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Kyle Heise
Skidmore College
Kyle Heise, an undergraduate student at Skidmore College, investigated whether sympathetic nervous system (SNS) activation induced by lower body negative pressure (LBNP) alters near-infrared spectroscopy vascular occlusion test (NIRS-VOT) responses. In 39 healthy adults, participants completed randomized trials while forearm muscle oxygen saturation (SMO₂) and central hemodynamics were measured. LBNP significantly altered cardiovascular parameters, including reduced heart rate, cardiac output, and stroke volume, and increased mean arterial pressure, but most NIRS-VOT measures of microvascular function remained unchanged. The only difference observed was a faster time-to-peak SMO₂, indicating enhanced reoxygenation during sympathetic activation. These findings suggest that SNS activation via LBNP does not meaningfully alter most NIRS-VOT indicators of microvascular function, though it may influence recovery kinetics. Kyle will present his research at the American Physiology Summit in Minneapolis, Minnesota in April.
ABSTRACT
Introduction: The Near-Infrared Spectroscopy Vascular Occlusion Test (NIRS-VOT) is a novel method for assessing microvascular function in vivo. The influence of acute sympathetic nervous system (SNS) activation on its outcomes remains unclear. Lower Body Negative Pressure (LBNP) is a safe model for cardiopulmonary baroreceptor unloading that increases SNS activity. Understanding whether SNS activation alters NIRS-VOT kinetics is essential for interpreting data in populations with elevated sympathetic tone, such as aging or disease. Purpose: To determine whether SNS activation via LBNP (–20 mmHg) alters NIRS-VOT microvascular metrics in healthy adults and to identify potential sex or inter-arm differences. It was hypothesized that LBNP would promote greater deoxygenation but lower reoxygenation slopes due to greater sympathetic activity and vasoconstriction. Methods: Healthy men and women (N = 39; 17 men, 22 women) completed three randomized trials (Control Right, LBNP Left, LBNP Right). NIRS-VOT was performed on both forearms to measure muscle oxygen saturation (SMO₂). Central hemodynamics and blood pressure were measured continuously. Results: LBNP decreased heart rate (p < 0.001, η²ₚ = 0.400), cardiac output (p < 0.001, η²ₚ = 0.501), stroke volume (p = 0.031, η²ₚ = 0.179), and increased mean arterial pressure (p < 0.001, η²ₚ = 0.396). No sex × condition interactions were observed. RMSSD decreased significantly (p = 0.012, η²ₚ = 0.41), whereas RR interval was unchanged (p = 0.814, η²ₚ = 0.03). Baseline SMO₂ (p = 0.415, η²ₚ = 0.019), Slope 1 (p = 0.683, η²ₚ = 0.005), Slope 2 SMO₂ (p = 0.987, η²ₚ ≈ 0), time to halfway (p = 0.867, η²ₚ ≈ 0), and peak SMO₂ (p = 0.555, η²ₚ = 0.010) were unchanged. LBNP reduced time-to-peak SMO₂ (p = 0.015, η²ₚ = 0.154), indicating faster recovery. Adjusted skinfold influenced time-to-peak (p = 0.038, η²ₚ = 0.114) and peak SMO₂ (p = 0.035, η²ₚ = 0.118), with no effects on other outcomes. Regression analyses showed body fat % predicted baseline SMO₂ in both Control (p = .001, R² = 0.71) and LBNP (p = .017, R² = 0.48). Under Control, Slope 2 SMO₂ was predicted by baseline RMSSD (p = .038). During LBNP, Slope 2 SMO₂ was predicted by body fat % (p = .016) and diastolic BP (p = .026), while time-to-peak SMO₂ was predicted by skinfold thickness (p = .023). Time-to-halfway was predicted by grip strength alone (p < .001) and together with skinfolds (p < .001). All other variables were excluded from final models. Conclusion: LBNP did not change microvascular function as measured by Slope 1, Slope 2 SMO₂, baseline SMO₂, time-to-halfway, or peak SMO₂. The only NIRS-VOT change was faster time-to-peak SMO₂, suggesting enhanced recovery kinetics under sympathetic activation. Individual characteristics including body fat %, diastolic BP, grip strength, and skinfold thickness influenced specific NIRS-VOT outcomes. No sex differences were observed. Funding: This work was funded by the AHA awarded to SJI (#24AIREA1247045).
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