21
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Is lactic acidosis a cause of exercise induced hyperventilation at the respiratory compensation point?

      British Journal of Sports Medicine
      Acidosis, Lactic, complications, physiopathology, Adult, Body Mass Index, Exercise, physiology, Exercise Test, methods, Humans, Hydrogen-Ion Concentration, Hyperventilation, etiology, Oxygen Consumption, Sodium Bicarbonate, administration & dosage

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The respiratory compensation point (RCP) marks the onset of hyperventilation ("respiratory compensation") during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body's buffering mechanisms which leads to metabolic (lactic) acidosis. It was intended to test this experimentally. During a first ramp-like exercise test on a cycle ergometer, RCP (range: 2.51-3.73 l x min(-1) oxygen uptake) was determined from gas exchange measurements in five healthy subjects (age 26-42; body mass index (BMI) 20.7-23.9 kg x m(-2); Vo(2peak) 51.3-62.1 ml x min(-1) x kg(-1)). On the basis of simultaneous determinations of blood pH and base excess, the necessary amount of bicarbonate to completely buffer the metabolic acidosis was calculated. This quantity was administered intravenously in small doses during a second, otherwise identical, exercise test. In each subject sufficient compensation for the acidosis, that is, a pH value constantly above 7.37, was attained during the second test. A delay but no disappearance of the hyperventilation was present in all participants when compared with the first test. RCP occurred on average at a significantly (p = 0.043) higher oxygen uptake (+0.15 l x min(-1)) compared with the first test. For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. However, it does not represent the only additional stimulus of ventilation during intense exercise. Muscle afferents and other sensory inputs from exercising muscles are alternative triggering mechanisms.

          Related collections

          Author and article information

          Comments

          Comment on this article