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1992b; Mancini et?al. 1992; Simonini et?al. 1996a,b; Delp et?al. 1997; Garnier et?al. 2003; Schrepper et?al. 2012). While there is clearly a HF-induced skeletal muscle myopathy contributing to exercise intolerance, some research has suggested that mitochondrial dysfunction could be the product of muscle disuse and deconditioning as a result of a diminished capacity to exercise rather than a HF-induced myopathy (Chati et?al. 1996; Mettauer et?al. 2001; Williams et?al. 2004; Toth et?al. 2012). In addition to determining how skeletal muscle mitochondria are involved in a HF-related myopathy, it is important to understand how they might respond to exercise training. While exercise has been [http://en.wikipedia.org/wiki/Ficain Ficain] shown to yield muscular oxidative improvements in people with HF (Minotti et?al. 1990; Hambrecht et?al. 1995; Wisloff et?al. 2007), the capacity for improvement has not been assessed. In fact, to our knowledge, no study has directly compared the magnitude of oxidative adaptations to endurance exercise training between participants with and without HF. Exercise training has been recommended for individuals with HF [http://www.selleckchem.com/products/CAL-101.html Idelalisib] as a safe and effective means of improving clinical, functional, and physiological outcomes (O'Connor et?al. 2009; Keteyian 2011; McMurray et?al. 2012; Ades et?al. 2013), thus, it is important to understand how muscle mitochondria in individuals with HF respond to exercise training. The first aim of this study was to measure and compare baseline skeletal muscle oxidative capacity of people with and without HF. The second aim of this study was to compare the magnitude of oxidative adaptations in response to endurance exercise in people with and without HF. We hypothesized that people with HF would have reduced oxidative capacity and impaired oxidative adaptations to endurance [http://www.selleckchem.com/small-molecule-compound-libraries.html Small molecule library chemical structure] exercise compared to controls. Materials and Methods Participants Sixteen participants with HF (13 male, 3 female) were recruited through a local cardiology clinic. Twenty healthy controls (6 male, 17 female) were recruited from the surrounding community. A subset of enrolled participants (n?=?7, n?=?5; for HF and control respectively) volunteered to participate in a 4-week long wrist-flexor training program, followed by 4?weeks of inactivity. One HF participant only completed the first 5?weeks of the program. One control participant completed the first 7?weeks of the program. HF participants with implanted cardioverter-defibrillators (ICDs) and reduced ejection fraction (