Navegando por Palavras-chave "Cinética do VO2"

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    Avaliação das cinéticas do consumo de oxigênio e da reoxigenação muscular esquelética na recuperação do exercício de alta intensidade em pacientes com miopatia mitocondrial: implicações sobre os mecanismos de intolerância ao exercício
    (Universidade Federal de São Paulo (UNIFESP), 2011-03-31) Bravo, Daniela Manzoli [UNIFESP]; Nery, Luiz Eduardo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Background: Mitochondrial Myopathy patients (MM) and Progressive External Ophthalmoplegia (PEO) present with respiratory chain dysfunction and inability to increase muscle oxygen extraction and aerobic ATP synthesis, leading to exercise intolerance and slower O2 kinetics. When oxygen extraction is impaired, in an attempt to maintain muscle oxygen uptake, these patients could increase oxygen delivery, thus exhibiting a hyperkinetic cardiovascular and ventilatory response. On the other hand, some evidence of oxygen delivery impairment was found in MM patients, such as a decrease in muscle blood flow in the forearm and a greater capacity for ATP production after oxygen supplementation. Recovery O2 kinetics provides information on tissue oxygen debt repayment and oxygen blood store replenishment after exercise. To our knowledge, recovery O2 kinetics has never been evaluated in MM patients, as well as its integration with the non-invasive cardiovascular and muscle reoxygenation responses. Objective: to contrast oxygen delivery and utilization dynamics on exercise recovery of MM patients and to identify the main pathophysiologic mechanisms of exercise intolerance in these subjects. Methods: Were evaluated in 12 MM patients and 12 healthy controls, the recovery kinetics of: (i) O2 (ii) deoxyhemoglobin variation ([HHb], measured by near-infrared spectroscopy - NIRS) in vastus lateralis, (iii) cardiac output (CO) by transthoracic bioimpedance, after a high-intensity constant work rate test (70% of maximal workload in a previous incremental test) to the limit of tolerance in a cycle ergometer. Results: We detected slower kinetics for [HHb] ([HHb] = 43.7 ± 21.2 vs. 27.5 ± 6.7) and for O2 ( O2 = 58.1 ± 25.1 vs. 38.8 ± 7.6) in MM patients compared to controls, respectively. Additionally, these responses were associated with a faster recovery CO kinetics in relation to O2 kinetics in MM patients compared to controls (T½DC*1,44 / O2 = 1,3 ± 0,4 vs. 1,7 ± 0,6). Conclusion: Patients with MM and PEO present with a higher oxygen debt and slower reoxygenation kinetics in the recovery of a high-intensity exercise test. Those responses were associated with a faster CO recovery in relation to O2 kinetics, indicating a microvascular oxygen transport deficit, besides the characteristic mitochondrial impairment observed in these patients.