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Maximum rate of oxygen consumption related to succinate dehydrogenase activity in skeletal muscle fibres of chronic heart failure patients and controls
Author(s) -
Bekedam Martijn A.,
Van BeekHarmsen Brechje J.,
Boonstra Anco,
Van Mechelen Willem,
Visser Frans C.,
Van Der Laarse Willem J.
Publication year - 2003
Publication title -
clinical physiology and functional imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.608
H-Index - 67
eISSN - 1475-097X
pISSN - 1475-0961
DOI - 10.1046/j.1475-0961.2003.00517.x
Subject(s) - skeletal muscle , medicine , heart failure , heart rate , oxygen , cardiology , myofibril , vo2 max , endocrinology , chemistry , blood pressure , organic chemistry
Summary Previous studies indicate that the low maximum rate of oxygen consumption ( V O 2max ) of chronic heart failure (CHF) patients is not because of impaired pump function of the heart. We hypothesize that V O 2 during maximum exercise is determined by the total oxidative capacity of skeletal muscle. V O 2max of six controls and 14 CHF patients, New York Heart Association class I–III, was determined using an incremental bicycle ergometer test. Cryostat sections of a biopsy from the quadriceps femoris muscle were incubated for succinate dehydrogenase (SDH) using quantitative histochemistry. V O 2max (range: 29 ml O 2 kg min −1 in a class III patient to 118 ml O 2 kg min −1 in a control subject) correlates with the mean SDH activity of skeletal muscle fibres ( r = 0·79 or r = 0·81, including or excluding oxygen uptake at rest, respectively; P <0·001). The relationship between V O 2max and SDH activity is similar to that determined previously using isolated single muscle fibres and myocardial trabeculae under hyperoxic conditions. From the product of SDH activity and the cross‐sectional area of the fibre (i.e. spatially integrated SDH activity), it is possible to calculate the maximum oxygen uptake rate per unit muscle fibre length. This uptake rate is linearly related to the number of capillaries per fibre ( r = 0·76, P <0·001) in all subjects, suggesting that oxidative capacity of skeletal muscle fibres in CHF patients decreases in proportion to the oxygen supply capacity of the microcirculation.