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 (O(2)) 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 O(2) uptake (Vo(2peak)) 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 O(2) delivery (~54%), arterial-venous O(2) difference (~10%), and muscle O(2) diffusive conductance (D(M)O(2)) (~39%) (assessed during KE), thereby increasing single-leg Vo(2peak) by ~53%, to a level exceeding that of the untrained controls. Post-training, during maximal cycling, O(2) delivery (~40%), arterial-venous O(2) difference (~15%), and D(M)O(2) (~52%) all increased, yielding an increase in Vo(2peak) of ~40%, matching the controls. CONCLUSIONS: In the face of continued central limitations, clear improvements in muscle structure, peripheral convective and diffusive O(2) transport, and subsequently, O(2) utilization support the efficacy of local skeletal muscle training as a powerful approach to combat exercise intolerance in CHF.
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 (O(2)) 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 O(2) uptake (Vo(2peak)) 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 O(2) delivery (~54%), arterial-venous O(2) difference (~10%), and muscle O(2) diffusive conductance (D(M)O(2)) (~39%) (assessed during KE), thereby increasing single-leg Vo(2peak) by ~53%, to a level exceeding that of the untrained controls. Post-training, during maximal cycling, O(2) delivery (~40%), arterial-venous O(2) difference (~15%), and D(M)O(2) (~52%) all increased, yielding an increase in Vo(2peak) of ~40%, matching the controls. CONCLUSIONS: In the face of continued central limitations, clear improvements in muscle structure, peripheral convective and diffusive O(2) transport, and subsequently, O(2) utilization support the efficacy of local skeletal muscle training as a powerful approach to combat exercise intolerance in CHF.
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