Skeletal Muscle Neurovascular Coupling, Oxidative Capacity, and Microvascular Function with 'One Stop Shop' Near-infrared Spectroscopy

Abstract

Exercise represents a major hemodynamic stress that demands a highly coordinated neurovascular response in order to match oxygen delivery to metabolic demand. Reactive hyperemia (in response to a brief period of tissue ischemia) is an independent predictor of cardiovascular events and provides important insight into vascular health and vasodilatory capacity. Skeletal muscle oxidative capacity is equally important in health and disease, as it determines the energy supply for myocellular processes. Here, we describe a simple, non-invasive approach using near-infrared spectroscopy to assess each of these major clinical endpoints (reactive hyperemia, neurovascular coupling, and muscle oxidative capacity) during a single clinic or laboratory visit. Unlike Doppler ultrasound, magnetic resonance images/spectroscopy, or invasive catheter-based flow measurements or muscle biopsies, our approach is less operator-dependent, low-cost, and completely non-invasive. Representative data from our lab taken together with summary data from previously published literature illustrate the utility of each of these end-points. Once this technique is mastered, application to clinical populations will provide important mechanistic insight into exercise intolerance and cardiovascular dysfunction.

The Association Between Contrast-Enhanced Ultrasound and Near-Infrared Spectroscopy-Derived Measures of Calf Muscle Microvascular Responsiveness in Older Adults

“…The magnitude of the O 2 Hb response in the present study is also similar to previous NIRS findings [15]. Post-occlusion hyperaemia is a homeostatic response to the oxygen deficit caused by arterial cuff occlusion, reflecting vasodilatory capacity [26]. As such, the magnitude of the response is related to the magnitude of the oxygen deficit, which is influenced by cuff-occlusion duration [19,21].…”

The 72-Hour Microcirculation Dynamics in Viable Free Flap Reconstructions

“…This results in reactive vasodilatation and hyperemia in response to the tissues increased metabolic needs after reanastomosis. 24 25 Moreover, the increase of flow compensates for a reduction in SO 2 , caused by increased tissue oxygen consumption postanastomosis. 16 17 26 However, it is without doubt that further research is required within the field of free flap physiology to fully understand the changes in microcirculation after anastomosis that account for the observed changes of flow and SO 2 measured using the O2C monitoring device.…”