Skeletal muscle reoxygenation after high-intensity exercise in mitochondrial myopathy

Abstract

This study addressed whether O-2 delivery during recovery from high-intensity, supra-gas exchange threshold exercise would be matched to O-2 utilization at the microvascular level in patients with mitochondrial myopathy (MM). Off-exercise kinetics of (1) pulmonary O-2 uptake (V) over dotO(2p)); (2) an index of fractional O-2 extraction by near-infrared spectroscopy (Delta[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 (V) over dotO(2p) were significantly slower in patients than controls (tau = 53.8 +/- 16.5 vs. 38.8 +/- 7.6 s, respectively; p < 0.05). Q'(T)0, however, declined at similar rates (s = 64.7 +/- 18.8 vs. 73.0 +/- 21.6 s; p > 0.05) being typically slower than (V) over dotO(2p) in both groups. Importantly, Delta[deoxy-Hb + Mb] dynamics (MRT) were equal to, or faster than, tau(V) over dotO(2p) in patients and controls, respectively. in fact, there were no between-group differences in tau(V) over dotO(2p)/MRTD[deoxy-Hb + Mb] (1.1 +/- 0.4 vs. 1.0 +/- 0.2, p > 0.05) thereby indicating similar rates of microvascular O-2 delivery. These data indicate that the slower rate of recovery of muscle metabolism after highintensity exercise is not related to impaired microvascular O-2 delivery in patients with MM. This phenomenon, therefore, seems to reflect the intra-myocyte abnormalities that characterize this patient population.