A. Coxon
University of Cambridge
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Featured researches published by A. Coxon.
The American Journal of Clinical Nutrition | 1992
S. Kreitzman; A. Coxon; Kalman F Szaz
Glycogen is stored in the liver, muscles, and fat cells in hydrated form (three to four parts water) associated with potassium (0.45 mmol K/g glycogen). Total body potassium (TBK) changes early in very-low-calorie diets (VLCDs) primarily reflect glycogen storage. Potassium released from glycogen can distort estimates of body composition during dieting. TBK changes due to glycogen mobilization were measured in 11 subjects after 4 d dieting with a VLCD. The influence of water-laden glycogen on weight fluctuations during the dieting process, the exaggerated regain if carbohydrate loading occurs, and the implications for weight control programs and overestimation of nitrogen losses with dieting are discussed.
Annals of Nutrition and Metabolism | 1991
D. A. Brodie; Roger G. Eston; A. Coxon; S. Kreitzman; Harold R. Stockdale; Alan N. Howard
Fat-free mass was measured by hydrodensitometry, electrical impedance and total body potassium before and after water and electrolyte loss induced by (a) the administration of the diuretic frusemide, and (b) sweat loss. All methods of measuring fat-free mass were shown by pilot experiments to have procedural reliability. The diuretic caused a reduction in apparent fat-free mass of 2.63 kg by the impedance method, of 2.33 kg by hydrodensitometry and of 1.8 kg by total body potassium. Water and electrolyte loss from sweating caused a fat-free loss of 2.3 kg, 2.7 kg and 1.3 kg by the same three procedures. Urinary potassium accounted for about one fifth of the observed 40K fat-free mass loss. Each method was thus clearly sensitive to the induced water loss. These data suggest that in evaluating the composition of weight loss, existing methods of measuring body composition do not distinguish between water and other more critical components of fat-free mass. It is thus essential that stable hydration levels are established for any longitudinal comparison of weight loss by these methods.
European Journal of Applied Physiology | 1992
Roger G. Eston; S. Shephard; S. Kreitzman; A. Coxon; D. A. Brodie; Kevin L. Lamb; Vasilios Baltzopoulos
SummaryThe effect of very low calorie diet (VLCD) on fat-free mass (FFM) and physiological response to exercise is a topic of current interest. Ten moderately obese women (aged 23–57 years) received VLCD (1695 kJ·day−1) for 6 weeks. FFM, estimated by four conventional techniques, and heart rate (fc), blood lactate (lab), mean arterial pressure (MAP), respiratory exchange ratio (R) and rating of perceived exertion (RPE) were measured during a submaximal cycle ergometry test 1 week bevore, in the 2nd and 6th week, and 1 week after VLCD treatment. Strength and muscular endurance of the quadriceps and hamstrings were tested by isokinetic dynamometry. The 11.5-kg reduction in body mass was approximately 63% fat and 37% FFM. The latter was attributed largely to the loss of water associated with glycogen. Whilst exercise fc increased by 9–14 beats·min−1 (P<0.01), there were substantial decreases (P<0.01) in submaximal MAP (1.07–1.73 kPa), lab (0.75–1.00 mmol·1−1 and R (0.07–0.09) during VLCD. R and fc returned to normal levels after VLCD. Gross strength decreased (P<0.01) by 9 and 13% at 1.05 rad·s−1 and 3.14 rad·ss−1, respectively. Strength expressed relative to body mass (Nm·kg−1) increased (P<0.01) at the lower contraction velocity, but there was no change at the faster velocity. Muscular endurance also decreased (P<0.01) by 62 and 82% for the hamstrings and quadriceps, respectively: We concluded that the strength decrease was a natural adaptation to the reduction in body mass as the ratio of strength to FFM was maintained. Despite the physiological alterations, subjects could tolerate short-term, steady-state exercise during VLCD, with only slight increases in RPE. However, greater fatigue is associated with long duration strength training exercises during VLCD.
The Lancet | 1989
A. Coxon; S. Kreitzman
1. Yanagisawa M, Kurihara H, Kimura S, et al. A novel potent vasoconstrictor peptide produced by vascular endothelial cells. Nature 1988; 332: 411-15. 2. Uchida Y, Ninomiya H, Saotome M, et al. Endothelin, a novel vasoconstrictor peptide, as potent bronchoconstrictor. Eur J Pharmacol 1988; 154: 227-28. 3. Nomura A, Uchida Y, Ohtsuka M, et al. Endothelium-derived polypeptide potently constricts human bronchi. Am Rev Respir Dis 1989, 139: A468. 4. Black PN, Ghatei MA, Bretherton-Watt D, Takahashi K, Krausz T, Bloom SR. Endothelin is formed by cultured tracheal epithelial cells. Am Rev Respir Dis 1989; 139: A52.
International Journal of Obesity | 1989
A. Lemons; S. Kreitzman; A. Coxon; A. Howard
International Journal of Obesity | 1989
A. Coxon; S. Kreitzman; D. A. Brodie; A. Howard
International Journal of Obesity | 1989
Roger G. Eston; D. A. Brodie; A. Coxon; S. Kreitzzman
International Journal of Obesity | 1989
D. A. Brodie; Roger G. Eston; S. Kreitzman; A. Coxon
International Journal of Obesity | 1989
J. Walls; J. Worzencraft; S. Kreitzman; A. Coxon; A. Howard
International Journal of Obesity | 1989
S. Kreitzman; A. Coxon; D. A. Brodie; Roger G. Eston; A. Howard