Biochemical changes in a 100 km run: carbohydrates, lipids, and hormones in serum.

During the 100 km race in Biel, Switzerland, seven-well trained men (age 33.3 +/- 3.5 years; V02 max. 59.9 +/- ml/kg) have been investigated. Their mean running time over the 100 km distance averaged 10.41 +/- 1.25 h. In contrast to almost unchanged blood glucose and lactate concentrations, blood lipids showed significant changes. Triglycerides decreased about two-fold, whereas glycerol and free fatty acids increased to extremely high concentrations (0.628 and 2.44 mmol/l respectively). Plasma insulin after the run was unaffected, whereas growth hormone, aldosterone and cortisol concentrations were significantly increased. With the exceptions of a still significantly elevated aldosterone and lactate concentration as well as a decreased triglyceride concentration all other values in the blood are restored to normal 24 h after completion of the run.

Biochemical changes in a 100 km run: free amino acids, urea, and creatinine.

Free amino acids, urea, and creatinine were analyzed in venous blood and urine of 11 trained (28--81 years old) male subjects before, immediately after, and 1 day after a 100 km running competition. The urinary excretion per minute of all amino acids was lowered after the contest. The renal clearance of creatinine was reduced from 116 to 60 ml/min and the clearance of most amino acids was reduced to a similar extent. However, for the amino acids with a resting clearance under 1 ml/min (x), a high relative clearance ratio (y in % of x) was seen post-exercise: y = -92.3 (log10 x) +23.1, r = -0.83, showing that their high reabsorption capacity had been impaired. Serum concentrations of most free amino acids, including the branched-chain amino acids and alanine, were reduced to 35--85% of the pre-race values. The sulfur amino acids were elevated either at the end of (cystine, to 180%) or 24 h after (methionine, to 155%) the race. Urea production increased by 44% while creatinine production tended to decrease. The production of 3-methylhistidine remained unchanged. These findings are compatible with a stimulation of gluconegenesis at the expense of the amino acid pool without induction of muscle protein catabolism.

Compartmentation of acetyl-coA in rat-liver mitochondria.

The ratio of the specific radioactivities of 3-hydroxybutyrate: citrate was determined in rat liver mitochondria which were incubated in the presence of [1-14C]palmitate, pyruvate, bicarbonate, ATP, phosphate and malonate. Without compartmentation this ratio would maximally be 2, however, under our conditions values of 2.5-3.7 were observed. In further experiments with mitochondria, the sensitivity of pyruvate carboxylase for acetyl-CoA produced from various precursors was tested. It was found that acetyl-CoA produced from L-acetylcarnitine or by oxidation from either pyruvate, octanoate or palmitylcarnitine but not from leucine led to a stimulation of pyruvate carboxylation. These results demonstrate a compartmentation of acetyl-CoA in liver mitochondria. The further finding that different mitochondrial fractions showed varying ratios of specific radioactivities of 3-hydroxybutyrate:citrate indicates that the observed compartmentation may be explained by the existence of different types of mitochondria with varying enzyme patterns and acetyl-CoA pools.