Relação entre a oferta e a utilização muscular periférica de oxigênio na transição do exercício leve para o intenso em pacientes com insuficiência cardíaca

Detalhes bibliográficos
Ano de defesa: 2010
Autor(a) principal: Sperandio, Priscila Cristina de Abreu [UNIFESP]
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Tese
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://repositorio.unifesp.br/handle/11600/10026
Resumo: Impaired muscle blood flow at the onset of heavy-intensity exercise may transiently reduce microvascular O2 pressure and decrease the rate of O2 transfer from capillary to mitochondria in chronic heart failure (CHF). However, advances in the pharmacological treatment of CHF (e.g., angiotensin-converting enzyme inhibitors and third generation of â-blockers) may have improved microvascular O2 delivery to an extent that intramyocyte metabolic inertia might become the main locus of limitation of O2 uptake ( O2) kinetics. We included 10 optimally treated sedentary patients (ejection fraction = 29 ± 8%) and 11 age-matched controls. We assessed the rate of change of pulmonary O2 ( O2p), tissue O2 extraction in the vastus lateralis estimated by concentration of deoxy-hemoglobin+myoglobin (~Ä[deoxy-Hb+Mb]) measured by near-infrared spectroscopy (NIRS), and cardiac output ( T) during highintensity exercise performed to the limit of tolerance (Tlim). Sluggish O2p and T kinetics in patients were significantly related to lower Tlim values (P = 0.05). The dynamics of Ä[deoxy-Hb+Mb] were faster in patients than controls (mean response time (MRT) = 15.9 ± 2.0 s vs. 19.0 ± 2.9 s; P = 0.05) with a subsequent response “overshoot” being found only in patients (7/10). Moreover, t O2p/MRT-Ä[deoxy- Hb+Mb] ratio was greater in patients (4.69 ± 1.42 s vs. 2.25 ± 0.77 s; P = 0.05) and related to T kinetics and Tlim (R = 0.89 and 0.78, respectively; P = 0.01). We conclude that despite the advances in the pharmacological treatment of CHF, disturbances in “central” and “peripheral” circulatory adjustments still play a prominent role in limiting O2p kinetics and tolerance to heavy-intensity exercise in nontrained patients.