高血圧ジャーナル: オープンアクセス

Matrix Metalloproteinase-9 and Augmentation Index are Reduced with an 8-Week Green-Exercise Walking Programme

Abstract

Jane ES Thompson, Richard Webb, Paul Hewlett, David Llewellyn, Barry J Mcdonnell

Objectives: MMP-9 is involved in degrading the Extracellular Matrix (ECM); specifically elastin, which provides elasticity to the arterial wall. Elastin degradation and restructuring of the ECM results in increased vascular remodelling and arterial stiffness. Conversely, exercise improves age-related vascular stiffening. Therefore, this study aimed to investigate whether participation in a green-exercise programme affects vascular haemodynamics and mRNA expression of MMP-9.

Methods: Thirty-six healthy, sedentary individuals (44 ± 2yrs; not taking any cardiovascular-acting medication) joining a moderate-intensity, aerobic green-exercise programme, were recruited. At baseline and 8-weeks into the programme, physical activity (measured in weekly MET-minutes [IPAQ]), supine Mean Arterial Blood Pressure (MAP), Augmentation Index (AIx) and aortic Pulse Wave Velocity (aPWV) data were collected and blood samples were obtained. Leukocytic MMP-9 mRNA expression (RT-PCR) and plasma protein levels (ELISA) were analysed; AIx and aPWV were measured via applanation tonometry (SphygmoCor, Atcor Medical, Australia).

Results: The cohort was split into those who adhered (n=17) and did not adhere (n=19) to the programme. MMP-9 expression, MAP and AIx all decreased significantly in the exercise-adherent group (cf. the non-adherent group), while significant correlations were seen between: (i) ΔMMP-9 expression and ΔMET-minutes/wk; (ii) ΔMMP-9 expression and ΔAIx; (iii) ΔAIx and ΔMET-minutes/wk (P<0.05 in all cases). aPWV did not change significantly between the groups.

Conclusions: These findings suggest that exercise-induced down-regulation of MMP-9 may contribute to reduced ECM degradation and therefore ameliorate vascular remodelling. Additional studies are needed to explore these findings further; however, these data may provide a biomolecular mechanism for aerobic exercises ability to delay age-related increases in arterial stiffening.