Skeletal muscle reoxygenation after high-intensity exercise in mitochondrial myopathy

Abstract

This study addressed whether O₂ delivery during recovery from high-intensity, supra-gas exchange threshold exercise would be matched to O₂ utilization at the microvascular level in patients with mitochondrial myopathy (MM). Off-exercise kinetics of (1) pulmonary O₂ uptake $(\dot{V}{\text{O}}_{2} {\text{p}}),$ (2) an index of fractional O₂ extraction by near-infrared spectroscopy (Δ[deoxy-Hb + Mb]) in the vastus lateralis and (3) cardiac output (Q ^′_T ) by impedance cardiography were assessed in 12 patients with biopsy-proven MM (chronic progressive external ophthalmoplegia) and 12 age- and gender-matched controls. Kinetics of $\dot{V}{\text{O}}_{2} {\text{p}}$ were significantly slower in patients than controls (τ = 53.8 ± 16.5 vs. 38.8 ± 7.6 s, respectively; p < 0.05). Q ^′_T , however, declined at similar rates (τ = 64.7 ± 18.8 vs. 73.0 ± 21.6 s; p > 0.05) being typically slower than $\dot{V}{\text{O}}_{2} {\text{p}}$ in both groups. Importantly, Δ[deoxy-Hb + Mb] dynamics (MRT) were equal to, or faster than, $\tau \dot{V}{\text{O}}_{2} {\text{p}}$ in patients and controls, respectively. In fact, there were no between-group differences in $\tau \dot{V}{\text{O}}_{2} {\text{p}}$/MRTΔ[deoxy-Hb + Mb] (1.1 ± 0.4 vs. 1.0 ± 0.2, p > 0.05) thereby indicating similar rates of microvascular O₂ delivery. These data indicate that the slower rate of recovery of muscle metabolism after high-intensity exercise is not related to impaired microvascular O₂ delivery in patients with MM. This phenomenon, therefore, seems to reflect the intra-myocyte abnormalities that characterize this patient population.