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Arterial H+ regulation during exercise in humans
Karlman Wasserman1, William L Beaver, Xing-Guo Sun
1Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90502, USA. kwasserman@LABiomed.org
Arterial H+ concentration is precisely regulated during exercise, shifting from respiratory to metabolic acidosis above the lactic acidosis threshold. This indicates a less sensitive but continuous regulation of acidity during intense physical activity.
Area of Science:
- Exercise Physiology
- Human Physiology
- Biochemistry
Background:
- Arterial H+ concentration ([H+]a) is tightly regulated at rest, despite high production rates.
- Understanding the precise regulation of [H+]a during exercise is crucial for interpreting physiological responses.
Purpose of the Study:
- To determine the precision of arterial H+ concentration ([H+]a) regulation during progressively increasing exercise workloads.
- To investigate the relationship between [H+]a, PaCO2, and ventilation (V˙(E)) across different exercise intensities.
Main Methods:
- Measurements of [H+]a, PaCO2, and V˙(E) in 16 healthy subjects during incremental exercise.
- Analysis of ventilatory and acid-base responses relative to exercise intensity and the lactic acidosis threshold (LAT).
Main Results:
- Ventilation (V˙(E)) increased with [H+]a, initially driven by PaCO2 below the LAT.
- Above the LAT, [H+]a increased more significantly relative to V˙(E), indicating a shift to metabolic acidosis.
- PaCO2 initially increased with work rate but decreased above the LAT, while [H+]a continued to rise.
Conclusions:
- Arterial H+ concentration ([H+]a) is regulated throughout the full range of exercise.
- The regulation of [H+]a becomes less sensitive above the lactic acidosis threshold (LAT).
- Exercise-induced acidosis transitions from primarily respiratory to metabolic as exercise intensity increases beyond the LAT.
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