Methylphenidate Enhances Grip Force and Alters Brain Connectivity

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A central fatigue theory proposes that force output during fatiguing exercise is limited to maintain homeostasis. The self-awareness of the body's homeostatic state is known as interoception. Brain regions thought to play a role in interoception, such as the insular and orbital frontal cortex, have been proposed as sites for the upstream regulation of fatiguing exercise. Methylphenidate (MPH) can improve force output during exercise and may alter central processes during fatiguing exercise. However, the ergogenic neural underpinnings of MPH are unknown. This study examines the effect of MPH on force output and brain functional connectivity during a muscle-fatiguing handgrip task.


In a double-blind, crossover design, 15 subjects (mean age = 28.4 ± 5.2; 9 males and 6 females) ingested MPH or placebo before performing a muscle-fatiguing handgrip task during functional magnetic resonance imaging. We examined force output and brain connectivity (psychophysiological interactions and functional connectivity) throughout the task as well as in the few seconds just before releasing the grip dynamometer (i.e., pretask failure).


We show that in the MPH condition, subjects increased grip force throughout but not during pretask failure. Brain connectivity was altered throughout the task between the insular and the hand motor cortex, as well as between the insular and the orbital frontal cortex. There were no differences in connectivity during pretask failure.


For the first time, we show that brain connectivity can be influenced by MPH during muscle-fatiguing exercise. This study provides additional support that the CNS acts to regulate motor drive subservient to homeostasis.

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