Aerobic training enhances muscle deoxygenation in early post-myocardial infarction

Exercise-induced skeletal muscle deoxygenation is startling by its absence in early post-myocardial infarction (MI) patients. Exercise training early post-MI is associated with reduced cardiovascular risk and increased aerobic capacity. We therefore investigated whether aerobic training could enhance the muscle deoxygenation in early post-MI patients. 21 +/- A 8 days after the first MI patients (n = 16) were divided into 12-week aerobic training (TR, n = 10) or non-training (CON, n = 6) groups. Before and after intervention, patients performed ramp bicycle exercise until exhaustion. Muscle deoxygenation was measured at vastus lateralis by near-infrared spectroscopy during exercise. Aerobic training significantly increased peak oxygen uptake (VO2) (18.1 +/- A 3.0 vs. 22.9 +/- A 2.8 mL/kg/min), decreased the change in muscle oxygen saturation from rest to submaximal and peak exercise (a dagger SmO2; 2.4 +/- A 5.7 vs. -7.0 +/- A 3.4 %), and increased the relative change in deoxygenated hemoglobin/myoglobin concentration from rest to submaximal (-1.5 +/- A 2.3 vs. 3.0 +/- A 3.6 mu mol/L) and peak exercise (1.1 +/- A 4.5 vs. 8.2 +/- A 3.5 mu mol/L). Change in total hemoglobin/myoglobin concentration in muscle was not significantly affected by training. In CON, no significant alterations were found after 12 weeks in either muscle deoxygenation or peak VO2 (18.6 +/- A 3.8 vs. 18.9 +/- A 4.6 mL/kg/min). An increase in peak VO2 was significantly negatively correlated with change in a dagger SmO2 (r = -0.65) and positively associated with change in a dagger deoxy-Hb/Mb at peak exercise (r = 0.64) in TR. In early post-MI patients, aerobic training enhanced skeletal muscle deoxygenation, and the enhancement was related to increased aerobic capacity.