Muscle Oxygenation of the Paretic and Nonparetic Legs During and After Arterial Occlusion in Chronic Stroke

Abstract

Oxygen delivery and demand are reduced in the paretic leg post-stroke, reflecting decreased vascular function and reduced muscle quantity and quality. However, it is unknown how muscle oxygenation, the balance between muscle oxygen delivery and utilization, is altered in chronic stroke during and after occlusion-induced ischemia. ObjectivesThe objective was to determine muscle oxygen consumption rate, microvascular responsiveness and reactive hyperemia in the paretic and nonparetic legs during and after arterial occlusion post-stroke. Materials and MethodsMuscle oxygen saturation was measured with near-infrared spectroscopy on the vastus lateralis of each leg during 3-minute arterial occlusion and recovery (3 min). Muscle oxygen consumption was derived from the desaturation slope during ischemia, microvascular responsiveness was derived from the resaturation slope after ischemia and reactive hyperemia was derived from the area under the curve above baseline after ischemia. Results: Eleven subjects (91% male; 32.2±6.1 months post-stroke; age 62.9±13.6 years) with a hemiparetic gait pattern participated. There was no significant between-leg muscle oxygenation difference at rest (paretic: 64.9±16.6%; nonparetic: 70.6±15.6%, p = 0.13). Muscle oxygen consumption in the paretic leg (-0.53±0.24%/s) was significantly reduced compared to the nonparetic leg (-0.70±0.36%/s; p = 0.03). Microvascular responsiveness was significantly reduced in the paretic leg compared to the nonparetic leg (paretic: 4.6±1.8%/s; nonparetic: 5.7±1.6%/s, p = 0.04). Reactive hyperemia was not significantly different between legs (paretic:4384±2341%·s; nonparetic: 3040±2216%·s, p = 0.07). ConclusionMuscle oxygen consumption and microvascular responsiveness are impaired in the paretic compared to the nonparetic leg, suggesting both reduced skeletal muscle aerobic function and reduced ability to maximally perfuse muscle tissue.