Autism-Open Access

Autism-Open Access
Open Access

ISSN: 2165-7890

Commentary - (2015) Volume 5, Issue 2

Exercise Alleviates Autism Spectrum Disorder Deficits

Trevor Archer*
Department of Psychology, University of Gothenburg, SE45030 Gothenburg, Sweden
*Corresponding Author: Trevor Archer, Department of Psychology, University of Gothenburg, SE45030 Gothenburg, Sweden, Tel: 46317864694 Email:

Introduction

Amongst other behavioral deficits, children afflicted with Autism Spectrum Disorders (ASDs) present an array of motor skill impairments [1-3]. These deficits include problems the planning and performance of goal-directed behaviors [4,5]. Simermeyer and Ketcham (2015) have studied aspects of motor planning ability in ASD-diagnosed children (aged 5-13 years) through application of a method consisting of fine and gross motor tasks and postural components through altering sensory input [6]. They observed that ASD children expressed greater variability in hand selection during the “dial-turning task” and a tendency to plan movements that were not in accordance with ‘end-state comfort’. These children displayed a reduced ability to imitate movements correctly, presented lower scores for both the drawing and stickler tasks, and required longer time to ‘bead the bracelet’ than the comparison control group. The notion of end-state comfort refers to planning movements that allow individuals to attain comfort at task completion despite an initial phase of no-comfort/discomfort [7]. In children presenting normal development, a near completion of end-state performance is reached by 10 years-of-age [8]. Thus, the impairments by ASD children described by Simermeyer and Ketcham (2015) imply a serious disadvantage. The purpose of this treatise is to examine the notion of physical exercise as intervention to facilitate a positive developmental trajectory, as has been observed both under normal conditions and those associated with developmental disturbance, e.g. ADHD [9-14]. Motor skills difficulties, such as balance, posture and gait and movement speed, are present in children diagnosed with ASD [15,16]. Some of the behaviors associated with ASD stereotypical, repetitive and counterproductive. Episodes of physical exercise and/or activity were found to reduce the stereotypies and increase positive behaviors, such as time spent on tasks [17,18]. Other deficits in ASD involve alterations in the neurophysiological response to stress, including impairments in heart rate adaptation to challenges set by attentional demands and social encounters [19-21]. In circumstances of physical exertion or stress that occur during exercise it has been observed repeatedly that individuals (children) presenting ASD generally displayed lowered physiologic, i.e., heart rate, adaptations [22-24]. Pace and Bricout (2015) have shown that in comparison with a group of healthy children, a group of ASD children (aged 10 +1.45 years) evidenced lowered heart rate: at pre-test, during physical evaluation and at maximal exertion [25]. The ASD children displayed also a higher number of falls on the balance test, lower force on the handgrip test, lower levels of performance on the plate tapping test, vertical and broad jump tests, the Euro fit sit-up test and the test of reactive speed. They required too a greater length of time to achieve the motor educational course. They concluded that the ASD children in the sample may be characterized by motor impairments, lower daily skills abilities, and deficits in cardiac adaptation to physical exertion. Nevertheless, the consensus of the findings implied that physical activity programs initiated early ought to be maintained into adulthood thereby ensuring against cardiovascular risks associated with a sedentary lifestyle. Perinatal administration of the anti-epileptic drug, valproic acid, has been applied as a neurobehavioral model of autism in rodents [26]. It induces symptoms of autism that involve social and cognitive deficits and repetitive behaviors, suppresses the number of BrdU-positive (5-bromo-2’-deoxyuridine-positive) cells, linked to reelin, in the hippocampus induced autistic-like behavior in male rats through administration of valproic acid (400 mg/kg) on postnatal day 14 [27-29]. They were assigned to either exercise or sedentary groups from postnatal day 28 onwards for four weeks. Treadmill exercise was maintained five times/week during a 30 min session each day. The treadmill exercise load was: 1st five-min period at a speed of 2 meters/min, 2nd five-min period 5 meters/min, and 8 meters/min over the final 20 min. In tests of social behavior, the heightened aggressive behavior of valproate-injected rats was reduced by the treadmill exercise regime concurrent with improved cognitive performance in an eight-arm, radial arm maze. Postnatal valproic acid reduced reelin, an extracellular matrix glycoprotein that regulates neuronal migration and positioning during brain development, in the hippocampus, whereas, the treadmill running intervention increased reelin expression in the valproate-treated rats. The utility of animal models of ASD needs to be exploited more completely since rodents adapt rapidly to treadmill type running exercise interventions thereby facilitating the examination of a multiple of symptom phenotypes and biomarkers of disorder [30]. Despite the promise of exercise intervention for the alleviation of ASD symptoms, several conditions require fulfillment for effective improvements to be obtained; these include:

(i) The notion of individual participation and compliance in physical exercise programmes.

(ii) The pervading presence of issues concerning balance impairments which require taylor-made exercise forms, and

(iii) The reality of auditory hypersensitivity which complicates the choice of exercise regimes.

A paucity of intervention studies have concentrated upon the notion of ‘individual participation’. Adair et al., (2015) have shown that individually-tailored, educational and mentoring programmes enhanced participation outcomes, particularly with regard to exercise regimes wherein in cases where participation was only a secondary outcome, little or no effect was registered [31]. Balance deficits are present in ASD and are exacerbated by alterations of stance yet these deficits were unrelated to symptom severity when age-of-subject was taken into account, the complications associated with interventions are under study [32,33]. Finally, in ASD children, auditory modality hypersensitivity presents an important feature of disability. The “listening project protocol” offers a new intervention, a form of ‘neural exercise’ that applies acoustic stimulation to recruit the neural regulation of the middle ear muscles [34]. Listening project protocol was hypothesized to reduce auditory hypersensitivities by increasing the neural tone to the middle ear muscles to functionally dampen competing sounds in frequencies lower than human speech. Their experimental trials demonstrated that listening project protocol, when contrasted to control conditions, selectively reduced auditory hypersensitivities. These findings are consistent with the polyvagal theory, which emphasizes the role of the middle ear muscles in social communication.

Despite the established genetic and neuroimmune connections, environmental factors, such as diet and gastrointestinal complications, are being taken into account increasingly [35-38]. The notion of “plural autisms” affecting the expressions of developmental trajectories focuses attention on influences of diet. For example, it appears that differing responses to the use of a gluten- and casein-free diet, defined as best- and non-response, has combined with some progress on determining the underlying genetic and biological correlates potentially related to such dietary elements [39]. Currais et al. have shown that the dietary glycemic index induces a marked impact upon ASD the phenotype [40]. In BTBR mice, a model of ASD, they found that the diet modulated plasma metabolites, neuroinflammation, and brain markers of neurogenesis to mimic the human condition. Puig-Alcaraz, et al. measured homocysteine, glutathione, methionine, and 3-nitrotyrosine in the urine of ASD children. They observed the increase in homocysteine was directly related to the severity of the communication skills deficits but the deficits in socialization skills or the preponderance of repetitive/restricted behaviors [41]. In an examination of several elements of dietary supplements in 56% of children presenting ASD, Stewart et al. found deficiencies in vitamin D and calcium; supplementation caused excess vitamin A, folate, and zinc, as well as vitamin C and copper (2–3 years), and manganese and copper (4–8 years) [42]. Thus, the dangers of dietary supplement ought to be observed.

References

  1. Dewey D, Cantell M, Crawford SG (2007) Motor and gestural performance in children with autism spectrum disorders, developmental coordination disorder, and/or attention deficit hyperactivity disorder. J IntNeuropsycholSoc 13: 246-256.
  2. Ghaziuddin M, Butler E (1998) Clumsiness in autism and Asperger syndrome: a further report. J Intellect Disabil Res 42: 43-48.
  3. Manjiviona J, Prior M (1995) Comparison of Asperger syndrome and high-functioning autistic children on a test of motor impairment. J Autism DevDisord 25: 23-39.
  4. Hovik KT, Egeland J, Isquith PK, Gioia G, Skogli EW, et al. (2014) Distinct Patterns of Everyday Executive Function Problems Distinguish Children With Tourette Syndrome From Children With ADHD or Autism Spectrum Disorders. J AttenDisord. 2014.
  5. Kriete T, Noelle DC (2015) Dopamine and the development of executive dysfunction in autism spectrum disorders. PLoS One 10: e0121605.
  6. Simermeyer JL, Ketcham CJ (2015) Motor planning and end-state comfort in children with autism spectrum disorders. Autism 5:138.
  7. Adalbjornsson CF, Fischman MG, Rudisill ME (2008) The end-state comfort effect in young children. Res Q Exerc Sport 79: 36-41.
  8. Thibaut JP, Toussaint L (2010) Developing motor planning over ages. J Exp Child Psychol 105: 116-129.
  9. Archer T (2015) Health benefits of physical exercise for children and adolescents. J Novel Physiother 4:203.
  10. Archer T, Garcia D (2014) Physical exercise influences academic performance and well-being in children and adolescents. Int J School CognPsychol 1:e102.
  11. Garcia D, Archer T (2014) Positive affect and age as predictors of exercise compliance. PeerJ 2: e694.
  12. Archer T, Kostrzewa RM (2012) Physical exercise alleviates ADHD symptoms: regional deficits and development trajectory. Neurotox Res 21: 195-209.
  13. Archer T, Garcia D (2015) Exercise and dietary restriction for promotion of neurohealth benefits. Health 7:136-152.
  14. Hannan AJ (2014) Environmental enrichment and brain repair: harnessing the therapeutic effects of cognitive stimulation and physical activity to enhance experience-dependent plasticity. Neuropath ApplNeurobiol 40: 13-25.
  15. Green D, Charman T, Pickles A, Chandler S, Loucas T, et al. (2009) Impairment in movement skills of children with autistic spectrum disorders. Dev Med Child Neurol 51: 311-316.
  16. MacDonald M, Lord C, Ulrich DA (2014) Motor skills and calibrated autism severity in young children with autism spectrum disorder. Adapt PhysActiv Q 31: 95-105.
  17. Levinson LJ (1993) The effects of exercise intensity on the stereotypic behaviours of individuals with autism. Adapt Phys Act Q 10:255-268.
  18. Rosenthal-Malek A, Mitchell S (1997) Brief report: the effects of exercise on the self-stimulatory behaviors and positive responding of adolescents with autism. J Autism DevDisord 27: 193-202.
  19. MarinoviÄ-Curin J, MarinoviÄ-TerziÄ I, Bujas-PetkoviÄ Z, Zekan L, SkrabiÄ V, et al. (2008) Slower cortisol response during ACTH stimulation test in autistic children. Eur Child Adolesc Psychiatry 17: 39-43.
  20. Althaus M, Mulder LJ, Mulder G, Aarnoudse CC, Minderaa RB (1999) Cardiac adaptivity to attention-demanding tasks in children with a pervasive developmental disorder not otherwise specified (PDD-NOS). Biol Psychiatry 46: 799-809.
  21. Corona R, Dissanayake C, Arbelle S, Wellington P, Sigman M (1998) Is affect aversive to young children with autism? Behavioral and cardiac responses to experimenter distress. Child Dev 69: 1494-1502.
  22. Jansen LM, Gispen-de Wied CC, Wiegant VM, Westenberg HG, Lahuis BE, et al. (2006) Autonomic and neuroendocrine responses to a psychosocial stressor in adults with autistic spectrum disorder. J Autism DevDisord 36: 891-899.
  23. Meng L, Lu L, Murphy KM, Yuede CM, Cheverud JM, et al. (2011) Neuroanatomic and behavioral traits for autistic disorders in age-specific restricted index selection mice. Neuroscience 189: 215-222.
  24. Verhoeven EW, Smeekens I, Didden R (2013) Brief report: suitability of the Social Skills Performance Assessment (SSPA) for the assessment of social skills in adults with autism spectrum disorders. J Autism DevDisord 43: 2990-2996.
  25. Pace M, Bricout VA (2015) Low heart rate response of children with autism spect rum disorders in comparison to controls during physical exercise. PhysiolBehav 141: 63-68.
  26. Wagner GC, Reuhl KR, Cheh M, McRae P, Halladay AK (2006) A new neurobehavioral model of autism in mice: pre- and postnatal exposure to sodium valproate. J Autism DevDisord 36: 779-793.
  27. Yochum CL, Bhattacharya P, Patti L, Mirochnitchenko O, Wagner GC (2010) Animal model of autism using GSTM1 knockout mice and early postnatal sodium valproate treatment. Behav Brain Res 210: 202-210.
  28. Yochum CL, Dowling P, Reuhl KR, Wagner GC, Ming X (2008) VPA-induced apoptosis and behavioral deficits in neonatal mice. Brain Res 1203: 126-132.
  29. Seo TB, Cho HS, Shin MS, Kim CJ, Ji ES, et al. (2013) Treadmill exercise improves behavioral outcomes and spatial learning memory through up-regulation of reelin signaling pathway in autistic rats. J ExercRehabil 9: 220-229.
  30. Archer T, Fredriksson A (2013) The yeast product Milmed enhances the effect of physical exercise on motor performance and dopamine neurochemistry recovery in MPTP-lesioned mice. Neurotox Res 24: 393-406.
  31. Adair B, Ullenhag A, Keen D, Granlund M, Imms C (2015) The effect of interventions aimed at improving participation outcomes for children with disabilities: A systematic review. Dev Med Child Neurol.
  32. Graham SA, Abbott AE, Nair A, Lincoln AJ, Müller RA, et al. (2015) The Influence of Task Difficulty and Participant Age on Balance Control in ASD. J Autism DevDisord 45: 1419-1427.
  33. Dutheil F, Chambres P, Hufnagel C, Auxiette C, Chausse P, et al. (2015) 'Do Well B.': Design Of WELL Being monitoring systems. A study protocol for the application in autism. BMJ Open 5: e007716.
  34. Porges SW, Bazhenova OV, Bal E, Carlson N, Sorokin Y, et al. (2014) Reducing auditory hypersensitivities in autistic spectrum disorder: preliminary findings evaluating the listening project protocol. Front Pediatr 2:80.
  35. Chapman NH, Nato AQ Jr, Bernier R, Ankenman K, Sohi H, et al. (2015) Whole exome sequencing in extended families with autism spectrum disorder implicates four candidate genes. Hum Genet.
  36. Estes ML, McAllister AK (2015) Immune mediators in the brain and peripheral tissues in autism spectrum disorder. Nat Rev Neurosci 16: 469-486.
  37. Michel M, Schmidt MJ, Mirnics K (2012) Immune system gene dysregulation in autism and schizophrenia. DevNeurobiol 72: 1277-1287.
  38. Gore AC, Martien KM, Gagnidze K, Pfaff D (2014) Implications of prenatal steroid perturbations for neurodevelopment, behavior, and autism.  Endocr Rev 35: 961-991.
  39. Whiteley P (2015) Nutritional management of (some) autism: a case for gluten- and casein-free diets? ProcNutrSoc 74: 202-207.
  40. Currais A, Farrokhi C, Dargusch R, Goujon-Svrzic M, Maher P (2015) Dietary glycemic index modulates the behavioral and biochemical abnormalities associated with autism spectrum disorder. Mol Psychiatry.
  41. Puig-Alcaraz C, Fuentes-Albero M, Calderón J, Garrote D, Cauli O (2015) Increased homocysteine levels correlate with the communication deficit in children with autism spectrum disorder. Psychiatry Res.
  42. Stewart PA, Hyman SL, Schmidt BL, Macklin EA, Reynolds A, et al. (2015) Dietary Supplementation in Children with Autism Spectrum Disorders: Common, Insufficient, and Excessive. J AcadNutr Diet 115: 1237-1248.
Citation: Archer T (2015) Exercise Alleviates Autism Spectrum Disorder Deficits. Autism Open Access 5:146.

Copyright: © 2015 Archer T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Top