Limbic System and Sport

The limbic system is composed of a group of brain structures associated with various functions, most notably emotion, cognition, fear, and motivation. There is considerable variation in what structures researchers  consider  to  constitute  the  limbic  system, though the two primary structures of the system are consistently noted to be the amygdala and hippocampus. It should be acknowledged that the concept  of  the  limbic  system  as  the  predominant view of the limbic system as the locus of emotional regulation  of  emotional  regulation  is  considered by  many  to  be  flawed  because  it  is  overly  simplistic.  Some  researchers  in  mainstream  psychology have suggested that the concept of the limbic system be abandoned altogether. Nonetheless, the key structures of the limbic system (i.e., the hippocampus and amygdala) play important regulatory roles in behavior and may factor into some of the psychological  effects  seen  with  exercise.  Both  the amygdala  and  hippocampus  have  demonstrated important  links  with  emotion,  cognition,  and  the adaptation to stress.

The Limbic System and the Stress Response

Perhaps  one  of  the  main  reasons  that  the  limbic system  is  associated  with  the  stress  response  and behavior is because of the direct links that it shares with  the  hypothalamic-pituitary-adrenal  (HPA) axis. The HPA axis, hippocampus, and amygdala (along with the autonomic nervous system [ANS] and  dorsal  raphe  nuclei)  all  respond  to  stressful stimuli.  Furthermore,  these  areas  also  influence corticotropin-releasing  hormone  (CRH),  serotonin,  and  other  endocrine  responses  associated with stressful stimuli. The stress responses appear to  be  mediated  through  mineralocorticoid  and glucocorticoid  receptors  in  target  organs  as  well as in the limbic system itself. In conjunction with serotonergic  input  from  the  dorsal  raphe  nuclei, the  amygdala  and  hippocampus  help  integrate cognitive  and  behavioral  responses  associated with  the  HPA  axis  during  exposure  to  stressors, including   exercise.   Neuroanatomic   pathways between the hippocampus and hypothalamus provide for integration of metabolic, emotional, and cognitive information.

As  further  evidence  of  the  link  between  the limbic  system  and  the  HPA  axis,  glucocorticoids have  structural  and  functional  impacts  on  the hippocampus.  Marked  impairment  of  cognition has  been  noted  with  chronic  exposure  to  stress. Additionally, chronic stress induces direct changes in  CRH  and  CRH  gene  expression  in  the  hippocampus  as  well  as  a  variety  of  morphological changes  associated  with  cognitive  impairments. It  appears  that  exercise,  along  with  other  positive stimuli such as an enriched environment, can counteract  these  deleterious  effects  and  promote neurogenesis.  Optimal  challenge  or  stimulation positively  influences  limbic  system  development. An  inverse-U  relationship  appears  to  exist  for the effects of stress on hippocampal function and structure. Stressors of a moderate intensity, such as exercise,  effectively  enhance  hippocampal-related cognitive  function.  On  the  other  hand,  excessive or chronic stressors impair cognition and, as noted previously, produce negative changes in the hippocampus and related gene expression.

The hippocampus plays a central role in regulating cognitive and endocrine responses and adaptations  to  stressors,  including  exercise.  Part  of  this regulatory role is derived from the inhibition that the hippocampus exerts over HPA axis activation. It is also important for terminating HPA axis activity  following  stressor  exposure  in  order  to  promote  systemic  recovery.  The  hippocampus  exerts negative  feedback  on  the  paraventricular  nucleus under  situations  of  high  glucocorticoid  secretion in order to decrease CRH secretion. Additionally, there  is  a  counter-regulatory  influence  by  the  glucocorticoids  on  hippocampal  activity  that  results from acute stress. Under these conditions, the link between  stress,  the  hippocampus,  and  the  amygdala  should  also  be  recognized  as  stressors  that impair  the  hippocampus  yet  enhance  amygdala activation.  This  enhanced  amygdala  activation is  particularly  pronounced  in  the  bed  nucleus  of the  stria  terminalis  (BNST),  which  is  a  key  projection site that has been associated with anxiety. Anxiety  may  manifest  itself  as  such  things  as excessive  worry  and  apprehension,  physical  tension,  heightened  cardiovascular  tone,  and,  in animal  models,  freezing  behaviors  and  decreased free-roaming.

Hippocampal Influences on Depression and Cognition

Dysfunction  in  the  limbic  system  has  been  implicated   in   the   development   of   depression   and stress-related  disorders.  One  of  the  mechanisms by  which  certain  antidepressants  appear  to  exert effects  is  through  upregulation  of  neurotrophic factors,  particularly  brain-derived  neurotrophic factor  (BDNF),  in  the  limbic  structures.  Further support for the link between the limbic system and depressive  etiology  is  the  fact  that  a  number  of morphological and metabolic changes occur in the hippocampus of individuals suffering from depression.  It  may  partly  be  through  this  pathway  that exercise exerts its effects on depression and anxiety. BDNF  increases  in  the  hippocampus  in  response to exercise and facilitates use-dependent neuronal growth. Despite the BDNF downregulation that is common during intense or prolonged stress, secretion  is  upregulated  during  exercise.  Furthermore, there  appear  to  be  at  least  33  exercise-regulated hippocampal  genes,  many  of  which  are  involved in growth factor and neurotrophic factor signaling and  production.  One  growth  factor  in  particular that is stimulated by exercise, VGF, appears to be involved in energy balance, synaptic plasticity, and has demonstrated antidepressant actions.

There  is  some  evidence  that  brain  uptake  of insulin-like  growth  factor-1  (IGF-1)  from  endocrine or paracrine sources is necessary for exercise-induced  hippocampal  neurogenesis.  Additionally, exercise  helps  halt  the  stress-induced  efflux  of glutamate from the hippocampus that can be detrimental  to  hippocampal  structure  and  function. Activity-related  increases  in  norepinephrine  and serotonin may also have mediating roles in neurogenesis and cell proliferation, respectively.

The Amygdala: Emotion and Adaptation

The  amygdala  attributes  emotional  valence  and arousal to external stimuli and integrates adaptive responses  to  stressors.  The  basolateral  region  of the amygdala integrates with the hippocampus to derive  contextual  information  from  stimuli.  The centromedial  area  has  projections  to  the  lateral hypothalamus to help control blood pressure and projections to the BNST to regulate HPA activation.  Because  of  these  anatomical  connections, amygdalar  activation  directly  stimulates  HPA axis  responses  and  allows  the  limbic  system  to play  a  key  role  in  regulating  psychological  and physiological  adaptations  to  stressors,  including exercise.

The  amygdala  plays  a  key  role  in  emotional behaviors, fear conditioning, reward, and nociception.  Much  like  the  hippocampus,  chronic  stress can  affect  neuronal  morphology  and  synaptic plasticity in the amygdala. This may be impacted significantly  with  exercise,  though  limited  data currently  exist  to  support  this.  The  amygdalar CRH systems appear to be activated by stressors of  a  predominantly  psychological  nature,  which may be related to cognitive interpretations of the nature of the exercise stimulus.

 

References:

  1. Hand, G. A., Phillips, K. D., & Wilson, M. A. (2006).Central regulation of stress reactivity and physical activity. In E. O. Acevedo & P. Ekkekakis (Eds.), Psychobiology of physical activity (pp. 189–201). Champaign, IL: Human Kinetics.
  2. LeDoux, J. E. (2000). Emotion circuits in the brain.Annual Review of Neuroscience, 23, 155–184.
  3. Sapolsky, R. M. (2003). Stress and plasticity in thelimbic system. Neurochemical Research, 28,1735–1742.

 

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