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Background  Regular exercise reduces cardiovascular and metabolic disease partly through improved aerobic fitness. The determinants of exercise-induced gains in aerobic fitness in humans are not known. We have demonstrated that over 500 genes are activated in response to endurance-exercise training, including modulation of muscle extracellular matrix (ECM) genes. Real-time quantitative PCR, which is essential for the characterization of lower abundance genes, was used to examine 15 ECM genes potentially relevant for endurance-exercise adaptation. Twenty-four sedentary male subjects undertook six weeks of high-intensity aerobic cycle training with muscle biopsies being obtained both before and 24 h after training. Subjects were ranked based on improvement in aerobic fitness, and two cohorts were formed (n = 8 per group): the high-responder group (HRG; peak rate of oxygen consumption increased by +0.71 ± 0.1 L min -1 ; p < 0.0001) while the low-responder group (LRG; peak rate of oxygen consumption did not change, +0.17 ± 0.1 L min -1 , ns). ECM genes profiled included the  angiopoietin 1  and related genes ( angiopoietin 2 ,  tyrosine kinase with immunoglobulin-like and EGF-like domains 1 (TIE1) and 2  ( TIE2 ),  vascular endothelial growth factor  ( VEGF ) and related receptors ( VEGF receptor 1, VEGF receptor 2 and neuropilin-1 ),  thrombospondin-4 ,  α2-macroglobulin  and  transforming growth factor β2 .    Results   neuropilin-1  (800%; p < 0.001) and  VEGF receptor 2  (300%; p < 0.01) transcript abundance increased only in the HRG, whereas levels of  VEGF receptor 1  mRNA actually declined in the LRG (p < 0.05).  TIE1  and  TIE2  mRNA levels were unaltered in the LRG, whereas transcription levels of both genes were increased by 2.5-fold in the HRG (p < 0.01). Levels of  thrombospondin-4  (900%; p < 0.001) and  α2-macroglobulin  (300%, p < 0.05) mRNA increased substantially in the HRG. In contrast, the amount of  transforming growth factor β2  transcript increased only in the HRG (330%; p < 0.01), whereas it remained unchanged in the LRG (-80%).    Conclusion  We demonstrate for the first time that aerobic training activates  angiopoietin 1  and  TIE2  genes in human muscle, but only when aerobic capacity adapts to exercise-training. The fourfold-greater increase in aerobic fitness and markedly differing gene expression profile in the HRG indicates that these ECM genes may be critical for physiological adaptation to exercise in humans. In addition, we show that, without careful demonstration of physiological adaptation, conclusions derived from gene expression profiling of human skeletal muscle following exercise may be of limited value. We propose that future studies should (a) investigate the mechanisms that underlie the apparent link between physiological adaptation and gene expression and (b) use the genes profiled in this paper as candidates for population genetic studies.

Modulation of extracellular matrix genes reflects the magnitude of physiological adaptation to aerobic exercise training in humans