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Press Release:
Targeting leg fatigue in heart failure
Doctors should not only treat the heart muscle in chronic heart failure patients, but also their leg muscles through exercise, say researchers in a major new study.
Heart failure causes breathlessness and fatigue that severely limits normal daily activities such as walking. The University of Leeds research team has, for the first time, shown that leg muscle dysfunction is related to the severity of symptoms in heart failure patients. These findings suggest that daily activity in patients with severe heart failure may not simply be limited by the failing heart, but also by an impairment in the leg muscles themselves.
In a series of experiments with chronic heart failure patients, the research team measured responses of the heart, lungs and leg muscles following a moderate exercise warm-up. Using a near-infrared laser to measure the oxygenation of the leg muscles, they found that warm-up exercise increased the activity of skeletal muscle enzymes that control energy production. However, this adaptation was less in patients with the most severe symptoms, showing that the heart failure condition had a negative impact on the normal function of the leg muscles.
Dr Harry Rossiter, of the University's Faculty of Biological Sciences says: "Many chronic heart failure patients complain of leg fatigue during exercise and this can prevent them from being active. Our study shows that by warming up properly, patients can improve the oxygenation and performance of their leg muscles, which is beneficial in promoting exercise tolerance."
"When your muscles don't use oxygen well, it causes an uncomfortable burning sensation during activity," says Dr Klaus Witte, the Leeds General Infirmary Cardiologist on the research team. "The effect of a warm up is to direct oxygen to the places that are going to need it, and make the muscles ready to use it when you start exercising."
Dr Rossiter says the next stage of this research will be to see whether training of the skeletal muscles can improve long-term overall outcomes for patients with chronic heart failure, and to discover more about the pathological changes in the leg muscles that may be a contributing factor in limiting exercise.
"Our main message is that exercise is safe and beneficial in patients with heart failure. By warming up the leg muscles properly, the exercise can be more comfortable and sustained for longer - affording great benefits for these patients," he says.
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The intramuscular contribution to the slow oxygen uptake kinetics during exercise in chronic heart failure is related to the severity of the condition
T. Scott Bowen, Daniel T. Cannon, Scott R. Murgatroyd, Karen M. Birch, Klaus K. Witte, and Harry B. Rossiter
Journal of Applied Physiology October 2011
The mechanism for slow pulmonary oxygen uptake (VO2) kinetics in patients with chronic heart failure (CHF) is presently unclear, but may be due to limitations in the intramuscular control of O2 utilization or O2 delivery. Recent evidence of a transient overshoot in microvascular deoxygenation supports the latter. Prior (or warm-up) exercise can increase O2 delivery in healthy individuals. We therefore aimed to determine whether prior exercise could increase muscle oxygenation and speed VO2 kinetics during exercise in CHF. Fifteen males with CHF (NYHA I-III) due to left ventricular systolic dysfunction performed two 6-min moderate-intensity exercise transitions (bout 1, bout 2) from rest to 90% lactate threshold on a cycle ergometer, separated by 6-min of rest. VO2 was measured using a turbine and mass spectrometer, and muscle tissue oxygenation index (TOI) by near-infrared spectroscopy. Prior exercise increased resting TOI by 5.3±2.4 % (P=0.001), attenuated the deoxygenation overshoot (-3.9±3.6 vs. -2.0±1.4 %; P=0.011), and speeded the VO2 time constant (τ; 49±19 vs. 41±16 s; P=0.003). Resting TOI was correlated to τVO2 before (R2=0.51; P=0.014) and after (R2=0.36; P=0.051) warm-up exercise. However, the mean response time of TOI was speeded between bouts in half of the patients (26±8 vs. 20±8 s) and slowed in the remainder (32±11 vs. 44±16 s): the latter group having greater NYHA scores (P=0.042) and slower VO2 kinetics (P=0.001). These data indicate that prior moderate-intensity exercise improves muscle oxygenation and speeds VO2 kinetics in CHF. The most severely limited patients, however, appear to have an intramuscular pathology that limits VO2 kinetics during moderate exercise.
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