Skeletal muscle deoxygenation abnormalities in early post-myocardial infarction.
cross_sectional · Level IV
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- Record sourced from PubMed, PMID 24621961.
- Also identified by DOI 10.1249/MSS.0000000000000334.
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Abstract
Reduced peak aerobic capacity in chronic heart failure can be partly explained by impaired peripheral factors. However, skeletal muscle deoxygenation responses during exercise and their relation to peak aerobic capacity have not been fully established in early post-myocardial infarction (MI) patients. Patients early post-MI (age, 61 ± 9 yr; n = 16; 21 ± 8 d after the first MI) and age-, height-, and weight-matched control participants (age, 61 ± 9 yr; n = 18) performed a ramp cycling exercise until exhaustion. Near-infrared spectroscopy at the belly of the vastus lateralis muscle in the left leg was recorded continuously for measurement of skeletal muscle deoxygenation responses during exercise. Peak oxygen uptake (18.4 ± 3.5 vs 28.2 ± 10.7 mL · kg(-1) · min(-1), P < 0.01) was significantly lower in MI. Change in muscle oxygen saturation from rest to peak exercise (ΔSmO2) was significantly greater in MI than that in controls (2.5% ± 5.6% vs -7.4% ± 3.4%, P < 0.01). Relative change in deoxygenated hemoglobin/myoglobin concentration from rest to peak exercise (Δdeoxy-Hb/Mb) was significantly lower in MI than that in controls (0.1 ± 3.6 vs 8.7 ± 6.4 μM, P < 0.01). In contrast, change in total hemoglobin/myoglobin, which is an indicator of blood volume, was not significantly different between groups. Peak oxygen uptake was negatively correlated with ΔSmO2 (r = -0.53, P < 0.05) and positively associated with Δdeoxy-Hb/Mb at peak exercise (r = 0.65, P < 0.01) in MI. Skeletal muscle deoxygenation abnormalities were observed during dynamic cycling exercise in early post-MI patients. These abnormalities were related to impaired peak aerobic capacity in early post-MI patients.
Medical subject headings
- Muscle, Skeletal
- Myocardial Infarction
- Oxygen Consumption