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Abstract

Combining near-infrared spectroscopy (NIRS) with a vascular occlusion test (VOT) is commonly used to assess the determinants of reactive hyperemia. However, the influence of exercise-induced metabolic demand on NIRS-derived outcomes remains unclear. Because reactive hyperemia is governed by redundant endothelial, myogenic, and metabolic factors, incorporating non-fatiguing exercise may provide an experimental approach to differentially emphasize their relative contributions. PURPOSE: Therefore, our purpose was to examine the effects of submaximal exercise on NIRS+VOT indices of skeletal muscle tissue oxygenation (StO2). METHOD: Twelve healthy adults ranging from 18 to 35 years old (6 males and 6 females; 25 ± 6 years; 72.7 ± 10.3 kg) participated in one experimental visit, which included a pre-exercise VOT, a handgrip exercise protocol, and a post-exercise VOT. The ischemic duration during each VOT was standardized to achieve a minimum StO2 of 40% or a maximum duration of 5 minutes. A NIRS probe was positioned over the dominant forearm flexors. Metrics calculated from each VOT included baseline StO2, the rate of desaturation during ischemia (downslope; first 30 s), the rate of resaturation during reperfusion (upslope; first 10 s), and the peak reperfusion saturation (StO2max). The exercise consisted of 30 intermittent handgrip contractions at 50% maximal voluntary contraction (MVC). RESULTS: Paired t-tests were used to compare pre- and post-exercise outcomes, with 95% confidence intervals (CI95%) reported for mean differences. A p ≤ 0.05 was considered significant. Mean force during exercise was 46.0 ± 10.2% MVC. Baseline StO2 significantly decreased (66.6 ± 3.9 vs. 64.2 ± 2.5%; p = 0.01; CI95% = 0.63 to 4.0%). Downslope increased significantly (p < 0.01), indicating faster deoxygenation (-0.112 ± 0.06 vs. -0.612 ± 0.21 %·s⁻¹; CI95% = 0.39 to 0.61%· s⁻¹), and accordingly, the ischemic duration decreased after exercise (223.9 ± 72.6 vs. 135.9 ± 122.8 s; p < 0.01, CI95% = 40.7 to 135.2 s). For the reactive hyperemia metrics, upslope increased (p < 0.01), reflecting faster reoxygenation (2.15 ± 0.66 vs. 2.60 ± 0.64 %· s⁻¹; CI95% = 0.31 to 0.60%· s⁻¹). In contrast, StO2max declined following exercise (79.3 ± 3.8 vs. 74.6 ± 3.4%; p < 0.01; CI95% = 3.6 to 5.8%). CONCLUSION: These findings suggest that moderate intensity handgrip exercise elevates metabolic vasodilator activity (e.g., K⁺, adenosine), accelerating resaturation, but simultaneously attenuates peak hyperemia, possibly through a blunted myogenic response to altered transmural pressure. Thus, this experimental model may help further specify the mechanisms provoking sex- and age-related differences commonly reported in the available NIRS+VOT literature. Future studies incorporating a time-matched, non-exercise control condition are warranted to strengthen these interpretations. Additionally, studies designed to determine whether these exercise-modified responses differ between men and women or across age groups are warranted.

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