Development of Surface-Coated Polylactic Acid/Polyhydroxyalkanoate (PLA/PHA) Nanocomposites.

This work reports on the design and development of nanocomposites based on a polymeric matrix containing biodegradable Polylactic Acid (PLA) and Polyhydroxyalkanoate (PHA) coated with either Graphite NanoPlatelets (GNP) or silver nanoparticles (AgNP). Nanocomposites were obtained by mechanical mixing under mild conditions and low load contents (<0.10 wt %). This favours physical adhesion of the additives onto the polymer surface, while the polymeric bulk matrix remains unaffected. Nanocomposite characterisation was performed via optical and focused ion beam microscopy, proving these nanocomposites are selectively modified only on the surface, leaving bulk polymer unaffected. Processability of these materials was proven by the fabrication of samples via injection moulding and mechanical characterisation. Nanocomposites showed enhanced Young modulus and yield strength, as well as better thermal properties when compared with the unmodified polymer. In the case of AgNP coated nanocomposites, the surface was found to be optically active, as observed in the increase of the resolution of Raman spectra, acquired at least 10 times, proving these nanocomposites are promising candidates as surface enhanced Raman spectroscopy (SERS) substrates.

Honeycomb Films with Core-Shell Dispersed Phases Prepared by the Combination of Breath Figures and Phase Separation Process of Ternary Blends.

Herein, we propose a strategy to fabricate core-shell microstructures ordered in hexagonal arrays by combining the breath figures approach and phase separation of immiscible ternary blends. This simple strategy to fabricate these structures involves only the solvent casting of a ternary polymer blend under moist atmosphere, which provides a facile and low-cost fabrication method to obtain the porous structures with a core-shell morphology. For this purpose, blends consisting of polystyrene (PS) as a major component and PS40-b-P(PEGMA300)48 amphiphilic copolymer and polydimethylsiloxane (PDMS) as minor components were dissolved in tetrahydrofuran and cast onto glass wafers under humid conditions, 70% of relative humidity. The resulting porous morphologies were characterized by optical and confocal Raman microscopy. In particular, confocal Raman results demonstrated the formation of core-shell morphologies into the ordered pores, in which the PS forms the continuous matrix, whereas the other two phases are located into the cavities (PDMS is the core while the amphiphilic copolymer is the shell). Besides, by controlling the weight ratio of the polymer blends, the structural parameters of the porous structure such as pore diameter and the size of the core can be effectively tuned.

Immobilization of Stimuli-Responsive Nanogels onto Honeycomb Porous Surfaces and Controlled Release of Proteins.

In this article, we describe the formation of functional honeycomb-like porous surfaces fabricated by the breath figures technique using blends of either amino-terminated poly(styrene) or a poly(styrene)-b-poly(acrylic acid) block copolymer with homopoly(styrene). Thus, the porous interfaces exhibited either amino or acid groups selectively located inside of the holes, which were subsequently employed to anchor stimuli-responsive nanogels by electrostatic interactions. These nanogels were prepared from poly(N-isopropylacrylamide) (PNIPAM) cross-linked with dendritic polyglycerol (dPG) and semi-interpenetrated with either 2-(dimethylamino)ethyl methacrylate (DMAEMA) or 2-acrylamido-2-methyl-1-propanesulfonic acid (AMPS) to produce positively and negatively charged nanogel surfaces, respectively. The immobilization of these semi-interpenetrated networks onto the surfaces allowed us to have unique stimuli-responsive surfaces with both controlled topography and composition. More interestingly, the surfaces exhibited stimuli-responsive behavior by variations on the pH or temperature. Finally, the surfaces were evaluated regarding their capacity to induce a thermally triggered protein release at temperatures above the cloud point temperature (T(cp)) of the nanogels.

Enzymatic Catalysis Combining the Breath Figures and Layer-by-Layer Techniques: Toward the Design of Microreactors.

Herein, we report the fabrication of microstructured porous surfaces with controlled enzymatic activity by combining the breath figures and the layer-by-layer techniques. Two different types of porous surfaces were designed based on fluorinated and carboxylated copolymers in combination with PS, using poly(2,3,4,5,6-pentafluorostyrene)-b-polystyrene (PS5F31-b-PS21) and polystyrene-b-poly(acrylic acid) (PS19-b-PAA10) block copolymers, respectively. For comparative purposes, flat surfaces having similar chemistry were obtained by spin-coating. Poly(sodium 4-styrenesulfonate)/poly(allylamine hydrochloride) (PSS/PAH) multilayers incorporating alkaline phosphatase (ALP) were built on these porous surfaces to localize the enzyme both inside and outside of the pores using PS/PS5F31-b-PS21 surfaces and only inside the pores on PS/PS19-b-PAA10 surfaces. A higher catalytic activity of ALP (about three times) was obtained with porous surfaces compared to the flat ones. The catalysis happens specifically inside the holes of PS/PS19-b-PAA10surfaces, where ALP is located. This opens the route for applications in microreactors.

Dendritic amphiphiles as additives for honeycomb-like patterned surfaces by breath figures: role of the molecular characteristics on the pore morphology.

The current study presents a library of honeycomb-like patterned surfaces developed from a variety of different water-soluble amphiphilic dendrons. When compared to commercial surfactants, the dendrons produce a wide variety of porous surfaces due to their well-defined branched structure. Different functionalities and generations of dendrons have been studied. A singular hierarchical distribution of the dendrons, forming small nanoparticles (micelles) only at the inner edges of the holes (coffee stain effect) is observed. Once the surfaces are fabricated, these dendrons can be easily recovered via simple aqueous washing. After this treatment, the surfaces exhibit a high hydrophobic character (up to 140°) due to the high porosity. This behavior can be described by the Cassie-Baxter model.

Measured maximal heart rates compared to commonly used age-based prediction equations in the Heritage Family Study.

OBJECTIVE: The purpose of this study was to examine how well two commonly used age-based prediction equations for maximal heart rate (HRmax ) estimate the actual HRmax measured in Black and White adults from the HERITAGE Family Study. METHODS: A total of 762 sedentary subjects (39% Black, 57% Females) from HERITAGE were included. HRmax was measured during maximal exercise tests using cycle ergometers. Age-based HRmax was predicted using the Fox (220-age) and Tanaka (208 - 0.7 × age) formulas. RESULTS: The standard error of estimate (SEE) of predicted HRmax was 12.4 and 11.4 bpm for the Fox and Tanaka formulas, respectively, indicating a wide-spread of measured-HRmax values are compared to their age-predicted values. The SEE (shown as Fox/Tanaka) was higher in Blacks (14.4/13.1 bpm) and Males (12.6/11.7 bpm) compared to Whites (11.0/10.2 bpm) and Females (12.3/11.2 bpm) for both formulas. The SEE was higher in subjects above the BMI median (12.8/11.9 bpm) and below the fitness median (13.4/12.4 bpm) when compared to those below the BMI median (12.2/11.0 bpm) and above the fitness median (11.4/10.3) for both formulas. CONCLUSION: Our findings show that based on the SEE, the prevailing age-based estimated HRmax equations do not precisely predict an individual's measured-HRmax .

Psoriasis and physical activity: a review.

Psoriasis is a common, chronic inflammatory skin disease that can cause significant discomfort and impairment to quality of life. Recent research indicates that individuals with moderate-to-severe psoriasis are likely at greater risk for chronic cardiometabolic co-morbidities such as cardiovascular disease, type 2 diabetes, obesity and metabolic syndrome. Physical activity can be an effective primary and adjunctive treatment for these maladies in other populations. Unfortunately, only a limited number of studies have examined physical activity in psoriasis, which are limited by poor design and lack of validated physical activity assessment methodologies. A variety of data suggest shared physiologic pathways between physical activity, psoriasis, and psoriasis cardiometabolic co-morbidities. Increased adiposity, inflammation, oxidative stress, adhesion molecules and lipids are physiologically linked to psoriasis, the risk of psoriasis cardiometabolic co-morbidities, and low levels of physical activity. In addition, epigenetic pathways are involved in psoriasis and could be influenced by physical activity. The physical and psychosocial impairments common in psoriasis may make it difficult to participate in regular physical activity, and future studies should aim to determine if physical activity interventions improve functioning and reduce co-morbidities in psoriasis.

Variations in the four and a half LIM domains 1 gene (FHL1) are associated with fasting insulin and insulin sensitivity responses to regular exercise.

AIMS/HYPOTHESIS: The expression of the four and a half LIM domains 1 gene (FHL1) is increased in the muscle of individuals who show an improvement in insulin sensitivity index (S(I)) after 20 weeks of exercise training. The aim of the present study was to investigate associations between three FHL1 single nucleotide polymorphisms (SNPs) and variables derived from an IVGTT, both in the sedentary state and in response to exercise training, in participants in the HERITAGE Family Study. MATERIALS AND METHODS: SNPs were typed using fluorescence polarisation methodology. Analyses were performed separately by sex and in black and white individuals. RESULTS: In black participants, no associations were found with any of the SNPs. In white women (n = 207), SNP rs9018 was associated with the disposition index (D(I)), which is calculated as S(I) generated from the MINMOD program (x10(-4) min(-1)[microU/ml](-1)) multiplied by acute insulin response to glucose (AIR(g); pmol/l x 10 min), and the glucose disappearance index (K(g)) training responses (p = 0.016 and p = 0.008, respectively). In white men (n = 222), all SNPs were associated with fasting glucose levels (p < or = 0.05) and SNP rs2180062 with the insulin sensitivity index (S(I)) (p = 0.04) in the sedentary state. Two SNPs were associated with fasting insulin training response. Fasting insulin decreased to a greater extent in carriers of the rs2180062 C allele (p = 0.01) and rs9018 T allele (p = 0.04). With exercise training, S(I) (x10(-4) min(-1)[microU/ml](-1): 0.68 +/- 0.20 vs -0.77 +/- 0.44, p = 0.046), D(I) (319 +/- 123 vs -528 +/- 260, p = 0.006) and K(g) (per 100 min: 0.09 +/- 0.04 vs -0.14 +/- 0.8, p = 0.03) improved more in the C allele carriers at rs2180062 than in the T allele carriers. CONCLUSIONS/INTERPRETATION: Fasting insulin and S(I) responses to exercise training were associated with DNA sequence variation in FHL1 in white men. Whether these associations exist only in white men remains to be investigated.

Changes in inflammatory biomarkers following one-year of moderate resistance training in overweight women.

BACKGROUND: Overweight individuals commonly demonstrate elevated levels of inflammatory and cell adhesion molecules. Elevated levels of inflammation and adhesion have been implicated in the pathogenesis of cardiovascular disease. Aerobic exercise has been shown to be effective in altering specific biomarkers of inflammation and cell adhesion; however, little is known regarding the effects of resistance training (RT) on these biomarkers. This study examined the effects of 1 year of moderate-intensity RT on biomarkers of inflammation and adhesion in healthy, overweight women. METHODS AND RESULTS: Participants included 28 (12 control, 16 RT) overweight (body mass index>or=25 kg/m2) women, aged 25-44 years, studied before and after 1 year of RT. C-reactive protein (CRP), interleukin-6 (IL-6), adiponectin, intracellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin were measured by standard enzyme-linked immunosorbent assays. Body composition, blood pressure, fasting blood lipids, glucose and insulin also were assessed. There were no significant changes in blood pressure, fasting blood lipids, glucose or insulin levels in either group after 1 year. There was also no change in body mass or fat mass in either group; however, there was a significant increase in lean body mass (P<0.05) in the RT group. Both CRP (P<0.01) and adiponectin (P<0.01) demonstrated significant improvements in the RT group, with no change in IL-6. Conversely, there were no associated changes in the biomarkers of cell adhesion in either group. CONCLUSIONS: This study demonstrates that moderate-intensity RT significantly results in modest improvements of inflammatory markers without affecting cell adhesion molecules in overweight women.

Scaling submaximal exercise cardiac output and stroke volume: the HERITAGE Family Study.

This study investigated different methods of scaling submaximal cardiac output (Q) and stroke volume (SV) to best normalize for body size (body surface area [BSA], height [Ht], weight [Wt], and fat-free mass [FFM]). Q and SV were measured at both an absolute (50 W) and a relative power output (60 % of VO2max) in 337 men and 422 women, 17 to 65 years of age. Traditional ratio scaling was examined in addition to allometric scaling, where scaling exponents ( B) were determined for each body size variable (x) that best normalized the physiological outcome variables (y) for body size (y = ax(b)). With ratio scaling, regardless of the body size variable (x = BSA, Ht, Wt, FFM), there was no evidence of a linear relationship between x and y (y = Q or SV). A linear relationship is a necessary condition for appropriate normalization. Further, when ratio-scaled variables (e.g., Q/BSA) were correlated to the body size variable (e.g., BSA) by which they were scaled, significant (p

Genome-wide scan to identify quantitative trait loci for baseline resting heart rate and its response to endurance exercise training: the HERITAGE Family Study.

Evidence of a genetic component for resting heart rate (RHR) has been found. Quantitative trait loci (QTLs) for baseline RHR have been reported, but not for RHR training response. It is of interest to identify QTLs that may harbor genes influencing RHR variation at baseline and in response to regular exercise training. Here, a multipoint variance components linkage scan using 654 markers was performed to search for QTLs that influence RHR adjusted for several covariates at baseline and in response to 20 weeks of endurance training (post-training minus baseline) in 99 White and 127 Black families in the HERITAGE Family Study. Potentially interesting linkages were revealed on 4 q and 11 p for baseline RHR, and on 1 q and 21 q for RHR training response in Whites. The QTLs on 2 q, 6 q, 7 q, 12 q, 14 q, and 15 q for baseline RHR, and on 3 p, 20 p and 21 q for RHR training response were found in Blacks. Promising linkages (lod scores >or= 1.75, p or= 135/80 mm Hg) subset of 40 White families suggesting a pleiotropic gene for BP and RHR with interactions. In conclusion, among QTLs on 1 q, 2 p, 3 p, 4 q, and 11 p that replicated across subsamples and studies, 11 p is most promising for dense mapping and association studies in HERITAGE and other cohorts.

Evidence of major genes for plasma HDL, LDL cholesterol and triglyceride levels at baseline and in response to 20 weeks of endurance training: the HERITAGE Family Study.

This study assessed major gene effects for baseline HDL-C, LDL-C, TG, and their training responses (post-training minus baseline) in 527 individuals from 99 White families and 326 individuals from 113 Black families in the HERITAGE Family Study. The baseline phenotypes were adjusted for the effects of age and BMI, and the training response phenotypes were adjusted for the effects of age, BMI, and their respective baseline values, within each of the sex-by-generation-by-race groups, prior to genetic analyses. In Whites, we found that LDL-C at baseline and HDL-C training response were under influence of major recessive genes (accounting for 2--30 % of the variance) and multifactorial (polygenic and familial environmental) effects. Interactions of these major genes with sex, age, and BMI were tested, and found to be nonsignificant. In Blacks, we found that baseline HDL-C was influenced by a major dominant gene without a multifactorial component. This major gene effect accounted for 45 % of the variance, and exhibited no significant genotype-specific interactions with age, sex, and BMI. Evidence of major genes for the remaining phenotypes at baseline and in response to endurance training were not found in both races, though some were influenced by major effects that did not follow Mendelian expectations or were with ambiguous transmission from parents to offspring. In summary, major gene effects that influence baseline plasma HDL-C and LDL-C levels as well as changes in HDL-C levels in response to regular exercise were detected in the current study.

Genome-wide linkage scans for prediabetes phenotypes in response to 20 weeks of endurance exercise training in non-diabetic whites and blacks: the HERITAGE Family Study.

AIMS/HYPOTHESIS: Impaired insulin secretion, insulin action, insulin-independent glucose effectiveness, glucose tolerance and the associated abnormalities in insulin and glucose metabolism phenotypes are precursors of type 2 diabetes. Genome-wide multipoint variance component linkage scans were carried out using 654 markers to identify quantitative trait loci for insulin sensitivity, acute insulin response to glucose, disposition index and glucose effectiveness training responses in whites and blacks in the HERITAGE Family Study. METHODS: These phenotypes were obtained from an IVGTT with the minimal model. The distributions of insulin sensitivity, acute insulin response to glucose and disposition index training responses (post-training minus baseline) were approximately normalised using a square-root transformation. All phenotypes were adjusted for the effects of age, BMI and their respective baseline values within sex and generation by race prior to linkage scans. RESULTS: In blacks, a promising linkage with a maximum lod score of 3.1 on 19q (54-62 Mb) for glucose effectiveness training response was found. Six interesting linkages with lod scores of at least 1.0 were found for disposition index training response in whites. They included 1p (30 Mb), 3q (152 Mb), 6p (23-42 Mb), 7q (95-96 Mb), 10p (15 Mb) and 12q (119-126 Mb). CONCLUSIONS/INTERPRETATION: Quantitative trait loci for 20 weeks of endurance exercise training responses in insulin action and glucose metabolism phenotypes were found on chromosome 19q as well as 6p and 7q, with nominal (6p, 7q) but consistent (6p) linkages across the races.

Generalized abdominal visceral fat prediction models for black and white adults aged 17-65 y: the HERITAGE Family Study.

OBJECTIVE: To determine if the relationship between abdominal visceral fat (AVF) and measures of adiposity are different between Black and White subjects and to develop valid field prediction models that accurately identify those individuals with AVF levels associated with high risk for chronic disease. DESIGN: Cross-sectional measurements obtained from 91 Black men, 137 Black women, 227 White men, and 237 White women subjects, ages 17-65 y, who were participants in the HERITAGE Family Study, both at baseline and following 20 weeks of endurance training. MEASUREMENTS: AVF, abdominal subcutaneous fat (ASF), abdominal total fat (ATF), and sagittal diameter (SagD) were measured by computed tomography (CT). Body density was determined by hydrostatic weighing and was used to estimate relative body fat. Arm, waist (WC), and hip circumferences and skinfold thickness measures were taken, and BMI was calculated from weight (kg) and height (m(2)). Since CT abdominal fat variables were skewed, a natural log transformation (Ln) was used to produce a normal distribution. The General Linear Model (GLM) procedure was used to test the relationship between AVF and two different groups of variables-CT and anthropometric. RESULTS: The AVF of White men and women was significantly higher than that of Black men and women, independent of BMI, WHR, WC, and age, and was greater for men than for women. The CT model showed that the combination of SagD, Ln (ASF), age, and race accounted for 84 and 75% of the variance in AVF in men and women, respectively. The anthropometric model provided two valid generalized field AVF prediction equations. The Field-I equation, which included BMI, WHR, age and race, had an r(2) of 0.78 and 0.73 for men and women, respectively. The Field-II equation, which included BMI (women only), WC, age, and race, had an r(2) of 0.78 and 0.72 for men and women, respectively. The field model equations became less accurate as the estimated AVF increased. CONCLUSIONS: (1) At the same age and level of adiposity, Black men and women have less AVF than White men and women. These differences are greater in men than in women. (2) The field regression equations can be generalized to the diverse group of adults studied, both in an untrained and trained state. However, their accuracy decreases with increasing levels of AVF.

Quantitative trait loci for maximal exercise capacity phenotypes and their responses to training in the HERITAGE Family Study.

The purpose of this study was to identify regions of the human genome linked to maximal oxygen uptake (VO2max) and maximal power output (MPO), and their response to a standardized 20-wk endurance-training program in sedentary black and white subjects. A total of 509 polymorphic markers covering the 22 autosomes were used in the genome-wide linkage scan. Baseline phenotypes were adjusted for age, sex, and body mass, whereas the training responses were adjusted for age, sex, and the baseline values. Regression-based single- and multipoint linkage analyses were used. In the sedentary state, a total of 351 and 102 sibling pairs were available for whites and blacks, respectively, and 329 and 90 sibling pairs, respectively, for the training response phenotypes. Baseline VO2max showed promising linkage (P < 0.0023) with 11p15.1 (whites), and suggestive evidence of linkage (0.01 > P > 0.0023) was found on 1p31, 7q32, and 7q36 (blacks). Baseline MPO exhibited promising linkage on 10q23 and suggestive evidence of linkage on 13q33 and 18q11-q12 (whites). VO2max training response yielded promising linkages with markers on 1p31 (blacks) and suggestive on 4q27, 7q34, and 13q12 (whites) and on 16q22 and 20q13.1 (blacks). Training-induced changes in MPO showed promising linkages on 5q23 (whites) and suggestive on 1q21, 4p15.1, and 4p13 (whites) and on 1q22 and 13q11 (blacks). In conclusion, the strongest evidence of linkage was found on chromosomal regions 11p15 and 10q23 for VO2 max and MPO in the sedentary state and on chromosomes 1p31 and 5q23 for their responsiveness to training. These chromosomal regions harbor several candidate genes that deserve further investigation.

Sex differences in the relationships of abdominal fat to cardiovascular disease risk among normal-weight white subjects.

The objectives of this study are to investigate the relationships between abdominal fat and risk factors for cardiovascular disease (CVD) among normal-weight (NW) white subjects and to determine how these relationships differ by sex. NW adults (177 males and 258 females) and overweight adults (133 males and 111 females) from the Québec Family Study and the HERITAGE Family Study were retained for this study. Risk factors included systolic and diastolic blood pressures, low-density lipoprotein and high-density lipoprotein cholesterols, triglycerides, and fasting glucose. Only in NW female adults, abdominal visceral fat (AVF) area assessed by computed tomography was significantly correlated with all risk factors, except for fasting glucose, even after age, study cohort, and fat mass were taken into account. NW female subjects with at least one risk factor had a significantly higher AVF than those without risk factors, although the difference was small. Thus, only NW female adults with more AVF tended to have a more adverse CVD risk factor profile.

Post-heparin lipolytic enzyme activities, sex hormones and sex hormone-binding globulin (SHBG) in men and women: The HERITAGE Family Study.

We tested the hypothesis that androgen, estrogen, and sex hormone-binding globulin (SHBG) levels would be significantly related to post-heparin hepatic lipase (HL) and lipoprotein lipase (LPL) activities in a sample of Caucasian men (n = 233) and women (n = 235) aged 17-64 years from the HERITAGE Family Study. Body composition (hydrostatic weighing), abdominal adipose tissue distribution (computed tomography), plasma lipid-lipoprotein and hormone levels, and post-heparin lipases activities were measured. HL activity was significantly higher in males, whereas LPL activity was higher in women (P < 0.005). In women only, HL activity was positively associated with body fat mass (r = 0.17, P < 0.05) and intra-abdominal adipose tissue area (r = 0.18, P < 0.05). Significant associations were also found between fasting insulin and LPL activity (r = -0.16, P < 0.05 and r = -0.18, P < 0.005) as well as HL activity (r = 0.22, P < 0.005, and r = 0.27, P < 0.0001) in men and women, respectively. A positive association between total testosterone and HL activity was noted in men (r = 0.13, P = 0.05). In women, plasma SHBG levels were negatively associated with HL activity (r = -0.48, P < 0.0001), and statistical adjustment for body fat mass, visceral adipose tissue area, and fasting insulin did not attenuate this correlation. In multivariate analyses with models including adiposity variables and measurements of the hormonal profile, insulin, and testosterone levels were both independent positive predictors of HL activity in men. In women, hormone use was a significant positive predictor, and SHBG level a strong negative predictor of HL activity, independent of plasma estradiol and testosterone concentrations. Fasting insulin was the only significant predictor of LPL activity in men (negative association), whereas menstrual status, fasting insulin (negative associations), and plasma SHBG levels (positive association) were all independent predictors of LPL activity in women. These results suggest that the postulated sensitivity of lipolytic enzymes to androgens and estrogens is reflected by a strong negative association between SHBG levels and HL, and a lower magnitude positive association of this hormonal parameter to LPL activity in women. These associations appear to be independent from concomitant variation in total adiposity or body fat distribution.

Evidence of major genes for exercise heart rate and blood pressure at baseline and in response to 20 weeks of endurance training: the HERITAGE family study.

Major gene effects on exercise heart rate (HR) and blood pressure (BP) measured at 50 W and 80 % maximal oxygen uptake (VO (2)max) were assessed in 99 White families in the HERITAGE Family Study. Exercise HR and BP were measured both before and after 20 weeks of endurance training. The baseline phenotypes were adjusted for the effects of age and BMI, whereas the training responses (post-training minus baseline) were adjusted for the effects of age, BMI and the corresponding baseline values, within four sex-by-generation groups. Baseline exercise HR at 50 W was under the influence of a major recessive gene and a multifactorial component, which accounted for 30 % and 27 % of the variance, respectively. The training response was found to be under the influence of a major dominant gene, which accounted for 27 % of the variance. These significant major gene effects were independent of the effects of cigarette smoking, baseline VO (2)max, and the resting HR levels. No significant interactions were found between genotype and age, sex, or BMI. No major gene effect was found for exercise BP. Instead, we found the baseline exercise BP at 50 W and 80 % VO (2)max and the training response at 50 W were solely influenced by multifactorial effects, which accounted for about 50 %, 40 % and 20 % of the variance, respectively. No familial resemblance was found for training responses in exercise HR or BP at 80 % VO (2)max. Segregation analysis also was carried out for exercise HR in Whites pooled with a small sample of Blacks in HERITAGE. Similar major effects were found, but the transmission from parents to offspring did not follow Mendelian expectations, suggesting sample heterogeneity. In conclusion, submaximal exercise HR at baseline and in response to endurance training was influenced by putative major genes, with no evidence of interactions with sex, age or BMI, in contrast to a multifactorial etiology for exercise BP.

Associations between cardiorespiratory responses to exercise and the C34T AMPD1 gene polymorphism in the HERITAGE Family Study.

The associations of the C34T polymorphism of the adenosine monophosphate deaminase 1 (AMPD1) gene with cardiorespiratory phenotypes were tested during cycling exercise at absolute and relative power outputs progressing to exhaustion before and after endurance training for 20 wk in the HERITAGE Family Study cohort (n = 779). Since no blacks were mutant homozygotes (TT), only whites were considered for analysis (400 normal homozygotes, CC; 97 heterozygotes, CT; and 6 TT). For sedentary state, cycling at the absolute power output of 50 W resulted in a higher rating of perceived exertion in TT (P < 0.0001). At the relative intensity of 60% of Vo(2 max), stroke volume was lower in TT (P < 0.05). Maximal values for power output, systolic blood pressure, heart rate, Vco(2), and respiratory exchange ratio were lower in TT (P < 0.05). The cardiorespiratory training response at 50 W and at 60% of Vo(2 max) was similar across C34T-AMPD1 genotypes. However, the maximal values for ventilation, Vo(2), and Vco(2) during exercise increased less in TT (P < 0.01). The results indicate that subjects with the TT genotype at the C34T AMPD1 gene have diminished exercise capacity and cardiorespiratory responses to exercise in the sedentary state. Furthermore, the training response of ventilatory phenotypes during maximal exercise is more limited in TT.

Strength training for obesity prevention in midlife women.

OBJECTIVE: The primary goal of this study was to assess whether increases in fat-free mass (FFM) and decreases in total and percentage fat mass from 15 weeks of twice weekly supervised strength training would be maintained over 6 months of unsupervised exercise in a randomized controlled trial. DESIGN: In all, 60 women aged 30-50 y, body mass index between 20 and 35 kg/m(2), were randomized to control or treatment groups. The treatment group performed twice-weekly supervised strength training followed by 6 months of unsupervised training. Measurements at baseline, 15, and 39 weeks included body weight and body composition by dual-energy X-ray absorptiometry. Repeated measures regression was used to assess between-group differences for changes over time. RESULTS: Almost 90% of prescribed exercise sessions were completed. The body composition treatment effects over 15 weeks were largely maintained over 6 months of unsupervised exercise. Over the total 39 weeks of strength training, the treatment group gained +0.89 kg more in FFM, lost -0.98 kg more in fat mass, and lost -1.63% more in percent body fat when compared to the control group. P-values for these between-group differences in 39-week changes were 0.009, 0.06, and 0.006, respectively. Strength training did not result in any significant weight loss or waist circumference attenuation. Adjustment for changes in energy intake and physical activity did not alter these results. CONCLUSIONS: Twice-weekly strength training is behaviorally feasible for busy midlife women and the favorable body composition changes resulting from supervised strength training can be maintained over time. These findings lay the groundwork for determining the long-term health benefits of this behaviorally feasible exercise prescription, potentially including prevention of age-associated fat gains.