Transient hypofrontality as a mechanism for the psychological effects of exercise

Abstract

Although exercise is known to promote mental health, a satisfactory understanding of the mechanism underlying this phenomenon has not yet been achieved. A new mechanism is proposed that is based on established concepts in cognitive psychology and the neurosciences as well as recent empirical work on the functional neuroanatomy of higher mental processes. Building on the fundamental principle that processing in the brain is competitive and the fact that the brain has finite metabolic resources, the transient hypofrontality hypothesis suggests that during exercise the extensive neural activation required to run motor patterns, assimilate sensory inputs, and coordinate autonomic regulation results in a concomitant transient decrease of neural activity in brain structures, such as the prefrontal cortex, that are not pertinent to performing the exercise. An exercise-induced state of frontal hypofunction can provide a coherent account of the influences of exercise on emotion and cognition. The new hypothesis is proposed primarily on the strength of its heuristic value, as it suggests several new avenues of research.

Introduction

Exercise is beneficial to mood and cognition (e.g., Colcombe and Kramer, 2003, Scully et al., 1998, Tomporowski, 2003). Extensive evidence shows that in the moderate, aerobic range, exercise reduces stress, decreases anxiety, and alleviates depression (Salmon, 2001). Despite decades of research attempting to explicate a neurochemical basis for these phenomena, a sound mechanistic explanation is still lacking. Previous research has concentrated heavily on alterations in neurotransmitter mechanisms such as norepinephrine (Dishman, 1997), endorphins (Hoffman, 1997), serotonin (Chaouloff, 1997), and most recently endocannabinoids (Sparling et al., 2003, Dietrich and McDaniel, 2004). Bearing on this long-standing gap in the medical knowledge base, it will be shown that established concepts in cognitive psychology and the neurosciences, coupled with recent findings intimating prefrontal cortex pathology in anxiety disorders and depression, can be synthesized to formulate a new hypothesis. This surprisingly simple hypothesis, “transient hypofrontality”, is based on functional neuroanatomy and should be regarded as complementary to explanations focusing on neurotransmitter changes. Importantly, this new theoretical framework yields a number of eminently testable hypotheses.