Anti-ageing and Therapeutic Effect of Exercise on Brain: A Neurophysiological Perspective.

                                

In this article I discuss about the effect of exercise on brain health. A huge number of research have studied the effect of exercise on cardio-vascular system,endocrine system and musculoskeletal system.Many studies have provided evidence for the positive and prophylactic effect of exercise on these systems in disease and health.However as of 2014 number of research have explored the effect of exercise on brain health. In this article I wish to provide a research based overview of neurophysiological effect and therapeutic effect of exercise on CNS health, Neurodegenerative diseases and aging.

A number of studies have observed beneficial neurophysiologial effect of acute and chronic exercise in Human and animals.A study published in 2005 in Journal of Neurobiology of Ageing by psychiatrist Ronald Stanton Duman PhD states that exercise and enriched environment increases neurotrophic support in human brain by increasing cerebral blood Flow (CBF),the expression of Neurotropic Factors like BDNF, IGF-1, VEGF , NT-3,FGF-2 , GDNF , EGF and NGF as well as the induction of pro-inflammatory process by exercise promote neurogenesis, angeogenesis and synaptogenesis. 

Studies have also shown that physical exercise modulates the major CNS neurotransmitters that are associated with ones state of alertness( Norepinephrine),pleasure and reward system(Dopamine) and the level of anxiety( serotonin).Besides that changes in the level of these neurotransmitters may have different consequences depending on the type of receptors and cortical areas that are activated (Sarbadhikari SN & Saha AK 2006). A study published in BJSM in 2004 by Dietrich, titled 'Endocannabenoids and exercise' says that regular physical exercise can cause a sense of well being and euphoria,anxiolytic effects,sedation and decreased sensitivity to pain in humans by promoting release of opioids and endocannabenoids. Systematic exercise and proper diet that is rich in anti-oxidants have very positive impact in brain health. Adhering to diet that is rich in anti-oxidants and anti-inflammatory components in combination with physical exercise participation would have significantly better results.Moreover,elevated Vascular Endothelial Growth Factor(VEGF) levels,accelerated metabolism might contribute to enhanced angeogenesis( Periera AC et all 2007).  

In the last decade a number of studies have come up with promising evidence for considering exercise as a supportive prophylactic and  therapeutic means in the treatment plans of Neuropsychatric diseases such as Major Depressive Disorder(MDD), Dementia and Parkinsons disease. Smaller hippocampal volume, which may be due to fewer Granule Neurons(GN) in the Dentate Gyrus(DG) is identified in patients suffering from MDD ( Boldrin M et all 2013). Exercise increases beta endorphin levels which might play a significant role in  enhancing the birth of new neurons in the Dentate Gyrus. exercise also increases levels of VEGF and BDNF that may play a critical role in promoting the survival of new neurons in the Denate Gyrus which is indicated to undergo pathologic changes in MDD (B.R.Christie2006). Rethorst et all reviewed  75 RCTs comparing exercise versus no treatment or wait list control. 58 of the 75 studies were included in a Meta-Analysis which showed a clinically significant effect of exercise on MDD.( ES:0.80,95%CI-0.90 to 0.67). 

  Clinical Studies in human demonstrate that various modalities and systematic exercise can improve cognitive capacity in patients with PD.Cognitive dysfunction in Parkinsons Disease(PD) is associated with impaired executive function( Higginson CI et all 2003). In 2013 Fisher et all published an RCT in Neuroreport. Which analysed whether Treadmill exercise promotes Striatal D2 binding potential in patients with early parkinsons disease. 4 patients with early PD where randomized to receive intensive exercise( treadmil training sessions/3/week for 8 weeks) or no exercise. 2 healthy age- matched individuals participated in treadmill training. Alterations in the DA-D2R binding potential as a marker for receptor expression were determined using PET imaging with (18F) Fallypride. Turning perfromance of the patients with PD as a measure for postural control  and UPDR scale scores pre-exercise and post exercise were determined. The results showed an exercise -induced inrease in 18F binding potential as well as improved postural control in patients with early PD who exercised. The researches concluded that exercise leads to positive  Neuroplasticty in dopamenergic signaling and contributes to improved postural control in early stage PD. 

A number of studies have also showed that Progressive Resistance Exercise also helps to enhance functionality and quality of life of patients with PD. Patients with mild to moderate PD can obtain increase in performance or strength similar to that of normal adults in the same age in a resistance training program. Resistance training can produce functional improvements in gait and may therefore be useful as part of a physical rehabilitation and/ or health maintenance program for patients with PD( Scabdalis et all 2001).

Caerphilly Cohort study, A study that monitored the health habits of 2235 men over a period of 35 years have confirmed exercise significantly reduces the risk of Dementia along with other 4 healthy behaviors low body weight, No-smoking, low alcohol , healthy diet.People who consistently followed 4 or 5 of these behaviors experienced a 60% decline in dementia and cognitive decline with exercise being the strongest mitigating factor( Peter Elwood et all 2013). A study  conducted by Yerokhvin et all in 2012  analysed whether strengthening exercise programs help to improve verbal memory in patients with early dementia.This study evaluated the effect of a 10 weeks strengthening exercise intervention on cognitive function and EEG in a sample of 13 older adults with early Dementia and 9 normative controls. Results revealed beneficial effect of strengthening exercise on verbal memory coupled with frontal beta and delta power asymmetries and N200 amplitude asymmetry. Results of the study showed that strength training programs helps to enhance cognitive efficiency in people with early stage dementia.Physical exercise improves the efficiency of the capillary system and and increases the O2 supply to the brain.Thus enhancing metabolic activity and oxygen uptake in neurons and increases neurotropin levels and resistance to stress. Regular exercise and active lifestyle during adulthood have been associated with reduced risk and protective effects for mild cognitive impairment and Alzheimer's disease( Perla Kaliman 2011). Apolipoprotein (APOE) is a gene that produces an important protein called Apoplipoprotein E which is essential for packing cholesterol and other fats and carrying them through the circulation. Carriers of an allelic variant of APOE gene called APOE epsilon4 are at increased risk of Alzheminer's Disease(AD).APOE e4 causes increased deposit of amyloid beta peptides and amyloid plaques in the brain tissue of carriers of this variant. Amyloid beta peptides and amyloid plaques causes progressive death of neurons in the brain and triggers signs of AD.In APOEe4 carriers compared to non-carriers greater level of physical activity may be more effective in reducing amyloid burden and are associated with greater activation of Semantic memory related neural circuits( J C Smith et all 2013).    

These research finding conclude that systematic exercise and healthy diet and way of living    is a prophylactic and supportive therapeutic means in promoting brain health, preventing or preventing the progress of Neuropsychatric and Neurodegenerative conditions and a supportive therapy for array of Neuropsychatric conditions. Systematic exercise and lifestyle is also a potent mediator of anti-ageing effect in ageing brain. I hope this article will provide a scientific understanding of the neurophysiological effect of exercise and a research based understanding of the prophylactic and therapeutic effect of exercise on brain health. The main purpose of this article is like my every other articles to promote evidence based practice of exercise science among Exercise Physiologists , Clinical Exercise Specialists, Health and Fitness Specialists and other Exercise Professionals. I hope everyone will find this article informative as well.        

Siby C Chacko BPE,MPE( Exercise Physiology)              

REFERENCES

1) Duman RS, Neurotropic factors and regulation of mood: Role of exercise science and metabolism.

    Neuro bio.ag. 1:88-93(2005).

2) Sarbadhikari SN & Saha AK,Moderate exercise and chronic exercise produces counteractive 

    effect on different areas of brain by acting through various neurotransmitter receptor sub-types: 

    A hypothesis. theor.bio&med model 3:33(2006).

3) Dietrich A, Mcdaniel WF, Endocannabenoids and exercise, BJSM , 38:536-541(2004).

4) Periera AC, Huddleston DE, Brickman AM, Sousunov AA,Hen R,McKhann GM, Sloan R,

    Gag FH, Brown TR, Small SA. An in vivo corelate of exercise induced neurogensis in adult 

     dentate gyrus. proc.natl.acad.sci USA 104:5638-5643(2007).

5) Boldrin M , Santiago AN, Hen R, Dwork AJ, Rosoklija GB, Tamir.H, Arango V and Johnmann J

    Hippocampal granule neurons number and dentate gyrus volume in anti-depressant treated and 

    Untreated Major Depression.38(6) 1068-1077 (2013).

6) B R Christie. Anti-Depressive effect of exercise evidence for an adult

     Neurogenesis hypothesis?.J.Pscyc.Neuroscience 31(2) 84-92 (2006).

7) Rethorst CD, Wipfli BM, Landers DM, The anti- depressive effect of exercise a meta-analysis of 

    randomized controlled Trials. Spot.MEd. 39: 491-511(2009).

8) Higginson CI , King DS, Levine D, Wheellock VL, Khamphay NO and Sigvardit KA.

    The relationship between verbal memory and Parkinson disease.Brain cogn 52(3) 343-352(2003).

9) FisherBE, Li Q, Nacca A, Saleem GJ, Song J, Yip J,Hui JS ,Jackowec MW and Petzinger GM.

     Treadmill exercise promotes Striatal D2 binding potential in patients with early parkinsons disease.

      Neuroreprt 24(10) 509-514 (2013).

10) Scandalis , Thomas A DO, Bosak, Andrew BA, Berliner,Jefrry C BS, Helman,Laura L BS, 

       Wells, Micheal R.Resistance training and Gait Function in patients with parkinosn's disease.

        AJPMR 80(1): 38-43( 2001).

11) Peter Elwood. Julieta Galanti, Janet Pickering, Stephen Phalmer, Antony Bayer, Yoav Ben Sholmo,

      Marcus Longly and John Gallacher. Healthy lifestyle reduces the incidence of chronic diseases and 

      dementia:Evidence from the Caerphilly Cohort study. DOI: 10.1371/journal pone.0081877( 2013).

12) Yerkhin V, anderson HC, Hogan MJ, Dunnam M, Huber D, Osborne S, Shulan M.

       Neuropsychological and Neurophysiological effect of strengthening exercise for early Dementia: 

       A pilot study. Ag. Neuropsycho&cog.J of normo& dysfunctional dev. VOl.19(3)380-401(20120.

13) P kaliman, Marcelina P , JF Lalanza, Antoni C, Rosa ME, Merce P. Neurophysiological and epigenetic 

       effect of Physical Exercise on the aging process.Ageing R Rev. 10(4) 475-486 (20110.

14) J C Smith,Kristy AN, John LW, M Seidenberg, SM rao.Physical activity and Brain function in older 

      adults at increased risk for Alzhemier's disease.Brain. sci.3:54-83(2013).

   

     

      

     

Molecular Cascades of Resistance Training induced Skeletal Muscle Hypertrophy: A Molecular Physiological perspective.

In this article I discuss of a relatively new topic,The Cellular and Molecular Cascades of Skeletal Muscle Hypertrophy. It is perhaps a hot area for research in Molecular Exercise Physiology and Exercise genetics in vogue. Exercise Physiologist and Exercise practitioners may be very familiar with the Physiological Mechanism of Skeletal muscle hypertrophy.Muscle hypertrophy can be considered distinct and separate from muscle hyperplasia. During hypertrophy contractile elements enlarge and the extracellular matrix expands to support growth (Vierck J et all 2000). However muscle volumaization depends on both hypertrophy and hyperplasia. This article will provide a research based understanding of biomolecular cross talks and cascades that regulate resistance training induced muscle growth.This article's prime focus is on IGF-1(Insulin Like Growth Factor-1) mediated skeletal muscle hypertrophy through the activation of sarcoplasmic (cellular) signaling pathway PI3k/Akt/mTOR ( Mammalian Target of Rapamycin).
 A profound understanding of molecular and genetic factors that mediate skeletal muscle hypertrophy and the impact of mechanical loading on such molecular processes will enable Nutritionists,exercise physiologists & practitioners to develop new and more effective supplements and training protocols for athletes to prevent Over Training Syndrome and recover from OTS. It will also be helpful for rehabilitation specialists,clinical exercise physiologist & HFS's to develop systematic therapeutic resistance training programs for the management and prevention of  Cancer Cachexia , HIV induced Cachexia , other diseases and againg induced muscle wasting.         

For a conceptual understanding of the topic, I will briefly discuss What IGF-1 is ? and What PI3k/Akt/mTOR pathway is ? accompanied by brief reviews of current research on the role of mechanical loading of skeletal muscle on the IGF-1 mediated PI3k/Akt/mTOR pathway activation & skeletal muscle Hypertrophy.

IGF-1

Insulin Like Growth Factor-1 or Somatomedian C is a protein that in human is encoded by IGF-1 gene.( Jansen.M et All 1983). It is a cellular signaling molecule which  has a molecular structure similar to that of insulin. In human it is chiefly secreted by liver and skeletal muscle tissue. It acts like growth hormone in both autocrine and paracrine manner on skeletal muscle tissue by binding to IGF-1r. It plays an important  anabolic role in adult skeletal muscle  growth. IGF-1 isforms  have  significant role in cellular processes of many tissue types. IGF-1r's are mainly expressed in satellite cell population. Satellite cells are the mononuclear progenitor cells of skeletal muscles.For several years research have focused on IGF-1 mediated skeleltal muscle growth in response to resistance exercise.Many studies have found exercise induces IGF-secretion.IGF-1 isoforms binds to specific receptors in muscles cell surface and activates growth stimulating pathway( PI3k/Akt/mTOR Path way).To date several isoforms of IGF-1 have been found in human and other animals. 
Of which IGF-1c isoform has been observed to be increasingly expressed at the onset of satellite cell proliferation in response to muscle cell damage induced by muscle lengthening contractions in human(McKay BR et all 2008).
IGF1/PI3k/Akt/mTORcomplex is a potent stimulator of sarcoplasmic growth.IGF1/PI3k/Akt/mTOR complex stimulates skeletal muscle hypertrophy by inhibiting the effect of a protein called Myostatin ( a member of TGF-beta family). Deletion or inhibition of Myostatin causes an increase in skeletal muscle size because myostatin acts both to inhibit the myoblast differentiation and to block the Akt pathway( David J Glass 2011). 

PI3k/Akt/mTOR pathway

It is an intracellular signaling pathway contributes to  Muscle Hypertrophy. It is activated by IGF-1 and has a number of downstream effects which either promote protein synthesis( proteogenesis) or prevent protein breakdown ( proteolysis). The IGF-1 mediated downstream signaling cascades of PI3k/Akt/mTOR pathway is complex and will be difficult for those with little back-ground in molecular physiology to understand. Therefore, I will try to present in a simple and comprehensible manner for Exercise Physiologist and exercise professionals in general. IGF-1 acts in a hormone like manner by binding to IGF-1r in skeletal muscle tissue, especially in satellite cells. Ligand binded IGF-1r activates intracellular signaling transducer enzyme PI3k ( phospho ionosetide 3 kinase) this in turn lead to the activation of Akt or PKB( Protein Kinase B).It is an enzyme that  plays key role in glucose metabolism, cell proliferation, transcription and cell migration. IGF-1/PI3k/Akt complex binds to mTOR or Mammalian Target of Rapamycin. Specifically to mTOR isoform Mammalian Target Of Rapamycin Complex-1. It is a protein that in human is encoded by MTOR gene.It act as a catalyst of Cell growth, proliferation, Cell motility , cell survival, protein synthesis and transcription.
 IGF-1's pro-hypertrophy activity comes predominantly through its ability to activate PI3k/Akt signaling pathway ( Glass DJ 2010). The IGF1/PI3k/Akt/mTOR pathway, which has been shown to induce, hypertrophy, prevent induction of requisite atrophy mediators namely the Muscle Specific Ubiquitin Ligases (MAFBx) and Muscle RING-finger protein1( MuRF1)(Trevor.M.Stitt et All 2004). Akt phosphoryates and inactivates Tuberosclerosis Complex 2 ( TSC2) resulting in the activation of mTOR. mTOR phosphorylates 70KDa ribosomal S6 protein kinase (p70S6K1) resulting in an increase in muscle protein synthesis( Peter Tiidus, A Russel Tupling,Michael Houston 2012). The Mammalian Target of Rapamycin complex 1(mTORC1) pathway is the primary regulator of skeletal muscle growth. Bodine et all in 2001 reported that the over expression of Akt in mice resulted in an astonishing amount of skeletal muscle hypertrophy mediated by the activation of mTORC1 signaling pathway.2011 Miyazaki et all demonstrated IGF-1/PI3k/Akt non-depended activation of mTORC1 and skeletal muscle hypertrophy in C57BL/6J mice.However so far no studies in human have reported supportive evidence for IGF-1/PI3k/Akt non- depended activation of mTORC1 pathway( mTOR).  
       

IGF-1/PI3k/Akt/mTOR Pathway 

     

                             

  

     Siby C Chacko BPE,MPE ( Exercise Physiology)

References

1) Vierck J, O'Reilly,B.Hossner,K.Antonio,J.Byrne,K.Bucci.L and Dodson, Satellite cell regulation
    Following miotruma caused by resistance exercise. Cell.Bio.Int. 24: 263-272 (2000)

2) Jansen.M, Van Schaic FM,Ricker AT,Bulock.B, Woods.DE, Gabby K H and Nussbum AL , Sequence of cDNA Human Insulin Like Growth factor - 1 precursor.Nature: 306(5943) 609-11.(1983).

3) David J Glass , PI3 kinase regulation of skeletal muscle hypertrophy and atrophy. curr.top.in.micro bio
   and immuno Vol. 346 pp 267-278(2010)

4) Mc Kay BR,O'Reilly,Philips SM, Tarnopolsky MA and Parise.G, Co- expression of IGF
    Family members with Myogenic regulatory factors with folowing acute damaging muscle  
    lengthening contractions in Human. J.Physio.586: 5549-5560 (2008).

5)  David J Glass , PI3 kinase regulation of skeletal muscle hypertrophy and atrophy. curr.top.in.micro bio
   and immuno Vol. 346 pp 267-278(2010). 

6) Trevor.N.Stitt, Doreen Drujan, Brian A Clark, Frank Panaro,David J Glass et all.
     The IGF-1?PI3k/Akt pathway Prevents expression of Muscle Atrophy induced Ubiquitin Ligases
      by inhibiting FOXO Transcription factors. Mollecular Cell Vol.14(3)pp-395-403 (2004).

7) Peter Tiidus, A Russel Tupling,Michael , Houston , Biochemistry Primer for exercise Science 4th edition
     chap-3 pp:39-70 (2012).

8) Bodine SC , Stitt.T.N, Gonzalez.M,Kline W.O,Glass DJ et all . Akt/mTOR pathway is a crucial 
    regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nat.cell.bio 3(11)1014-1019(2001).

Systematic Exercise: A non-pharmaceutical approach for enhancing Adult Neuroplastcity and Reducing Cognitive Decline

                                 

So far it has been hypothesized that systematic exercise programs and Active Lifestyle has a very significantly positive effect on enhancing human cognition,executive functions and memory in both adult and pediatric population. A number of research have come up with significant evidence for supporting this notion. Physical exercise is an efficient non-pharmaceutical approach that can be used to enhance and maintain cognitive function in healthy older adults and patients suffering from mild cognitive impairment ( Louis Beher& Kirk.L.Erickson 2013).

In a study conducted in 2012 by Lindsay.S.Nagamatsu et all showed that Physical activity helps to improve verbal and spatial memory in older adults with probable mild cognitive impairment.In this study 86 women aged between subjective memory complaints completed one of the 3 interventions twice/ week for 6 months resistance training, aerobic training and or balance and tone. They tested verbal memory using Rey Auditory Verbal Learning Test (RAVLT) and spatial memory using computerized test before and after trial completion. Both exercise groups showed significant improvement in memory performance which was not observed in the control group.
A single blinded RCT conducted in 2010 by Teresa Liu-Ambrose et all concluded that once weekly or twice weekly resistance training benefited the executive cognitive functions of selected attention and conflict resolution among senior woman. In this study 155 community dwelling woman aged(65-75) were randomly allocated into once weekly(n=54) twice weekly(n=52) resistance training group and twice weekly balance and tone training group(n=49) (control group). The primary outcome measure was performance on the Stroop Test, an executive cognitive test of selective attention and Conflict resolution. The secondary outcome measures were working memory, verbal memory, brain volume, gait speed and muscular function.The results were very remarkable. Both resistance training groups significantly improved there performance on the Stroop test compared with those in the control group ( P≤ .03). Task performance improved by 12.6% and 10.9% in the once weekly and twice weekly resistance training group. where as it reduced by 0.5% in the control group.Enhanced selective attention and conflict resolution was significantly associated with increased gait speed. However the study also found reduction in brain volume in both the experimental groups as compared to control group.

These evidences flash light on the fact that structured and scientifically designed exercise programs help to enhance neuroplasticty and neurogenesis in aging Maintaining functional pasticity of the Cortex is essential for healthy aging. Aerobic exercise and resistance training may be an effective behavioral intervention to promote functional plasticity among seniors. Teresa Liu-Ambrose et all have showed in 2011 that 12 months of twice  weekly  resistance training caused functional changes and increase in hemodynamic activity in 2 cortical regions associated with response inhibition process. the cortical areas are left middle temporal gyrus and the left anterior insular extending into lateral orbital cortex. 

Research performed by Takao Suzuki et all in 2013 showed that exercise intervention are beneficial  for improving logical memory and maintaining general cognitive function and reducing whole brain cortical atrophy in older adults with amenstic mild cognitive impairment(MCI). Subjects were 100 100 adults ( mean age 75)with MCI.The subjects were classified into amnestic MCI group ( n=50) with neuroimaging measures and other MCI group (N=50) before the randomization.Subjects in each groups were randomized to either a multicomponent exercise or an education control group using a ratio of 1:1. The exercise group exercise for 90min./day, 2day/wk/40 times for 6 months.These exercise program was  conducted under multi-task condition to simulate working memory and attention.The control group attended 2 education class.A repeated measure ANOVA revealed that no group into x time interactions in the cognitive test and brain atrophy in MCI patients.A sub analysis of amnestic MCI patients for group x time interactions revealed that the exercise group exhibited significantly better mini mental state examination (p=.04) and logical memory scores (p=.04) and reducing whole brain cortical atrophy(p<.05) compared to the control group.

All these evidences points to the fact that exercise interventions needs to be incorporated into the geriatric and amenestic populations treatment plans and daily life routines.It is also necessary that exercise specialists and clinicians should update the current research and promote multidisciplinary approach in  geriatric and aging population management.Just like the Medical community exercise science professionals also should  give emphasis to evidence based practice of exercise physiology , clinical exercise physiology and exercise science.One of the main goal of this article is to promote evidence based practice among exercise science professionals. 

Siby C Chacko BPE, MPE (Exercise Physiology)       

REFERENCES

1) Louis Behar, Kirk.L.Erickson and Teresa Liu Ambrose , Physical exercise and brain function in 

     older adults (2013) Journal of aging research ch:1,p.no-1 to 3.

2) Lindsay.S.Nagamastu ,Alison Chan, Jennifer.C.Devis, Lynn Beattie, Physical activity improves verbal

    and spatial memory in older adults with probable mild cognitive impairment: A 6 month RCT (2013)

     J.of Aging Res. Article ID 861893.pp-10.

3) Teresa Liu Ambrose et all , Resistance Training and Executive Functions: A12 month RCT (2010)JAMA      vol.-170,No.2 

4) T.Suzuki,Shimada.H, Makizako.H,Doi.T, Yoshida.D, A RCT of Multicomponent Exercise in Older 

     adults with Mild Cognitive Impairment.( 2013) PloS one: 2013, 8(4): g61483.

      

Functional Anatomy of Human Rexed laminae.

                                                         

There are 10 Rexed Laminae identified by Swedish Neuroscientist Bore Rexed in 1950. These are gray matter layers widely distributed in Dorsal , ventral and lateral columns of the Spinal cord at various level.

Lamina I
It is located in the dorsal hone. It consist of scattered large neurons that receive afferent connections from Lissauer's Tract.These neurons are mainly involved in Noceception ( pain Sensation). Pain sensation relayed here can not be modulated.

Laminae II&III
Lamina II with overlap with Lamina III approximately conterminous with the Substantia Gelatinosa of Rolando.These lamina contain inter-neurons that receive pain and temperature afferents from Lissauer's Tract.But make no contributions to the DCML pathway.

Lamina IV
It contains polymodal sensory neurons , That are activated by many different sensory stimuli. Cells in Lamia IV gives rises to the Contralaeral Spinothalamic Tract.

Laminae V & VI
These layers are indistinguishable in humans. Cells in lamina IV and V to VI make up the Nucleus Proprious. It is involved in pain and temperature sensation.

Lamina VII
It is the most extensive Cytoarchetectonic Layer in human spinal cord.Between C8 and L3 the medial portion of the lamina VII contains dorsal Nucleus of Clark.Degeneration of Neurons in Clarks Nucleus is indicated in friedreich's Ataxia.Cells in Nucleus Dorsalis of Clark gives rise to Dorsal spino cerbellar tract.Intermedio- lateral gray column of the lamina VII contains preganglionic sympathetic neurons between T1 and L2 and preganglionic parasympathetic neurons between S2 and S4.

Lamina VIII
It contains interneurons involved in motor control including Renshaw cells that receives collaterals from nearby Lamina IX.

Lamina IX
It contains the Alpha Motor Neurons. There is a Nuclear group at all levels that innervates axial and proximal Muscles and a lateral Nuclear group at cervical and Lumbar enlargements that innervates distal extremity muscles.

Lamina X
It surrounds the central spinal canal.It contains neurons that receives visceral afferent information.


REFERENCES

1) William. W. Cambell, DeJong's the neurological Examination 7th edition (2012)ch:24 pp: 379-381

2) Brent .L.Fogal, Randlop.W.Evans, Clinical Neurogenetics (2013)

Effects of Exercise Training and Rehabilitation Programs in Stroke Survivors

                                                 

This article is based on American heart Association's scientific statement on post stroke exercise to enhance stroke survives Activities of Daily Living(ADLs) and general Fitness.I hope this article will really give essential understanding on this topic to all Exercise Specialists dealing with stroke survivors.This will also help to promote evidence based practice of exercise science.

The link between exercise training and improved cardiovascular fitness and health has been well established in the general population. Whether the training-induced health and fitness benefits can be extrapolated to persons who are disabled by stroke remained unclear until recently. Evidence now suggests that the exercise trainability of stroke survivors may be comparable, in many ways, to that of their age-matched, healthy counterparts.

In a RCT that involved 42 hemiparetic stroke survivors, vigorous aerobic exercise training 3 times per week for 10 weeks evoked significant improvements in peak oxygen consumption and workload, submaximal exercise blood pressure response, exercise time, and sensorimotor function; moreover, the latter was significantly related to improvement in aerobic capacity.The findings demonstrated that stroke patients can increase their cardiovascular fitness by a magnitude that is similar to that of healthy older adults who engage in endurance training programs.

The effect of 6 months of treadmill aerobic exercise training on the energy expenditure and cardiovascular demands of moderate aerobic exercise with a graded treadmill for ambulation was studied in stroke patients with chronic hemiparetic gait. The program elicited significant reductions in submaximal energy expenditure; these reductions were progressive with continued exercise training. An important implication of this study was that it extended the observation of a potential benefit from task-oriented aerobic exercise training to the clinically relevant task of hemiparetic ambulation. The data suggest that aerobic exercise training and improved cardiovascular fitness might enable activities of daily living to be performed at a lower percentage of the aerobic capacity.Recently, the effects of a 1-hour-per-day, 3-day-per-week, 12-week exercise program of combined cardiovascular, strength, and flexibility training was studied in 35 stroke patients with multiple comorbidities.Compared with controls, the exercise group demonstrated significant gains in peak oxygen uptake and strength and improvements in body composition. 

The effect of a 6-month home exercise training program was investigated in a prospective, randomized, controlled clinical trial that involved 88 men with CAD and disability, two thirds of whom were stroke survivors.The subjects demonstrated significant increases in peak left ventricular ejection fraction and high-density lipoprotein cholesterol and decreases in resting heart rate and total serum cholesterol with exercise training.

In a 12-week cycle-ergometer training study, exercise capacity and self-concept improved in 7 hemiparetic stroke patients. However, there were no direct measurements of cardiorespiratory fitness, and motor function improvements were characterized by subjective descriptions rather than standardized functional evaluations.

Collectively, these findings support the use of regular aerobic exercise to improve cardiovascular health and fitness after stroke, which is consistent with recent consensus statements on exercise for able-bodied individuals. Strength training also has been found to have beneficial effects in patients with stroke. Several studies have shown strong associations between paretic knee-extension torque and locomotion ability and between both hip flexor and ankle plantar flexor strength of the paretic limb and walking speed after stroke.
A recent investigation evaluated the effects of a 12-week, twice-per-week, progressive resistance-training program on muscle strength, gait, and balance in stroke subjects.Lower-limb strength increased 68% on the affected side and less so on the intact side. Transfer time, motor performance, and static and dynamic balance also showed improvements. These results confirmed those of a previous study that showed benefits of strength training of the hemiparetic knee.

Traditional stroke rehabilitation programs emphasize functional training as a means to help the individual gain and maintain as much independence as possible. Training in the performance of mobility and personal care tasks, together with attempts to improve muscle strength and coordination, continue to form the central areas of focus of most rehabilitation programs. Whether these exercise-training programs enhance aerobic fitness is not clear. The heightened degree of physical skill required to perform these tasks and the physiological stress placed on the deconditioned individual’s cardiovascular system while performing activities of daily living suggest that a physiological training effect is likely to occur when these movements are performed in a sustained and systematic manner. Because increased levels of physical activity are associated with a reduced risk for stroke and cardiovascular disease and enhanced physical and psychosocial performance, such interventions performed in a stroke rehabilitation program may have a favorable effect on the prevention of recurrent stroke and cardiovascular events.

A recent study evaluated the relative cardiovascular stress of physical therapy and occupational therapy sessions in 20 patients undergoing a stroke rehabilitation program.The time per session in which the achieved heart rate was within the prescribed target heart rate zone was found to be extremely low, which suggests that these sessions elicited inadequate cardiovascular stress to induce a training effect.
Both of these last 2 studies found that activities that evoked the greatest heart rate increases were performed in the upright position and involved transitional movements. Approximately one third to one half of the treatment time was apportioned to standing activities.

Some researchers have raised concerns that occupational therapy sessions for poststroke patients may involve periods of intense isometric work that induce excessive cardiovascular demands. In contrast, others have suggested that workloads for stroke patients who participated in physical therapy were appropriate, evoking relatively low levels of cardiovascular stress. Moreover, it has been theorized that the predominantly static nature of most stroke rehabilitation programs might contribute to the low physical endurance of poststroke patients.

Extrapolation of what is known about the training effect of regular exercise by able-bodied individuals suggests that certain levels of exercise that are achieved during many stroke rehabilitation programs may improve aerobic fitness and thereby help reduce the risk for recurrent stroke and cardiovascular events. Accordingly, professionals who design and conduct stroke rehabilitation programs should consider allocating more time to aerobic exercise training to optimize patient outcomes.

References

1) Neil F. Gordon, MD, PhD, Cochair; Meg Gulanick, PhD, APRN, Cochair; Fernando Costa, MD; Gerald Fletcher, MD; Barry A. Franklin, PhD; Elliot J. Roth, MD; Tim Shephard, RN, MSN , Physical Activity and Exercise Recommendations for Stroke Survivors.Circulation.2004.pp.no-2033-2034.

2) Potempa K, Lopez M, Braun LT, et al. Physiological outcomes of aerobic exercise training in hemiparetic stroke patients. Stroke. 1995; 26: 101–105.

3) Macko RF, Smith GV, Dobrovolny CL, et al. Treadmill training improves fitness reserve in chronic stroke patients. Arch Phys Med Rehabil. 2001; 82: 879–884.

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