Publications

To evaluate the effect of intensity of physical activity on body fatness and fat distribution, observations of 1366 women and 1257 men who participated in the 1981 Canada Fitness Survey were analyzed. Subjects were tested for energy expenditure of leisure-time activities and estimated maximal oxygen uptake (VO2max), body fatness was measured by subcutaneous skinfold thicknesses, and anthropometric measurements were made. Subjects of both sexes were categorized into four subgroups on the basis of their participation in leisure-time activities of various intensities. In general, subjects practicing vigorous activities on a regular basis had lower subcutaneous skinfold thicknesses and waist-to-hip ratios (WHRs) than those not performing these activities. These differences remained statistically significant after a covariance analysis was used to remove the effect of total energy expenditure of leisure-time activities on subcutaneous fat and fat distribution. Moreover, the WHR remained significantly lower in subjects performing high-intensity exercise after the effect of subcutaneous fat on fat distribution was adjusted for.

The authors report a severe neurological deficit with transient quadriplegia which appeared in a critically burned patient subsequently to resuscitation. The diagnosis of central pontine myelinolysis is confirmed thanks to the MRI. The lesion could be related to a serious and too quickly corrected hyponatremia and/or to a cerebral edema. Prevention and diagnosis of this disease in burn patients are discussed.

No abstract is provided for this article.

A major gene hypothesis for heparin releasable plasma lipoprotein lipase (PH-LPL) activity was assessed using segregation analyses of data on 495 members in 98 normolipidemic sedentary families of Caucasian descent who participated in the HERITAGE Family Study. Segregation analyses were performed on PH-LPL adjusted for age, and on PH-LPL activity adjusted for age and fasting insulin. Prior to adjustment for insulin, neither a major gene effect nor a multifactorial component could be rejected, and support for a major gene was equivocal i.e. neither the Mendelian transmission nor the no transmission (equal τs) models were rejected. However, after adjusting for the effects of insulin, a major gene effect on PH-LPL activity was unambiguous. The putative locus accounted for 60% of the total phenotypic variance, and the homozygous recessive form affected 10% (q 2)of the sample (i.e. gene frequency (q)=0.31), and led to a low PH-LPL value. The lack of a significant multifactorial effect suggested that the familial etiology of PH-LPL activity adjusted for insulin was likely to be primarily a function of the major locus. In conclusion, the present study is the first to report segregation analyses on PH-LPL activity prior to and after adjusting for insulin, and suggests that there is an indication of a pleiotropic genetic effect on PH-LPL activity and insulin, in addition to a major gene effect on PH-LPL activity alone.

Abdominal obesity is associated with numerous metabolic alterations, such as hypertriglyceridemia and low levels of high density lipoprotein (HDL) cholesterol. However, compared with abdominally obese white individuals, abdominally obese black individuals have been characterized by higher plasma HDL cholesterol levels, suggesting that the impact of abdominal fat accumulation on the lipoprotein-lipid profile may differ among ethnic groups. Therefore, we have compared the associations between body fatness, visceral adipose tissue (AT) accumulation, and metabolic risk variables in a sample of 247 white men and 240 white women versus a sample of 93 black men and 143 black women. Although no difference in mean total body fatness was found between the 2 race groups, white men had higher levels of visceral AT than did black men (P<0.001). Despite the fact that black women had a greater body fat content than did white women, black women had levels of visceral AT that were similar to those of white women, suggesting a lower susceptibility to visceral obesity in black women. This lower accumulation of visceral AT in blacks was accompanied by significantly reduced apolipoprotein B concentrations and ratios of total cholesterol to HDL cholesterol as well as higher plasma HDL cholesterol levels (P<0.05) compared with those values in whites. Irrespective of sex, higher postheparin plasma hepatic lipase (HL) and lower lipoprotein lipase (LPL) activities were found in whites, resulting in an HL/LPL ratio that was twice as high in whites as in blacks (P<0.005). Although differences in lipoprotein-lipid levels were noted between whites and blacks, results from multiple regression analyses revealed that after control for morphometric and metabolic variables of the study (body fat mass, visceral AT, LPL, HL, and age), ethnicity had, per se, only a minor contribution to the variance in plasma lipoprotein levels. Thus, our results suggest that the higher plasma HDL cholesterol levels and the generally more cardioprotective plasma lipoprotein profile found in abdominally obese black versus white individuals are explained, at least to a certain extent, by a lower visceral AT deposition and a higher plasma LPL activity in black individuals.

Recent data suggest that hyperinsulinemia with euglycemia may favor the restoration of energy balance when one gains body weight. To test the validity of this concept in humans, the data of 24 young men who had been exposed to a 353-MJ overfeeding protocol for 100 d and who were remeasured after a 4-mo follow-up were analyzed. The sample was subdivided in two groups on the basis of the overfeeding-induced change in postprandial plasma insulin. The increase in postprandial energy expenditure induced by overfeeding was significantly greater in high than in low postprandial insulin responders (P < 0.05) but not after body fat gain was controlled for. After the overfeeding protocol, the loss of subcutaneous adiposity was greater in high than in low postprandial insulin responders. However, this difference was no more significant after the gain in fat mass was controlled for. There was no difference between the two groups in post-overfeeding loss of body weight, fat mass, or fat-free mass. These results partly agree with the idea that hyperinsulinemia resulting from a long-term positive energy balance and its associated fat gain exert a regulatory role promoting the restoration of energy balance.

The relationships between habitual physical activity and fitness parameters and fasting serum high density lipoprotein cholesterol (HDL-C), total cholesterol (TC), and triglycerides (TG) were assessed in 357 men aged 30–59 years (mean 44, SD 5). A progressive submaximal power output test (PWC150), a 1-min sit-up test, and a 3-day activity energy expenditure record were obtained for each subject. HDL-C, TG, and HDL-C/TC were significantly associated with the fitness indices (PWC150 and sit-ups), but not with the mean daily energy expenditure computed from a 3-day activity record. However, when the subjects were stratified according to the maximal level of intensity reported in the work and leisure energy expenditure record, a relationship between maximal exercise or work intensity and the concentration of HDL-C and TG, and the ratio HDL-C/TC was found. When adjusted by multiple regression procedures for age, alcohol consumption, cigarette smoking, socio-economic status, fatness level, and TC, or TG, or HDL-C, as appropriate, these relationships became nonsignificant, with the exception of TG and PWC150. These results suggest that habitual physical activity of light intensities is not a major determinant of HDL-C, TC, and HDL-C/TC; it could, however, have a small but significant role in TG. In addition, data suggest that periods of exercise of higher intensity, i.e. with an energy cost of about 6 mets and more, could be a sensible mean to influence serum blood lipid levels.

Objective. To derive optimal body mass index (BMI) and waist circumference thresholds for children and adolescents, to predict risk factor clustering. Design. Cross-sectional receiver operating characteristic curve analysis. Setting. The Bogalusa Heart Study, a community-based study of cardiovascular disease risk factors in early life. Participants. A total of 2597 black and white children and adolescents, 5 to 18 years of age, who were examined between 1992 and 1994. Main Outcome Measures. The presence or absence of ≥3 age-adjusted risk factors (low high-density lipoprotein cholesterol level, high low-density lipoprotein cholesterol level, high triglyceride level, high glucose level, high insulin level, and high blood pressure) was predicted from age-adjusted BMI and waist circumference values. Results. The areas under the receiver operating characteristic curves were significantly different from 0.5 for both BMI and waist circumference for all gender/race groups, ranging from 0.73 to 0.82. The optimal BMI thresholds were at the 53rd and 50th percentiles for white and black male subjects, respectively, and at the 57th and 51st percentiles for white and black female subjects, respectively. Similarly, the optimal waist circumference thresholds were at the 56th and 50th percentiles for white and black male subjects, respectively, and at the 57th and 52nd percentiles for white and black female subjects, respectively. The sensitivity and specificity at the thresholds were similar for all gender/race groups, ranging from 67% to 75%. Conclusions. The use of BMI and waist circumference for the prediction of risk factor clustering among children and adolescents has significant clinical utility. In this sample, race and gender differences in the optimal thresholds were minimal.

Physical activity and molecular ageing presumably interact to precipitate musculoskeletal decline in humans with age. Herein, we have delineated molecular networks for these two major components of sarcopenic risk using multiple independent clinical cohorts. We generated genome-wide transcript profiles from individuals (n = 44) who then undertook 20 weeks of supervised resistance-exercise training (RET). Expectedly, our subjects exhibited a marked range of hypertrophic responses (3% to +28%), and when applying Ingenuity Pathway Analysis (IPA) up-stream analysis to ∼580 genes that co-varied with gain in lean mass, we identified rapamycin (mTOR) signaling associating with growth (P = 1.4×10−30). Paradoxically, those displaying most hypertrophy exhibited an inhibited mTOR activation signature, including the striking down-regulation of 70 rRNAs. Differential analysis found networks mimicking developmental processes (activated all-trans-retinoic acid (ATRA, Z-score = 4.5; P = 6×10−13) and inhibited aryl-hydrocarbon receptor signaling (AhR, Z-score = −2.3; P = 3×10−7)) with RET. Intriguingly, as ATRA and AhR gene-sets were also a feature of endurance exercise training (EET), they appear to represent "generic" physical activity responsive gene-networks. For age, we found that differential gene-expression methods do not produce consistent molecular differences between young versus old individuals. Instead, utilizing two independent cohorts (n = 45 and n = 52), with a continuum of subject ages (18–78 y), the first reproducible set of age-related transcripts in human muscle was identified. This analysis identified ∼500 genes highly enriched in post-transcriptional processes (P = 1×10−6) and with negligible links to the aforementioned generic exercise regulated gene-sets and some overlap with ribosomal genes. The RNA signatures from multiple compounds all targeting serotonin, DNA topoisomerase antagonism, and RXR activation were significantly related to the muscle age-related genes. Finally, a number of specific chromosomal loci, including 1q12 and 13q21, contributed by more than chance to the age-related gene list (P = 0.01–0.005), implying possible epigenetic events. We conclude that human muscle age-related molecular processes appear distinct from the processes regulated by those of physical activity.

A genome-wide linkage scan was performed for genes affecting submaximal exercise cardiac output (Q) and stroke volume (SV) in the sedentary state and their responses to a standardized 20-wk endurance training program. A total of 509 polymorphic markers were used, and 328 pairs of siblings from 99 white nuclear families and 102 sibling pairs from 105 black family units were available. Q and SV were measured in relative steady state during exercise at 50 W (Q50 and SV50, respectively). Baseline phenotypes were adjusted for age, sex, and body surface area (BSA), and the training responses (post-training − baseline, Δ) were adjusted for age, sex, baseline BSA, and baseline value of the phenotype. Three analytical strategies were used: a multipoint variance components linkage analysis using all the family data, and regression-based single- and multipoint linkage analyses using pairs of siblings. In whites, baseline SV50 and ΔSV50 showed promising linkages ( P &lt; 0.0023) with markers on chromosomes 14q31.1 and 10p11.2, respectively. Suggestive evidence of linkage (0.01 &gt; P &gt; 0.0023) for ΔSV50 and Δ Q50 was detected on chromosome 2q31.1 and for baseline SV50 and Q50 on chromosome 9q32-q33. In blacks, markers on 18q11.2 showed promising linkages with baseline Q50. Suggestive evidence of linkage was found in three regions for baseline SV50 (1p21.3, 3q13.3, 12q13.2) and one for baseline SV50 and Q50 (10p14). All these chromosomal regions include several potential candidate genes and therefore warrant further studies in the HERITAGE cohort and other studies.