Abstract
During incremental work rate exercise, ventilation (V̇E) typically increases in proportion to the metabolic rate until the onset of a progressive metabolic acidemia induces an additional compensatory hyperpnea. We examined the control characteristics of this compensatory mechanism in seven healthy subjects performing incremental cycle ergometry to their limit of tolerance at different levels of lower-body positive pressure (LBPP) at 0, 15, 30, and 45 Torr in order to determine if LBPP could alter the occurrence of the ventilatory threshold. Ventilatory responses and pulmonary gas exchange variables were measured breath-by-breath while 'arterialized'-venous blood was sampled from the dorsum of the heated hand for determination of [lactate], pH, and [K+]. The ventilatory threshold was progressively reduced with increasing levels of LBPP: Ventilatory threshold = 2.33 - (0.0173 · LBPP); (r2 = 0.59, P < 0.001). Ventilatory equivalents for oxygen (V̇E/V̇O2 ) and carbon dioxide (V̇E/V̇CO2 ) were systematically elevated at work rates above 50 W by increases in respiratory frequency which also resulted in lower PetCO2 and higher PetO2 values. As [lactate] was only slightly elevated above control (dGlactate<1 mEq·L-1) while pH and [K+] were unchanged, it seems unlikely that the LBPP-induced hyperpnea can be attributed to activation of peripheral arterial or central chemoreceptors. These findings suggests a ventilatory stimulus may be generated by an LBPP-induced reduction in perfusion with the subsequent accumulation of intramuscular metabolites at the working limb and/or a direct effect of increased intramuscular tissue pressure.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 121-135 |
| Number of pages | 15 |
| Journal | Respiration Physiology |
| Volume | 94 |
| Issue number | 2 |
| DOIs | |
| State | Published - 1993 |
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Keywords
- Control of breathing
- Exercise, hyperpnea
- Mammals, humans
- Pressure, lower body
ASJC Scopus subject areas
- Physiology
- Pulmonary and Respiratory Medicine
Cite this
Evidence for an intramuscular ventilatory stimulus during dynamic exercise in man. / Williamson, J. W.; Raven, P. B.; Foresman, B. H.; Whipp, B. J.
In: Respiration Physiology, Vol. 94, No. 2, 1993, p. 121-135.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Evidence for an intramuscular ventilatory stimulus during dynamic exercise in man
AU - Williamson, J. W.
AU - Raven, P. B.
AU - Foresman, B. H.
AU - Whipp, B. J.
PY - 1993
Y1 - 1993
N2 - During incremental work rate exercise, ventilation (V̇E) typically increases in proportion to the metabolic rate until the onset of a progressive metabolic acidemia induces an additional compensatory hyperpnea. We examined the control characteristics of this compensatory mechanism in seven healthy subjects performing incremental cycle ergometry to their limit of tolerance at different levels of lower-body positive pressure (LBPP) at 0, 15, 30, and 45 Torr in order to determine if LBPP could alter the occurrence of the ventilatory threshold. Ventilatory responses and pulmonary gas exchange variables were measured breath-by-breath while 'arterialized'-venous blood was sampled from the dorsum of the heated hand for determination of [lactate], pH, and [K+]. The ventilatory threshold was progressively reduced with increasing levels of LBPP: Ventilatory threshold = 2.33 - (0.0173 · LBPP); (r2 = 0.59, P < 0.001). Ventilatory equivalents for oxygen (V̇E/V̇O2 ) and carbon dioxide (V̇E/V̇CO2 ) were systematically elevated at work rates above 50 W by increases in respiratory frequency which also resulted in lower PetCO2 and higher PetO2 values. As [lactate] was only slightly elevated above control (dGlactate<1 mEq·L-1) while pH and [K+] were unchanged, it seems unlikely that the LBPP-induced hyperpnea can be attributed to activation of peripheral arterial or central chemoreceptors. These findings suggests a ventilatory stimulus may be generated by an LBPP-induced reduction in perfusion with the subsequent accumulation of intramuscular metabolites at the working limb and/or a direct effect of increased intramuscular tissue pressure.
AB - During incremental work rate exercise, ventilation (V̇E) typically increases in proportion to the metabolic rate until the onset of a progressive metabolic acidemia induces an additional compensatory hyperpnea. We examined the control characteristics of this compensatory mechanism in seven healthy subjects performing incremental cycle ergometry to their limit of tolerance at different levels of lower-body positive pressure (LBPP) at 0, 15, 30, and 45 Torr in order to determine if LBPP could alter the occurrence of the ventilatory threshold. Ventilatory responses and pulmonary gas exchange variables were measured breath-by-breath while 'arterialized'-venous blood was sampled from the dorsum of the heated hand for determination of [lactate], pH, and [K+]. The ventilatory threshold was progressively reduced with increasing levels of LBPP: Ventilatory threshold = 2.33 - (0.0173 · LBPP); (r2 = 0.59, P < 0.001). Ventilatory equivalents for oxygen (V̇E/V̇O2 ) and carbon dioxide (V̇E/V̇CO2 ) were systematically elevated at work rates above 50 W by increases in respiratory frequency which also resulted in lower PetCO2 and higher PetO2 values. As [lactate] was only slightly elevated above control (dGlactate<1 mEq·L-1) while pH and [K+] were unchanged, it seems unlikely that the LBPP-induced hyperpnea can be attributed to activation of peripheral arterial or central chemoreceptors. These findings suggests a ventilatory stimulus may be generated by an LBPP-induced reduction in perfusion with the subsequent accumulation of intramuscular metabolites at the working limb and/or a direct effect of increased intramuscular tissue pressure.
KW - Control of breathing
KW - Exercise, hyperpnea
KW - Mammals, humans
KW - Pressure, lower body
UR - http://www.scopus.com/inward/record.url?scp=0027486616&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027486616&partnerID=8YFLogxK
U2 - 10.1016/0034-5687(93)90042-9
DO - 10.1016/0034-5687(93)90042-9
M3 - Article
C2 - 8272585
AN - SCOPUS:0027486616
VL - 94
SP - 121
EP - 135
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
SN - 1569-9048
IS - 2
ER -