The aim of this study was to examine the effect of brisk walking on cardiometabolic risk profile and on the gene expression (ie, messenger RNA [mRNA] levels) of inflammatory and thrombotic markers in abdominal and femoral subcutaneous adipose tissues (SATs) among sedentary overweight to obese women with different menopause statuses.
Sixteen late premenopausal (mean [SD] age, 49  y; mean [SD] body mass index, 31.9 [3.0] kg/m2) and 14 early postmenopausal (53  y; 30.8 [1.9] kg/m2) women were involved in a 16-week walking program (three sessions of 45 min/wk at 60% of heart rate reserve). Glucose-insulin homeostasis, lipid-lipoprotein profile, and inflammatory (tumor necrosis factor-α, interleukin-6 [IL-6], and adiponectin) and thrombotic (plasminogen activator inhibitor-1) SAT mRNA and plasma levels were measured before and after the intervention.
Glucose area under the curve was reduced in all participants (P = 0.03) after the walking program. Increases in plasma tumor necrosis factor-α were observed in both groups (P = 0.001), whereas increases in plasminogen activator inhibitor-1 levels were found in postmenopausal women only (P = 0.014). However, plasma IL-6 and adiponectin levels remained unchanged after the intervention (0.07 < P < 0.98). Although femoral SAT adiponectin mRNA levels decreased in postmenopausal women only (P = 0.008), abdominal SAT IL-6 mRNA levels were reduced in both groups (P = 0.01).
Taken together, our results show that, despite a reduced abdominal SAT IL-6 expression, brisk walking does not seem to exert a favorable impact on the cardiometabolic risk profile of overweight to obese women, irrespective of their menopause status.
From the 1Faculty of Physical Education and Sports, University of Sherbrooke, Sherbrooke, Canada; 2Research Center on Aging, Le Centre de santé et de services sociaux, Institut universitaire de gériatrie de Sherbrooke, Sherbrooke, Canada; 3Institut National de Santé Publique de Québec, Québec, Canada; 4Department of Kinesiology, Faculty of Medicine, Université Laval, Québec, Canada; 5Centre de recherche de l’Institut Universitaire de Cardiologie et de Pneumologie de Québec, Université Laval, Québec, Canada; and 6Lipid Research Center and 7Diabetes Research Unit, Centre de Recherche du Centre Hospitalier Universitaire de Québec, Québec, Canada.
Received February 19, 2012; revised and accepted June 14, 2012.
Funding/support: This study was supported by the Canadian Institutes of Health Research (grant MOP 77572 to P.M.).
Financial disclosure/conflicts of interest: None reported.
The authors alone are responsible for the content and writing of this article.
E.R. performed data collection, statistical analyses, and figure and manuscript preparation. S.T. was responsible for supervision of training, part of data collection, and manuscript preparation. M.L. and F.P. performed recruitment, supervision of laboratory experiments and data collection, and manuscript preparation. M.C. carried out part of data collection (plasma adiponectin levels) and manuscript revision. J.D. and J.S.W. were coinvestigators and performed physical examination of all participants throughout the study, supervision of adipose tissue biopsies, and manuscript revision. J.-P.D. and J.B. were collaborators and carried outpart of data collection (plasma high-sensitivity C-reactive protein, fibrinogen, adipokine, and plasminogen activator inhibitor-1 levels) and manuscript revision. P.M. was principal investigator and senior writer, and performed study design, supervision of data collection and analyses, manuscript preparation, and revision.
Address correspondence to: Pascale Mauriège, PhD, Department of Kinesiology, Faculty of Medicine, Laval University, Québec, Canada G1V 0A6. E-mail: Pascale.Mauriege@kin.ulaval.ca