Preserved contribution of nitric oxide to baseline vascular tone in deconditioned human skeletal muscle

Abstract

Deconditioning is a risk factor for cardiovascular disease. Exercise reduces this risk, possibly by improving the vascular endothelial nitric oxide (NO) pathway. The effect of deconditioning on the NO pathway is largely unknown. This study was designed to assess baseline NO availability in the leg vascular bed after extreme, long-term deconditioning (spinal cord-injured individuals, SCI) as well as after moderate, short-term deconditioning (4 weeks of unilateral lower limb suspension, ULLS). For this purpose, seven SCI were compared with seven matched controls. Additionally, seven healthy subjects were studied pre- and post-ULLS. Leg blood flow was measured by venous occlusion plethysmography at baseline and during infusion of 5 incremental dosages of N(G)-monomethyl-L-arginine (L-NMMA) into the femoral artery. Sodium nitroprusside (SNP) was infused to test vascular responsiveness to NO. Baseline leg vascular resistance tended to be higher in SCI compared with controls (37+/-4 versus 31+/-2 arbitrary units (AU), P=0.06). Deconditioning altered neither the vasoconstrictor response to L-NMMA (increase in resistance in SCI versus controls: 102+/-33% versus 69+/-9%; pre- versus post-ULLS: 95+/-18% versus 119+/-15%), nor the vascular responsiveness to NO. In conclusion, two human in vivo models of deconditioning show a preserved baseline NO availability in the leg skeletal muscle vascular bed.

Figure 1. Change in leg vascular resistance in response to l-NMMA (0.025–0.05–0.1–0.2–0.4 mg min⁻¹ dl⁻¹ of leg tissue), SNP (0.06–0.2–0.6 μg min⁻¹ dl⁻¹), and angiotensin II (Ang II 0.25–0.5–2.0 ng min⁻¹ dl⁻¹)

A, spinal cord-injured individuals versus matched controls (• and ○, respectively). B, healthy subjects before and after ULLS (○ and •, respectively). Data represent means and s.e.m.