Exercise intolerance in HFpEF may be driven by impaired skeletal muscle oxidative metabolism rather than impaired cardiac reserve.
Skeletal muscle oxidative impairment may underlie exercise intolerance in compensated HFpEF despite preserved cardiac reserve; leaves open need for interventional trials before practice change.
Contrary to our hypothesis, cardiac reserve is not significantly impaired in well-compensated outpatients with HFpEF. The abnormal haemodynamic response to exercise (decreased peak VO(2), increased ΔQ(c)/ΔVO(2) slope) is similar to that observed in patients with mitochondrial myopathies, suggesting an element of impaired skeletal muscle oxidative metabolism. This impairment may limit functional capacity by two mechanisms: (i) premature skeletal muscle fatigue and (ii) metabolic signals to increase the cardiac output response to exercise which may be poorly tolerated by a left ventricle with impaired diastolic function.
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Bhella et al. (2011) studied this question.