Methylphenidate alters brain connectivity after enhanced physical performance.

Muscle fatigue is a disturbed homeostatic state characterized by a temporary inability to maintain force output and has lasting effects on the brain in the period immediately after exercise, such as decreased interhemispheric functional connectivity (FC). Stimulants that increase dopamine and norepinephrine neurotransmission can enhance performance during muscle fatiguing exercise (i.e. are ergogenic). We recently demonstrated that methylphenidate (MPH) increased force output and increased FC between the insular (IC) and hand motor cortex during a fatiguing handgrip task. However, whether resting FC is altered in the recovery period after enhanced force is unknown. The objective of these follow-up analyses was to examine the effects of performing a fatiguing handgrip task with MPH on subsequent resting state FC. In a double-blind counter-balanced design, participants ingested placebo or MPH and in a magnetic resonance imaging scanner performed: a six-minute pre-task resting scan, a fatiguing handgrip task during scanning, and then a six-minute post-task resting scan. We investigated task-related force and resting state FC pre- and post-task between: (1) interhemispheric motor cortices (M1) and (2) the right IC and left hand motor area. We found 1) a post-task reduction in M1 interhemispheric FC and that the extent of reduciton was negatively correlated with enhanced mean trial force in MPH conditions. 2) MPH but not placebo increased post-task FC between the right IC and left hand motor area. This study demonstrates that using MPH during a muscle fatiguing task has lasting effects on the brain that are markedly different from drug naïve conditions.

Methylphenidate Enhances Grip Force and Alters Brain Connectivity.

INTRODUCTION: 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. METHODS: 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). RESULTS: 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. CONCLUSION: 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.

The role of information processing between the brain and peripheral physiological systems in pacing and perception of effort.

This article examines how pacing strategies during exercise are controlled by information processing between the brain and peripheral physiological systems. It is suggested that, although several different pacing strategies can be used by athletes for events of different distance or duration, the underlying principle of how these different overall pacing strategies are controlled is similar. Perhaps the most important factor allowing the establishment of a pacing strategy is knowledge of the endpoint of a particular event. The brain centre controlling pace incorporates knowledge of the endpoint into an algorithm, together with memory of prior events of similar distance or duration, and knowledge of external (environmental) and internal (metabolic) conditions to set a particular optimal pacing strategy for a particular exercise bout. It is proposed that an internal clock, which appears to use scalar rather than absolute time scales, is used by the brain to generate knowledge of the duration or distance still to be covered, so that power output and metabolic rate can be altered appropriately throughout an event of a particular duration or distance. Although the initial pace is set at the beginning of an event in a feedforward manner, no event or internal physiological state will be identical to what has occurred previously. Therefore, continuous adjustments to the power output in the context of the overall pacing strategy occur throughout the exercise bout using feedback information from internal and external receptors. These continuous adjustments in power output require a specific length of time for afferent information to be assessed by the brain's pace control algorithm, and for efferent neural commands to be generated, and we suggest that it is this time lag that crates the fluctuations in power output that occur during an exercise bout. These non-monotonic changes in power output during exercise, associated with information processing between the brain and peripheral physiological systems, are crucial to maintain the overall pacing strategy chosen by the brain algorithm of each athlete at the start of the exercise bout.