Abstract
This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. Endtidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles in the brain elicit the hyperventilation observed during intense exercise.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 991-994 |
| Number of pages | 4 |
| Journal | Journal of Applied Physiology Respiratory Environmental and Exercise Physiology |
| Volume | 52 |
| Issue number | 4 |
| State | Published - Oct 25 1982 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Physiology
- Endocrinology
Cite this
Exercise hyperventilation in patients with McArdle's disease. / Hagberg, J. M.; Coyle, E. F.; Carroll, James Edwin; Miller, J. M.; Martin, W. H.; Brooke, M. H.
In: Journal of Applied Physiology Respiratory Environmental and Exercise Physiology, Vol. 52, No. 4, 25.10.1982, p. 991-994.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Exercise hyperventilation in patients with McArdle's disease
AU - Hagberg, J. M.
AU - Coyle, E. F.
AU - Carroll, James Edwin
AU - Miller, J. M.
AU - Martin, W. H.
AU - Brooke, M. H.
PY - 1982/10/25
Y1 - 1982/10/25
N2 - This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. Endtidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles in the brain elicit the hyperventilation observed during intense exercise.
AB - This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. Endtidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles in the brain elicit the hyperventilation observed during intense exercise.
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M3 - Article
C2 - 6953061
AN - SCOPUS:0019968393
VL - 52
SP - 991
EP - 994
JO - Journal of Applied Physiology Respiratory Environmental and Exercise Physiology
JF - Journal of Applied Physiology Respiratory Environmental and Exercise Physiology
SN - 8750-7587
IS - 4
ER -