Biomedical subjects

T A St Amand

Publications and source records attributed to T A St Amand.

3 recordsLinked to original sources

PubMed2000

Pyruvate overrides inhibition of PDH during exercise after a low-carbohydrate diet.

The effects of carbohydrate deprivation on the regulation of pyruvate dehydrogenase (PDH) were studied at rest and during moderate-intensity exercise. An inhibitory effect of a chronic low-carbohydrate diet (LCD) on the active form of PDH (PDHa) mediated by a stable increase in PDH kinase (PDHK) activity has recently been reported (Peters SJ, Howlett RA, St. Amand TA, Heigenhauser GJF, and Spriet LL. Am J Physiol Endocrinol Metab 275: E980-E986, 1998.). In the present study, seven males cycled at 65% maximal O(2) uptake for 30 min after a 6-day LCD. Exercise was repeated 1 wk later after a mixed diet (MD). Muscle biopsies were sampled from the vastus lateralis at rest and at 2 and 30 min of exercise. At rest, PDHa activity (0.18 +/- 0.04 vs. 0.63 +/- 0.18 mmol x min(-1) x kg wet wt(-1)), muscle glycogen content (310.2 +/- 36.9 vs. 563.9 +/- 32.6 mmol/kg dry wt), and muscle lactate content (2.6 +/- 0.3 vs. 4.2 +/- 0.6 mmol/kg dry wt) were significantly lower after the LCD. Resting muscle acetyl-CoA (10.8 +/- 1.9 vs. 7.4 +/- 0.8 micromol/kg dry wt) and acetylcarnitine (5.3 +/- 1.4 vs. 1.6 +/- 0.3 mmol/kg dry wt) contents were significantly elevated after the LCD. During exercise, PDHa, glycogenolytic rate (LCD 5.8 +/- 0.4 vs. MD 6.9 +/- 0.2 mmol x min(-1) x kg dry wt(-1)), and muscle concentrations of acetylcarnitine, pyruvate, and lactate increased to the same extent in both conditions. The results of the present study suggest that inhibition of resting PDH by elevated PDHK activity after a LCD may be overridden by the availability of muscle pyruvate during exercise.

3-Hydroxybutyric Acid↗

PubMed2000

Symptom perception during acute bronchoconstriction.

The hypothesis underlying the present study was that some of the variability in symptom intensity seen during acute bronchoconstriction may result from varying intensities of several stimuli yielding several sensations that can be identified by specific descriptive expressions (symptoms). A total of 232 subjects inhaled methacholine in doubling concentrations to a 20% decrease in FEV(1), or 64 mg/ml. The study identified the prevalence of dyspnea, nonspecific discomfort associated with the act of breathing, and 10 specific symptom expressions. Each symptom intensity was rated in Borg scale units. The contribution of the specific symptoms to the intensity of dyspnea is illustrated in the following equation (r = 0. 84): Dyspnea = 0.44 + 0.19 Difficult breathing + 0.41 Chest tightness + 0.20 Breathlessness + 0.14 Labored breathing + 0.11 Chest pain. Dyspnea was more intense with broncho-constriction, baseline pulmonary impairment, weight, and sex (being female). Dyspnea was less intense with age (being older) and as airway responsiveness to methacholine increased (p < 0.05 for all factors). Chest tightness and chest pain were at polar extremes on the discrimination scale, i.e., easily discriminated; chest tightness, difficult and labored breathing were not easily discriminated.

Adult↗

PubMed1998

Human skeletal muscle pyruvate dehydrogenase kinase activity increases after a low-carbohydrate diet.

To characterize human skeletal muscle enzymatic adaptation to a low-carbohydrate, high-fat, and high-protein diet (LCD), subjects consumed a eucaloric diet consisting of 5% of the total energy intake from carbohydrate, 63% from fat, and 33% from protein for 6 days compared with their normal diet (52% carbohydrate, 33% fat, and 14% protein). Biopsies were taken from the vastus lateralis before and after 3 and 6 days on a LCD. Intact mitochondria were extracted from fresh muscle and analyzed for pyruvate dehydrogenase (PDH) kinase, total PDH, and carnitine palmitoyltransferase I activities and mitochondrial ATP production rate (using carbohydrate and fat substrates). beta-Hydroxyacyl CoA dehydrogenase, active PDH (PDHa), and citrate synthase activities were also measured on whole muscle homogenates. PDH kinase (PDHK) was calculated as the absolute value of the apparent first-order rate constant of the inactivation of PDH in the presence of 0.3 mM Mg2+-ATP. PDHK increased dramatically from 0.10 +/- 0.02 min-1 to 0.35 +/- 0.09 min-1 at 3 days and 0.49 +/- 0. 06 min-1 after 6 days. Resting PDHa activity decreased from 0.63 +/- 0.17 to 0.17 +/- 0.04 mmol. min-1. kg-1 after 6 days on the diet, whereas total PDH activity did not change. Activities for all other enzymes were unaltered by the LCD. In summary, severe deficiency of dietary carbohydrate combined with a twofold increase in dietary fat and protein caused a rapid three- to fivefold increase in PDHK activity in human skeletal muscle. The increased PDHK activity downregulated the amount of PDH in its active form at rest and decreased carbohydrate metabolism. However, an increase in the activities of enzymes involved in fatty acid oxidation did not occur.

3-Hydroxyacyl CoA Dehydrogenases↗