Fluid Movement ◽  
Hypotonic Fluid ◽  
Vascular Space ◽  
Relative Exercise Intensity ◽  
Graded Exercise ◽  
The Relationship

To test the hypothesis that acute hypoxia does not modify the relationship between plasma vasopressin concentration ([AVP]p) and plasma osmolality (Posmol) during exercise and that the increase in [AVP]p during exercise is due mainly to the exercise intensity-dependent increase in Posmol, we examined [AVP]p during a graded exercise in a hypoxic condition (13% O2, N2 balance) in seven healthy male subjects. A graded exercise in a normoxic condition on a separate day served as the control. Hypoxia reduced peak aerobic power (V˙o 2 peak) by 32.4 ± 2.7%. Blood samples obtained during rest and at around 25, 45, 65, 80, and 100% ofV˙o 2 peak of each of the respective conditions were used for analyses of intravascular water and electrolyte balance. The pattern of the changes in fluid and electrolyte balance in response to percentV˙o 2 peak was similar between the two conditions. Plasma volume decreased linearly as percentV˙o 2 peak increased while Posmol increased in a curvilinear fashion with a steep increase occurring at above ∼66%V˙o 2 peak. Above this relative exercise intensity, plasma sodium, potassium, and lactate concentrations also increased, whereas plasma bicarbonate concentration decreased. Thus transvascular fluid movement at above ∼66%V˙o 2 peak was due to the net efflux of hypotonic fluid out of the vascular space in both conditions. The relationship between [AVP]p and Posmol during exercise in response to relative exercise intensity was similar between the two conditions. The results indicate that acute mild hypoxia itself has no direct effect on vasopressin release, and it does not modify the relationship between [AVP]p and Posmol during exercise. The results also support the hypothesis that exercise-induced vasopressin release is primarily stimulated by increased Posmol produced by hypotonic fluid movement out of the vascular space in a relative exercise intensity-dependent manner.

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