Methylphenidate Hydrochloride Increases Energy Expenditure in Healthy Adults

Abstract

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

Energy expenditure in obesity associated with craniopharyngioma

“…One of these three was also taking methylphenidate for attention-deficit disorder. Methylphenidate is reported to increase REE and suppress food intake [19, 20]. In spite of this, our patients still had a lower than expected REE indicating that these medicines were unlikely to be confounders in our analysis.…”

Physiological responses in rock climbing with repeated ascents over a 10-week period

“…The Weir (1949) and Zuntz (1901) equations have been used previously in research in different fields, including Public Health (Doucet et al 2003;Lorello et al 2008;Shew et al 2000) and Sport Sciences (Brugniaux et al 2010;McDaniel et al 2002;Stewart and Stewart 2007;Westerterp et al 1992). Within the Sport Sciences, these EE equations have been used in the study of disciplines such as ultra-endurance running (Stewart and Stewart 2007), cycling (McDaniel et al 2002) and mountaineering (Westerterp et al 1992).…”

Approaches to obesity management

“…The noradrenergic sympathomimetic agent phentermine is approved as a short‐duration (<3 months) adjunct to lifestyle modification, although it should be noted that combination phentermine/topiramate ER is indicated for long‐term treatment in the United States. The exact mechanism of action of phentermine is unknown, but it appears to act within the hypothalamus to upregulate noradrenaline, resulting in the stimulation of β 2 ‐adrenergic receptors to induce appetite suppression; it also appears to inhibit monoamine oxidase, potentiating the effect of serotonin and possibly increasing basal metabolic rate . Phentermine is associated with a 3.6 kg (95% confidence interval (CI), 0.6–6.0 kg) greater weight loss compared with placebo in studies …”

“…Adverse effects related to phentermine are attributable to its stimulant properties and include dry mouth, agitation, insomnia and decreased concentration . Significant cardiovascular and neurocognitive complications were also historically attributed to this therapy; however, a recent meta‐analysis of phentermine monotherapy studies concluded that phentermine is not associated with any serious adverse events .…”