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97 Increasing skeletal muscle oxygenation by prior moderate-intensity exercise increases aerobic energy provision in chronic heart failure
  1. T S Bowen,
  2. D T Cannon,
  3. S R Murgatroyd,
  4. K K Witte,
  5. H B Rossiter
  1. University of Leeds, Leeds, UK

Abstract

Rapid adaptation of pulmonary oxygen uptake (VO2) at exercise onset reduces the reliance on limited anaerobic energy stores and is associated with increased exercise tolerance. These VO2 kinetics, however, are slow in patients with chronic heart failure (CHF). This could be due to limitations in the control of muscle O2 consumption and/or O2 delivery. Recent evidence in CHF of a transient overshoot in microvascular deoxygenation at exercise onset supports the latter. As prior exercise is known to increase muscle blood flow in healthy individuals, we examined whether it could attenuate the fall in microvascular deoxygenation and speed VO2 kinetics on transition to moderate exercise in CHF patients. Thirteen CHF patients (NYHA class I: n=3, II: n=9, and III: n=1) performed a ramp test on a cycle ergometer for estimation of lactate threshold (LT) and VO2max. Patients subsequently repeated two 6-min moderate-intensity exercise transitions (bout 1, bout 2) from rest to 90%LT, separated by 6-min of rest. Measurements included breath-by-breath VO2 using a turbine and mass spectrometer (MSX, NSpire, UK), and tissue oxygenation index (TOI) of the vastus lateralis by spatially resolved near-infrared spectroscopy (NIRO200, Hamamatsu, Japan). The exponential time-constant (τ) for TOI and phase II VO2 were estimated using non-linear least-squares regression. The τVO2/τTOI, or “kinetic index”, was taken to reflect the relative matching of muscle oxygenation to its instantaneous requirement. LT and VO2max were 9.9±1.7 (mean±SD) and 15.0±3.2 ml/kg/min, respectively. Prior exercise increased resting TOI by 10±3% (p<0.05), attenuated the transient overshoot in muscle deoxygenation by ∼50% (p<0.05) and slowed the rate of deoxygenation in the transient (τTOI: 10±1 vs 21±13 s; p<0.05). Both τVO2 (46±20 vs 39±18 s; p<0.05) and the kinetic index (4.5±1.8 vs 2.2±0.9; p<0.05) were reduced following prior exercise. τVO2 was well correlated to the kinetic index (R2=0.92) in bout 1. However, although a lower τVO2 was typically reflected in a reduced kinetic index in bout 2, VO2 kinetics remained slowed in 4 patients. These patients had a higher NYHA class (2.3±0.5 vs 1.6±0.5; p=0.06) and greater initial τVO2 (62±17 vs 33±9 s; p<0.05) than the others. In CHF prior moderate-intensity exercise improved the dynamic matching of muscle oxygenation to its instantaneous requirement and speeded VO2 kinetics in all patients. This suggests that slow VO2 kinetics in CHF are due, at least in part, to a dynamic limitation in O2 delivery. However, this approach revealed an apparent limitation in the control of muscle O2 consumption in the most severe patients, which was only partly ameliorated by improving O2 delivery. Nevertheless, these findings suggest that an acute intervention to improve muscle oxygenation can increase aerobic energy provision on transition to exercise in CHF patients.

  • Blood flow
  • near-infrared spectroscopy
  • oxygen uptake kinetics

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