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

S van Ginkel1,2, S Ruoss3, P Valdivieso3

  • 1School of Healthcare Science, Manchester Metropolitan University, Manchester, UK.

Scandinavian Journal of Medicine & Science in Sports
|September 27, 2015
PubMed
Summary
This summary is machine-generated.

Endurance exercise enhances muscle metabolism, but ACE inhibition with lisinopril shifts gene expression towards angiogenesis. This suggests a hypoxia-related mechanism regulates exercise-induced gene responses.

Keywords:
Muscleangiotensinexercisegenehypertensionhypoxialisinoprilperfusion

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Area of Science:

  • Exercise Physiology
  • Molecular Biology
  • Pharmacology

Background:

  • Skeletal muscle adapts to endurance exercise through enhanced metabolic pathways and gene expression.
  • Tissue perfusion and oxygenation are key modulators of these exercise-induced adaptations.
  • The role of angiotensin-converting enzyme (ACE) inhibition in modulating these responses is not fully understood.

Purpose of the Study:

  • To investigate the impact of ACE inhibition (lisinopril) on exercise-induced gene and protein expression related to angiogenesis and oxygen metabolism in human skeletal muscle.
  • To determine if vasoconstriction influences the expression of pro-angiogenic and oxygen metabolism factors post-exercise.
  • To explore the potential hypoxia-related ACE-dependent mechanism in exercise adaptation.

Main Methods:

  • A single bout of standardized one-legged bicycle exercise was performed by 14 male Caucasians.
  • Seven participants received lisinopril for 3 days prior to exercise.
  • Muscle biopsies from the m. vastus lateralis were collected pre- and 3 hours post-exercise for molecular analysis.

Main Results:

  • Exercise increased mRNA for COX4I1, COX4I2, and HIF-1α, and protein levels for HIF-1α in the non-lisinopril group.
  • In the lisinopril group, exercise specifically increased VEGF mRNA and protein, with a trend for tenascin-c mRNA.
  • These findings suggest ACE inhibition alters the molecular response to exercise.

Conclusions:

  • Exercise-induced expression of angiogenesis and mitochondrial energy metabolism transcripts are partly regulated by a hypoxia-related, ACE-dependent mechanism.
  • ACE inhibition may shift the adaptive response of skeletal muscle to endurance exercise.
  • Further research is warranted to elucidate the precise pathways involved.