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Acute Inactivity Impairs Glycemic Control but Not Blood Flow to Glucose Ingestion


Medicine & Science in Sports & Exercise: May 2015 - Volume 47 - Issue 5 - p 1087–1094
doi: 10.1249/MSS.0000000000000508
Applied Sciences

Purpose Insulin-stimulated increases in skeletal muscle blood flow play a role in glucose disposal. Indeed, 7 d of aerobic exercise in patients with Type 2 diabetes increased blood flow responses to an oral glucose tolerance test (OGTT) and improved insulin sensitivity. More recent work suggests that reduced daily physical activity impairs glycemic control (GC) in healthy individuals. Herein, we sought to determine whether an acute reduction in daily activity (from >10,000 to <5000 steps per day) for 5 d (RA5) in healthy individuals reduced insulin-stimulated blood flow and GC in parallel and if a 1-d return to activity (RTA1) improved these outcomes.

Methods OGTT were performed as a stimulus to increase insulin in 14 healthy, recreationally active men (24 ± 1.1 yr) at baseline, RA5, and RTA1. Measures of insulin sensitivity (Matsuda index) and femoral and brachial artery blood flow were made during the OGTT. Free-living measures of GC including peak postprandial glucose (peak PPG) were also made via continuous glucose monitoring.

Results Femoral and brachial artery blood flow increased during the OGTT but neither was significantly impacted by changes in physical activity (P > 0.05). However, insulin sensitivity was decreased by RA5 (11.3 ± 1.5 to 8.0 ± 1.0, P < 0.05). Likewise, free-living GC measures of peak PPG (113 ± 3 to 123 ± 5 mg·dL−1, P < 0.05) was significantly increased at RA5. Interestingly, insulin sensitivity and GC as assessed by peak PPG were not restored after RTA1 (P > 0.05).

Conclusions Thus, acute reductions in physical activity impaired GC and insulin sensitivity; however, blood flow responses to an OGTT were not affected. Further, a 1-d return to activity was not sufficient to normalize GC after 5 d of reduced daily physical activity.

1Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO; 2Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO; and 3Division of Gastroenterology and Hepatology, Department of Medicine, University of Missouri, Columbia, MO

Address for correspondence: John P. Thyfault, Ph.D., Department of Nutrition and Exercise Physiology and Medicine, University of Missouri School of Medicine, One Hospital Drive, NW502 Health Sciences Building, Columbia, MO 65212; E-mail:

Submitted for publication June 2014.

Accepted for publication September 2014.

© 2015 American College of Sports Medicine