Linear model results on the 24 selected SNPs in the SAPHIR, KORA F3 and CoLaus study using an additive genetic model, adjusted for age, sex and BMI, as well as the combined fixed effects meta-analysis results.

<p>Effect estimates and standard errors (for the combined as well as sex-specific analyses) are based on the original adiponectin scale, whereas p-values are taken from the linear regression on log(adiponectin).</p

Characteristics of the 24 SNPs in SAPHIR, KORA F3 and CoLaus, including genotype quality (call rate or imputation quality RSQR).

*<p>Minor and Major alleles based on the plus-strand.</p>**<p>Number of homozygotes for the major allele/heterozygotes/homozygotes for the rare allele; For KORA F3 and CoLaus, where imputed genotype scores have been used, this are the numbers of the “best guess” genotypes (KORA F3) and rounded sum of genotype scores.</p>***<p>Based on exact test of Hardy-Weinberg Equilibrium (HWE).</p

Schematic structure of <i>SREBF1</i> gene.

<p>Exons are numbered indicating the alternatively spliced -a and -c variants. Genomic location of the analyzed single nucleotide polymorphisms are marked. The single nucleotide polymorphisms highlighted in yellow showed a strongly associated with adiponectin levels in our study. The single nucleotide polymorphism highlighted in grey showed a significant association in a previous study <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0052497#pone.0052497-Felder1" target="_blank">[26]</a> and was only borderline significantly associated in the present study (p = 0.004).</p

Linkage disequilibrium structure across the <i>SREBF1</i> single nucleotide polymorphisms.

<p>The pair wise linkage disequilibrium (R² and D’) is given for each pair of single nucleotide polymorphisms. Color-coding is based on R². The diagonal line indicates the physical position of the single nucleotide polymorphisms relative to each other.</p

Clinical characteristics of the subjects from SAPHIR, KORA F3 and CoLaus studies (means ± SD or numbers (%)), for whom all relevant variables and genotypes are available.

<p>Clinical characteristics of the subjects from SAPHIR, KORA F3 and CoLaus studies (means ± SD or numbers (%)), for whom all relevant variables and genotypes are available.</p

Fibre type composition and capillarisation.

<p>Example of serial cross-sectional images of <i>vastus lateralis</i> muscle biopsies immunostained for (A) slow myosin heavy chain (MHC), (B) fast MHC, and (C) the endothelial cell marker CD31. Numbers mark identical slow muscle fibres in the section series. Scale bar: 50 μm.</p

Effect of genotype and 10-weeks supervised stationary cycling on anthropometric variables, aerobic capacity and power, myocellular variables and mitochondria enzyme activity.

<p>Values are paired differences ± SE from paired sample <i>t</i>-Test after testing with general linear model for repeated measures; <i>p</i> = significant interaction between time and genotype; *<i>p</i>≤.05, **<i>p</i>≤.01 and ***<i>p</i> ≤.001 indicate significant differences of pre vs. post measures within group; ns, not significant; for other abbreviations see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0123881#pone.0123881.t001" target="_blank">Table 1</a>.</p><p>Effect of genotype and 10-weeks supervised stationary cycling on anthropometric variables, aerobic capacity and power, myocellular variables and mitochondria enzyme activity.</p

Relative changes [%] of muscle characteristics in response to the 10 weeks endurance training programme.

<p>(A) Control individuals (GT1) show a significant increase of the slow fibre proportion after training while carriers of SNP Gly482Ser (GT2) are unaffected. (B) There is no difference between GT1 and GT2 in the increase of capillaries. (C) Controls (GT1) and SNP carriers (GT2) exhibit no significant differences in the training-induced increases in volume density of slow fibre mitochondria and intramyocellular lipid (IMCL). (D) The increases of fast fibre mitochondria and IMCL are also similar in GT1 and GT2. (E) Similarly, post-training increases in amounts of mitochondria as indicated by the activities of CS and OXPHOS enzymes do not significantly diverge between GT1 and GT2. GT1 (n = 13), GT2 (n = 15); data given as means ± SE; * intergroup differences significant at <i>p < 0</i>.<i>05</i>.</p

Baseline characteristics of whole sample and genotypes.

<p>Values are means ±S.E. after one-way ANOVA; GT1 = major allele type in <i>PPARGC1A</i> (G/G, wild type), GT2 = homozygous and heterozygous for minor allele frequency in <i>PPARGC1A</i> (A/A, G/A); BM = body mass, BMI = body mass index; VO_2-RCP = oxygen uptake at respiratory compensation point (RCP, second ventilatory threshold, aerobic capacity), VO_2-peak = peak oxygen uptake at cessation (aerobic power), P_RCP = mechanical power at RCP in Watt, P_max = maximum mechanical power in Watt; SF = slow fibre (MHC slow+/MHC fast-); HF = slow-fast hybrid fibre (MHC slow+/MHC fast+); cap/SF = capillaries per slow fibre; Mito-SF = mitochondria in slow fibre; Mito-FF = mitochondria in fast fibre; Lip-SF = lipid droplets in slow fibre; Lip-FF = lipid droplets in fast fibre; mtDNA = mitochondrial DNA; CS = citrate synthase; C I—V = complex I—V; COX = cytochrome c oxidase; <i>p</i> = significance level between the genotype (GT) groups; <i>ns</i> = not significant.</p><p>Baseline characteristics of whole sample and genotypes.</p