This study sought to elucidate the mechanisms responsible for the benefits of small muscle mass exercise training in patients with chronic heart failure (CHF).
How central cardiorespiratory and/or peripheral skeletal muscle factors are altered with small muscle mass training in CHF is unknown.
We studied muscle structure, and oxygen (O2) transport and metabolism at maximal cycle (whole-body) and knee-extensor exercise (KE) (small muscle mass) in 6 healthy controls and 6 patients with CHF who then performed 8 weeks of KE training (both legs, separately) and repeated these assessments.
Pre-training cycling and KE peak leg O2 uptake (Vo2peak) were ∼17% and ∼15% lower, respectively, in the patients compared with controls. Structurally, KE training increased quadriceps muscle capillarity and mitochondrial density by ∼21% and ∼25%, respectively. Functionally, despite not altering maximal cardiac output, KE training increased maximal O2 delivery (∼54%), arterial-venous O2 difference (∼10%), and muscle O2 diffusive conductance (DMO2) (∼39%) (assessed during KE), thereby increasing single-leg Vo2peak by ∼53%, to a level exceeding that of the untrained controls. Post-training, during maximal cycling, O2 delivery (∼40%), arterial-venous O2 difference (∼15%), and DMO2 (∼52%) all increased, yielding an increase in Vo2peak of ∼40%, matching the controls.
In the face of continued central limitations, clear improvements in muscle structure, peripheral convective and diffusive O2 transport, and subsequently, O2 utilization support the efficacy of local skeletal muscle training as a powerful approach to combat exercise intolerance in CHF.