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C Reece

Publications and source records attributed to C Reece.

10 recordsLinked to original sources
PubMed1994

Effects of exercise training modality on glucose tolerance in men with abnormal glucose regulation.

To determine the effects of exercise training modality on glucose tolerance in men with untreated abnormal glucose regulation, 26 untrained men (age 54 +/- 9 years; mean +/- SD) with either non-insulin-dependent diabetes mellitus (N = 8), impaired glucose tolerance (IGT) (N = 12) or hyperinsulinemia with normal glucose tolerance (N = 6) were studied before and after 20 wk of either strength training (ST) (N = 8), aerobic (treadmill walk/jog) training (AT) (N = 8), or no exercise (control group; N = 10). Plasma concentrations of glucose and insulin were measured after a 12-14 hr fast and during a standard oral glucose tolerance test (OGTT) before and after training. The ST program significantly reduced total plasma glucose area (mmol.l-1.120 min-1) under the OGTT curve (1348 +/- 251 vs 1190 +/- 329, p < 0.05), and plasma glucose levels (mmol.l-1) at 60 min (p < 0.05), 90 min (P < 0.05), and 120 min (p < 0.05) after glucose ingestion. Strength training also lowered the total plasma insulin area (pmol.l-1.120 min-1) under the OGTT curve (60082 +/- 25467 vs 46727 +/- 11273, p < 0.05) as well as plasma insulin levels (pmol.l-1) at fasting (p < 0.05) and at 90 min (p < 0.01) and 120 min (p < 0.05) after glucose ingestion. All men with IGT (four in each training group) normalized their glucose tolerance following the training. There were no significant differences in OGTT results between ST and AT and no changes were observed in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1993

Aerobic versus strength training for risk factor intervention in middle-aged men at high risk for coronary heart disease.

To compare the effects of strength training (ST) to those of aerobic training (AT) for coronary heart disease (CHD) risk factor intervention, we studied 37 previously untrained males (aged 50 +/- 9 years, mean +/- SD) before and after 20 weeks of either ST (N = 14), AT (walk/jog, N = 13), or no exercise (inactive controls, N = 10). Lipoprotein and lipid profiles, blood pressure, and glucose and insulin responses to an oral glucose tolerance test (OGTT) were assessed before and after the training period in all three groups. The ST program produced significant reductions in plasma glucose levels at 60, 90, and 120 minutes (P < .05) after glucose ingestion, whereas the AT program resulted in significant reductions only at 90 and 120 minutes (P < .05). ST also decreased insulin levels during fasting (P < .05) and at 90 and 120 minutes (P < .01) after glucose ingestion. AT decreased insulin levels at 90 and 120 minutes (P < .01) after glucose ingestion. Both training programs reduced the total area under the glucose tolerance curve for glucose (both P < .05) and insulin (both P < .05), but there were no significant differences in these changes between the two groups. None of the glucose or insulin values were significantly altered in the control group. There were no significant changes in lipoprotein and lipid profiles or blood pressure in any of the three groups. These results suggest that ST and AT have comparable effects on risk factors for CHD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Short-chain acyl-coenzyme A dehydrogenase activity, antigen, and biosynthesis are absent in the BALB/cByJ mouse.

BALB/cByJ (J) mice have short-chain acyl-CoA dehydrogenase (SCAD) deficiency and an organic aciduria similar to that of human SCAD deficiency. [9,10(n)-3H]- and [15,16(n)-3H]palmitate oxidations in J mouse fibroblasts were 96 and 35% of control, respectively, consistent with an isolated SCAD defect. Acyl-CoA dehydrogenase activities were assayed in muscle and fibroblast mitochondria from BALB/cBy controls (Y) and SCAD-deficient J mice. Medium-chain acyl-CoA dehydrogenase (MCAD) activities were comparable in both J and Y mice from all tissues. In the presence of MCAD antiserum, SCAD activities in J mice were undetectable in both tissues. Apparent Km and Vmax values in liver mitochondria suggested a somewhat increased affinity of MCAD for butyryl-CoA in J mice, as compared with MCAD from other species. Immunoblot studies using mitochondria revealed identical apparent SCAD molecular weight in liver, muscle, and fibroblasts from Y mice and no detectable SCAD antigen in J mice; MCAD antigen was detected in comparable amounts from both Y and J mice. Radiolabeling and immunoprecipitation studies in J mouse fibroblasts revealed no SCAD synthesis, but normal MCAD synthesis. These data argue against the existence of tissue-specific SCAD isoforms in the mouse and confirm that this mouse strain is a model for the human organic aciduria resulting from this beta-oxidation defect.

Acyl-CoA Dehydrogenase↗
PubMed1992

Bremsstrahlung imaging using the gamma camera: factors affecting attenuation.

Quantitative imaging of bremsstrahlung from pure beta emitters is proposed as a means for in vivo management of antibody therapy. The method involves the use of high-energy collimation, an empirically selected broad photon energy window to enhance detector sensitivity, and a Wiener restoration filter to compensate for system blur. The measured and filtered data were obtained for an idealized scattering medium and isolated spherical sources. An effective linear attenuation coefficient of about 0.13 cm-1 was determined from the raw image data of 32P. A coefficient of 0.14 cm-1 was determined after the images were restored using the Wiener filter. The measured attenuation was not significantly dependent on the size of the region of interest or the size of the source. Its variation was within the experimental error of measurement (+/- 5%). The measured sensitivity (6 x 10(-6) cps/Bq) was sufficient for imaging therapy doses of 32P or 90Y.

Filtration↗
PubMed1991

Strength training does not improve lipoprotein-lipid profiles in men at risk for CHD.

Sixteen untrained males, age 46 +/- 11 yr (mean +/- SD), were studied to determine the effects of 20 wk of strength training on lipoprotein-lipid profiles and post-heparin lipase activities. All subjects had abnormal lipoprotein-lipid profiles and at least two other risk factors for coronary heart disease (CHD). To control for day-to-day variations in blood lipoprotein levels, baseline values were established by taking at least two blood samples on separate days from the training and control groups. The training program resulted in a 50% increase in upper body strength (P less than 0.001) and a 37% increase in lower body strength (P less than 0.001) as measured by the one repetition maximum test (1-RM). No changes in the 1-RM test were observed in the control group. There were no significant changes in VO2max (34.5 +/- 6.4 vs 36.2 +/- 7.4 ml.kg-1.min-1 or percent fat (25.4 +/- 4.2 vs 24.9 +/- 4.1%) with training. There were also no significant changes in plasma concentrations of triglyceride (193 +/- 96 vs 171 +/- 101 mg.dl-1), total cholesterol (231 +/- 22 vs 210 +/- 22 mg.dl-1), and HDL-C (35 +/- 6 vs 36 +/- 8 mg.dl-1), or LDL-C (139 +/- 16 vs 139 +/- 21 mg.dl-1). Furthermore, the activities of post-heparin lipoprotein lipase (9 +/- 4 vs 13 +/- 5 moles.ml-1.h-1) and hepatic lipase (35 +/- 10 vs 35 +/- 9 moles.ml-1.h-1) did not change with training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

A case of glutaric acidemia type II (severe multiple acyl-CoA dehydrogenation disorder) with subsequent prenatal exclusion in a sibling.

A case of severe multiple acyl-CoA dehydrogenation disorder is described. This is the second such case reported to have had an elevated maternal serum alpha-fetoprotein and normal amniotic alpha-fetoprotein. The child's 3-day extrauterine life was characterized by intractable acidosis, respiratory distress, and ventricular fibrillation. The characteristic biochemical, morphologic, and microscopic findings of this condition are reviewed. A subsequent pregnancy was evaluated using chorionic villus sampling and analysis of cultured trophoblasts. The trophoblasts were biochemically normal, and a normal child was subsequently delivered. Since the manifestations of this disorder developed in utero, prenatal diagnosis and therapy offer the only hope for a more prolonged survival.

Acidosis↗
PubMedDate not supplied

Black self-concept.

Explore the source record for details and available documents.

Adolescent↗