Near-infrared assessments of skeletal muscle oxidative capacity in persons with spinal cord injury.

After spinal cord injury (SCI) skeletal muscle decreases in size, increases in intramuscular fat, and has potential declines in mitochondrial function. Reduced mitochondrial function has been linked to the development of metabolic disease. The aim of this study was to measure mitochondrial function in persons with SCI using near-infrared spectroscopy (NIRS). Oxygen consumption of the vastus lateralis muscle was measured with NIRS during repeated short-duration arterial occlusions in nine able-bodied (AB) and nine persons with motor complete SCI. Skeletal muscle oxidative capacity (V max) was evaluated with two approaches: (1) rate constant of the recovery of oxygen consumption after exercise and (2) extrapolated maximum oxygen consumption from a progressive work test. V max as indicated by the rate constant (k) from the recovery kinetics test was lower in SCI compared with AB participants (k: SCI 0.7 ± 0.3 vs. AB 1.9 ± 0.4 min(-1); p < 0.001). Time constants were SCI 91.9 ± 37.8 vs. AB 33.6 ± 8.3 s. V max from the progressive work test approached a significant difference between groups (SCI 5.1 ± 2.9 vs. AB 9.8 ± 5.5 % Hb-Mb/s; p = 0.06). NIRS measurements of V max suggest a deficit of 50-60 % in participants with SCI compared with AB controls, consistent with previous studies using (31)P-MRS and muscle biopsies. NIRS measurements can assess mitochondrial capacity in people with SCI and potentially other injured/diseased populations.

There's more to flow-mediated dilation than nitric oxide.

Flow-mediated dilation (FMD) is the standard tool used to assess endothelial function. The premise behind the standard FMD test is that it serves as an endothelial-dependant nitric oxide bioassay; however, the endothelium may release additional dilatory molecules which contribute to FMD, most notably prostacyclin and endothelial-derived hyperpolarizing factor. The relative importance of these molecules to the dilatory response may vary substantially among individuals, particularly in response to a number of diseased states. This review discusses how each of these molecules may contribute to vasodilation, and considers the circumstances in which they may vary.