The effect of thiamine and its metabolites on the activity of tissue and purified lactate dehydrogenase

It is shown that thiamine and its metabolites effect lactate dehydrogenase activity and lactate content in the tissues. Thiochrome and thiamine phosphate increase the lactate level in the liver and small intestine. The given effect correlates with the inhibition of the tissue and purified lactate dehydrogenase by thiochrome.     

Post-competition blood lactate concentrations in collegiate swimmers.

The purpose of this investigation was to quantitate post-competition lactate (LA) concentrations of swimmers during a competitive collegiate meet. Blood LA was measured by an enzymatic method on 23 subjects 5 min after each race event. The largest mean LA concentration of 25.7 mM/L was observed in swimmers after competing in the 200-yd individual medley. Swimmers in the 200-yd butterfly, back, breast and freestyle races had similar mean blood LA concentrations (ranging from 16.4 to 20.6 mM/L). Swimmers in the two longest events, the 500-yd and 1,000-yd free style races, had mean LA concentrations of 15.6 and 10.0 mM/L, respectively. To account for the effects of motivation, LA concentrations were measured following maximal effort noncompetitive 100 and 200-yd swims. LA concentrations were slightly greater in conjunction with faster performances for the competitive as compared to the noncompetitive 100 and 200-yd swims.     

Influence of moderate cold exposure on blood lactate during incremental exercise.

This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30 degrees C or at 10 degrees C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO2) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la-]b. The VO2 was identical under both environments. At 10 degrees C, as compared to 30 degrees C, the lactate anaerobic threshold (Than,la-) occurred at an exercise intensity 15 W higher and [la-]b was lower for submaximal intensities above the Than,la-. Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10 degrees C [15.60 (SEM 3.15) nmol.l-1] than at 30 degrees C [8.64 (SEM 2.37) nmol.l-1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la-]b observed for submaximal high intensities during severe cold exposure.     

Presence of lactate dehydrogenase and lactate racemase in Megasphaera elsdenii grown on glucose or lactate.

Activity of D-lactate dehydrogenase (D-LDH) was shown not only in cell extracts from Megasphaera elsdenii grown on DL-lactate, but also in cell extracts from glucose-grown cells, although glucose-grown cells contained approximately half as much D-LDH as DL-lactate-grown cells. This indicates that the D-LDH of M. elsdenii is a constitutive enzyme. However, lactate racemase (LR) activity was present in DL-lactate-grown cells, but was not detected in glucose-grown cells, suggesting that LR is induced by lactate. Acetate, propionate, and butyrate were produced similarly from both D- and L-lactate, indicating that LR can be induced by both D- and L-lactate. These results suggest that the primary reason for the inability of M. elsdenii to produce propionate from glucose is that cells fermenting glucose do not synthesize LR, which is induced by lactate.     

Effect of respiratory alkalosis during exercise on blood lactate

A biofeedback model of hyperventilation during exercise was used to assess the independent effects of pH, arterial CO2 partial pressure (PaCO2), and minute ventilation on blood lactate during exercise. Eight normal subjects were studied with progressive upright bicycle exercise (2-min intervals, 25-W increments) under three experimental conditions in random order. Arterialized venous blood was drawn at each work load for measurement of blood lactate, pH, and PaCO2. Results were compared with those from reproducible control tests. Experimental conditions were 1) biofeedback hyperventilation (to increase pH by 0.08-0.10 at each work load); 2) hyperventilation following acetazolamide (which returned pH to control values despite ventilation and PaCO2 identical to condition 1); and 3) metabolic acidosis induced by acetazolamide (with spontaneous ventilation). The results showed an increase in blood lactate during hyperventilation. Blood lactate was similar to control with hyperventilation after acetazolamide, suggesting that the change was due to pH and not to PaCO2 or total ventilation. Exercise during metabolic acidosis (acetazolamide alone) was associated with blood lactate lower than control values. Respiratory alkalosis during exercise increases blood lactate. This is due to the increase in pH and not to the increase in ventilation or the decrease in PaCO2.     

Inhibition of thiamine transport in Saccharomyces cerevisiae by thiamine disulfides.

Both thiamine disulfide and O-benzoyl thiamine disulfide, which are thiolfrom derivatives of thiamine, strongly inhibited thiamine transport in Saccharomyces cerevisiae. The inhibition appeared to be due to a high affinity of the analogs for yeast cell membranes, in which thiamine transport component(s) may be integrated.     

Relationship between turnover rate and blood concentration of lactate in exercising dogs.

Steady-state blood lactate concentrationss and lactate turnover, or entry, rates were determined by use of constant infusion of L(+)-[14C]lactate in seven anesthetized dogs before and during electrically induced exercise. Lactate entry rates increased during exercise in all dogs with or without the infusion of additional exogenous cold lactate. Blood lactate concentrations, on the other hand, rose to levels considerably below those predicted for these entry rates in a previous study of the relationship in normal nonexercising dogs. It is concluded that improved efficiency of lactate removal during exercise allows low blood concentrations despite large increases in entry rates.     

Acute altitude exposure and altered acid-base states. II. Effects on exercise performance and muscle and blood lactate

This study examined the influence of the respiratory alkalosis of acute altitude (AL) exposure alone or in combination with metabolic acid-base manipulations on exercise performance and muscle and blood lactate accumulation. Four subjects exercised for 10 min at 50% and 75% and to exhaustion at 90% of ground level (GL) VO2max, and at the same relative exercise intensities during three exposures to a simulated altitude of 4200 m; (i) normal (NAL), (ii) following 0.2 g.kg-1 ingestion of sodium bicarbonate (BAL), and (iii) following 0.5 g.day-1 ingestion of acetazolamide for 2 days prior to exposure (AAL). Muscle and blood lactate values were similar throughout exercise for GL and NAL. Although muscle lactates were similar among AL conditions blood lactate was reduced for AAL and increased following exhaustive exercise for BAL compared with NAL. Time to exhaustion at 90% VO2max was increased for NAL (10.4 +/- 1.6 min) compared with GL (7.1 +/- 0.2 min). Performance time was decreased for AAL (6.3 +/- 2.8 min) compared with NAL and BAL (12.4 +/- 4.2 min). These data suggest that the induced respiratory alkalosis of acute AL exposure may enhance exercise performance at high relative intensities. In contrast, the ingestion of acetazolamide before AL exposure would have detrimental effects on performance. The mechanism responsible for these changes may relate to the possible influence of altered extracellular acid-base states on intracellular hydrogen ion accumulation and lactate release.