Abstract
ObjectiveResting metabolic rate (RMR) is the component of energy expenditure that explains the largest proportion of total daily energy requirements. Since RMR is determined largely by fat-free mass and a low RMR predicts weight gain in healthy adults, identifying the role of muscle atrophy following stroke on RMR may help identify ways to mitigate the development of obesity post-stroke.MethodsThirty-nine stroke survivors with chronic hemiparesis (mean ± SEM: age: 61 ± 1 years, latency from stroke: 107 ± 40 months, BMI: 31 ± 3 kg/m2) underwent DXA scans for measurement of body composition, including total, paretic, and non-paretic leg lean mass and fasted, 30-min indirect calorimetry for measurement of RMR.ResultPredicted RMR was calculated by the Mifflin-St Jeor equation, which considers weight, height, and age for both men and women. RMR was 14% lower than predicted (1438 ± 45 vs. 1669 ± 38 kcals/24 hrs; P<0.01). Total (r=0.73, P<0.01), paretic (r=0.72, P<0.01) and non-paretic (r=0.67, P<0.01) leg lean mass predicted RMR.ConclusionThese data indicate that muscle atrophy post stroke may lead to a reduced RMR. This substantiates the need to attenuate the loss of lean mass after a stroke to prevent declines in RMR and possible weight gain common post-stroke.
Highlights
Stroke is the leading cause of long-term disability [1]
Resting metabolic rate (RMR) is the component of energy expenditure that explains the largest proportion of total daily energy requirements
Since it is well established that resting metabolic rate (RMR) is determined largely by fat-free mass, accounting for ~60–70% of RMR [22] and large proportion of total body lean mass is found in the extremities, we hypothesis that muscle atrophy of the lower extremity may contribute to a reduced RMR post-stroke
Summary
Stroke is the leading cause of long-term disability [1]. We have previously shown that resultant hemiparesis leads to lean tissue wasting and decreased strength [2,3], which may impair and delay post-stroke recovery. Loss of muscle may contribute to declines in energy expenditure [7] and the subsequent weight gain [8] observed post-stroke. Independent of changes in lean mass, do not appear to result in a decrease in RMR [16]; loss of muscle mass observed with other (non-stroke) chronic diseases [17], aging [18], prolonged bed rest [19], and detraining [20] are associated with a reductions in RMR. Since it is well established that RMR is determined largely by fat-free mass, accounting for ~60–70% of RMR [22] and large proportion of total body lean mass is found in the extremities, we hypothesis that muscle atrophy of the lower extremity may contribute to a reduced RMR post-stroke.
Sign-in/Register to view highlights & summary 
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
