lactic acid/hypoxia

The extracellular pH defense against the lactic acidosis resulting from exercise can be estimated from the ratios -delta[La].delta pH-1 (where delta[La] is change in lactic acid concentration and delta pH is change in pH) and delta[HCO3-].delta pH-1 (where delta[HCO3-] is change in bicarbonate

To evaluate the role of mineralized tissues of the leopard frog in buffering acid, we analyzed the composition of femur and auditory capsule, the latter of which encloses a portion of the endolymphatic lime sacs, and investigated the extent to which these tissues are involved in buffering lactic

Objective. To study the effect of acute moderate hypoxia on plasma lactic acid (LA) and lactic dehydrogenase (LDH) content in pilots. Method. Concentrations of plasma LA and LDH were measured by colorimetry in 16 healthy male pilots in the early morning (6:00 a.m.), following acute moderate hypoxic

We measured O2 uptake (VO2), CO2 output (VCO2), and net lactic acid output (L) during a 30-min period of repetitive 1/s isotonic tetanic contractions of the dog gastrocnemius-plantaris muscle group. The conditions were modest ischemic hypoxia (ischemia), hypoxia hypoxia (hypoxia), and free-flow

In mice, changes of body temperature and concentration of lactic acid in the blood were studied after three modes of barochamber hypoxia (altitude 8000 m) at the temperatures +10, +20 and +36 degrees C. The greatest drop of body temperature occurred at +10 degrees C, the least one at +36 degrees C.

The data obtained with the aid of additional hypoxic load (blood loss, ascending in a barochamber) reveal a considerable lactacidemia occurring prior to erythropoiesis activation which corroborates the theory of activation of the erythropoietin formation with lactic acid. The degree of lactacidemia

Hypoxemia transiently inhibits the incidence of fetal breathing movements (FBM), but their incidence returns to normal after several hours despite maintained hypoxemia. We hypothesized that the lactic acidosis associated with prolonged systemic hypoxemia might mediate the adaptation of the hypoxemic

Most hypoxia-induced malformations are caused by a syndrome involving tremendous edema followed by formation of clear blisters and hematomas. These, in turn, mechanically interfere with development. Studies of blood pH and lactic acid indicate that lactate accumulation initiates this syndrome. The

During hypoxia cardiac contraction declines and there is an intracellular acidosis. We find that, if this acidosis is abolished by decreasing pCO2 there is little restoration of force. Therefore the acidosis is not the major cause of the decline of force. The acidosis may partly result from the

Hypoxic pretreatment (3 kPa oxygen) of maize (Zea mays L.) root tips improved their survival time in a subsequent anoxic incubation from 10 h to more than 3 d, provided that glucose was added to the medium to sustain metabolism. The glycolytic flux (lactate + ethanol) was the same in both pretreated

Melanoma is the most aggressive form of skin cancer. Hypoxia is a feature of the tumor microenvironment that reduces efficacy of immuno- and chemotherapies, resulting in poor clinical outcomes. Lactococcus lactis is a facultative anaerobic gram-positive lactic acid bacterium (LAB) that is

Lactic acid (LA) is present in tumors, asthma, and wound healing, environments with elevated IL-33 and mast cell infiltration. Although IL-33 is a potent mast cell activator, how LA affects IL-33-mediated mast cell function is unknown. To investigate this, mouse bone marrow-derived mast cells were

Albino rats of the Wistar family were raised from the time of birth in the normobaric hypoxic environment. They were subjected at two subsequent equal trials of muscular work: the first in hypoxic normobaric conditions; the second in hypoxic hypercapnic conditions (CO2 = 2%). The modifications of

Albino rats of the Wistar family were subjected at three subsequent equal trials of muscular work: the first in normoxyc conditions; the second in hypoxic normobaric conditions; the third in hypoxic-hypercapnic normobaric conditions. The modifications of the lactacidemia, pyruvicemia and acid-base