Key result
Post-exercise phosphocreatine recovery was slower in CHF patients compared with healthy controls, with even slower muscle tissue re-oxygenation.
Why the study?
Is muscle metabolic recovery following submaximal exercise in patients with CHF limited by O2 delivery or O2 utilization compared to healthy controls?
Observational (n=21)
Is muscle metabolic recovery following submaximal exercise in patients with CHF limited by O2 delivery or O2 utilization compared to healthy controls?
Prolonged metabolic recovery in CHF patients is associated with slower muscle tissue re-oxygenation, suggesting that impaired exercise capacity depends more on reduced muscle blood flow than on limitations in O2 utilization.
Answers are grounded in this paper and cite their sources.
Reduced muscle blood flow may predominate over O2 utilization deficits in CHF; supports mechanistic studies but leaves open clinical translation.
CHF (chronic heart failure) is associated with a prolonged recovery of skeletal muscle energy stores following submaximal exercise, limiting the ability to perform repetitive daily activities.However, the pathophysiological background of this impairment is not well established. The aim of the present study was to investigate whether muscle metabolic recovery following submaximal exercise in patients with CHF is limited by O2 delivery or O2 utilization. A total of 13 stable CHF patients (New York Heart Association classes II-III) and eight healthy subjects, matched for age and BMI (body mass index), were included. All subjects performed repetitive submaximal dynamic single leg extensions in the supine position. Post-exercise PCr (phosphocreatine) resynthesis was assessed by 31P-MRS (magnetic resonance spectroscopy). NIRS (near-IR spectroscopy) was applied simultaneously, using the rate of decrease in HHb (deoxygenated haemoglobin) as an index of post-exercise muscle re-oxygenation. As expected, PCr recovery was slower in CHF patients than in control subjects (time constant, 47+/-10 compared with 35+/-12 s respectively; P=0.04). HHb recovery kinetics were also prolonged in CHF patients (mean response time, 74+/-41 compared with 44+/-17 s respectively; P=0.04). In the patient group, HHb recovery kinetics were slower than PCr recovery kinetics (P=0.02), whereas no difference existed in the control group(P=0.32). In conclusion, prolonged metabolic recovery in CHF patients is associated with an even slower muscle tissue re-oxygenation, indicating a lower O(2) delivery relative to metabolic demands. Therefore we postulate that the impaired ability to perform repetitive daily activities in these patients depends more on a reduced muscle blood flow than on limitations in O(2) utilization.
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Kemps et al. (2009) conducted an observational in Chronic heart failure (n=21). Repetitive submaximal dynamic single leg extensions vs. Healthy subjects was evaluated on Post-exercise phosphocreatine (PCr) recovery time constant (s) (p=0.04). Post-exercise phosphocreatine recovery was slower in CHF patients compared with healthy controls, with even slower muscle tissue re-oxygenation.
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