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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.

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 (P < 0.008) constant error (CE) and total error (TE) values that were too large to be of practical value (TE > 4.0%BF). The BP produced a significantly (P < 0.008) 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 (P > 0.008) 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.

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; P>0.05), 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, P<0.05) 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, P<0.05) 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, P>0.05) and LDLc (2.6+/-0.1 mmol/l vs. 2.8+/-0.1 and 2.8+/-0.2 mmol/l, P<0.05) 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 purpose of this study was to examine the effects of 28 days of beta-alanine (b-Ala) and creatine monohydrate (CrM) supplementation on the onset of neuromuscular fatigue by using the physical working capacity at neuromuscular fatigue threshold (PWC(FT)) test in untrained men. Fifty-one men (mean age +/- SD = 24.5 +/- 5.3 years) volunteered to participate in this 28-day, double-blind, placebo-controlled study and were randomly assigned to 1 of 4 groups: placebo (PLA; 34 g dextrose; n = 13), CrM (5.25 g CrM plus 34 g dextrose; n = 12), b-Ala (1.6 g b-Ala plus 34 g of dextrose; n = 12), or b-Ala plus CrM (CrBA; 5.25 g CrM plus 1.6 g b-Ala plus 34 g dextrose; n = 14). The supplement was ingested 4 times per day for 6 consecutive days, then twice per day for 22 days before posttesting. Before and after the supplementation, subjects performed a continuous incremental cycle ergometry test while a surface electromyographic signal was recorded from the vastus lateralis muscle to determine PWC(FT). The adjusted mean posttest PWC(FT) values (covaried for pretest PWC(FT) values) for the b-Ala and CrBA groups were greater than those for the PLA group (p < or = 0.05). However, there were no differences between the CrM vs. PLA, CrBA vs. b-Ala, CrM vs. b-Ala, or CrM vs. CrBA groups (p > 0.05). These findings suggested that b-Ala supplementation may delay the onset of neuromuscular fatigue. Furthermore, there appeared to be no additive or unique effects of CrM vs. b-Ala alone on PWC(FT).