Search

To study the effect of menstrual cycle phase and carbohydrate ingestion on glucose kinetics and exercise performance, eight healthy, moderately trained, eumenorrheic women cycled at 70% of peak [O.sub.2] consumption for 2 h and then performed a 4 kJ/kg body wt time trial. A control (C) and a glucose ingestion (G) trial were completed during the follicular (F) and luteal (L) phases of the menstrual cycle. Plasma substrate concentrations were similar before the commencement of exercise. Glucose rates of appearance and disappearance were higher (P [is less than] 0.05) during the 2nd h of exercise in FC than in LC. The percent contribution of carbohydrate to total energy expenditure was greater in FC than in LC, and subjects performed better (13%, P [is less than] 0.05) in FC. Performance improved (19% and 26% in FG and LG compared with FC and LC, respectively, P [is less than] 0.05) with the ingestion of glucose throughout exercise. These data demonstrate that substrate metabolism and exercise performance are influenced by the menstrual cycle phase, but ingestion of glucose minimizes these effects. estrogen; progesterone; carbohydrate metabolism; endurance exercise

To examine the roles of 17 [Beta]-estradiol ([E.sub.2]) and progesterone (Prog) in lipid metabolism, skeletal muscle enzyme activities were studied in female Sprague-Dawley rats. Groups included sham-operated rats (C) and ovariectomized rats treated with placebo (O), [E.sub.2] (E), Prog (P), both hormones at physiological doses (P + E), or both hormones with a high dose of [E.sub.2] (P + HiE). Hormone (or vehicle only) delivery was via time-release pellets inserted at the time of surgery, 15 days before metabolic testing. Results demonstrated that carnitine palmitoyltransferase maximal activity was 19, 21, and 19% lower (P [is less than] 0.01) in O, P, and P + E rats, respectively, compared with C rats. Conversely, activity in E and P + HiE rats was 14 and 19% higher (P [is less than] 0.01) than in C. [Beta]-Hydroxyacyl-CoA dehydrogenase ([Beta]-HAD) maximal activity was 20% lower (P [is less than] 0.01) in O than in C rats; similarly, P and P + E rats were 18 and 19% lower, respectively (P [is less than] 0.01); however, treatment with E2 returned [Beta]-HAD activity to C levels. These results suggest that [E.sub.2] plays a role in lipid metabolism by increasing the maximal activity of key enzymes in the fat oxidative pathway of skeletal muscle. ovariectomy; estrogen; progesterone; lipid metabolism

To examine the effect of exercise and adrenergic blockade on lymphocyte cytokine production, six men ingested either a placebo (control) or an [Alpha]- (prazosin hydrochloride) and [Beta]-adrenoceptor antagonist (timolol malate) capsule (blockade, or BLK) 2 h before performing 19 [+ or -] 1 min of supine bicycle exercise at 78 [+ or -] 3% peak pulmonary uptake. Blood was collected before and after exercise, stimulated with phorbol 12-myristate 13-acetate and ionomycin, and surface stained for T ([CD3.sup.+]) and natural killer [NK ([CD3.sup.-][CD56.sup.+])] lymphocyte surface antigens. Cells were permeabilized, stained for the intracellular cytokines interleukin (IL)-2 and interferon (IFN)-[Gamma], and analyzed using flow cytometry. BLK had no effect on the resting concentration of stimulated cytokine-positive T and NK lymphocytes or the amount of cytokine they were producing. Exercise resulted in an increase (P [is less than] 0.05) in the concentration of stimulated T and NK lymphocytes producing cytokines in the circulation, but these cells produced less (P [is less than] 0.05) cytokine post- compared with preexercise. BLK attenuated (P [is less than] 0.05) the elevation in the concentration of lymphocytes producing cytokines during exercise; however, BLK did not affect the amount of IL-2 and IFN-[Gamma] produced. These results suggest that adrenergic stimulation contributes to the exercise-induced increase in the concentration of lymphocytes in the circulation; however, it does not appear to be responsible for the exercise-induced suppression in cytokine production. T cells; natural killer cells; interleukin-2; interferon-[Gamma]

Starkie, R. L., J. Rolland, D. J. Angus, M. J. Anderson, and M. A. Febbraio. Circulating monocytes are not the source of elevations in plasma IL-6 and TNF-[Alpha] levels after prolonged running. Am J Physiol Cell Physiol 280: C769-C774, 2001.--The present study was undertaken to examine the effect of prolonged running on monocyte intracellular cytokine production and plasma cytokine concentration. Blood samples were collected 1 h before, immediately after, 2 h after, and 24 h after a competitive marathon run. There was no change in the number of cells spontaneously producing tumor necrosis factor (TNF)-[Alpha] however, there was a decrease in the number of cells producing interleukin (IL)-1[Alpha] and IL-6 (P [is less than] 0.01) postexercise. In contrast, there was an increase in the number of monocytes that responded to lipopolysaccharide stimulation by producing IL-1[Alpha], TNF-[Alpha], and IL-6 (P [is less than] 0.01) immediately and 2 h postexercise; however, these cells contained less cytokine (P [is less than] 0.05). Plasma IL-6, TNF-[Alpha], epinephrine, norepinephrine, and cortisol concentrations were markedly increased (P [is less than] 0.01) postexercise. These data demonstrate that circulating monocytes are not the source of elevated levels of plasma IL-6 and TNF-[Alpha] after prolonged running. In addition, it is likely that stress hormones result in a decrease in the amount of cytokine produced by LPS-stimulated cells postexercise. flow cytometry; epinephrine; cortisol