ACE inhibition modifies exercise-induced pro-angiogenic and mitochondrial gene transcript expression.

Skeletal muscle responds to endurance exercise with an improvement of biochemical pathways that support substrate supply and oxygen-dependent metabolism. This is reflected by enhanced expression of associated factors after exercise and is specifically modulated by tissue perfusion and oxygenation. W...

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Publicado en:Scandinavian Journal of Medicine & Science in Sports (John Wiley & Sons, Inc.) Vol. 26; no. 10; pp. 1180 - 1188
Autores principales: Ginkel, S., Ruoss, S., Valdivieso, P., Degens, H., Waldron, S., Haan, A., Flück, M.
Formato: pictorial research tables/charts Journal Article
Publicado: John Wiley & Sons, Inc. Oct2016
Acceso en línea:Ver este registro en EBSCOhost
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      jtl: Scandinavian Journal of Medicine & Science in Sports (John Wiley & Sons, Inc.)
      issn: 16000838
      maglogo: N
    pubinfo:
      dt: Oct2016
      vid: 26
      iid: 10
      pid: 52269
      pub: John Wiley & Sons, Inc.
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        118370254
        10.1111/sms.12572
        118370254
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        atl: ACE inhibition modifies exercise-induced pro-angiogenic and mitochondrial gene transcript expression.
      aug:
        au:
          Ginkel, S.
          Ruoss, S.
          Valdivieso, P.
          Degens, H.
          Waldron, S.
          Haan, A.
          Flück, M.
        affil: School of Healthcare Science, Manchester Metropolitan University, Manchester UK
      sug:
        subj:
          Gene Expression
          Angiotensin-Converting Enzyme Inhibitors Therapeutic Use
          Exercise Physiology
          Muscle, Skeletal Metabolism
          Transcription Factors
          Adaptation, Physiological
          Vasoconstriction
          Biopsy
          Vascular Endothelial Growth Factors
          Cycling
          Blood Pressure
          Aerobic Capacity
          Exercise Test
          Prospective Studies
          Data Analysis Software
          Paired T-Tests
          Analysis of Variance
          P-Value
          Clinical Assessment Tools
          Adult
          Male
          Human
          Adult: 19-44 years
          Male
      ab: Skeletal muscle responds to endurance exercise with an improvement of biochemical pathways that support substrate supply and oxygen-dependent metabolism. This is reflected by enhanced expression of associated factors after exercise and is specifically modulated by tissue perfusion and oxygenation. We hypothesized that transcript expression of pro-angiogenic factors ( VEGF, tenascin- C, Angpt1, Angpt1 R) and oxygen metabolism ( COX4I1, COX4I2, HIF-1α) in human muscle after an endurance stimulus depends on vasoconstriction, and would be modulated through angiotensin-converting enzyme inhibition by intake of lisinopril. Fourteen non-specifically trained, male Caucasians subjects, carried out a single bout of standardized one-legged bicycle exercise. Seven of the participants consumed lisinopril in the 3 days before exercise. Biopsies were collected pre- and 3 h post-exercise from the m. vastus lateralis. COX4I1 ( P = 0.03), COX4I2 ( P = 0.04) m RNA and HIF-1α ( P = 0.05) m RNA and protein levels ( P = 0.01) showed an exercise-induced increase in the group not consuming the ACE inhibitor. Conversely, there was a specific exercise-induced increase in VEGF transcript ( P = 0.04) and protein levels ( P = 0.03) and a trend for increased tenascin-c transcript levels ( P = 0.09) for subjects consuming lisinopril. The observations indicate that exercise-induced expression of transcripts involved in angiogenesis and mitochondrial energy metabolism are to some extent regulated via a hypoxia-related ACE-dependent mechanism.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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