Considering that a deleterious effect on in vitro myosin mechanical function due to myosin carbonylation has been reported in skeletal muscle of rats with CHF (Coirault et al., 2007), and that in vivo performance is negatively affected by excessive ROS production (Kuwahara et al., 2010), it is reasonable to hypothesize that in mice with CHF protein carbonylation could be responsible, at least in part, for the development of skeletal muscle dysfunction and physical activity decline. Here, MYH14 is linked to congestive heart failure.