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Rauramaa, Rainer FACSM; Väisänen, Sari; Rankinen, Tuomo; Gagnon, Jacques; Bouchard, Claude FACSM Author Information
It was hypothesized that more accurate equations for estimating submaximal VO2 during cycle ergometry could be developed if more independent variables were used in the equation.The purposes of this study were: (1) to develop new equations for estimating submaximal VO2 during cycle ergometry; and (2) to examine the accuracy of the newly developed equations and those of the American College of Sports Medicine (1995), Berry et al. (1993), Lang et al. (1992), Latin and Berg (1994), and Londeree et al. (1997).Subjects (715 men and women, ages 16-65 yr, from the HERITAGE Family Study) completed a maximal cycle ergometry test, two submaximal trials at 50 W and 60% of VO2max, hydrostatic weighing, and stature and body mass measures before and after 20 wk of cycle ergometry training. Regression analysis generated prediction equations using pretraining data from the 60% trials.No equation with more independent variables was better than an equation that used only power output. This equation, HERITAGE-1, with only power output was cross-validated using the "jackknife" technique. Paired t-tests, mean differences, SEEs, and Es were used to compare the VO2 estimated by HERITAGE-1 and those of previously published equations with the measured VO2 at 60% of VO2max.HERITAGE-1 was slightly better than the equations of ACSM, Lang et al., and Latin and Berg using pretraining data but was not better when using post-training data. All four of these equations were superior to the equations of Berry et al. and Londeree et al.
No abstract is provided for this article.
No abstract is provided for this article.
1 The aims of the present study were to determine whether long-term 5-hydroxytryptamine (5-HT) reuptake blockade and inhibition of type-A monoamine oxidase (MAO-A) lead to an enhancement of the electrically evoked release of tritium from guinea-pig brain slices preloaded with [3H]-5-HT, and to assess the sensitivity of the terminal 5-HT1D autoreceptor, the α2-adrenoceptor also located on 5-HT terminals, and the 5-HT3 receptor that modulates 5-HT release following these two types of antidepressant treatments. 2 The electrically evoked release of tritium was significantly enhanced following a 21-day treatment with the 5-HT reuptake blocker, paroxetine and the reversible MAO-A inhibitor, befloxatone, in preloaded slices of the hypothalamus, hippocampus and frontal cortex 48 h after removal of the osmotic minipumps used to deliver the drugs. 3 The inhibitory effect of the terminal 5-HT autoreceptor agonist, 5-methoxytryptamine, on the evoked release of tritium was attenuated in slices of the hypothalamus, hippocampus, but not frontal cortex, following the paroxetine treatment. In the befloxatone group, the effectiveness of 5-methoxytryptamine was unaltered in the same brain structures. 4 The sensitivity of the α2-adrenoceptor on 5-HT terminals, assessed using UK 14.304, was attenuated in hypothalamus, hippocampus, but not frontal cortex slices prepared from befloxatone-treated guinea-pigs and preloaded with [3H]-5-HT. The paroxetine treatment did not alter the sensitivity of this α2-adrenoceptor in the hypothalamus. 5 The sensitivity of the α2-adrenoceptor on noradrenaline terminals, also assessed using UK 14.304, was not altered in hippocampus and hypothalamus slices preloaded with [3H]-noradrenaline following the long-term befloxatone treatment. 6 In frontal cortex slices, [3H]-5-HT uptake was no longer significantly attenuated after a 21-day treatment with paroxetine, whereas it was still markedly inhibited in hypothalamus slices. The enhancing effect of paroxetine on the evoked release of [3H]-5-HT in the superfusion medium was no longer evident in frontal cortex slices of the paroxetine group. These data indicate that long-term 5-HT reuptake blockade desensitized the 5-HT transporter in the frontal cortex. 7 The capacity of the 5-HT3 receptor agonist, 2-methyl-5-HT, to enhance the electrically evoked release of tritium was not altered in hypothalamus, hippocampus, and frontal cortex slices prepared from befloxatone-treated guinea-pigs, but was significantly attenuated in the paroxetine group also treated for 21 days. Following a 2-day paroxetine treatment, the enhancing effect of 2-methyl-5-HT on tritium release was unaltered in frontal cortex slices.
No abstract is provided for this article.
No abstract is provided for this article.
Our objective was to determine threshold values of waist girth, waist-to-hip ratio (WHR), and sagittal diameter corresponding to an accumulation of visceral adipose tissue of 130 cm2 and to verify whether these threshold values could be influenced by sex, age, menopausal status, and the degree of obesity. From the regression equations computed in the total sample of 213 men [aged (mean+/- SD) 37.8 +/- 12.2 y] and 190 women (aged 37.3 +/- 12.1 y), a waist girth of approximately 95 cm in both sexes, WHR values of 0.94 in men and of 0.88 in women, and sagittal diameters of 22.8 cm in men and 25.2 cm in women corresponded to a visceral adipose tissue area of 130 cm2. In both sexes, threshold values of waist girth corresponding to critical amounts of visceral adipose tissue were generally lower in subjects who were > or = 40 y old (approximately 90 cm) than in younger individuals (approximately 100 cm). Similar differences were found for WHR and sagittal diameter threshold values. Finally, threshold values of waist girth corresponding to critical amounts of visceral adipose tissue were essentially similar in normal-weight and overweight men and women, whereas threshold values of WHR were in general higher in normal-weight than in overweight subjects. In conclusion, our results suggest that the relations of anthropometric variables to visceral adipose tissue accumulation are age-specific. However, waist girth is likely to be a more convenient anthropometric correlate of visceral adipose tissue than the WHR because threshold values of waist girth corresponding to critical amounts of visceral adipose tissue do not appear to be influenced by sex or by the degree of obesity.
No abstract is provided for this article.
Four types of human obesities are defined by topography of fat deposition. The focus of the paper is on the genetic determinants and the nongenetic correlates of the first type, which is commonly defined as excess weight-for-height or excess body fat without a particular concentration of fat in a given area of the body. The heritability of fat mass or percent body fat derived from underwater-weighing assessment of body density reaches ∼25% of the age- and gender-adjusted pheno-typic variance. The within-identical-twin-pair resemblance in the response to a standardized overfeeding protocol emphasizes the importance of the genotype in determining individual differences in body weight and body composition. In this regard, the proneness to store energy primarily as fat or as lean tissue is a major determinant of the response to a caloric surplus.
