<a name="home"></a>The decreased oxygen uptake during progressive exercise in ischemia-induced heart failure is due to reduced cardiac output rate

Abstract

We tested the hypothesis that the inability to increase cardiac output during exercise would explain the decreased rate of oxygen uptake (VO 2 ) in recent onset, ischemia-induced heart failure rats. Nine normal control rats and 6 rats with ischemic heart failure were studied. Myocardial infarction was induced by coronary ligation. VO 2 was measured during a ramp protocol test on a treadmill using a metabolic mask. Cardiac output was measured with a flow probe placed around the ascending aorta. Left ventricular end-diastolic pressure was higher in ischemic heart failure rats compared with normal control rats (17 ± 0.4 vs 8 ± 0.8 mmHg, P = 0.0001). Resting cardiac index (CI) tended to be lower in ischemic heart failure rats (P = 0.07). Resting heart rate (HR) and stroke volume index (SVI) did not differ significantly between ischemic heart failure rats and normal control rats. Peak VO 2 was lower in ischemic heart failure rats (73.72 ± 7.37 vs 109.02 ± 27.87 mL min -1 kg -1 , P = 0.005). The VO 2 and CI responses during exercise were significantly lower in ischemic heart failure rats than in normal control rats. The temporal response of SVI, but not of HR, was significantly lower in ischemic heart failure rats than in normal control rats. Peak CI, HR, and SVI were lower in ischemic heart failure rats. The reduction in VO 2 response during incremental exercise in an ischemic model of heart failure is due to the decreased cardiac output response, largely caused by depressed stroke volume kinetics. Correspondence

Functional capacity in a rat model of heart failure: impact of myocardial infarct size

“…Evidence indicates that HF provokes a muscle fibre type shift from type I to type II and a reduction in muscle weight, and these alterations can explain, at least in part, the reduced in HF (Rolim et al . ).…”

“…Skeletal muscles composed of slow-twitch fibres are affected in HF (Lunde et al 2001). Evidence indicates that HF provokes a muscle fibre type shift from type I to type II and a reduction in muscle weight, and these alterations can explain, at least in part, the reducedV O 2 max in HF (Rolim et al 2006).…”

VEGF165 Gene Therapy Improves Left Ventricular Function and Exercise Capacity in Diabetic Rats after Myocardial Infarction: Impact on Mortality Rate

“…Although we did not evaluate the cardiac output in the present study, it is possible that the increase in left ventricular function is associated with the improvement of this variable and, consequently, better VO 2 max. In fact, Rolim et al [36] previously showed that the reduction in VO 2 response during incremental exercise in an ischemic model of heart failure is closely related to the decreased cardiac output response, largely caused by depressed stroke volume kinetics.…”

Curso temporal das avaliações morfofuncionais e hemodinâmicas em ratos diabéticos e infartados

“…na prática clínica tem sido considerada um importante indicador prognóstico em indivíduos com insuficiência cardíaca (IC), uma vez que oferece padrões fidedignos para o diagnóstico clínico. A avaliação das respostas cardiorespiratórias ao exercício agudo e crônico, de forma semelhante ao realizado em humanos, tem sido uma prática comum na investigação de modelos animais de diferentes patologias (Wisloff et al, 2001;Rodrigues et al, 2007;Rolim et al, 2006).…”

“…Estes resultados corroboram dados da literatura, nos quais animais com 5 semanas após IM apresentaram reduções no consumo máximo de oxigênio e do débito cardíaco o que limita o transporte de oxigênio para a musculatura esquelética, promovendo um desbalanço entre oferta e necessidade de oxigênio em relação aos incrementos de esforço (Rolim et al, 2006). Além disso, mudanças no tipo de fibra muscular (tipo 1 para 2) e a redução da massa muscular, além da reduzida vasodilatação periférica, podem contribuir para o decréscimo da capacidade de esforço e VO 2 máx.…”