TY - JOUR
T1 - Isolated quadriceps training increases maximal exercise capacity in chronic heart failure
T2 - The role of skeletal muscle convective and diffusive oxygen transport
AU - Esposito, Fabio
AU - Reese, Van
AU - Shabetai, Ralph
AU - Wagner, Peter D.
AU - Richardson, Russell S.
PY - 2011/9/20
Y1 - 2011/9/20
N2 - Objectives: This study sought to elucidate the mechanisms responsible for the benefits of small muscle mass exercise training in patients with chronic heart failure (CHF). Background: How central cardiorespiratory and/or peripheral skeletal muscle factors are altered with small muscle mass training in CHF is unknown. Methods: 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. Results: 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. Conclusions: 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.
AB - Objectives: This study sought to elucidate the mechanisms responsible for the benefits of small muscle mass exercise training in patients with chronic heart failure (CHF). Background: How central cardiorespiratory and/or peripheral skeletal muscle factors are altered with small muscle mass training in CHF is unknown. Methods: 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. Results: 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. Conclusions: 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.
KW - blood flow
KW - cardiac output
KW - hyperoxia
KW - oxygen supply
KW - oxygen utilization
KW - skeletal muscle
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U2 - 10.1016/j.jacc.2011.06.025
DO - 10.1016/j.jacc.2011.06.025
M3 - Article
C2 - 21920265
AN - SCOPUS:80053018209
VL - 58
SP - 1353
EP - 1362
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 13
ER -