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

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Summary

Introduction

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.

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