BACKGROUND: Vascular occlusion tests (VOT) provide a useful index of microvascular function, which is a known predictor of cardiovascular disease (CVD). Handgrip (HG) strength has emerged as a valuable metric to assess CVD risk. However, little remains known regarding VOT responses among adults of various strength levels. Therefore, our purpose was test for differences between groups of low and high strength, as quantified by HG. METHODS: Fifty (50% female), midlife to older adults (64±9 yr) completed a VOT (3 min baseline, 5 min occlusion, 3 min reperfusion) with a near-infrared spectroscopy device attached to the forearm. This test provided an index of skeletal muscle oxygenation (StO2, %) during periods of transient ischemia and the immediate post-occlusion period of reactive hyperemia (RH) (e.g., marker of microvascular function). To describe RH, the initial (1st ten s) rate of reperfusion was calculated via simple linear regression. Additionally, the maximum value observed post-occlusion was defined as StO2max. Participants were separated into high and low strength groups based on the 50th percentile for both sexes. That is, men and women were equally distributed into the low and high groups. Independent t-tests were used to examine mean differences, and p≤0.05 was considered significant. RESULTS: The high group exhibited significantly greater HG strength than the low strength group (36.1 ± 7.8 vs. 25.6 ± 5.9 kg; p<0.001). However, there were no differences (p>0.05) between the groups for baseline StO2 (68.1 ± 4.0 vs. 65.3 ± 6.1%) or rate of desaturation during ischemia (-0.103 ± 0.03 vs. -0.118 ± 0.03%∙s-1). For RH, the stronger group demonstrated significantly greater StO2max (79.5 ± 3.4 vs. 77.0 ± 4.0%; p=0.019), but interestingly, the lower strength group resulted in a faster rate of reperfusion (1.83 ± 0.7 vs. 2.27 ± 0.7%∙s-1;p=0.032). CONCLUSIONS: There were inconsistent RH responses between the high and low strength groups. Thus, the initial rate of reperfusion and StO2max likely reflect different underlying mechanisms and may not be equally influenced by HG strength. Additionally, our low strength group may have been above a clinical HG strength threshold (e.g., 19 kg cut-off) such that those individuals still presented with relatively low risks. Future studies are needed to further understand HG sensitivity in qualifying CVD risks, especially as it relates to the peripheral microvasculature.

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