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Haischer, MH, Cooke, DM, Carzoli, JP, Johnson, TK, Shipherd, AM, Zoeller, RF, Whitehurst, M, and Zourdos, MC. Impact of cognitive measures and sleep on acute squat strength performance and perceptual responses among well-trained men and women. J Strength Cond Res 35(2S): S16-S22, 2021-This study assessed the efficacy of currently used assessments for sleep, anxiety, and stress in predicting 1-repetition maximum (1RM) back squat performance. Fifty-three men (age, 23 ± 3 years; body mass, 86.67 ± 13.93 kg; training age, 6.0 ± 2.5 years; 1RM = 163.5 ± 39.5 kg) and 15 women (age, 21 ± 1.5 years; body mass, 63.34 ± 9.6 kg; training age, 4 ± 1.5 years; 1RM = 81.5 ± 12.5 kg) participated. Subjects completed the Daily Analysis of Life Demands for Athletes (DALDA), the revised Competitive State Anxiety Inventory-2 (CSAI-2R), and Oviedo Sleep Questionnaire (OSQ) to evaluate stress, anxiety, and sleep, respectively. Subjects then completed the perceived self-efficacy (PSE) scale, to predict what loads they were 100, 75, and 50% confident that they could lift for a 1RM; then completed 1RM testing with rating of perceived exertion (RPE) and average concentric velocity (ACV) obtained on each attempt. The performance-dependent variable was calculated by subtracting the PSE responses from the actual 1RM (1RM-PSE difference). Bootstrapping with 1,000 replicate samples was used with linear regression to increased robustness of the statistical analyses, and 95% confidence intervals (CIs) were calculated. Hours of sleep was an inverse predictor of ACV (p = 0.014; 95% CI = 0.046 to-0.011) and a positive predictor of RPE (p = 0.005; 95% CI = 0.068-0.342). Furthermore, the hypersomnia subscale of the OSQ was a negative predictor of 1RM-PSE difference at 50% confidence (p = 0.028; 95% CI = -3.507 to -0.528), and CSAI-2R total score was a negative predictor of RPE at 1RM (p = 0.043; 95% CI = -0.041 to -0.003); however, the DALDA did not exhibit any significant relationships. These data highlight the importance of monitoring anxiety and sleep when assessing readiness for maximal strength performance.

This study examined the time course of recovery following resistance exercise sessions in the back squat, bench press, and deadlift. Twelve well-trained males (age: 24.5 ± 3.8 years, body mass: 84.01 ± 15.44 kg, training age: 7.1 ± 4.2 years) performed 4 sets to failure at 80% of a 1-repetition maximum (1RM) on the squat, bench press, and deadlift in successive weeks. The bench press was always performed in week 2 with the squat and deadlift order counterbalanced between weeks 1 and 3. Indirect muscle damage and performance fatigue was assessed immediately before and after exercise and at 24 h, 48 h, 72 h, and 96 h postexercise. Outcome measures included limb swelling, joint range of motion, delayed onset muscle soreness, average concentric velocity (ACV) at 70% of 1RM, creatine kinase, lactate dehydrogenase, and cell-free DNA (cfDNA). Most measures demonstrated a main time effect (p < 0.05) within conditions; however, no between condition (p > 0.05) differences existed. ACV decreased in the squat condition for up to 72 h (p = 0.02, –8.61%) and in the bench press (p < 0.01, –26.69%) immediately postexercise but did not decline during the deadlift condition (p > 0.05). There was a main time effect for increased cfDNA in the squat (p < 0.01) and bench press (p < 0.05), but not the deadlift (p = 0.153). Further, immediately postexercise increases in cfDNA were directly related (p < 0.05) to changes in ACV in all 3 conditions. These results suggest that the deadlift does not result in greater muscle damage and recovery time than the squat and bench press following volume-type training in well-trained men. Further, acute changes in cfDNA may predict performance during the recovery period.

Purpose: To examine the validity of 2 linear position transducers, the Tendo Weightlifting Analyzer System (TWAS) and Open Barbell System (OBS), compared with a criterion device, the Optotrak Certus 3-dimensional motion-capture system (OC3D). Methods: A total of 25 men (age, 25 [3] y; height, 174.0 [6.7] cm; body mass, 89.0 [14.7] kg; squat 1-repetition maximum [1RM], 175.8 [34.7] kg) with ≥2 y of resistance-training experience completed a back 1RM and 1 set to failure at 70% of 1RM. Average concentric velocity (ACV) and peak concentric velocity (PCV) were recorded by all 3 devices during the final warm-up set, all 1RM attempts, and every repetition during the 70% set. Results: In total, 575 samples were obtained. Bland–Altman plots, mountain plots, a 1-way analysis of variance, SEM, and intraclass correlation coefficients were used to analyze validity. The analysis of variance showed no difference (P = .089) between devices for ACV. However, for PCV, TWAS was significantly different (ie, inaccurate) from OC3D (P P = .001), but OBS was similar (P = .412) to OC3D. For ACV, intraclass correlation coefficients were higher for OBS than for TWAS. Bland–Altman plots showed agreement for ACV for both devices against OC3D but large limits of agreement for PCV for both devices. Mountain plots showed valid ACV for both devices, however, but slightly greater ACV and PCV accuracy with OBS than TWAS. Conclusions: Both devices may provide valid ACV measurements, but some metrics suggest more accurate ACV with OBS vs TWAS. For PCV, neither device is particularly accurate; however, OBS seems to be more accurate than TWAS.

Background Interleukin‐15 (IL‐15) is a myokine associated with muscle strength, possibly by attenuating protein breakdown. A variant in the alpha‐receptor (IL‐15Rα 1775 A>C, rs2228059) partially modulates the muscle strength and size response to resistance training. We examined if this polymorphism associated with habitual physical activity among European‐American adults. Methods Men (n = 240, 23.7 ± 0.3 year, body mass index [BMI] 25.3 ± 0.3 kg/m2) and women (n = 292, 23.2 ± 0.3 year, 24.0 ± 0.3 kg/m2) were genotyped. Physical activity phenotypes were derived from the Paffenbarger Physical Activity Questionnaire. Analysis of covariance (ancova) tested log‐transformed differences between the IL‐15Rα genotype and physical activity phenotypes by gender with age and BMI as covariates. Results Men with the IL‐15Rα 1775AA genotype spent more time in light intensity physical activity (39.4 ± 2.4 hr/week) than men with the CC genotype (28.6 ± 2.3 hr/week, (p = .009). Conclusion Further research is needed to confirm our finding and determine the possible mechanisms by which the IL‐15Rα variant modulates light intensity physical activity.

Cooke, DM, Haischer, MH, Carzoli, JP, Bazyler, CD, Johnson, TK, Varieur, R, Zoeller, RF, Whitehurst, M, and Zourdos, MC. Body mass and femur length are inversely related to repetitions performed in the back squat in well-trained lifters. J Strength Cond Res 33(3): 890-895, 2019-The purpose of this research note was to examine whether relationships existed between anthropometrics (body mass, body fat percentage [BF%], and femur length) and descriptive characteristics (age and sex) with repetitions performed to failure at 70% of 1 repetition maximum (1RM) in the back squat. Fifty-eight subjects (males = 43, females = 15; age: 23 ± 3 years, training age: 5.5 ± 2.5 years, body mass: 80.65 ± 16.34 kg, BF%: 10.98 ± 3.53%, and femur length: 47.1 ± 2.6 cm) completed a 1RM squat followed by one set to failure at 70% of 1RM. Total repetitions performed at 70% of 1RM were 14 ± 4 (range: 6-26). Bivariate correlations showed significant inverse relationships between body mass (r = -0.352, p = 0.003), BF% (r = -0.278, p = 0.014), and femur length (r = -0.265, p = 0.019), with repetitions performed. No significant relationships existed between age and sex (p > 0.05), with repetitions performed. All these variables entered into a standard multivariate regression. The model R was 0.200, and body mass had the largest influence (p = 0.057) because relative importance analysis demonstrated body mass to contribute to 43.87% of the variance (of the R) in repetitions performed. No other variable was significant or approached significance (p > 0.05). Our results reveal that body mass, BF%, and femur length all are inversely related to repetitions performed at 70% of 1RM in the back squat.

Background and aim Fibroblast growth factor 21 (FGF21) is positively associated with body mass index, potentially as a compensatory mechanism to mediate obesity related metabolic and inflammatory insult due to chronic low-grade elevations of the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). Therefore, FGF21 response in obese subjects and the associations with increased pro-inflammatory cytokines, insulin resistance, and energy utilization warrants investigation. Methods and results Twenty four untrained subjects (12 obese and 12 normal-weight) performed 30 min of continuous submaximal aerobic exercise. Following exercise, obese subjects exhibited a blunted FGF21 response to exercise compared to normal-weight subjects as indicated by area-under-the-curves "with respect to increase" (AUCi) analyses ( p = 0.005). Furthermore, while exercise-induced plasma FGF21 was not associated with any inflammatory cytokine (IL-6 and TNF-α) response, FGF21 AUCi was positively correlated with glucose AUCi (r = 0.495, p = 0.014), total relative energy expenditure (r = 0.562, p = 0.004), and relative maximal oxygen consumption (VO 2max ; r = 0.646, p = 0.001) in all subjects. Conclusion Impaired cardiorespiratory fitness may influence the sensitivity of FGF21 response to acute exercise in obese individuals, potentially contributing to the attenuated metabolic response (e.g., glucose) and total exercise energy expenditure. Therefore, exercise training aimed at improving cardiorespiratory fitness and/or body composition may augment cardioprotective properties against obesity-associated CVD through enhanced FGF21 flux.

The overarching aim of this study was to compare volume-equated high-repetition daily undulating periodization (DUPHR) versus a low-repetition daily undulating periodization (DUPLR) program for muscle performance. Sixteen college-aged (23 ± 3 years) resistance-trained males were counterbalanced into 2 groups: (i) DUPHR (n = 8), with a weekly training order of 12 repetitions (Day 1), 10 repetitions (Day 2), and 8 repetitions (Day 3); and (ii) DUPLR (n = 8), with a weekly training order of 6 repetitions (Day 1), 4 repetitions (Day 2), and 2 repetitions (Day 3). Both groups trained 3 times/week for 8 weeks on nonconsecutive days, with pre- and post-training testing during weeks 1 and 8. Participants performed only squat and bench press exercises each session. Changes in one-repetition maximum (1RM) strength, muscle thickness (MT), and muscular endurance (ME) were assessed. Both groups significantly increased 1RM strength for both squat and bench press (p < 0.01), and no group differences existed (p > 0.05). Similarly, both groups experienced significant increases in chest, lateral quadriceps distal, and anterior quadriceps MT (p < 0.05), but no change was present in either group for lateral quadriceps mid MT (p < 0.05). No group differences were discovered for changes in MT (p > 0.05). ME did not significantly change in the squat or bench press for either group (p > 0.05); however, for squat ME, a moderate effect size was observed for DUPHR (0.57) versus a trivial effect size for DUPLR (0.17). Our findings suggest that in previously trained males, training volume is a significant contributor to strength and hypertrophy adaptations, which occur independently of specific repetition ranges.

Recently, a genome-wide association study (GWAS) that identified eight single-nucleotide polymorphisms (SNPs) associated with BMI highlighted a possible neuronal influence on the development of obesity. We hypothesized these SNPs would govern the response of BMI and subcutaneous fat to resistance training in young individuals (age = 24 years). We genotyped the eight GWAS-identified SNPs in the article by Willer et al. in a cohort (n = 796) that undertook a 12-week resistance-training program. Females with a copy of the rare allele (C) for rs17782313 (MC4R) had significantly higher BMIs (CC/CT: n = 174; 24.70 ± 0.33 kg/m2, TT: n = 278; 23.41 ± 0.26 kg/m2, P = 0.002), and the SNP explained 1.9% of overall variation in BMI. Males with a copy of the rare allele (T) for rs6548238 (TMEM18) had lower amounts of subcutaneous fat pretraining (CT/TT: n = 65; 156,534 ± 7,415 mm3, CC: n = 136; 177,825 ± 5,139 mm3, P = 0.019) and males with a copy of the rare allele (A) for rs9939609 (FTO) lost a significant amount of subcutaneous fat with exercise (AT/AA: n = 83; −798.35 ± 2,624.30 mm3, TT: n = 47; 9,435.23 ± 3,494.44 mm3, P = 0.021). Females with a copy of the G allele for a missense variant in the SH2B1 (rs7498665) was associated with less change of subcutaneous fat volume with exercise (AG/GG: n = 191; 9,813 ± 2,250 mm3 vs. AA: n = 126; 770 ± 2,772 mm3; P = 0.011). These data support the original finding that there is an association between measures of obesity and a variant near the MC4R gene and extends these results to a younger population and implicates FTO, TMEM18, and SH2B1 polymorphisms in subcutaneous fat regulation.

Emerging data have revealed a negative association between adiposity and muscle quality (MQ). There is a lack of research to examine this interaction among young, healthy individuals, and to evaluate the contribution of adiposity to adaptation after resistance exercise (RE).The purpose of this investigation was to examine the influence of subcutaneous adipose tissue (SAT) on muscle function among non-obese individuals before and after RE.Analyses included 634 non-obese (body mass index30 kg m(-2)) subjects (253 males, 381 females; age=23.3 ± 5.2 years). SAT and muscle mass (magnetic resonance imaging-derived SAT and biceps muscle volume), isometric and dynamic biceps strength, and MQ (strength/muscle volume), were analyzed at baseline and after 12 weeks of unilateral RE.At baseline, SAT was independently associated with lower MQ for males (β=-0.55; P0.01) and females (β=-0.45; P0.01), controlling for body mass and age. Adaptation to RE revealed a significant negative association between SAT and changes for strength capacity (β=-0.13; p=0.03) and MQ (β=-0.14; P0.01) among males. No attenuation was identified among females. Post-intervention SAT remained a negative predictor of MQ for males and females (β=-0.47; P0.01).The findings reveal that SAT is a negative predictor of MQ among non-obese, healthy adults, and that after 12 weeks of progressive RE this association was not ameliorated. Data suggest that SAT exerts a weak, negative influence on the adaptive response to strength and MQ among males.

Baseline muscle size and muscle adaptation to exercise are traits with high variability across individuals. Recent research has implicated several chemokines and their receptors in the pathogenesis of many conditions that are influenced by inflammatory processes, including muscle damage and repair. One specific chemokine, chemokine (C-C motif) ligand 2 (CCL2), is expressed by macrophages and muscle satellite cells, increases expression dramatically following muscle damage, and increases expression further with repeated bouts of exercise, suggesting that CCL2 plays a key role in muscle adaptation. The present study hypothesizes that genetic variations in CCL2 and its receptor ( CCR2) may help explain muscle trait variability. College-aged subjects [ n = 874, Functional Single-Nucleotide Polymorphisms Associated With Muscle Size and Strength (FAMUSS) cohort] underwent a 12-wk supervised strength-training program for the upper arm muscles. Muscle size (via MR imaging) and elbow flexion strength (1 repetition maximum and isometric) measurements were taken before and after training. The study participants were then genotyped for 11 genetic variants in CCL2 and five variants in CCR2. Variants in the CCL2 and CCR2 genes show strong associations with several pretraining muscle strength traits, indicating that inflammatory genes in skeletal muscle contribute to the polygenic system that determines muscle phenotypes. These associations extend across both sexes, and several of these genetic variants have been shown to influence gene regulation.

Converging lines of evidence suggest that AKT1 is a major mediator of the responses to insulin, insulin-like growth factor 1 (IGF1), and glucose. AKT1 also plays a key role in the regulation of both muscle cell hypertrophy and atrophy. We hypothesized that AKT1 variants may play a role in the endophenotypes that make up metabolic syndrome. We studied a 12-kb region including the first exon of the AKT1 gene for association with metabolic syndrome-related phenotypes in four study populations [FAMUSS cohort (n = 574; age 23.7 ± 5.7 years), Strong Heart Study (SHS) (n = 2,134; age 55.5 ± 7.9 years), Dynamics of Health, Aging and Body Composition (Health ABC) (n = 3,075; age 73.6 ± 2.9 years), and Studies of a Targeted Risk Reduction Intervention through Defined Exercise (STRRIDE) (n = 175; age 40–65 years)]. We identified a three SNP haplotype that we call H1, which represents the ancestral alleles at the three loci and H2, which represents the derived alleles at the three loci. In young adult European Americans (FAMUSS), H1 was associated with higher fasting glucose levels in females. In middle age Native Americans (SHS), H1 carriers showed higher fasting insulin and HOMA in males, and higher BMI in females. In older African-American and European American subjects (Health ABC) H1 carriers showed a higher incidence of metabolic syndrome. Homozygotes for the H1 haplotype showed about twice the risk of metabolic syndrome in both males and females (p

Previous studies have reported associations of polymorphisms in the IGF1 gene with phenotypes of body composition (BC). The purpose of this study was to identify phenotypes of BC and physical function that were associated with the IGF1 promoter polymorphism (rs35767, −C1245T). Subjects from the Health, Aging, and Body Composition Study, white males and females (n = 925/836) and black males and females (533/705) aged 70–79 years were genotyped for the polymorphism. Phenotypes of muscle size and function, bone mineral density, and BC were analyzed for associations with this polymorphism. To validate and compare these findings, a cohort of young (mean age = 24.6, SD = 5.9) white men and women (n = 173/296) with similar phenotypic measurements were genotyped. An association with BC was identified in elderly females when significant covariates (physical activity, age, smoking status, body mass index) were included. White women with C/C genotype had 3% more trunk fat and 2% more total fat than those with C/T (P

The present study examined associations between the ciliary neurotrophic factor (CNTF) 1357 G → A polymorphism and the muscle strength response to a unilateral, upper arm resistance-training (RT) program among healthy, young adults. Subjects were 754 Caucasian men (40%) and women (60%) who were genotyped and performed a training program of the nondominant (trained) arm with the dominant (untrained) arm as a comparison. Peak elbow flexor strength was measured with one repetition maximum, isometric strength with maximum voluntary contraction, and bicep cross-sectional area with MRI in the trained and untrained arms before and after training. Women with the CNTF GG genotype gained more absolute isometric strength, as measured by MVC (6.5 ± 0.3 vs. 5.2 ± 0.5 kg), than carriers of the CNTF A1357 allele in the trained arm pre- to posttraining ( P < 0.05). No significant associations were seen in men. Women with the CNTF GG genotype gained more absolute dynamic (1.0 ± 0.1 vs. 0.6 ± 0.1 kg) and allometric (0.022 ± 0.0 vs. 0.015 ± 0.0 kg/kg−0.67) strength, as measured by 1 RM, than carriers of the CNTF A1357 allele in the untrained arm pre- to posttraining ( P < 0.05). No significant associations were seen in men. No significant associations, as measured by cross-sectional area, were seen in men or women. The CNTF 1357 G → A polymorphism explains only a small portion of the variability in the muscle strength response to training in women.

The purpose of this study was to assess the association of age with muscle mass and strength in a group of young adults before and after 12 weeks of progressive resistance training. Eight hundred twenty-six young males and females (age 24.34 +/- 5.69 yr, range 18-39 yr) completed a strictly supervised 12-week unilateral resistance training program of the nondominant arm. Isometric (maximal voluntary contraction [MVC]) and dynamic strength (1 repetition maximum [1RM]) of the elbow flexors and cross-sectional area (CSA) of the biceps-brachii using magnetic resonance imaging (MRI) scans were measured before and after training. Pearson correlation coefficients were calculated for size and strength variables and age. In addition, the cohort was divided into groups according to decade of life and differences assessed by analysis of variance. Age correlated significantly and positively with all pretraining measures of muscle size and strength (CSA: r = 0.191, p < 0.001; MVC: r = 0.109, p = 0.002; 1RM: r = 0.109, p = 0.002). Age was not related to the training-induced changes in CSA or MVC but was negatively associated with the change in 1RM (r = -0.217, p < 0.001). The study indicates that age does have a significant positive relationship with muscle size and strength in untrained young adults. Although age was negatively associated with improvements in 1RM, the effect of age was small relative to the improvements induced through resistance training, thus suggesting age does not limit response to training in any practical way during early adulthood.

KOSTEK, M. A., T. J. ANGELOPOULOS, P. M. CLARKSON, P. M. GORDON, N. M. MOYNA, P. S. VISICH, R. F. ZOELLER, T. B. PRICE, R. L. SEIP, P. D. THOMPSON, J. M. DEVANEY, H. GORDISH-DRESSMAN, E. P. HOFFMAN, and L. S. PESCATELLO. Myostatin and Follistatin Polymorphisms Interact with Muscle Phenotypes and Ethnicity. Med. Sci. Sports Exerc., Vol. 41, No. 5, pp. 1063–1071, 2009. Purpose: We examined associations among myostatin (MSTN) 2379 A 9 G and 163 G 9 A and follistatin (FST) j5003 A 9 T and j833 G 9 T single nucleotide polymorphisms (SNP) on the muscle size and the strength response to resistance training (RT). Methods: Subjects (n = 645, age = 24.1 T 0.2 yr, body mass index [BMI] = 24.2 T 0.2 kgIm j2 ) self-disclosed themselves as Caucasian (78.9%), African American (3.6%), Asian (8.4%), Hispanic (5.0%), or Other (4.2%). They were genotyped for MSTN 2379 A 9 G( n = 645), MSTN 163 G 9 A( n = 639), FST j5003 A 9 T( n = 580), and FST j833 G 9 T( n = 603). We assessed dynamic (one repetition maximum [1RM]) and isometric (maximum voluntary contraction [MVC]) muscle strength and size (crosssectional area [CSA]) of the elbow flexors before and after 12 wk of unilateral upper-arm RT. Repeated-measures ANCOVA tested associations among genetic variants and muscle phenotypes with age and BMI as covariates. Results: Baseline MVC was greater among African Americans who were carriers of the MSTN G 2379 allele (AG/GG, n = 15) than the A2379A homozygotes (n = 8; 64.2 T 6.8 vs 49.8 T 8.7 kg). African Americans who were carriers of the FST T j5003 allele (n = 12) had greater baseline 1RM (11.9 T 0.7 vs 8.8 T 0.5 kg) and CSA (24.4 T 1.3 vs 19.1 T 1.2 cm 2 ) than African Americans with the A-5003A genotype (n = 14; P G 0.05). No MSTN or FST genotype and muscle phenotype associations were found among the other ethnic groups (P Q 0.05). Conclusion: MSTN 2379 A 9 G and FST j5003 A 9 T were associated with baseline muscle strength and size among African Americans only. These ethnic-specific associations are hypothesis generating and should be confirmed in a larger sample of African Americans.

The purposes of this study were to (1) derive and test allometric scaling models of biceps isometric strength using body mass (BM) and muscle cross-sectional area (CSA) as the scaling variables, (2) assess the influence of body mass index (BMI) by separating the cohort by BMI (normal25 kg/m(2) vs. overweight/obeseor =25 kg/m(2)) and repeating step 1, and (3) assess the effect of BMI on isometric strength allometrically adjusted for differences in CSA by comparing scaled strength between normal weight versus overweight/obese women. The participants were 183 women (18-39 years old) who reported no strength training in the prior year. Isometric strength and CSA of the biceps were assessed on the non-dominant arm. The CSA allometric model met all statistical criteria and produced a scaling exponent of 0.44. The BM model did not meet these criteria until the entire cohort was separated by BMI. The scaling exponents for normal weight and overweight/obese women were 1.48 and 0.35, respectively. These data suggest that BMI exerted an influence on the relationship between BM and allometrically scaled isometric strength and may be explained by previous studies demonstrating greater contribution of fat mass (FM) versus fat-free mass (FFM) to BMI in overweight/obese women. As such, allometric scaling models of isometric strength, especially in populations that are heterogeneous with regard to body composition, must be carefully tested and examined across the range of BMI. Isometric strength relative to CSA was not significantly different between groups. However, allometrically scaled strength, using CSA as the criterion variable, was significantly greater in overweight/obese women compared to those of normal weight. These data suggest that isometric strength in women is not completely determined by CSA and other factors such as intramuscular fat and muscle fiber type may be confounding or contributing factors.

The purpose of this study was to validate the percentage of body fat (%BF) values estimated from the BOD POD (BP) with those obtained from hydrostatic weighing (HW) in athletic American high school boys. Additionally, the %BF values measured via near-infrared interactance (NIR), bioelectrical impedance (BIA), and skinfold (SF) were compared to HW to determine the validity of these measures. Thirty white boys (mean age +/- SD = 15.8 +/- 1.0 years) who where currently participating in organized sports volunteered to have their %BF estimated. Measurements were obtained from NIR, BP, BIA, and SF in random order and concluded with HW. The findings from the present study indicated that the NIR and BIA instruments produced significant (P0.008) constant error (CE) and total error (TE) values that were too large to be of practical value (TE4.0%BF). The BP produced a significantly (P0.008) higher CE with acceptable TE values compared to HW, but compared to all three SF estimations, the BP TE values were higher. Two of the SF equations were nonsignificant (P0.008) and had the lowest TE values compared to HW. These data suggest that the BP can produce acceptable body fat measures for athletic white boys but is not superior to estimates made by the SF equations used in this study.

Glucocorticoid receptor (NR3C1) polymorphisms associate with obesity, muscle strength, and cortisol sensitivity. We examined associations among four NR3C1 polymorphisms and the muscle response to resistance training (RT). European-American adults (n = 602, 23.8±0.4yr) completed a 12 week unilateral arm RT program. Maximum voluntary contraction (MVC) assessed isometric strength (kg) and MRI assessed biceps size (cm2) pre- and post-resistance training. Subjects were genotyped for NR3C1 -2722G>A, -1887G>A, -1017T>C, and +363A>G. Men carrying the -2722G allele gained less relative MVC (17.3±1.2vs33.5±6.1%) (p = 0.010) than AA homozygotes; men with -1887GG gained greater relative MVC than A allele carriers (19.6±1.4vs13.2±2.3%) (p = 0.016). Women carrying the -1017T allele gained greater relative size (18.7±0.5vs16.1±0.9%) (p = 0.016) than CC homozygotes. We found sex-specific NR3C1 associations with the muscle strength and size response to RT. Future studies should investigate whether these associations are partially explained by cortisol’s actions in muscle tissue as they interact with sex differences in cortisol production.

Apolipoprotein B (apoB) concentration and age are independently associated with an increased risk for cardiovascular disease. Age is also associated with increased apoB concentration. The purpose of this study was to determine the effects of exercise on apoB and examine the association between age and lipoproteins. Forty-one sedentary individuals exercised for 6 months, four times/week for 40 min between 60 and 85% of their maximal heart rate. Lipids were determined three times: before training, 24 and 72 h after the last training session. Exercise did not alter apoB (1.2+/-0.05 g/l vs. 1.2+/-0.05 g/l; P0.05), or other lipids or lipoproteins. When participants were sequestered by baseline low density lipoprotein cholesterol (LDLc), total cholesterol (TC) was decreased at 24 h post (6.3+/-0.2 mmol/l vs. 6.0+/-0.2 mmol/l, P0.05) and LDLc after 24 and 48 h post (4.3+/-0.1 mg/dl vs. 3.9+/-0.1 and 4.1+/-0.2 mg/dl, P0.05) in the high LDLc group. In the low LDLc group both TC (4.4+/-0.2 mmol/l vs. 4.6+/-0.2 and 4.6+/-0.2 mmol/l, P0.05) and LDLc (2.6+/-0.1 mmol/l vs. 2.8+/-0.1 and 2.8+/-0.2 mmol/l, P0.05) were elevated at 24 h and remained elevated at 72 h post compared to baseline. Age does not affect apoB or lipoproteins in response to exercise. Individuals with high baseline LDLc experienced acute reduction in TC and LDLc produced by each exercise session.

The effect of beta-alanine (beta-Ala) alone or in combination with creatine monohydrate (Cr) on aerobic exercise performance is unknown. The purpose of this study was to examine the effects of 4 weeks of beta-Ala and Cr supplementation on indices of endurance performance. Fifty-five men (24.5 +/- 5.3 yrs) participated in a double-blind, placebo-controlled study and randomly assigned to one of 4 groups; placebo (PL, n = 13), creatine (Cr, n = 12), beta-alanine (beta-Ala, n = 14), or beta-alanine plus creatine (CrBA, n = 16). Prior to and following supplementation, participants performed a graded exercise test on a cycle ergometer to determine VO(2peak), time to exhaustion (TTE), and power output, VO(2), and percent VO(2peak) associated with VT and LT. No significant group effects were found. However, within groups, a significant time effect was observed for CrBa on 5 of the 8 parameters measured. These data suggest that CrBA may potentially enhance endurance performance.

Exercise affects lipoprotein metabolism and apolipoprotein E (Apo E) genotype may alter changes in lipoprotein subclasses that occur with exercise. The present study examined the effects of Apo E genotype (APOE) on the response of lipoprotein subclass concentrations to long-term exercise. A prospective longitudinal study, conducted at seven centers, genetically screened 566 individuals to create three cohorts of healthy adults, equal for gender and the most common APOE variants: E2/3 (n = 35), E3/3 (n = 40), and E3/4 (n = 31). Subjects with body mass index (BMI) > or = 31 or evidence of dyslipidemia or metabolic disease were excluded. All subjects exercised aerobically at 75% of maximal heart rate for 40 min, four times weekly for 6 months. Fasting lipoprotein subpopulations were measured before and after exercise training using proton nuclear magnetic resonance spectroscopy. Serum lipids for the entire cohort did not change with exercise training, but the LDL subpopulation response varied by APOE. Small-sized LDL particles decreased only in the APOE3 homozygotes whereas medium-sized LDL particles increased only in this group. These changes were directionally different from the responses in the E2/3 and E3/4 subjects (p < 0.05). Neither exercise nor APOE variant affected overall LDL or HDL size or cholesterol concentration, but exercise decreased VLDL diameter by 3.5 nm (p < 0.001) attributable to decreases in large VLDL in each APOE group. In conclusion, APOE variants influence the serum LDL subpopulation response to exercise training in normolipidemic subjects. Subjects homozygous for APOE3 experienced the most beneficial lipid effects from exercise training.

Purpose: To examine associations among the angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism and the response to a 12-wk (2 d·wk-1) unilateral, upper-arm resistance training (RT) program in the trained (T, nondominant) and untrained (UT, dominant) arms. Methods: Subjects were 631 (mean ± SEM, 24.2 ± 0.2 yr) white (80%) men (42%) and women (58%). The ACE ID genotype was in Hardy-Weinberg equilibrium with frequencies of 23.1, 46.1, and 30.8% for ACE II, ID, and DD, respectively (?2 = 1.688, P = 0.430). Maximum voluntary contraction (MVC) and one-repetition maximum (1RM) assessed peak elbow flexor muscle strength. Magnetic resonance imaging measured biceps muscle cross-sectional area (CSA). Multiple variable and repeated-measures ANCOVA tested whether muscle strength and size differed at baseline and pre- to post-RT among T and UT and ACE ID genotype. Results: Baseline muscle strength and size were greater in UT than T (P < 0.001) and did not differ among ACE ID genotype in either arm (P = 0.05). In T, MVC increases were greater for ACE II/ID (22%) than DD (17%) (P < 0.05), whereas 1RM (51%) and CSA (19%) gains were not different among ACE ID genotype pre- to post-RT (P = 0.05). In UT, MVC increased among ACE II/ID (7%) (P < 0.001) but was similar among ACE DD (2%) pre- to post-RT (P = 0.05). In UT, 1RM (11%) and CSA (2%) increases were greater for ACE DD/ID than ACE II (1RM, 7%; CSA, -0.1%) (P < 0.05). ACE ID genotype explained approximately 1% of the MVC response to RT in T and approximately 2% of MVC, 2% of 1RM, and 4% of CSA response in UT (P < 0.05). Conclusion: ACE ID genotype is associated with the contralateral effects of unilateral RT, perhaps more so than with the muscle strength and size adaptations that result from RT.

Angiotensin-converting enzyme (ACE) has two common genetic variants: the insertion (I) and deletion (D) forms. ACE levels are greater in subjects with the D allele, and several studies suggest superior endurance performance in subjects with the I allele. The authors recently reported the results of a 6-month exercise training protocol examining the effect of apolipoprotein E on the lipid response. The present report examines the relationship of ACE genotype and exercise adherence. DNA samples were available for 110 subjects: 14 I/I, 52 I/D, and 44 D/D. Baseline and change in maximal oxygen uptake, body mass index, skinfold thickness, and serum lipids did not differ by ACE genotype, but adherence to exercise training was higher in I carriers than in D homozygotes. These preliminary results suggest that ACE genotype affects exercise adherence and raises the possibility that superior endurance capacity in subjects with the I allele is related to a genetic propensity to adhere to an exercise regimen.

THOMPSON, P. D., N. MOYNA, R. SEIP, T. PRICE, P. CLARKSON, T. ANGELOPOULOS, P. GORDON, L. PESCATELLO, P. VISICH, R. ZOELLER, J. M. DEVANEY, H. GORDISH, S. BILBIE, and E. P. HOFFMAN. Functional Polymorphisms Associated with Human Muscle Size and Strength. Med. Sci. Sports Exerc., Vol. 36, No. 7, pp. 1132–1139, 2004. Introduction: Skeletal muscle is critically important to human performance and health, but little is known of the genetic factors influencing muscle size, strength, and its response to exercise training. The Functional single nucleotide polymorphisms (SNP) Associated with Muscle Size and Strength, or FAMuSS, Study is a multicenter, NIH-funded program to examine the influence of gene polymorphisms on skeletal muscle size and strength before and after resistance exercise training. Methods: One thousand men and women, age 18 – 40 yr, will train their nondominant arm for 12 wk. Skeletal muscle size (magnetic resonance imaging) and isometric and dynamic strength will be measured before and after training. Individuals whose baseline values or response to training deviate 1.5 SD will be defined as outliers and examined for genetic variants. Initially candidate genes previously associated with muscle performance will be examined, but the study will ultimately attempt to identify genes associated with muscle performance. Conclusion: FAMuSS should help identify genetic factors associated with muscle performance and the response to exercise training. Such insight should contribute to our ability to predict the individual response to exercise training but may also contribute to understanding better muscle physiology, to identifying individuals who are susceptible to muscle loss with environmental challenge, and to developing pharmacologic agents capable of preserving muscle size and function. Key Words: SKELETAL MUSCLE, GENETICS, QUANTITATIVE TRAIT LOCI (QTL), HYPERTROPHY, GENOMICS

Brain-derived neurotrophic factor (BDNF) serves as a vital regulator of neuronal proliferation and survival, and has been shown to regulate energy homeostasis, glucose metabolism and body weight maintenance. Elevated concentrations of plasma BDNF have been associated with obesity and type 2 diabetes mellitus. Acute aerobic exercise transiently increases circulating BDNF, potentially correcting obesity-related metabolic impairment. The present study aimed to compare acute aerobic exercise elicited BDNF responses in obese and normal-weight subjects. Furthermore, we aimed to investigate whether acute exercise-induced plasma BDNF elevations would be associated with improved indices of insulin resistance, as well as substrate utilization [carbohydrate oxidation (CHOoxi) and fat oxidation (FAToxi)]. Twenty-two healthy, untrained subjects [11 obese (four men and seven women; age = 22.91 ± 4.44 years; body mass index = 35.72 ± 4.17 kg/m(2)) and 11 normal-weight (five men and six women; age = 23.27 ± 2.24 years; body mass index = 21.89 ± 1.63 kg/m(2))] performed 30 min of continuous submaximal aerobic exercise at 75% maximal oxygen consumption. Our analyses showed that the BDNF response to acute aerobic exercise was similar in obese and normal-weight subjects across time (time: P = 0.015; group: P = not significant) and was not associated with indices of IR. Although no differences in the rates of CHOoxi and FAToxi were found between both groups, total relative energy expenditure was significantly lower in obese subjects compared to normal-weight subjects (3.53 ± 0.25 versus 5.59 ± 0.85; P < 0.001). These findings suggest that acute exercise-elicited BDNF elevation may not be sufficient to modulate indices of IR or the utilization of either carbohydrates or fats in obese individuals.

The authors wish to thank Dr. Weijers (1) for his insightful comments on our article (2). Dr. Weijers is correct that most genetic variants identified using genome-wide association studies (GWAS) are not yet currently used in clinical practice to predict disease risk. Manolio et al. (3) addressed this lack of clinical use in an exquisite review in Nature Reviews Genetics . Their review …

The purpose of this study was to examine whether leptin levels affect the response of leptin to exercise training (ET) and whether this is also affected by C-reactive protein (CRP) or the three common Apolipoprotein E genotypes (APOE). Ninety-seven (male = 45, female = 52) sedentary individuals underwent 6 months of supervised ET. Blood was sampled before the initiation of ET, and again 24 and 72 hr after completion of the final training session. ET resulted in a small reduction in body mass (80.47 ± 18.03 vs 79.42 ± 17.34 kg, p < .01). Leptin was reduced 24 hr after the final exercise session (p < .01), but returned to normal after 72 hr (p > .05)—Pre: 13.51 ± 12.27, 24hr: 12.14 ± 12.34, 72hr: 12.98 ± 11.40 ng/ml. The most hyperleptinemic individuals had a greater initial response, which was sustained through to 72 hr after the final session in the pooled study population (p < .01), and in both males (p < .05) and females (p < .05) separately. CRP was related to leptin independently of body weight and positively related to the reductions in leptin. APOE genotype was not related to leptin levels and did not affect the response to ET. Leptin levels may only be reduced by ET in those with hyperleptinemia. In addition, both the initial extent of hyperleptinemia and the subsequent reduction in leptin may be related to low grade chronic systemic inflammation.

AB Purpose: An osteopontin (OPN; SPP1) gene promoter polymorphism modifies disease severity in Duchenne muscular dystrophy, and we hypothesized that it might also modify muscle phenotypes in healthy volunteers. Methods: Gene association studies were carried out for OPN (rs28357094) in the FAMuSS cohort (n = 752; mean +/- SD age = 23.7 +/- 5.7 yr). The phenotypes studied included muscle size (MRI), strength, and response to supervised resistance training. We also studied 147 young adults that had carried out a bout of eccentric elbow exercise (age = 24.0 +/- 5.2 yr). Phenotypes analyzed included strength, soreness, and serum muscle enzymes. Results: In the FAMuSS cohort, the G allele was associated with 17% increase in baseline upper arm muscle volume only in women (F = 26.32; P = 5.32 x 10-7), explaining 5% of population variance. In the eccentric damage cohort, weak associations of the G allele were seen in women with both baseline myoglobin and elevated creatine kinase. The sexually dimorphic effects of OPN on muscle were also seen in OPN-null mice. Five of seven muscle groups examined showed smaller size in OPN-null female mice, whereas two were smaller in male mice. The query of OPN gene transcription after experimental muscle damage in mice showed rapid induction within 12 h (100-fold increase from baseline), followed by sustained high-level expression through 16 d of regeneration before falling to back to baseline. Conclusion: OPN is a sexually dimorphic modifier of muscle size in normal humans and mice and responds to muscle damage. The OPN gene is known to be estrogen responsive, and this may explain the female-specific genotype effects in adult volunteers.

Purpose We investigated the influence of Leptin ( LEP ) and leptin receptor ( LEPR ) SNPs on habitual physical activity (PA) and body composition response to a unilateral, upper body resistance training (RT) program. Methods European-derived American volunteers (men = 111, women = 131, 23.4 ± 5.4 yr, 24.4 ± 4.6 kg·m − 2 ) were genotyped for LEP 19 G>A (rs2167270), and LEPR 326 A>G (rs1137100), 668 A>G (rs1137101), 3057 G>A (rs1805096), and 1968 G>C (rs8179183). They completed the Paffenbarger PA Questionnaire. Arm muscle and subcutaneous fat volumes were measured before and after 12 wk of supervised RT with MRI. Multivariate and repeated measures ANCOVA tested differences among phenotypes by genotype and gender with age and body mass index as covariates. Results Adults with the LEP 19 GG genotype reported more kcal/wk in vigorous intensity PA (1273.3 ± 176.8, p = 0.017) and sports/recreation (1922.8 ± 226.0, p LEP 19 GG genotype spent more h/wk in light intensity PA (39.7 ± 1.6) than A allele carriers (35.0 ± 1.4, p = 0.03). In response to RT, adults with the LEPR 668 G allele gained greater arm muscle volume (67,687.05 ± 3186.7 vs. 52,321.87 ± 5125.05 mm 3 , p = 0.01) and subcutaneous fat volume (10,599.89 ± 3683.57 vs. − 5224.73 ± 5923.98 mm 3 , p = 0.02) than adults with the LEPR 668 AA genotype, respectively. Conclusion LEP 19 G>A and LEPR 668 A>G associated with habitual PA and the body composition response to RT. These LEP and LEPR SNPs are located in coding exons likely influencing LEP and LEPR function. Further investigation is needed to confirm our findings and establish mechanisms for LEP and LEPR genotype and PA and body composition associations we observed.

The measurement of heart rate variability (HRV) is often applied as an index of autonomic nervous system (ANS) balance and, therefore, myocardial stability. Previous studies have suggested that relaxation or mind-body exercise can influence ANS balance positively as measured by HRV but may act via different mechanisms. No studies, to the authors' knowledge, have examined the acute response in HRV to interventions combining relaxation and mind-body exercise. The objective of this study was to compare the acute HRV responses to Yoga Nidra relaxation alone versus Yoga Nidra relaxation preceded by Hatha yoga.This was a randomized counter-balanced trial.The trial was conducted in a university exercise physiology laboratory.Subjects included 20 women and men (29.15±6.98 years of age, with a range of 18-47 years).Participants completed a yoga plus relaxation (YR) session and a relaxation only (R) session.The YR condition produced significant changes from baseline in heart rate (HR; beats per minute [bpm], p0.001) and indices of HRV: R-R (ms, p0.001), pNN50 (%, p=0.009), low frequency (LF; %, p=0.008) and high frequency (HF; %, p=0.035). The R condition produced significant changes from baseline in heart rate (bpm, p0.001) as well as indices of HRV: R-R (ms, p0.001), HF (ms(2), p=0.004), LF (%, p=0.005), HF (%, p=0.008) and LF:HF ratio (%, p=0.008). There were no significant differences between conditions at baseline nor for the changes from baseline for any of the variables.These changes demonstrate a favorable shift in autonomic balance to the parasympathetic branch of the ANS for both conditions, and that Yoga Nidra relaxation produces favorable changes in measures of HRV whether alone or preceded by a bout of Hatha yoga.

Ankyrin repeat domain 6 (ANKRD6) is a ubiquitous protein that associates with early development in mammals and is highly expressed in the brain, spinal cord, and heart of humans. We examined the role of 8 ANKRD6 single-nucleotide polymorphisms (SNPs) on muscle performance and habitual physical activity (PA). Single-nucleotide polymorphisms were 545 T>A (rs9362667), 485 M>L (rs61736690), 233 T>M (rs2273238), 128 I>L (rs3748085), 631 P>L (rs61739327), 122 Q>E (rs16881983), 197805 G>A (rs9344950), and 710 L>X (NOVEL). This study consisted of 922 healthy, untrained, European-derived American men (n = 376, 23.6 ± 0.3 years, 25.0 ± 0.2 kg·m-2) and women (n = 546, 23.2 ± 0.2 years, 24.0 ± 0.2 kg·m-2). Muscle strength (maximum voluntary contraction [MVC] and 1 repetition maximum [1RM]) and size (cross-sectional area [CSA]) were assessed before and after 12 weeks of unilateral resistance training (RT). A subsample (n = 536, 23.4 ± 0.2 years, 24.6 ± 0.2 kg·m-2) completed the Paffenbarger Physical Activity Questionnaire. Associations among ANKRD6 genotypes and muscle phenotypes were tested with repeated measure analysis of covariance (ANCOVA) and PA phenotypes with multivariate ANCOVA, with age and body mass index as covariates. ANKRD6 122 Q>E was associated with increased baseline biceps CSA. ANKRD6 545 A>T and ANKRD6 710 L>X were associated with increased 1RM and MVC in response to RT, respectively. ANKRD6 631 P>L was associated with increased biceps CSA response to RT and time spent in moderate-intensity PA among the total sample and women. ANKRD6 genetic variants were associated with the muscle size and strength response to RT and habitual PA levels. Further research is needed to validate our results and explore mechanisms for the associations we observed.

Genome-wide association studies (GWAS) have identified polymorphic loci associated with coronary artery disease (CAD) risk factors (i. e. serum lipids) in adult populations (42–69 yrs). We hypothesized that younger populations would show a greater relative genetic component due to fewer confounding variables. We examined the influence of 20 GWAS loci associated with serum lipids and insulin metabolism, in a university student cohort (n=548; mean age= 24 yrs), and replicated statistically associated results in a second study cohort of primary school students (n=810, mean age= 11.5 yrs). 19 loci showed no relationship with studied risk factors in young adults. However, the ancestral allele of the rs646776 (SORT1) locus was strongly associated with increased low density lipoprotein cholesterol {LDL (C)} in young adults (TT: 97.6 ± 1.0 mg/dL {n=345}, vs. CT/CC: 87.3 ± 1.0 mg/dL {n=203}; p = 3 × 10−6) and children (TT: 94.0 ± 1.3 mg/dL {n=551}, vs. CT/CC: 84.7 ± 1.4 mg/dL {n=259}; p = 4 × 10−6). This locus is responsible for 3.6% of population variance in young adults and 2.5% of population variance in children. The effect size of the SORT1 locus is considerably higher in young populations (2.5%–4.1%) compared to older subjects (1%).

Hepatic lipase (HL) and lipoprotein lipase (LPL) activities (HLA, LPLA) modify lipoproteins and facilitate their binding to hepatic receptors. Apolipoprotein E (APOE) physically interacts with the lipases, and the three common haplotypes of the APOE gene (ε2, ε3, and ε4) yield protein isoforms (E2, E3, and E4, respectively) that are functionally different. Lipase activities themselves differ by sex and exercise training status. The interaction of APOE genotype, exercise training, and sex effects on lipase activities has not been studied. We measured postheparin plasma lipase activities in normolipidemic men and women with the three most common APOE genotypes, which are the haplotype combinations ε2/ε3 ( n = 53 ), ε3/ε3 ( n = 62), and ε4/ε3 ( n = 52), enrolled in 6 mo of aerobic exercise training. These haplotype combinations comprise an estimated 11.6, 62.3, and 21.3% of the population, respectively. Baseline HLA was 35% lower in women than in men ( P < 0.0001). In men but not women, HLA was higher in ε2/ε3 group compared with ε4/ε3 ( P = 0.01) and ε3/ε3 ( P = 0.05). Neither sex nor APOE genotype affected baseline LPLA. Training decreased HLA by 5.2% ( P = 0.018) with no APOE effect. The apparent increase in LPLA following exercise was significant and APOE dependent only when corrected for baseline insulin ( P < 0.05). Exercise decreased LPLA by 0.8 μmol free fatty acid (FFA)·ml−1·h−1(−6%) in ε3/ε3 compared with the combined increases of 6.6% in ε2/ε3 and 12% in ε4/ε3 ( P = 0.018 vs. ε3/ε3). However, these differences were statistically significant only after correcting for baseline insulin. We conclude that common APOE genotypes interact with 1) sex to modulate HLA regardless of training status, with ε2/ε3 men demonstrating higher HLA than ε3/ε3 or ε4/ε3 men, and 2) aerobic training to modulate LPLA, regardless of sex, with ε3/ε3 subjects showing a significant decrease compared with an increase in ε2/ε3 and ε3/ε4 after controlling for baseline insulin.

ZOELLER, R. F., T. J. ANGELOPOULOS, B. THOMPSON, M. WENTA, T. B. PRICE, P. D. THOMPSON, N. M. MOYNA, R. L. SEIP, P. CLARKSON, P. M. GORDON, L. S. PESCATELLO, J. DEVANEY, H. GORDISH-DRESSMAN, E. P. HOFFMAN, and P. S. VISICH. Vascular Remodeling in Response to 12 wk of Upper Arm Unilateral Resistance Training. Med. Sci. Sports Exerc., Vol. 41, No. 11, pp. 2003–2008, 2009. Participation in regular aerobic exercise has been shown to increase arterial size and that exercise-induced vascular remodeling may be regional rather than systemic. However, these issues have been minimally investigated concerning resistance training. Purposes: To determine whether 1) resistance training of the nondominant arm elicits an increase in diameter of the brachial artery and 2) unilateral training induces arterial remodeling in the contralateral arm. Methods: Twenty-four previously untrained participants, consisting of 18 females (aged 22.3 T 5.1 yr) and 6 males (aged 21.7 T 1.8 yr), participated in unilateral strength training of the biceps and triceps for 12 wk using their nondominant arm. Isotonic (one-repetition maximum, 1RM) and isometric (ISO) strength of the biceps were assessed before and after training on both arms. Brachial artery diameter and biceps muscle cross-sectional area (CSA) of both arms were also measured before and after training using magnetic resonance imaging (MRI). Results: Brachial artery diameter increased 5.47% (P G 0.05) in the nondominant trained arm with no change observed in the dominant untrained arm. Biceps CSA increased 18.3% (P G 0.05) in the trained arm with no change (P 9 0.05) in the untrained limb. Nondominant 1RM and ISO strength increased by 35.1% and 16.8%, respectively (P G 0.05 for both), although there were no significant changes (P 9 0.05) in the contralateral arm. A modest correlation was found between the increases in CSA and in brachial artery diameter (r 2 = 0.19, P = 0.039). Conclusions: These results indicate that upper arm vascular remodeling, manifesting as increased brachial artery diameter, can result from resistance training and that these changes are localized to the trained

A classic morphogen, bone morphogenetic protein 2 (BMP2) regulates the differentiation of pluripotent mesenchymal cells. High BMP2 levels promote osteogenesis or chondrogenesis and low levels promote adipogenesis. BMP2 inhibits myogenesis. Thus, BMP2 synthesis is tightly controlled. Several hundred nucleotides within the 3' untranslated regions of BMP2 genes are conserved from mammals to fishes indicating that the region is under stringent selective pressure. Our analyses indicate that this region controls BMP2 synthesis by post-transcriptional mechanisms. A common A to C single nucleotide polymorphism (SNP) in the BMP2 gene (rs15705, +A1123C) disrupts a putative post-transcriptional regulatory motif within the human ultra-conserved sequence. In vitro studies indicate that RNAs bearing the A or C alleles have different protein binding characteristics in extracts from mesenchymal cells. Reporter genes with the C allele of the ultra-conserved sequence were differentially expressed in mesenchymal cells. Finally, we analyzed MRI data from the upper arm of 517 healthy individuals aged 18-41 years. Individuals with the C/C genotype were associated with lower baseline subcutaneous fat volumes (P = 0.0030) and an increased gain in skeletal muscle volume (P = 0.0060) following resistance training in a cohort of young males. The rs15705 SNP explained 2-4% of inter-individual variability in the measured parameters. The rs15705 variant is one of the first genetic markers that may be exploited to facilitate early diagnosis, treatment, and/or prevention of diseases associated with poor fitness. Furthermore, understanding the mechanisms by which regulatory polymorphisms influence BMP2 synthesis will reveal novel pharmaceutical targets for these disabling conditions.

C-reactive protein (CRP) is a marker for systemic inflammation and increased cardiovascular disease risk. Regular exercise may decrease CRP. Apolipoprotein E (apo E) has 3 common genotype variants--E2/3, 3/3, and 3/4--that modulate lipid metabolism and may have other metabolic physiologic roles, including some evidence that the genotype affects CRP levels. We assessed fasting serum CRP in 117 (male = 51, female = 66) healthy adults who volunteered for a 6-month aerobic exercise program. Both pre- and posttraining measurements were available in 71 (male = 31, female = 40) subjects. At baseline and follow-up, the numbers of subjects in the 3 groups were approximately equal: 2/3, n = 33 and 20; 3/3, n = 41 and 26; and 3/4, n = 43 and 25. At baseline, CRP levels differed by apo E genotype: means +/- SD were 2.84 +/- 2.18, 2.59 +/- 2.34, and 1.90 +/- 2.13 mg/L for E2/3, 3/3, and 3/4 subjects, respectively (3/4 vs 2/3, P.05). In women, CRP was higher than that in men (3.14 +/- 2.49 vs 2.12 +/- 2.13 mg/L, P.006). Exercise failed to affect CRP in the entire cohort (2.68 +/- 2.38 vs 2.52 +/- 2.48 mg/L) or in any apo E genotype group, and the apo E genotype effect observed at baseline persisted after training. In a largely white study cohort, CRP is higher in apo E3/3 than in 3/4 subjects and in women compared with men, but remains unchanged by 6 months of standard aerobic exercise training of the volume and higher intensity promoted by national organizations to reduce cardiovascular disease risk. How apo E genotype affects CRP is not known.

The aims of this study were to examine associations between two SNPs in the human IL-15 gene and three SNPs in the IL-15Ralpha gene with predictors of metabolic syndrome and phenotypes in muscle, strength, and bone at baseline and in response to resistance training (RT). Subjects were Caucasians who had not performed RT in the previous year and consisted of a strength cohort (n=748), volumetric cohort (n=722), and serum cohort (n=544). Subjects completed 12 weeks of unilateral RT of the non-dominant arm, using their dominant arm as an untrained control. ANCOVA analyses revealed gender-specific associations with: (1) IL-15 SNP (rs1589241) and cholesterol (p=0.04), LDL (p=0.02), the homeostasis model assessment (HOMA; p=0.03), and BMI (p=0.002); (2) IL-15 SNP (rs1057972) and the pre- to post-training absolute difference in 1RM strength (p=0.02), BMI (p=0.008), and fasting glucose (p=0.03); (3) IL-15Ralpha SNP (rs2296135) and baseline total bone volume (p=0.04) and the pre- to post-training absolute difference in isometric strength (p=0.01); and 4) IL-15Ralpha SNP (rs2228059) and serum triglycerides (p=0.04), baseline whole muscle volume (p=0.04), baseline cortical bone volume (p=0.04), and baseline muscle quality (p=0.04). All associations were consistent in showing a potential involvement of the IL-15 pathway with muscle and bone phenotypes and predictors of metabolic syndrome.

Background Of the five sub-phenotypes defining metabolic syndrome, all are known to have strong genetic components (typically 50–80% of population variation). Studies defining genetic predispositions have typically focused on older populations with metabolic syndrome and/or type 2 diabetes. We hypothesized that the study of younger populations would mitigate many confounding variables, and allow us to better define genetic predisposition loci for metabolic syndrome. Methods We studied 610 young adult volunteers (average age 24 yrs) for metabolic syndrome markers, and volumetric MRI of upper arm muscle, bone, and fat pre- and post-unilateral resistance training. Results We found the PPARα L162V polymorphism to be a strong determinant of serum triglyceride levels in young White males, where carriers of the V allele showed 78% increase in triglycerides relative to L homozygotes (LL = 116 ± 11 mg/dL, LV = 208 ± 30 mg/dL; p = 0.004). Men with the V allele showed lower HDL (LL = 42 ± 1 mg/dL, LV = 34 ± 2 mg/dL; p = 0.001), but women did not. Subcutaneous fat volume was higher in males carrying the V allele, however, exercise training increased fat volume of the untrained arm in V carriers, while LL genotypes significantly decreased in fat volume (LL = -1,707 ± 21 mm3, LV = 17,617 ± 58 mm3 ; p = 0.002), indicating a systemic effect of the V allele on adiposity after unilateral training. Our study suggests that the primary effect of PPARα L162V is on serum triglycerides, with downstream effects on adiposity and response to training. Conclusion Our results on association of PPARα and triglycerides in males showed a much larger effect of the V allele than previously reported in older and less healthy populations. Specifically, we showed the V allele to increase triglycerides by 78% (p = 0.004), and this single polymorphism accounted for 3.8% of all variation in serum triglycerides in males (p = 0.0037).

It is believed spot reduction, the exercise-induced localized loss of subcutaneous fat, does not occur as a result of an exercise program; however, evidence as a whole has been inconsistent. To reexamine this concept, we compared subcutaneous fat measurements before and after resistance training among 104 subjects (45 men, 59 women).Subjects participated in 12 wk of supervised resistance training of their nondominant arm. Magnetic resonance imaging and skinfold calipers examined subcutaneous fat in the nondominant (trained) and dominant (untrained) arms before and after resistance training. Repeated-measures ANCOVA tested for subcutaneous fat differences within and between arms before, after, and from before to after resistance training by gender and measurement technique, with BMI and age as covariates. Simple linear regression compared subcutaneous fat changes before and after resistance training as assessed by MRI and skinfold.Subcutaneous fat, measured by skinfold, decreased in the trained arm and not the untrained arm in the men (P0.01); it was similar in the total sample and in the women (P0.05). MRI determinations of subcutaneous fat changes were not different between arms in the total sample and by gender (P0.05).Subcutaneous fat changes resulting from resistance training varied by gender and assessment technique. Skinfold findings indicate that spot reduction occurred in men but not in women. In contrast, MRI found a generalized subcutaneous fat loss independent of gender, supporting the notion that spot reduction does not occur as a result of resistance training. MRI, sensitive to changes along the entire upper arm, detected greater variation in resistance training responses, preventing significant differences between trained and untrained arms. Variation in upper-arm resistance training response was not evident from a single skinfold measurement at the belly of the muscle.

Purpose: The purposes of this study were 1) derive allometric scaling models of isometric biceps muscle strength using pretraining body mass (BM) and muscle cross-sectional area (CSA) as scaling variables in adult males, 2) test model appropriateness using regression diagnostics, and 3) cross-validate the models before and after 12 wk of resistance training. Methods: A subset of FAMuSS (Functional SNP Associated with Muscle Size and Strength) study data (N = 136) were randomly split into two groups (A and B). Allometric scaling models using pretraining BM and CSA were derived and tested for group A. The scaling exponents determined from these models were then applied to and tested on group B pretraining data. Finally, these scaling exponents were applied to and tested on group A and B posttraining data. Results: BM and CSA models produced scaling exponents of 0.64 and 0.71, respectively. Regression diagnostics determined both models to be appropriate. Cross-validation of the models to group B showed that the BM model, but not the CSA model, was appropriate. Removal of the largest six subjects (CSA > 30 cm2) from group B resulted in an appropriate fit for the CSA model. Application of the models to group A posttraining data showed that both models were appropriate, but only the body mass model was successful for group B. Conclusion: These data suggest that the application of scaling exponents of 0.64 and 0.71, using BM and CSA, respectively, are appropriate for scaling isometric biceps strength in adult males. However, the scaling exponent using CSA may not be appropriate for individuals with biceps CSA > 30 cm2. Finally, 12 wk of resistance training does not alter the relationship between BM, CSA, and muscular strength as assessed by allometric scaling.

Pescatello, L.S., B.K. Kelsey, T.B. Price, R.L. Seip, T.J. Angelopoulos, P.M. Clarkson, P.M. Gordon, N.M. Moyna, P.S. Visich, R.F. Zoeller, H.A. Gordish-Dressman, S.M. Bilbie, P.D. Thompson, and E.P. Hoffman. The muscle strength and size response to upper arm, unilateral resistance training among adults who are overweight and obese. J. Strength Cond. Res. 21(2):307-313. 2007.-Overweight and obesity result in musculoskeletal impairments that limit exercise capacity. We examined if the muscle strength and size response to resistance training (RT) differed among 687 young (mean ± SEM, 24.2 ± 0.2 years) overweight and obese (OW) compared to normal weight (NW) adults as denoted by the body mass index (BMI). Subjects were 449 NW (22.0 ± 0.1 kg·m?2, 23.4 ± 0.3 years) and 238 OW (29.2 ± 0.2 kg·m?2, 25.6 ± 0.4 years) men (n = 285) and women (n = 402) who underwent 12 weeks (2 d·wk?1) of RT of the nondominant arm. Maximum voluntary contraction (MVC) and 1 repetition maximum (1RM) assessed peak elbow flexor strength. Magnetic resonance imaging measured the biceps muscle cross sectional area (CSA). Multiple dependent variable analysis of covariance tested if muscle strength and size differed among BMI groups pre-, post-, and pre-to-post-RT. Overweight and obese had greater MVC, 1RM, and CSA than NW pre- and post-RT (p < 0.001). Maximum voluntary contraction and 1RM gains were not different between BMI groups pre- to post-RT (p 0.05). When adjusted for baseline values, NW had greater relative MVC (21.2 ± 1.0 vs. 17.4 ± 1.4%) and 1RM (54.3 ± 1.5 vs. 49.0 ± 2.0%) increases than OW (p < 0.05). Normal weight also had greater allometric MVC (0.48 ± 0.02 kg·kg?0.67 vs. 0.40 ± 0.03 kg·kg?0.67) and 1RM (0.25 ± 0.00 vs. 0.22 ± 0.01 kg·kg?0.67) gains than OW (p < 0.05). CSA gains were greater among OW than NW (3.6 ± 0.2 vs. 3.2 ± 0.1 cm2) (p < 0.001); however, relative CSA increases were not different between BMI groups (19.4 ± 0.5 vs. 18.4 ± 0.7%) (p 0.05). Despite similar relative muscle size increases, relative and allometic strength gains were less among OW than NW. These findings indicate the short-term relative and allometric muscle strength response to RT may be attenuated among adults who are overweight and obese.

Objective: The biological function of resistin (RST) is unknown, although it may have roles in obesity, diabetes, and insulin resistance. The objective of this study was to examine the effects of single nucleotide polymorphisms (SNPs) in the human RST gene on muscle, bone, and adipose tissue phenotypes and in response to resistance training (RT). Research Methods and Procedures: Subjects were white and consisted of strength (n = 482) and size (n = 409) cohorts who had not performed RT in the previous year. Subjects completed 12 weeks of structured, unilateral upper arm RT aimed at increasing the size and strength of the non-dominant arm, using their dominant arm as an untrained control. Strength measurements were taken pre- and post-12-week RT and consisted of elbow flexor isometric strength and one-repetition maximum during a biceps curl using free weights. Whole muscle, subcutaneous fat, and cortical bone volumes were measured by magnetic resonance imaging. Six RST SNPs were identified. Analysis of covariance was used to test for effects of the SNPs on pre- and post-muscle strength and whole muscle, fat, and bone volumes independent of gender, age, and body weight. Results: Five RST SNPs (−537 A>C, −420 C>G, 398 C>T, 540 G>A, 980 C>G) were associated with measured phenotypes among subjects when stratified by BMI (

This study examined the effects of 28 days of beta-alanine supplementation on the physical working capacity at fatigue threshold (PWCFT), ventilatory threshold (VT), maximal oxygen consumption (VO2-MAX), and time-to-exhaustion (TTE) in women. Twenty-two women (age+/-SD 27.4+/-6.1 yrs) participated and were randomly assigned to either the beta-alanine (CarnoSyn) or Placebo (PL) group. Before (pre) and after (post) the supplementation period, participants performed a continuous, incremental cycle ergometry test to exhaustion to determine the PWCFT, VT, VO2-MAX, and TTE. There was a 13.9, 12.6 and 2.5% increase (p0.05) in VT, PWCFT, and TTE, respectively, for the beta-alanine group, with no changes in the PL (p0.05). There were no changes for VO2-MAX (p0.05) in either group. Results of this study indicate that beta-alanine supplementation delays the onset of neuromuscular fatigue (PWCFT) and the ventilatory threshold (VT) at submaximal workloads, and increase in TTE during maximal cycle ergometry performance. However, beta-alanine supplementation did not affect maximal aerobic power (VO2-MAX). In conclusion, beta-alanine supplementation appears to improve submaximal cycle ergometry performance and TTE in young women, perhaps as a result of an increased buffering capacity due to elevated muscle carnosine concentrations.

Zoeller RF, Riechman SE, Dabayebeh IM, Goss FL, Robertson RJ, Jacobs PL. Relation between muscular strength and cardiorespiratory fitness in people with thoracic-level paraplegia. Objectives To determine the relation between muscular strength, aerobic power (Vo 2 peak), submaximal blood lactate accumulation, and endurance performance in people with thoracic-level paraplegia. Design Participants performed tests of isokinetic strength, a graded exercise test, and 2 endurance performance tests. A Latin square counterbalanced design was used to determine the order of testing. Setting Research laboratory in a university setting. Participants Ten adult male volunteers with thoracic-level paraplegia. Interventions Not applicable. Main Outcome Measures The relations between strength, Vo 2 peak, submaximal blood lactate accumulation, and endurance were determined by correlation analysis. Results Shoulder flexion strength correlated with Vo 2 peak and power output at Vo 2 peak. Shoulder strength accounted for 68.4% of the variation in performance time. Greater isokinetic elbow flexion and extension strength was associated with higher Vo 2 and power output at a blood lactate concentration of 4mmol/L (flexion) and with a greater power output at Vo 2 peak (extension). Conclusions These findings suggest that in this population, greater muscular strength is associated with greater aerobic power and endurance. Greater muscular strength could exert a positive influence on exercise performance by enabling higher levels of cardiorespiratory stress as the result of reduced or delayed local muscle fatigue.

Ratings of perceived exertion (RPE) are used for exercise programming of cardiac rehabilitation patients, whenever it is difficult to use heart rate to set intensity due to medication or other factors. This investigation examined the physiological responses to two stepping exercise modes (upright and recumbent) at the same RPE. Analysis indicated significant physiological differences between the modes of exercise which may be mediated by postural differences. Specifically, the physiological responses to the recumbent exercise, but not the upright exercise, had the expected relationship with RPE, with recumbent stepping requiring less physiological effort than the upright stepping at the same RPE. As such, we cannot recommend with confidence that the prescription for upright exercise be made based on data from recumbent exercise or vice-versa.

This study assessed variability in muscle size and strength changes in a large cohort of men and women after a unilateral resistance training program in the elbow flexors. A secondary purpose was to assess sex differences in size and strength changes after training.Five hundred eighty-five subjects (342 women, 243 men) were tested at one of eight study centers. Isometric (MVC) and dynamic strength (one-repetition maximum (1RM)) of the elbow flexor muscles of each arm and magnetic resonance imaging (MRI) of the biceps brachii (to determine cross-sectional area (CSA)) were assessed before and after 12 wk of progressive dynamic resistance training of the nondominant arm.Size changes ranged from -2 to +59% (-0.4 to +13.6 cm), 1RM strength gains ranged from 0 to +250% (0 to +10.2 kg), and MVC changes ranged from -32 to +149% (-15.9 to +52.6 kg). Coefficients of variation were 0.48 and 0.51 for changes in CSA (P = 0.44), 1.07 and 0.89 for changes in MVC (P0.01), and 0.55 and 0.59 for changes in CSA (P0.01) in men and women, respectively. Men experienced 2.5% greater gains for CSA (P0.01) compared with women. Despite greater absolute gains in men, relative increases in strength measures were greater in women versus men (P0.05).Men and women exhibit wide ranges of response to resistance training, with some subjects showing little to no gain, and others showing profound changes, increasing size by over 10 cm and doubling their strength. Men had only a slight advantage in relative size gains compared with women, whereas women outpaced men considerably in relative gains in strength.

The α-actinin 3 (ACTN3) gene encodes a protein of the Z disk of myofibers, and a polymorphism of ACTN3 results in complete loss of the protein. The ACTN3 genotype (R577X) has been found to be associated with performance in Australian elite athletes (Yang N, MacArthur DG, Gulbin JP, Hahn AG, Beggs AH, Easteal S, and North K. Am J Hum Genet 73: 627–631, 2003). We studied associations between ACTN3 genotype and muscle size [cross-sectional area of the biceps brachii via magnetic resonance imaging (MRI)] and elbow flexor isometric (MVC) and dynamic [1-repetition maximum (1-RM)] strength in a large group of men ( N = 247) and women ( N = 355) enrolled in a 12-wk standardized elbow flexor/extensor resistance training program of the nondominant arm at one of eight study centers. We found no association between ACTN3 R577X genotype and muscle phenotype in men. However, women homozygous for the ACTN3 577X allele (XX) had lower baseline MVC compared with heterozygotes ( P < 0.05) when adjusted for body mass and age. Women homozygous for the mutant allele (577X) demonstrated greater absolute and relative 1-RM gains compared with the homozygous wild type (RR) after resistance training when adjusted for body mass and age ( P < 0.05). There was a trend for a dose-response with genotype such that gains were greatest for XX and least for RR. Significant associations were validated in at least one ethnic subpopulation (Caucasians, Asians) and were independent of training volume. About 2% of baseline MVC and of 1-RM strength gain after training were attributable to ACTN3 genotype (likelihood-ratio test P value, P = 0.01), suggesting that ACTN3 is one of many genes contributing to genetic variation in muscle performance and adaptation to exercise.

High density lipoprotein cholesterol (HDL-C) is a primary risk factor for cardiovascular disease. Apolipoprotein A-1 (apoA1) is the major HDL-associated apolipoprotein. The −75 G/A single nucleotide polymorphism (SNP) in the apolipoprotein A1 gene (APOA1) promoter has been reported to be associated with HDL-C concentrations as well as HDL-C response to dietary changes in polyunsaturated fat intake. We examined the effect of this APOA1 SNP on exercise-induced changes in HDL subfraction distribution. From a cohort of healthy normolipidemic adults who volunteered for 6 months of supervised aerobic exercise, 75 subjects were genotyped for the −75 G/A SNP. Of these, 53 subjects were G homozygotes (G/G) and 22 were A carriers (A/G and A/A). HDL subfractions were measured by nuclear magnetic resonance (NMR) spectroscopy by adding categories HDL-C 1 + 2 for the small subfraction, and HDL-C 3+4+5 for the large. Thechange in total HDL-C after exercise was 0.8 ± 7.2 mg/dL (+1.7%), and was not statistically significant. HDL subfraction amounts also did not significantly change with exercise training in the total cohort or in G homozygotes or A carriers. The amount of the large HDL subfraction increased in the G homozygotes and decreased in the A carriers (mean ± S.E.M., 1.8 ± 6.6 mg/dL versus −6.1 ± 2.3 mg/dL, p < 0.0005). In contrast, the amount of the small HDL subfraction decreased in G homozygotes and increased in A carriers (−1.3 ± 6.6 mg/dL versus 4.7 ± 1.2 mg/dL, p < 0.005). These results show that genetic variation at the APOA1 gene promoter is associated with HDL subfraction redistribution resulting from exercise training. © 2005 Elsevier Ireland Ltd. All rights reserved.

Physical activity improves lipid levels by altering triglyceride (TG) metabolism. Apolipoprotein E (Apo E) facilitates TG clearance by mediating lipoprotein binding to hepatic receptors, but Apo E also has less defined roles in skeletal muscle and nervous tissue. This study examined if variants in Apo E genotype affect the lipid and physiologic response to exercise training. Seven centers genetically screened 566 individuals to recruit 120 subjects into 6 gender-specific cohorts equal for the most common Apo E genotypes: E2/3, E3/3, and E3/4. Anthropometics, exercise capacity (Vo(2)max), serum lipids, and post heparin (PH) plasma lipase activities were measured before and after 6 months of supervised exercise training. Difference in the response (Delta) to training among the Apo E genotypes was the primary outcome variable. Differences in pretraining serum lipids among the Apo E genotypes mimicked those observed in population studies: TGs were slightly higher in E2/3 subjects, whereas low-density lipoprotein (LDL)-cholesterol (C) was lower (P = not significant [NS] ). TGs decreased 11% with training for the entire cohort (P.0001) and 7%, 12%, and 14% for the Apo E 2/3, 3/3 and 3/4 groups, respectively (P = NS for Delta). LDL-C did not change in the entire cohort, but decreased slightly in the 2/3 and 3/3 subjects and increased 4% in the 3/4 group (P = NS for Delta). High-density lipoprotein (HDL)-C increased 2% for the entire cohort (P =.06) due to a 6% increase in the 3/3 group (P =.07 for Delta). Total cholesterol (TC)/HDL and LDL/HDL decreased with training in the 2/3 and 3/3 groups, but increased in the 3/4 subjects and these responses differed among the genotypes (P.05 for Delta). Vo(2)max increased 9% to 10% for the entire cohort, but only 5% in the 3/3 subjects versus 13% in the 2/3 and 3/4 groups and these differences were significantly different among the genotypes (P.01 for Delta). This is the first prospective study to demonstrate that the serum lipid response to exercise training differs by Apo E genotype in a pattern consistent with known metabolic differences among the variants. Surprisingly, Apo E genotype also affected the increase in aerobic capacity produced by exercise training possibly via undefined effects on nerve and skeletal muscle function.