Immature Ixodes scapularis infestation and Borrelia burgdorferi infection of wild small mammals were studied from June to October in 2007 and from May to October in 2008 at 71 study sites in a zone where I. scapularis populations and environmental Lyme disease risk are emerging in southwestern Quebec. Seasonal host-seeking activity of immature I. scapularis was similar to patterns reported previously in Canada and the USA: nymphal activity peaked in spring while larval activity peaked in late summer. Synchronous activity of nymphs with some larvae was observed in late spring, which could favour establishment of B. burgdorferi strains that cause short-lived infections in their hosts. White-footed mice (Peromyscus leucopus), deer mice (P. maniculatus), chipmunks (Tamias striatus), and red squirrels (Tamiasciurus hudsonicus) carried 92.0% of the larvae and 94.2% of the nymphs collected. Adult male white-footed mice carried significantly larger numbers of both larval and nymphal I. scapularis than other species and classes of small mammals (different demographic groups or physiological status: age, sex, sexual activity). We conclude that seasonality and host association were comparable to previous studies in North America, even in the context of a newly endemic pattern of low infection prevalence and low densities of host-seeking and feeding I. scapularis in southwestern Quebec. Our studies suggest that B. burgdorferi transmission cycles are focused on adult male mice (which carried 35% of all feeding ticks collected in the study), so control methods targeting this class of hosts may be particularly effective. However, our study also suggested that habitats containing a diverse host structure may dilute transmission cycles by partitioning of nymphal and larval ticks on different host species.
The role of the genotype in the response to short-term overfeeding was assessed by submitted six pairs of male monozygotic twins to a 4.2 MJ (1000 kcal) per day energy intake surplus for a period of 22 consecutive days. Individual differences in fat mass and fat-free mass gains were observed in response to overfeeding but they were not randomly distributed. Indeed, the within-pair resemblance in the response was striking when compared to the heterogeneity found among the pairs in adiposity and fat-free mass gains. The intrapair resemblance in the response to overfeeding as assessed by the intraclass coefficient computed with the individual changes, reached 0.88 for total fat mass and 0.76 for fat-free mass. A similar trend for a genetically determined pattern of adaptation to overfeeding was observed for resting metabolic rate (intraclass = 0.63), thermic effect of a meal (intraclass = 0.62), and energy cost of submaximal exercise (intraclass = 0.78) when the data were analysed in terms of changes in oxygen uptake. On the other hand, no major alterations in glucose and insulin response to a glucose load or a test meal, in cardio-pulmonary adaptation to submaximal exercise and in maximal exercise tolerance were found with overfeeding. In contrast, the response of suprailiac fat cell lipolysis (intraclass of about 0.7) and heparin releasable adipose tissue lipoprotein lipase (intraclass - 0.82) varied among individuals but was highly homogeneous within genotypes. Similarly, a genotype-overfeeding interaction effect was seen for serum triglycerides (intraclass = 0.69), HDL-cholesterol (intraclass = 0.85), and the HDL-cholesterol to total cholesterol ratio (intraclass = 0.82). Multiple correlation analyses suggest that much of the variance in the response of fat mass (R = 0.65) and fat-free mass (R = 0.81) is accounted for by alterations in the energy expenditure components assessed in the study. If one takes into account the measurement errors always present in such complex studies and the fact that only a limited fraction of the energy expenditure of activity was considered by design, one can conclude that the genotype determines to a large extent the response variation to short-term overfeeding. In particular, the genotype-overfeeding interaction effect for body composition changes seems to be mediated by the various energy expenditure components, themselves characterized by significant genotype-overfeeding interaction effects.(ABSTRACT TRUNCATED AT 400 WORDS)
Des progrès considérables ont été accomplis au cours des dix dernières années dans la compréhension des bases génétiques de l’obésité et des complications métaboliques qui lui sont associées. Il est maintenant bien établi que les différentes formes d’obésité constituent des états ayant tendance à se concentrer dans les familles et que les ressemblances familiales qu’on observe sont en partie déterminées par les gènes. Le nombre de gènes potentiellement impliqués dans le développement de l’obésité ne cesse de croître. Cet article fait le point sur le rôle de l’hérédité dans l’obésité et sur les gènes et locus qui ont, à ce jour, été associés à l’obésité au sein de l’étude des familles de Québec.
Nine pairs of monozygotic twins of both sexes were submitted to a 20 week endurance training program, five times per week, 40 min per session, at an average of 80% of maximal heart rate reserve. Testing and training were performed on cycle ergometers. ˙VO2max was measured before (T1) and after (T4) the training program, as well as at the 7th (T2) and 14th (T3) week. Training significantly (p<0.01) increased ˙VO2max (Mean± SD; T1:2.6 ± 0.7; T2: 2.8 ± 0.7; T3: 2.8 ± 0.8 and T4: 3.0 ± 0.7 L·min-1). The time course of˙VO2max response to training is shown in thetable. Average increases in ˙VO2max reached 0.13, 0.31 0.42 after 7, 14 and 20 weeks of training, respectively. However, these changes were not randomly distributed among pairs, as about 2 to 6 times(F ratio) more variance was found between pairs than within pairs in the˙VO2max response to training. The intraclass correlations quantifying the intrapair resemblance in the response to training reached 0.31(p=.20) for the changes observed after 7 and 14 weeks of training and 0.71(p=.008) after 20 weeks. These results indicate that the response of˙VO2max to endurance training is genotype dependent and that this genotype-training interaction effect increases with the duration of training.
Skeletal muscle fiber type distribution is quite heterogeneous, with about 25% of North American Caucasian men and women having either less than 35% or more than 65% of type I fiber in their vastus lateralis muscle. To what extent human skeletal muscle fiber type proportion is under the control of genetic factors is examined in this paper. The results summarized here suggest that about 15% of the total variance in the proportion of type I muscle fibers in human is explained by the error component related to muscle sampling and technical variance, that about 40% of the phenotype variance is influenced by environmental factors, and the remaining variance (about 45%) is associated with inherited factors. These estimates suggest that a difference of about 30% in type I fibers among individuals could be explained exclusively by differences in the local environment and level of muscular contractile activity. However, unidentified genetic factors would have to be invoked to account for the observation that the skeletal muscle of about 25% of the North American Caucasian population have either less than 35% or more than 65% of type I fibers.—Simoneau, J.-A., Bouchard, C. Genetic determinism of fiber type pro-portion in human skeletal muscle. FASEB J. 9, 1091-1095 (1995)
0063 The intensity guidelines for prescribing aerobic exercise were recently revised by ACSM to use %VO2reserve (%VO2R) rather than %VO2max. PURPOSE: The current study investigated the relationship of %VO2max and %VO2R with %Heart Rate Reserve (%HRR) in 630 initially sedentary individuals (ages 17 to 65). METHODS: Each participant completed 2 graded cycle tests to exhaustion before and after 20 weeks of training. VO2 and HR data were collected at the end of each stage. Resting HR and estimated resting VO2 (3.5 ml•kg−1•min−1) were additionally used to determine linear regressions of %HRR vs. %VO2max and %HRR vs. %VO2R. Slope and intercept were determined pre- and post-training for the total cohort and for subjects grouped by gender, race, age and baseline fitness (VO2max). RESULTS: Overall, and in all sub-groups, both pre- and post-training, the slope and intercepts were significantly different from 1.0 and 0, respectively for both %HRR vs. %VO2max and %HRR vs. %VO2R. However, the slopes and intercepts for %HRR vs. %VO2max were closer to the line of unity than were the slopes and intercepts of %HRR vs. %VO2R (p< 0.01 to 0.0001). More importantly, the calculated HR values for %HRR vs. %VO2max were closer (p<0.001) at 50% (+0.4±2.2 bpm) and 85% (+3.8 ± 3.2) than the values for %HRR vs. % VO2R at 50% (+8.2 ± 2.6 bpm) and 85% (+6.6 ± 3.4 bpm). Posttraining data differences were similar, though of smaller magnitude, with HR values at 50 and 85% VO2max more similar (p<0.01) to %HRR than were %VO2R HR values to %HRR. CONCLUSION: These results differ from those of Swain et al. who studied young adults during treadmill (n = 50) and cycle (n = 57) testing. Since %VO2R is a more difficult calculation than %VO2max and is less understood and since the differences in HR values within the normal aerobic training range were significantly closer using %VO2max, %VO2max is the better measure for prescribing exercise intensity. Supported by multiple grants from NIH/NHLBI.
