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Blood hydrogen ion and lactate concentrations during strenuous exercise in the horse
Author(s) -
KRONFELD D. S.,
FERRANTE PAMELA L.,
TAYLOR LYNN E.,
CUSTALOW S. ELIZABETH
Publication year - 1995
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.1111/j.2042-3306.1995.tb04934.x
Subject(s) - alkalosis , acidosis , glycogen , bicarbonate , acid–base homeostasis , horse , lactate threshold , medicine , venous blood , metabolic acidosis , ventilation (architecture) , arterial blood , zoology , respiration , chemistry , endocrinology , blood lactate , biology , heart rate , blood pressure , anatomy , mechanical engineering , paleontology , engineering
Summary Exceptional findings in horses, such as metabolic alkalosis during exercise and an apparent absence of a distinct lactate threshold, led us to apply Stewart's acid‐base system and to develop a new statistical model for investigating lactate threshold. The lactate threshold was clearly demonstrated by an incremental exercise test using up to 14 steps. Lactate threshold was increased by training and by fat adaptation (prolonged interval training and a 10% corn oil diet). Fat adaptation appears to facilitate the metabolic regulation of glycolysis, sparing glucose and glycogen at work of low intensity, but promoting lactate production when power is needed for high intensity exercise. The blood lactate response to exercise was enhanced by fat adaptation and by oral supplementation of sodium bicarbonate. The synergistic effect of the combination suggested that inclusion of fat may enhance the advantage of a diet with a high cation‐anion balance. The lower CO 2 production of fat‐adapted horses could be of benefit under hot and humid conditions, especially in horses with reduced pulmonary function. During repeated sprints, central venous [H + ] increased (acidosis) but arterial [H + ] decreased (alkalosis). These changes were consistent with concurrent changes in venous and arterial PCO 2 but not [SID]. Arterial PO 2 remained constant. These findings suggest that increasing ventilation to maintain arterial PO 2 incidentally reduced PCO 2 , hence arterial [H + ]. In terms of homeostatic priorities, regulation of respiration took precedence over regulation of acid‐base status.