Objective: To examine the effects of methylphenidate hydrochloride (MPH) on resting energy expenditure (REE) and postprandial energy expenditure (PEE) and substrate partitioning. Methods and Procedures: Seven healthy men and seven healthy women participated in this double-blind, randomized, placebo-controlled, crossover study. MPH (0.5 mg/kg) or placebo was administered orally in the fasting state, 60 min before a REE measurement, and 90 min before a standardized breakfast of ~650 kcal. REE, PEE, and respiratory exchange ratio (RER) were obtained from indirect calorimetry. Body composition was measured using DEXA. Vital signs (blood pressure (BP) and heart rate (HR)) were assessed pre-and post-administration of MPH or placebo in every session. Results: During the, MPH condition, REE increased over values observed during the placebo session (7%, P < 0.001).No changes in fasting RER were noted. Although PEE continually decreased with time as expected, MPH treatment resulted in significantly greater PEE values at 90 min (5%, P < 0.01). No significant effects of MPH were found for vital signs (HR, systolic, and diastolic BP). Discussion: MPH causes a significant increase in both REE and PEE without the significant changes in HR and BP that are commonly associated with psychostimulant use. Recent findings from both animal and human studies suggest that rapid reuptake/metabolism of intrasynaptic dopamine (DA) resulting in reduced brain DA transmission may be related to the development of obesity (1,2). A method of increasing DA levels is using orally administered methylphenidate hydrochloride (MPH) which slows the reuptake of intrasynaptic DA allowing it to have a prolonged effect (3-5). Of interest to this study is the potential of MPH to increase both central and peripheral levels of DA and norepinephrine (NE) by blocking their respective transporters (6). Further, injected DA at a rate of 5 and 10 µg/min/kg, increased resting energy expenditure (REE) by 6 and 15%, respectively, in nonobese subjects (7). The main objective of this study was thus to investigate the effects of fast-release MPH on REE and postprandial energy expenditure (PEE), and substrate oxidation in human subjects.
Methods and procedures participantsSeven healthy men and seven healthy women were recruited by local advertisement. Inclusion criteria included men or women between the ages of 18 and 40; BMI ≥ 20 (normal weight or higher) and body weight <120 kg to accommodate the recommended maximum dosage of MPH of 60 mg/day; nonsmoker; body weight has not varied >2 kg in recent 6 months; no history of previous MPH use; no history of attention deficit hyperactivity disorder or current diagnosis of an axis 1 psychiatric disorder (e.g., depressive or anxiety disorders); no current use of thyroid medication; normal blood pressure (BP