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Exercise and Ageing

Muscle mass, pain and the immune system


by Martin Krause: uploaded ~2001, updated Dec 2004, April 2005, June 2012, November 2013

- have you ever looked upon muscle as an important source of protein for the immune system?

- have you wondered whether exercise could enhance the immune response?

- have you considered the role of pain and inflammation during exercise and the immune response?


Body Mass Index

- do you commonly use strength training for the prevention of metabolic syndrome?




T lymphocyte immune responses

Muscle as a source of protein for immune function

Heat shock protein (HSP)

Muscle glutamine and inflammatory-immune response

Implications for exercise training and immune function



Exericise and age related decline in vasodilation

Exercise and Pain

Pain and the central sympathetic nervous system



As we age, our adaptive immune system develope's specific responses as a result of antigen exposure. The ability to develop these responses is in part dependent upon protein-telomere shortening of eukaryotic carrier sites. These carrier sites represent protein endings which are splice off through mRNA. Subsequently, as we age, the protein sequences shorten. There is a finite limit to this shortening-splicing process. Therefore, the greater the protein mass in our youth, the greater the ability to respond to novel antigen exposure throughout life. Unfortunately, the aging process (beyond the 3rd decade) also reduces protein quality and quantity in the greatest store of protein in our body i.e. muscle. Furthermore, the innate immune system is also compromised by reduced muscle mass as the amount of natural killer (NK) cells are directly proportional to muscle mass in the aged population. This is particularly the case in people who commit to muscle atrophy through sedentary lifestyles, as well as those who deal poorly with psychogenic stressors which release catabolic hormones. Therefore the importance of regular exercise cannot be underestimated. A variety of exercise including cardiovascular, progressive resistance training and mind-body awareness (e.g. Yoga, Chi Gong, etc) is recommended.

There is direct relationship with muscle mass and immune function. The better your muscle mass the better the reservoir of proteins for the immune system to use at times of need. However, when in vigorous training and/or over-training the protein is being used for muscle recuperation and repair and therefore little is left over for the immune system. Moreover, animal experiments have demonstrated impaired proliferative responses of mononuclear or spleen cells to mitogens (Sacerdote P et al 1994 Brain Behav Immun, 8, 251-260) and IgG antibody responses to novel antigen exposure (Laudenslager ML et al 1988 Brain Behav Immun, 2, 92-101 cited in Pain Clinical Updates XIII, No1) in the presence of intermittent pain. Plausibly, immune suppression is more evident when you are doing potentially muscle damaging stuff such as downhill running, plyometrics , etc. I find it beneficial before doing such exercise to do an eccentric stretching regime as well as afterwards doing concentric X's such as bike riding. Additionally, mind-body awareness and relaxation through yoga can be particularly useful. These factors may then aid in reducing pain and inflammation associated with eccentric exercise. Also keep in mind that if you've hit the flu season, plenty of freshly squeezed oranges are great and better than the bottled stuff. Drink it within minutes of squeezing, otherwise the enzymes (due to lack of added preservatives and exposure to oxygen) start to break down the goodness. Naturally, all other essential dietary vitamins and minerals are also important. Emphasis has been placed on the omega 3 and 6 FFA's such as fish oil and evening primrose oil (EPO), anti-oxidants such as Vit E (slightly controversial recently), magnesium and Vitamin B's. However, there are a plethora of other minerals which help catalyze metabolic reactions (e.g. Zinc, Molybdenum, etc). Therefore, athletes should seek advice from a qualified sports dietician.

Progressive resistance training (PRT) can enhance muscle function by creating hypertrophy of muscle tissue. 40-60 minutes of PRT, 3 times per week, using a gym based weights programme can enhance your ability to fight infection by increasing the protein reservoir residing in your muscle mass. Ideally, 6-8 exercises are chosen which incorporate the largest muscle groups e.g. quadriceps, calfs, gluteals, pectorals, deltoids and trapezius. Since cachexia is a cascade of cytokine-immune responses, then eccentric exercises should also be chosen, as this may 'fine tune' the regulation of the cytokinine-immune response from the microtrauma induced by exercise. Additionally, such exercises can provide better functional stability and balance for ADL. Concentric exercise such as cycling can enhance muscle bulk. Ergogenic aids such as protein-carbohydrate supplementation, as well as creatine phosphate - HMB preparations taken during and/or within 20 minutes after cessation of exercise aids the restorative-regenerative training effect. Creatine phosphate is also thought to improve insulin sensitivity. Similarly, moderate exercise every 72 hours is thought to reduce the susceptibility to metabolic syndrome (i.e. hypertension, hyper-cholesterol, hyper-lipidemia, artherosclerosis, cardiovascular disease, & insulin resistant diabetes) . Since magnesium acts as an antithesis to calcium, it's supplementation may also aid in the prevention of injury, by improving the rate of muscle relaxation thereby reducing the chance of stiffening up and/or cramping during exercise as well enhancing the rate of recovery.


Sarcopenia is characterized by the reduction in muscle mass and may contribute to immunosenescence, as it is thought that muscle provides an important reservoir of heat shock proteins (HSP) and glutamine as well as act as a site for the action of insulin. HSPs are the cellular link, which activate T lymphocyte proliferation. Exercise can activate HSPs and may provide the 'danger signal' for T lymphocyte re-activation after a period of quiescence. Muscle glutamine appears to be important for inter-organ transport as well being a precursor for anti-oxidant activity. Dose specific exercise is thought to improve immune function through an improved ratio of TNF-a: IL-6, which may promote the anabolic effects of IGF-1 and insulin thereby possibly improving muscle mass, leading to enhanced mechanical loading tolerance. Additionally, older people with preserved muscle mass have the highest number of NK cells. The weight of evidence suggests that the preservation of muscle mass and/or reversal of sarcopenia through exercise could be a useful anabolic method to provide a protein reservoir for later use when the older person is exposed to infection, inflammation and/or severe trauma. Click on diagram for PDF file


Sarcopenia is characterized by reduced muscle mass [1]. This is significant as skeletal muscle contains 50-75% of all proteins in the human body and represents a store of energy and nitrogen which becomes a vital supply of fuel for the immune system, as well as a substrate for wound healing during malnutrition, injury and disease [2]. Loss of muscle mass may result in immunosenescence, which is characterized by impaired cellular immune function concomitant with increased inflammatory activity [3]. Little is known about the effects of exercise on the senescent immune system [3]. Moreover, exercise has been suggested as a prototype for studying the effects of stress factors on the cellular immune system, because several other physical stressors, such as burns, surgery, acute myocardial infarction and hyperthermia induce similar immune responses [3].

Muscle accounts for 90% of the cross sectional area in active young men, but only 30% of that area in frail older women [4]. The prevalence of clinically significant sarcopenia is estimated to range from 8.8% in 'young old' women to 17.5% in 'old old' men [1]. This review will entertain the notion that the loss of muscle mass due to sarcopenia attenuates the inflammatory-immune response due to the lack of protein stores (glutamine [5], heat shock protein [HSP] [6]). Cytokines such as Interleukin-6 (IL-6) could enhance the immune response through inhibition of Tumor Necrosis Factor ? (TNF-aplha) production and insulin resistance [7]. TNF-alpha is considered to enhance protein degradation through the activation of HSP [8], whereas Insulin [9, 10] and Insulin like Growth Factor (IGF-1) [11] are thought to enhance protein synthesis. Additionally, it will be hypothesized that dose specific exercise training can ameliorate some of the effects of sarcopenia as well as enhance immune function by balancing protein synthesis with proteolysis.

T lymphocyte immune responses

Cytokines are a group of low molecular weight regulatory proteins secreted by white blood cells and a variety of other cells which generally function as intercellular messenger molecules [12]. Proliferation of T lymphocytes is essential for the first step in an adaptive immune response [3]. Essentially there are 2 types of immune cells, the 'memory cells' and 'virgin cells'. With age, the percentage of memory cells increases with a corresponding decrease in virgin cells [3]. Consequently, a reduction in naïve cell responses, and a resulting shift to memory cell proliferative response has been shown in the older person [13]. Fortunately, with advancing age a progressive increase in natural killer (NK) cell number appears to compensate for a decreased number and function of T lymphocytes [14]. More importantly, these findings suggest that cells from older individuals do not suffer from a quantitative decline in cytokine production on a per cell basis [13]. Indeed, centenarians and nonagenarians who presented with the highest number of NK cells and best preserved cytolytic function, also had preserved integrity of muscle mass [14]. Therefore, this suggests that the maintenance of muscle cell mass could preserve the immune response to environmental stressors.

Muscle as a source of protein for immune function

Since muscle represents approximately 40% of body weight, it is thought to be an important reservoir of proteins [8], which may be called upon by the immune system in response to injury [10]. Even a 10% loss in lean body mass (LBM) corresponds with impaired immune function [15] and a loss of approximately 30% of the body proteins can result in death [2]. During severe trauma, such as burns, the need for essential amino acids drives the catabolic loss of protein from skeletal muscle, which can be as high as 1% per day of illness [16]. Accelerated muscle proteolysis is the primary cause of this loss of lean body mass characteristic of many diseases [17]. Some peptides generated by the breakdown of cell proteins are transported to the cell surface where they are presented to cytotoxic lymphocytes, which destroy cells presenting foreign (eg viral) peptides [17]. This may partially explain why successful aging has been associated with the preservation of muscle mass [14] as this would endow these individuals to draw on their store of protein for inflammatory-immune responses.

Increased cytokine activity has been associated with aging and muscle weakness [18], possibly resulting in inactivity. This age associated progressive dysregulation of immune response [19], is seen in older women with high IL-6 serum levels who have a higher risk of developing physical disability and experience steeper declines in walking ability than those with lower levels [18]. However, the statistical interaction of IL-6 concentration with disability was non-linear and the progression of disability and IL-6 concentration over time was not investigated [18]. Therefore, it is difficult to conclude whether elevated levels of IL-6 are the cause or the effect of skeletal muscle weakness, as the progressive withdrawal of a number of anabolic stimuli, also causes skeletal muscle weakness [18]. Furthermore, high levels of TNF-? and IL-6 have been shown to be associated with classical risk factors such as smoking, physical inactivity and body mass index (BMI) [20]. It is difficult to conclude whether the high levels of cytokines lead to inactivity or whether they are the result of reduced skeletal muscle loading capacity from inactivity. However a cycle of inactivity and chronic inflammatory-immune response is plausible.

Heat shock protein (HSP)

Numerous attempts to link exercise to meaningful alterations in immune function have been largely unconvincing [21]. It has been argued that it is local as opposed to the global immune system activation by HSPs, which is at the core of immune effects of exercise [21]. It is thought that HSPs on a cells surface activate T lymphocyte proliferation when accompanied by a co-stimulatory 'danger signal' [21]. These T lymphocytes can switch between the active and quiescent memory states, to be later re-activated in the presence of an antigen and co-stimulatory 'danger signal' [21]. Decreases in HSP72, a heat shock protein specifically related to skeletal muscle [22], is considered to promote apoptosis [23] possibly due to the lack of this secondary 'danger signal' [21]. Not surprisingly, apoptosis has been linked with sarcopenia [24]. HSP are involved in protein folding and sorting, in the assembly of protein complexes as well as binding of denatured proteins and are primarily induced in response to stress [6]. Impaired recovery from acute complications and the reduced renewal of damaged and toxic proteins are potential undesired consequences of low-protein turnover [25]. Indeed, critically ill patients have been shown to have low protein synthesis in skeletal muscle correlating with metabolic status and clinical indices of the severity of the disease [26]. Conversely, specific adaptation in muscle associated with enhanced proteolysis can occur [17], whereby HSPs provide a link between immune response to infection and autoimmunity during fever [27]. In fact older people have been shown to have a reduced incidence of fever in response to injury [28]. Although, exercise induced HSP activity has been described [6, 22] it is uncertain what level of exercise can provide the 'danger signal' required to enhance immune function [21].

Exercise may provide a hormonal stimulus to regulate HSP proteolysis. Recently, rodent investigations have demonstrated that Insulin-Like Growth Factor 1 (IGF-1) inhibits both lysosomal and ubiqitin-proteasome dependent stress protein breakdown in skeletal muscle [11] thus suggesting a hormonal regulating mechanism. Increased IGF-1 concentrations have been demonstrated near the Z-bands in the elderly after resistance training regime [29]. In particular, eccentric exercises have been associated with damage to these Z-bands [30]. Therefore, IGF-1 production in muscle may be responsible for the regulation of protein synthesis after HSP induced proteolysis as a result of exercise induced trauma.

Muscle glutamine and inflammatory-immune response

Skeletal muscle may represent an important source of anti-oxidants. Alterations of respiration in mitochondria of muscle cells has been associated with aging and sarcopenia [10, 31-34]. Interestingly, the muscle protein glutamine is a substrate for glutathione, which acts as an endogenous scavenger with an ability to counteract oxidative injury from oxygen free radicals [16]. This may be particularly important, as the level of oxidative stress imposed on the aging muscle is influenced by two fundamental biological processes: the increased generation of reactive oxygen species (ROS) and age-associated changes in antioxidant defense [33, 35]. Therefore, since glutamine accounts for nearly two thirds of the free intracellular amino acid pool and is abundant in skeletal muscle [16] it is likely to be an important source of anti-oxidants.

It is thought that TNF may mediate protein degradation in cachexia through a ubiquitin-proteasome pathway [8]. This skeletal muscle proteolysis seen in response to severe injury has been speculated to be for the provision of precursors for glutamine synthesis [16]. Glutamine is also thought to be a significant inter-organ nitrogen and carbon transporter as well as being important in glycogen metabolism and therefore can presumably affect mitochondrial oxidative responses [16]. Additionally, in the fasting state, an increase in glucocorticoids and reduction in insulin results in muscle proteolysis [17] presumably through an inter-organ mechanism. During acidosis, some amino acids from muscle protein are converted to glutamine, which is used by the kidneys in acid excretion and energy metabolism [17] (figure 1). Therefore, muscle may represent an important anti-oxidative organ during an inflammatory-immune response. Hence, in the presence of sarcopenia, reduced ability to counteract damage by oxidative radicals may be expected due to reduced glutamine stores.

Implications for exercise training and immune function

Investigators have recently demonstrated that muscle contractions induce the production and release of IL-6 but not TNF-alpha into the circulation [7]. Contrary to the conclusions of Ferrucci et al (2002) [18], other authors suggested that muscle-derived IL-6 contributes to mediate the beneficial metabolic effects of exercise and may inhibit TNF-alpha production and insulin resistance [7]. Administration of insulin has been shown to promote protein synthesis [9]. Furthermore, resistance exercise training has been shown to attenuate the catabolic effect of TNF by suppressing skeletal muscle TNF-alpha expression [36]. However, a 12 week high intensity progressive resistance training program did not affect immune function in healthy older people or subjects with systemic inflammation [37]. Yet, eccentric exercise is associated with an increase in pro-inflammatory cytokines [3, 30]; whereas concentric exercise has been associated with inflammation from oxidative stress [32] and hydrogen ion accumulation due to hypoperfusion [5]. Furthermore, a recent review concluded that older people have a preserved ability to recruit T lymphocytes and NK cells in response to exercise [3]. However, the cells recruited had a replicative history suggesting they were memory cells. Additionally, a lack of investigations into circulating levels of pro-inflammatory cytokines during eccentric exercise in older versus young populations was lamented by these authors [3]. Nevertheless, it would appear that resistance training could be beneficial for IL-6 production as well as TNF-alpha suppression post exercise.

Although investigators have demonstrated enhanced muscle size with resistance training in older people [38], there is little evidence to suggest that this change in size is sufficient to improve immune function [3, 39]. Yet, resistance training has been shown to significantly increase lean body mass and strength in HIV associated muscle wasting [40], therefore indicating a role for exercise in the presence of protease inhibitors and retroviral activity. Additionally, improved lean body mass and reduced fat has been shown to enhance IGF-1 levels during endurance training [41]. Consensus indicates that 'moderate exercise' may enhance immune function and may reduce the incidence of infection while long term exhaustive exercise results in immuno-suppression and an increased susceptibility to infections [12, 42-45]. This is consistent with Ji [33] who suggest that the major benefit of non-exhaustive exercise is to induce a mild oxidative stress that stimulates the expression of antioxidant enzymes, as well as the induction of IGF-1 [11] seen in resistance training [29,46]. Additionally, resistance training accompanied by nutritional supplementation has been shown to result in significant muscle hypertrophy [47]. Biomechanical principles dictate that for the same force, the strain in a skeletal muscle is reduced proportional to the skeletal muscle's cross sectional area [48]. Therefore, if contractile skeletal muscle mass is maintained or enhanced, then it is plausible that a greater spectrum of 'moderate exercise' can be entertained.

Nitrogen imbalance

Highly conditioned elderly humans seem to have a better preserved immune system, although it is not possible to conclude if this is linked to training or other lifestyle-related factors [3]. Specifically, a bi-directional neuro-immune system has been implicated for exercise induced modulation of immune function through the autonomic nervous system [49]. Importantly, the effect of exercise on immune function requires future investigation using dose specific criteria [39, 50] as over-training is characterized by reduced catecholamine levels, decreases in neutrophil function, serum and salivary immunoglobulin concentrations and NK cell numbers and possibly cytotoxic activity in peripheral blood, at least in younger individuals [51]. In particular, the 2-4 hours post exercise have been shown to demonstrate inflammation with concomitant suppression of immune function, especially after high intensity, eccentric exercise in young populations [5, 12]. If these findings can be extrapolated to older people then the periodization of training and careful selection of the type, volume, frequency, duration and intensity of exercise would appear to be important to gain the maximum anabolic and minimum catabolic effect. Presumably, this anabolic effect would reduce the prevalence of sarcopenia through the prevention or reversal of muscle mass loss thereby concomitantly ameliorating immunosenescence.


Sarcopenia is characterized by the reduction in muscle mass and may contribute to immunosenescence as muscle is thought to provide an important reservoir of heat shock proteins and glutamine as well as to represent a site for the action of insulin. HSPs are the cellular link, which activate T lymphocyte proliferation. Exercise can activate HSPs and may provide the 'danger signal' for T lymphocyte re-activation after a period of quiescence. Muscle glutamine appears to be important for inter-organ transport as well being a precursor for anti-oxidant activity. Gathering evidence suggests that dose specific exercise could improve immune function through an improved ratio of TNF-alpha: IL-6, which promotes the anabolic effects of IGF-1 and insulin thereby improving muscle mass, which can lead to enhanced mechanical loading tolerance. Additionally, older people with preserved muscle mass have the highest number of NK cells. Taken together the evidence suggests that the preservation of muscle mass and/or reversal of sarcopenia through exercise could improve the protein reservoir for a person to draw upon when they are exposed to infection, inflammation and/or severe trauma.

Exercise and Age-Related Decline in Arterial Vasodilation

Ageing has been associated with reduced arterial vasodilation and hypertension. Elevation of free oxygen radicals are thought to inactivate Nitrous Oxide (NO). Using a severe hand-gripping model, Shoemaker et al (Am J Physiol, 1997; 273, H23488-95) were able to demonstrate 7% vasodilation in young subjects versus only 3% brachial vasodilation in older individuals. Anecdotal evidence supporting the use of oral antioxidant supplementation comes from Japanese, Scandinavian and Italian populations where a high incidence of centenarians has been associated with diet. However, the use of oral antioxidants alone, in the abscence of exercise, has not been shown to reduce the risk of cardiovascular disease. Paradoxically, administration of high levels of Vitamin C after exercise seem to reduce the vasodilatory effect of exercise, suggesting some positive 'down-stream'  effects of oxygen free radicals on cardiovascular health (Wry et al 2011, Exerc & Sp Sci Rev, 39, 2, 68-76). Alternatively, the chronic balance of oxygen free radicals and their complementary antioxidants may be more important, suggesting regular exercise and dietry function rather than extremes of either are more significant contributors to cardiovascular health. Investigations, using small muscle mass oxidative stress such as knee extension training, which have minimal central cardiovascular responses, have demonstrated positive cardiovascular effects on blood pressure function (Richardson et al 2004, Am J Resp Crit Care Med, 169, 1, 89-96; Shephard et al 1997, Sports Medicine, 23, 2, 75-92). Such findings are important in subjects with central cardiovascular compromise, but moreover have an impact on exercise adherence where subjects do not enjoy whole body high oxidative stress exercise. Furthermore, although blood pressure wasn't shown to be effected by acute antioxidant supplementation, the muscle perfusion post exercise was 30-40% greater in the older individuals receiving supplementation (Wry et al 2009, Clin Sci (Lond.), 116, 5, 433-41). Moreover, phosphate markers of post exercise skeletal muscle energetics suggests further positive benefits of antioxidant supplementation in older individuals (Wry et all 2011, Exerc & Sp Sci Rev, 39, 2, 68-76). Therefore, regardless of the reduction in perfusion during exercise, post exercise effects of antioxidant supplemenation and the known increased functional capacity of trained individuals suggest efficient physiological musculoskeletal compensation, to mitigate against the aging process.

Exercise and pain

Individuals may exhibit reduced physical activity due to pain related 'fear-avoidance' behaviour. Unfortunately, this results in a viscous cycle of muscle atrophy and predisposition to muscle inflammation and injury. Cardiovascular training may stimulate the carotid sinus reflex, which via the ventral noradrenegic bundles (VNB) of the Locus Coeruleus to the Solitary Nucleus (Nucleus Tractus Solitarius) can provide descending modulation of pain in the neurons of the spinal cord.

The Locus Coeruleus is the origin of most noradrenergic neurons in the CNS. This pontine nucleus resides bilaterally next to the 4th ventricle. There are both dorsal and ventral bundles of neurones which have descending, ascending and cerebellar projections. The dorsal noradrenergic bundle (DNB) projects throughout the limbic system and neocotex and therefore has substantial influence on higher level brain activity. Any stimulus that threatens the biological, psychological or psychosocial integrity of the individual increases the firing of the Locus Coeruleus (LC). Thus, the LC is responsible for global vigilance for threatening and harmful stimuli. Interestingly the LC remains active during waking and non-REM sleep. Therefore, REM sleep is probably important for replenishing noradrenergic stores in the LC during suppression of sympathetic tone.

Does a relationship with chronic fatigue, bone density, thyroid function and the peripheral sympathetic nervous system exist? ? ?

The central sympathetic nervous system, osteoporosis and menstrual dysfunction (amenorrhea) as a consequence of over-training

Neurons in the medullary reticular formation project to the hypothalamus via the ventral noradrenergic bundle of the the LC. The hypothalamic paraventricular nucleus (PVN) coordinates the HPA axis. Neurons of the PVN receive afferent information from the ventrolateral medulla, dorsal raphe nucleus, nucleus raphe magnus, LC, dorsomedial nucleus and nuclues tractus solitarius. The PVN sends direct projections to the sympathetic intermediolateral cell column of the spinal cord, which in turn sends projections to the peripheral sympathetic nervous system. The peripheral sympathetic nervous system innervates the lymphatic glands. Prolonged nociception may cause sustained stress responses. Clinically this may manifest as fatigue, dysphoria, myalgia, nonrestorative sleep, somatic hypervigilence, reduced apetite and libido, impaired physical functioning and reduced concentration. Interestingly, these are also the signs and symptoms of over training. Well structured training regimes have the capacity to engage the body's capacity to regenerate and repair.

Anterior cruciate ligament (ACL) and the menstrual cycle

The ACL is designed to prevent forward shearing of the shin bone (tibia) on the thigh bone (femur).  Anterior knee laxity (AKL) and hyperextension of the knees were shown to be significant predictors of anterior tibial translation (ATT) in both males and females. Interestingly the restraining structures to knee hyperextension are the posterior cruciate ligament (PCL) and popliteus muscle, suggesting that the knee in non weight bearing is in a relative posterior position and hence allows for greater total anterior excursion of the tibia. Notably, if a females AKL changes as much as 3mm across her menstrual cycle the ATT changes by 2mm which represented a change of approx 30% in mean magnitude of the ATT (Schultz et al 2011 Med Sc Sp Ex, 43, 2, 287-295). Furthermore, in another investigation, the same authors demonstrated increased absolute and relative magnitudes of multiplanar knee laxity changes. These were seen as increased valgus coupled with relatively greater external rotation of the tibia, making the knee more susceptible to injury on ground contact and early in the landing phase (Schultz et al 2012 Med Sc Sp Ex, 44, 5, 900-909)

Muscle activation around the patella and the menstrual cycle

The initial firing rate is lower in the VMO (vastus medialis oblique) compared with VM (vastus medialis) in women not men. The firing rate is affected by the menstrual cycle, showing increases in initial firing during the early follicular phase through tp the late luteal phase. The initial firing was lower in VMO compared to VM during ovulatory and midluteal phases (Tenan et al 2013, Ex Sc Sp Ex, 45, 11, 2151-2157). This could play a bearing on anterior knee pain due to an increased lateral gliding of the patella over the femur, leading to patellofemoral syndrome.

Rises in Estrogen levels around ovulation have recently been demonstrated to increase the risk of traumatic knee injury in athletes. Furthermore, researchers hypothesized that oral monophasic contraceptive pill may reduce the incidence of cruciate ligament rupture. See the ABC website Catalyst for transcript, Thursday, 7th April 2005.

Young active female athletes frequently suffer from menstrual dysfunction, with late onset of menstruation (menarche), and/or amenorrhea which manifests as irregular menstrual cycles with disruption of the luteal phase of the cycle where it has been hypothesised that a surging luteal hormone phase competes with an endogenous opioid phase which affects bone mineral activity resulting in osteopenia in very young women (teenagers) which can lead to premature osteoporosis later in life. Additionally, nitrogen imbalance as welll as general negative energy imbalance have also been implicated in creating hormonal imbalances.


Predicting the failure of disc surgery by a hypofunctional HPA axis: evidence from a prospective study on patients undergoing disc surgery

Andrea Geiss, Nicolas Rohleder, Clemens Kirschbaum, Klaus Steinbach, Heinz W. Bauer and Fernand Anton


Patients with postoperative ongoing sciatic pain have been shown to exhibit reduced cortisol levels along with enhanced IL-6 levels. The aim of the present study was to clarify the relationship between a reduced cortisol secretion and enhanced cytokine levels by performing a prospective study on patients with disc herniation. Twenty-two patients were examined before and after their disc surgery. Twelve healthy, pain-free subjects matched for age, education and gender constituted the control group. The preoperative examinations included the assessment of the diurnal pattern of cortisol secretion and the feedback sensitivity of the hypothalamus-pituitary-adrenal (HPA) axis. Patients' subjective stress levels also were assessed during the preoperative examination. The diurnal pattern of cortisol secretion was again assessed during the postoperative examination. Furthermore, blood samples were collected to measure catecholamine, adrenocorticotropic hormone (ACTH)- and interleukin-6 (IL-6) levels before and after measuring the pressure pain thresholds (PPTs). An assessment of the sensitivity of circulating monocytes to the immunosuppressive effects of glucocorticoids was further included in the postoperative examinations. Failed back syndrome (FBS) patients ( n =12) showed a reduced cortisol secretion in the morning hours and enhanced feedback sensitivity of the HPA axis. Furthermore, FBS patients displayed an increased in-vitro production of proinflammatory cytokines and a relative glucocorticoid resistance of pro-inflammatory cytokine producing monocytes as compared to non-FBS patients ( n =10) and controls. After PPT measurement FBS patients exhibited an increased norepinephrine but decreased epinephrine response, together with lower ACTH levels and a four times higher plasma IL-6 response. These findings suggest that chronically stressed patients are at a higher risk for a poor surgical outcome as their reduced cortisol secretion promotes the postoperative ongoing synthesis of proinflammatory cytokines.

Keywords: Sciatic pain; Hypothalamus-pituitary-adrenal axis; Localized glucocorticoid resistance; Proinflammatory cytokines; Chronic stress

Corresponding author. Address: Department of Orthopaedics, Sahlgrenska Academy, Göteborg University, SE-41345 Gothenburg, Sweden. Tel.: +46 31 342 6086; fax: +46 31 416816

Exercise, allostasis, cognitive behavioural therapy and immune responses

See also : Dworkin RH, Beitbart WS (2004) Psychosocial aspects of pain: a handbook for health care providers.  IASP Press

ISBN 0-931092-48 to 5

Additionally see : DeLeo JA, Yezierski RP (2001)  The role of neuroinflammation and neuroimmune activation in persistent pain. Pain, 90, 1 to 6

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35. Wei Y.-H. Oxidative stress and mitochondrial DNA mutations in human aging. Proceedings of the Society for Exp Biol Med (Maywood). 1998;217:53 to 63.

36. Greiwe JS, Cheng BO, Rubin DC, Yarasheski KE, Semenkovich CF. Resistance exercise decreases skeletal muscle tumor necrosis factor [alpha] in frail elderly humans. FASEB Journal. 2001;15:475 to 482.

37. Rall LC, Roubenoff R, Cannon JG, Abad LW, Dinarello CA, Meydani SN. Effects of progressive resistance training on immune response in aging and chronic inflammation. Med Sci Sports Exercise. 1996;28:1356 to 1365.

38. Zinna EM, Yarasheski KE. Exercise treatment to counteract protein wasting of chronic diseases. Curr Opin Clin Nutr Metab Care. 2003;6:87-93.

39. Woods JA, Lowder TW, Keylock KT. Can Exercise Training Improve Immune Function in the Aged? Ann N Y Acad Sci. 2002;959:117 to 127.

40. Roubenoff R, McDermott A, Weiss L et al . Short-term progressive resistance training increases strength and lean body mass in adults infected with human immunodeficiency virus. AIDS. 1999;13:231-239.

41. Sun G, Gagnon J, Chagnon YC, Pérusse L et al. Association and linkage studies between the IGF-1 gene and body composition: the heritage family study. Med Sci Sports Exercise. 1998; 30:7.

42. Gleeson M, Overview: Exercise immunology. Immunol Cell Biol. 2000;78:483 to 484.

43. Woods JA, Lowder TW, Keylock KT. Exercise and cellular innate immune function. Med Sci Sports Exercise. 1999;31:57 to 66

44. Dressendorfer RH, Petersen SR, Moss Lovshin SE, Hannon JL, Lee SF, Bell GJ. Performance enhancement with maintenance of resting immune status after intensified cycle training. Clin J Sport Med. 2002;12:301 to 307.

45. Armstrong LE, VanHeest JL. The unknown mechanism of the overtraining syndrome: clues from depression and psychoneuroimmunology. Sports Med. 2002;32:185 to 209.

46. Fiatarone Singh MA, Ding W, Manfredi TJ et al. Insulin-like growth factor I in skeletal muscle after weight-lifting exercise in frail elders. Am J Physiol Endocrinol Metab. 1999;277:E136 to E143.

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References for Neuroendocrinology, Fibromyalgia, Thyroid, Pituitary, Hypothlamic-Gonadal axis, and Superior Cervical Ganglion

Alafou et al (1985). Origin and distribution of noradrenergic and NPY containing nerves in cerebral blood vessels of the gerbil. J.Cerebral Blood Flow, 5, S543 to 544

Acheson et al (1991). Detection of BDNF like activity in fibroblasts and Schwann cells: inhibition by antibodies to NGF. Neuron, 7, 265 to 275

Bennett et al (1989) Thyroid releasing hormone - catecholamine interactions in brain and spinal cord. Ann. NY Acad. Sci, 553, 106 to 120

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Bilezckian et al (1991). The influence of hyperthyroidism & hypothyroidism on alpha and beta adrenergic receptor systems and adrenergic responsiveness. Endo Reviews, 4, 378 to 388

Boada et al (1991). Evidence suggesting that the sympathetic nervous system mediates thyroidal depression in turpintine induced non thyroidal illness syndrome. Neuroendocrinology, 53, 360 to 364

Bijlsma et al (1984). Neurotrophic factors and nerve regeneration in the peripheral nervous system. Psychoneuroendocrinology, 9, 199 to 215

Bijlsma et al (1983a). Stimulation by ACTH 4-10 of nerve fibre regeneration following sciatic nerve crush. Muscle & Nerve, 6, 104 to 112

Bronk (1939) Synaptic mechanisms in sympathetic ganglion. J Neurophysiology, 2, 380 to 401

Brown & McAfee (1937) Long term potentiation in the superior cervical ganglion. Am J Physiol, 119, 221 to 235.

Brown et al (1989). Changes in blood pressure and plasma noradrenaline in short term hypothyroidism. Clinical Endocrinology, 30, 635 to 638

Butler et al (1982) Relationship of beta adrenoceptor density to fitness in athletes. Nature (London), 298, 60 to 62

Cardinali et al (1982). Efferent neuroendocrine pathways of the superior cervical ganglion (early depression of the pituitary-thyroid axis after ganglionectomy) Neuroendocrinology, 35, 248 to 254

Chanoine et al (1992) The role of transthyretin in the transport of thyroid hormone to cerebrospinal fluid and brain. Acta Med Austriaca, 19, Suppl 1, 25to 28

Chunhabundit et al (1992) Microvasculaturization of the rat superior cervical ganglion : a 3 dimensional observation. Acta Anatomica, 143, 54to 58

Danielson et al (1986). Experimental hyperthyroidism stimulates axonal growth in mesothelial chambers. Exp Neuro, 94, 54 to 65

de Florida et al (1991). Modulated long term potentiation in the cat superior cervical ganglion in vivo. Brain Res, 544, 203 to 210

Dessein et al (2000) Neuroendocrine deficiency-mediated development and persistence of pain in fibromyalgia : a promising paradigm? Pain, 86, 213-215

Fagius et al (1990) Baroreflex governed sympathetic outflow to muscle vasculture is increased in hypothyroidism. Clin Endo, 33, 177 to 185

Fogelfeld & Schneider (1990). Inhibition of chondroitin sulphate incorporation into human thyroglobulin Endo, 126, 1064 to 1069

Fone et al (1987) Regional distribution of substance P and thyrotropin releasing hormone like immunoreactivity and indoleamines in the rabbit spinal cord. J. Neurochem, 48, 1027-10323

Gillberg & Askmark (1991) Changes in Cholinergic and opioid receptors in the rat spinal cord, dorsal root and sciatic nerve after ventral and dorsal root lesion J Neural Transmission (Gen Sect), 85, 31 to 39

Landa et al (1991) In vitro effects of thyroxine on cholinergic neurotransmission in rat sympathetic superior cervical ganglion. Neuroendocrinology, 54, 552 to 558

Lehman et al (1992) Decreased nocturnal catecholamine excretion : parameter for an overtraining syndrome in athletes? Int. J. Sports Med, 12, 444 to 452

Lindvall et al (1978) Sympathetic nervous control of cerebrospinal fluid production from the choroid plexus. Science, 201, 176 to 8

Marcocci et al (1987) Norepinephrine and thyrotropin stimulation of iodide efflux in FRTL-5 thyroid cells involves metabolites of arachadonic acid and is associated with the iodination of thyroglobulin. Endocrinology, 120, 1127 to 1133

Mekhail et al (1990) Portal-like microcirculation in rat sympathetic ganglia. Acta Anatomica, 138, 200 to 207

Oleshansky et al (1990). The influence of fitness on neuroendocrine responses to exhaustive treadmill exercise. Euro. J. Appl. Physiol, 59, 405 to 410

Ratge et al (1987) Nebenwirkung und verhalten von Noradrenaline und Adrenaline in Plasma beim intravenoesen thyroliberin test bei Personen mit normaler und gestoerter Schilddruesen funktion. J. Clin. Chem & Clin Biomech, 25, 393 to 400

Stelmack & Kiernan (1977). Effects of triiodothyronine on the normal and regenerating facial nerve of the rat. Acta Neuropathologica, 40, 151 to 155

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Immunohormonal responses to musculoskeletal injury initially conceptualised by Martin Krause 1991-3.  Submitted to Cumberland College, Sydney University as a possible Masters Research topic but rejected.

Endurance Training

©Martin Krause 2004-2005

Last update : 22 July 2006



Trending @ Back in B Physio

  • Sun 15 Oct 2017

    Neuroplasticity in Tendon Dysfunction

    Neuroplasticity in Tendinopathy by Martin Krause A multitude of contributing factors to altered motor control must be addressed when treating tendon dysfunction. What we have failed to consider in the past when dealing with chronic or recurrent tendon issues are motor control problems encompassing corticospinal control of excitation and inhibition as well as belief systems about pain and contextual factors related to imaging.  Research by Ebonie Rio et al (2015) (BJSM Sept 25, 10.1136/bjsports-2015-095215) suggest that the pain state sets up an adaptive pathway whereby the ipsilateral kinetic chain is directly inhibited by reflexogenic pathways, as well as being inhibited by contralateral hemispheric activity. Simultaneously excitation is enhanced in the opposite limb as well as in least in the case of enhanced excitation of the hamstrings in quadricep tendinopathy. If this is true, then so much for training the contralateral limb for 'cross training' purposes! This may also explain why a lot of people seem to have "all their injuries on the same side" (of the body). Furthermore, they recommend enhancing corticospinal drive through the use of 30-60 second isometric holds at 70-80% MVC to load the muscle whilst using isokinetics to load the tendon. Moreover, they recommend the use of a metronome at 60bpm (stages 1 and 2) with a count of 3 up, 2 down for quads, and 2 up, 3 down for calf isokinetics to optimally engage corticospinal drive through the visual and auditory stimuli (also shown by Kohei et al 2012 for motor imagery and M1 stimulation) more Cortical mapping of infraspinatus muscle in chronic shoulder pain demonstrating higher motor thresholds (aMT= activation MT) and hence reduced excitability on the affected side (39 vs 35) (Ngomo et al 2015 Clinical Neurophysiol, 126, 2, 365-371) Cortical mapping of pain and fear. Lots of overlap suggesting that taking away the fear from the pain with clear clinical explanations and a focused goal directed program using specific functional outcomes is important.  ndividuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036,  Uploaded : 18 October 2017 Read More
  • Mon 09 Oct 2017


    Do I need a scan? "a picture tells a thousand words" - not really! by Martin Krause A scan, in it's self, will not improve anyone's condition. The purpose of a scan is to gain more information about the pathology. Sometimes this information may be irrelevant to the management of a patient's condition. For example, if you knocked your elbow on a door frame and suffered a bruise, which was already beginning to resolve, an ultrasound scan may show some minor soft tissue damage, but that was already obvious by the fact of the bruise, and the information gained from the scan has not helped nor changed the management of the bruise. Therefore, the main reason for getting a scan would be because there is concern that the presence of certain pathologies may lead to a change in the medical management. For example, sometimes a rolled ankle can be more than sprained ligaments, and may require surgey or immobilisation in a boot. If the therapists suspects this might be the case, then they will recommend or refer for a scan (probably an X-Ray) to check the integrity of the bones (especially the fibular and talar dome), because if there is no bony damage then the patient can be managed conservatively with taping, exercises, ultrasound, massage, joint mobilisations etc. However, if there is boney damage, for example, then it might be necessary for the ankle to be immobilised in a boot for three - six weeks, for example. This dramatically different medical management depends on the results of a scan, and it is therefore worth doing. However, scans have no predictive value to the presence or severity of pain. Thirty-three articles reporting imaging findings, in the low back, for 3110 asymptomatic individuals were investigated for pathology. The prevalence of disk degeneration in asymptomatic individuals increased from 37% of 20-year-old individuals to 96% of 80-year-old individuals. Disk bulge prevalence increased from 30% of those 20 years of age to 84% of those 80 years of age. Disk protrusion prevalence increased from 29% of those 20 years of age to 43% of those 80 years of age. The prevalence of annular fissure increased from 19% of those 20 years of age to 29% of those 80 years of age. (Brinjikji, W et al Spine Published November 27, 2014 as 10.3174/ajnr.A4173). Hence, the results of imaging need to be assessed within the context of the entire clinical picture. Frequently too much emphasis is placed on the imaging not only by the clinician but also by the patient. Some people react to pathology seen on scanning as an affirmation of their problem and can either use it to gain clarity and become better or conversely become worse. Moreover, some people find imaging with inconclusive results as a 'panic moment' - "no one knows what is wrong". Similarly, ultrasound imaging of the tendond has good predictive diagnostic and aids in clinical reasoning when it comes to full tears. However, with partial tears it is a totally different 'ball game'. Ultrasound is highly user dependent, with specifically trained musculoskeletal radiologists able to produce high-quality images that may provide more clinically relevant information than those produced by clinicians with less experience in imaging. Sean Docking, a leading tendon researcher at Monash University, cited 7 authors who found pathological tendon chnages in 59% of asymptomatic individuals, whereas he found that 52% of asymptomatic elite AFL sportsmen had tendon pathology on imaging! Furthermore, symptomatic individuals who improved clinically to the point of resuming play, weren't shown to have improvements on imaging. Again, the clinical context and the clinical reasoning can in many instances prove to be the 'gold standard' not the imaging itself, when considering management options. Shoulder supraspintatus tendon pathology, in the abscence of trauma, is known, in many instances, to be a disorder of immune-metabolic compromise of the tendon and bursa. Imaging may show some changes in signal intensity but, unless it's a complete tear, it can reveal neither the intensity nor the severity of pain when taken outside of the clinical context. A thorough physical and subjective examination integrating all the clinical dimensions of the problem will have far greater value than any one single imaging modality. Yet, imaging still should be used in instances of progressive rapid deterioration and suspected serious pathology which may require surgery and/or immediate medical intervention. In summary, sometimes it is worthwhile getting a scan, because the information gained from that scan will determined the type of medical management that is employed. However, at other times, the scan may be unneccessary, because the information may be irrelevant or lead to an incorrect change in medical management, due to over-reporting of 'false positives'. You will be able to make this decision on the advice of your health care professional. On occasions it can actually be detrimental to have a scan, because some patients can become overly obsessed with the medical terms used to describe their scan results, which then can become the major focus for the clinician and the patient, rather than the more prefereable focus on their symptoms and functional abilities. For example, many people have lumbar buldging discs yet have no symptoms, yet sometimes when these patients have an MRI or CT scan, they can develop symptoms because they think they should have pain if the scan says so! Conversely, for some people the results of imaging can have a positive and reassuring affect. Therefore, it is very important to assess a clients attitude to scans before prescibing them so that the patient's expectations are managed appropriately, and not burdened by the additional, sometimes confusing, information supplied by a scan. Uploaded : 10 October 2017 Read More
  • Thu 14 Sep 2017

    Cervical Spine implications in concussion

    Neck aetiology, autonomic and immune implications, exercise and diet in the musculoskeletal physiotherapy management of Post Concussion Syndrome (PCS) by Martin Krause, MAPA, Titled member Musculoskeletal Physiotherapy Association of Australia  A 14 year old boy presented to A&E, in August 2016, after receiving an impact to the head during AFL (Australian Rules Football). Although his SCAT3 scores were relatively mild, he went on to suffer severe lethergy, resulting in a lengthy abscence from school, culminating in a return to school for exams in the first week of December 2016. Even by December, even a 30 minute walk was extremely fatiguing. To place this into perspective, he had been playing elite academy grade AFL for several seasons and was an extremely fit outdoor adventurer. Confounding Variables : end of season injury and hence no follow up from the academy suffers from Hypermobile Joint Syndrome (HJS) and possibly Ehlers Danlos Syndrome (EDS), however Beighton score 4/9. suffers from food intolerances, particularly to Glutin and diary, but also some other foods. Potential IBS and autoimmune issues. had just gone through a growth spurt (190cm) Imaging : Brain MRI normal Medical Examination : Balance remained impaired to tandem walking and single leg stance. The vestibular occular motor scale showed significant accomodation deficit of 15cm and there was a mild exacerbation of symptoms. ImPACT testing revealed adequate scores and reaction time of 0.65 which is within acceptable range. History : School holidays December - January. Return to school and was placed in the lower classes. Prior to his concussion he was a top 10 student at an academically selective high school. Took up basketball and rowing as summer sports. Academic results tanked. Several Basketball injuries (Feb - April 17') as a result of what apppeared to be muscular imbalances from the relatively recent growth spurt, as well as taking on a new sport. Showed little interest in returning to AFL as no-one had followed him up during the previous year.  Current History : September 2017 showed a continued decline in academic levels. School teachers noted an inability to concentrate. Academic results still well below pre-concussion levels. Fatigue continuing to be problematic.  Literature Review : Post Concussion Syndrom (PCS) is defined as "cognitive deficits in attention or memory and at least three or more of the following symptoms: fatigue, sleep disturbances, headache, dizziness, irritability, affective disturbance, apathy, or personality change"  Further complications of PCS also appear to be an increased risk of musculoskeletal injury Nordstrom et al (2014, BMJ Sports Med, 48, 19, Predictors of PCS are uncertain. However, the following clinical variables are considered factors at increasing risk. These include prior history of concussion, sex (females more prominant), younger age, history of cognitive dysfunction, and affective disorders such as anxiety and depression (Leddy et al 2012, Sports Health, 4, 2, 147-154). Unlike the 'old days' which recommended a dark room and rest for several weeks post concussion, the consensus appears to be a graded return to exercise in order to restore metabolic homeostasis. Incredibly, highly trained young individuals can find even exercises in bed extremely demanding. Kozlowski et al (2013, J Ath Train, 48, 5, 627-635) used 34 people 226 days post injury to conclude significant physiological annomalies in response to exercise which may be the result of 'diffuse cerebral swelling'. Researchers have noted lower systolic and higher diastolic blood pressure in PCS (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Due to autonomic dysfunction manifested in altered cardiovascular and pulmonary responses (Mossberg et 2007, Arch Phys Med Rehab, 88, 3, 15-320) some clinicians have recommended the use of the exercise program for POTS (Postural Orthostatic Tachycardia Syndrome). This is a 5 month program which recommends mainly exercise in the horizontal and sitting positions for 1-4 months, including recumbent bike, rowing ergometer and swimming laps or kicking laps with a kick board. Month 4 upright bike and Month 5 upright training such as a elliptical trainer or treadmill. Other progressive exercise therapies have also included 20 minutes per day, 6 days per week, for 12 weeks of either treadmill or home gym exercises at 80% of the heart rate at which their concussion symtoms are exacerbated. Their programs were individually modified as the heart rate provoking symptoms increased. When compared to the 'control group', this intervention was shown to improve cerebral perfusion on fMRI, increase exercise tolerance at a higher heart rate, less fatigue and were showing activation patterns in areas of the brain on performing math processing test which were now normalised (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Graded exercises could also have included 'motor imagery' as espouse by the NOI group and the work of Lorrimer Moseley (University South Australia) when dealing with chronic pain. Ongoing Symptoms : The literature review by Leddy et al (2012) found that ongoing symptoms are either a prolonged version of concussion pathophysiology or a manifestation of other processes, such as cervical injury, migraine headaches, depression, chronic pain, vestibular dysfunction, visual disturbance, or some combination of conditions. Physiotherapy Assessment : One year PCS, fatigue continued to persist. Cognitive deficits with school work were reported to becoming more apparent. Assessment using various one leg standing tests employing oscillatory movement aroud the hips and knees for kinetic limb stability and lumbopelvic stability, which had been employed 6 months previously for his Basketball injuries were exhibiting deficits, despite these being 'somewhat good' previously. Physical Examination : cervical and thoracic spine Due to the Joint Hypermobility Syndrome (JHS) it was difficult to ascertain neck dysfunction based on range of movement testing. ROM were unremarkable except for lateral flexion which demonstrated altered intervertebral motion in both directions. Palpation using Australian and New Zealand manual therapy techniques such as passive accessory glides (upslopes and downslopes and traction) exhibited muscles spasms in the upper right cervical spine. Eye - Neck proprioceptive assessment using blind folds and laser pointer also  revealed marked variance from the normal. Repositioning error using the laser pointer with rotation demonstrated marked inability to reposition accurately from the left, tending to be short and at times completely missing the bullseye. Gaze stability with body rotation was NAD. Gaze stability whilst walking displayed some difficulty. Laser pointer tracing of the alphabet was wildly inaccurate. Thoracic ring relocation testing also revealed several annomalies, which may have also accounted for some autonomic dysfunction.  Occulomotor assessment and training Headache : Commonly referred to as cervicogenic headaches, one in five headaches in the general population are thought to be due to the cervical spine. The Upper Cervical Spine is particularly vulnerable to trauma because it is the most mobile part of the vertebral column, with a complex proprioceptive system connecting the vestibular apparatus and visual systems. It also coincides with the lower region of the brainstem and fourth ventricle. The brainstem houses many neurones associated with autonomic responses to pain and balance. Imaging of the fourth ventricle for swelling of the 'tonsils' and Arnold Chiari malformations are recommended when symptoms persist. In particular, children and adolescents are more vulnerable to neck contusions due to the proportionately larger head and less developed musculature. Cervical vertigo and dizziness after whiplash can mimic symptoms of PCS.. Mechanoreceptor dysfunction and vertebrobasilar artery insufficiency should be part of the differential diagnosis. Mechanical instability of the Upper Cervical Spine should also not be missed. Cervicogenic Headaches Further Interventions : Neurocognitive rehabilitation of attention processes. Psychological intervention using cognitive behavioural therapy (CBT). Neuro-opthalmologist to assess and treat smooth pursuit eye tracking. Naturopath for food intolerances and dietician for the optimisation of diet. Diet :  In cases with chronic fatiguing factors, nutrition can be become a vital aspect into the reparative process. This may include energy and mineral rich foods such as bananas, green leafy vegetables for iron and magnesium (200-300mg), oranges for vitamin C (anit-oxidant and helps with the absorption of iron), anti-oxidant rich foods such as EPA/DHA (1000mg) fish oil, curcumin (tumeric), Cats Claw, Devils Claw, Chia seeds, fruits of the forest (berries), and CoQ10 with Vitamin B. Folate and Ferritin levels should also be checked. Calorific energy intake should balance with energy exependiture. However, as we are often dealing with young individuals, as in this case, some form of comfort food may be appropriate such as, nuts, legumes, homus and sushi. Protein intake prior to carbohydrate intake may help ameliorate any blood suger fluctuations due to Glycemic Index factors, however simple carbohydrates (high GI) should be avoided wherever practical. Even oats need to be soaked overnight and cooked briefly, otherwise they become a high GI food and may even affect the absorption of iron. The type of rice used can also influence GI, hence the addition of protein such as fish. Protein supplementations are generally over-used. Daily protein intake should not exceed 1.2g per kg of body weight per day. Dosage for children is less than that for adults. See Nutritional Section of this Site Conclusion  Investigations, into people with persisting PCS, demonstrated that they applied more force over time to control balance. Helmich et al (2016, Med Sc Ex Sp, 48,  12, 2362-2368) proposed that in regard to cognitive processes, the increase of cerebral activation indicates an increase of attention demanding processes during postural control in altered environments. This is relevant in so far as individuals with post concussive symptomatology have a variety of symptoms including headache, dizziness, and cognitive difficulties that usually resolve over a few days to weeks. However, a subgroup of patients can have persistent symptoms which last months and even years. Complications in differential diagnosis, can arise clinically, when neck dysfunction and altered motor control occur concurrently due to both neck and cerebral pathology. For example, Whiplash and other traumatic head and neck injuries can result in pathology to both regions, whereas, more discreet altered cognitive processing from concussion can result in altered neck motor control. Musculoskelatal Physiotherapy can play a vital part in the treatment of neck dysfunction including the re-establishment of occulomotor proprioception and managing localized strength and cardiovascular exercise regimes. A total body, multi-disciplinary approach which is well co-ordinated amongst practitioners is vital to an optimal outcome.    Uploaded : 17 October 2017 Read More
  • Thu 24 Aug 2017

    Pain in the Brain - neural plasticity

    Pain in the Brain and Neural Plasticity by Martin Krause There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Pain can be the result of peripheral sensitisation from peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation through descending modulation at the peripheral receptor and in the spinal cord and through transcortical mechanisms depending on the 'meaning' and 'context given to the pain. Moreoever, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state.  Paradoxically, representation of body parts such as limbs and individual muscles can reduce in perceived size. In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Evidence for this neural plasticity comes from imaging studies, where brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens has been shown in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.  further reading Peripheral input is a powerful driver to neuroplasticity. Information gathered by touch, movement and vision, in the context of pain can lead to mal-adaptive plasticity, including the reorganisation of the somatosensory, and motor cortices, altered cortical excitability and central sensitisation. Examples of somatosensory reorganisation come from the work of Abrahao Baptista when investigating chronic anterior knee pain, who not only demonstrated reduced volume of Vastus Medialis but also is cortical translocation to another part of the cortex. ndividuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036,   AKP = anterior knee pain The same researcher (Abrahao Baptista) has shown that maximal tolerable electrical stimulation (eg TENS) of muscles can induce normalisation of the cortical changes through a process called 'smudging'. Transcortical stumilation has also been applied as a cortical 'primer' prior to the application of more traditional therapy such as motor re-training, exercise, and manipulation. Body illusions are another novel way to promote the normalisation of cortical function through adaptive neuroplasticity. Examples come from people with hand athritis, whose perception of their hand size is underestimated (Gilpin et al 2015 Rheumatology, 54, 4, 678-682). Using a curved mirror, similar to that in theme parks, the visual input can be increased to perceive the body part as larger (Preston et al 2011 DOI: 10.1093/rheumatology/ker104 · Source:PubMed ) . Irrespective of size, watching a reflection of the hand while performing synchronised movements enhances the embodiment of the reflection of the hand (Whitkopf et al 2017, Exp Brain res, 23, 5, 1933-1944). These visual inputs are thought to affect the altered functional connectivity between areas of the brain thereby affecting the 'pain matrix'. Another, novel way of looking at movement and pain perception is the concept of the motor engram. This has been defined as motor skill acquisition through the modification and organisation of muscle synergies into effective movement sequences. The learning process is thought to be acquired as a child through experientially based play activity. The specific neural mechanisms involved are unknown, however they are thought to include motor map topography reflecting the capacity for skilled movement reorganisation of motor maps in a manner that reflects the kinematics of aquired skilled movement map plasticity is supported by a reorganisation of cortical microcircuitry involving changes in synaptic efficacy motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience (Monfils 2005 Neuroscientist, 11, 5, 471-483). Interestingly, it is an intriguing notion that accessing motor engrams from patterns aquired prior to the pain experience might lead a normalisation of brain activity. My personal experience of severe sciatica with leg pain, sleepness nights and a SLR of less than 30 degrees, happened to coincide with training my 9 year old sons soccer training. I was noticing that the nights after i trained the children, I slept much better and my range of movement improved. I commenced a daily program of soccer ball tricks which i had been showing the kids, including 'juggling', 'rainbows' and 'around the worlds'. Eventually, I even took up playing soccer again after a 30 year abscence from the sport. Other than new activity related pain issues (DOMS), four years on, the sciatica hasn't returned. I can only conclude that this activity activated dormant childhood motor engram, worked on global balance, mobilised my nerve, encouraged cross cortical activity and turned my focus into finctional improvement. Further explainations for my expereience comes from evidence suggesting that a peripheral adaptive pain state is initiated, whereby transcortical inhibiton occurs by the contralaleral hemisphere to the one which controls the affected limb. Additionally, excitation cortical (M1) drive of the muscles of the contralateral limb to the one which is in pain also occurs. In such cases re-establishement of motor drive to the affected side is important. In terms of tendon rehabilitation, external audtory and visual cues using a metronome have been employed and are showing promising results (Ebonie Rio et al 2017 Personal communication). In terms of my experience with the soccer ball tricks, the external visual cues and the cross talk from using left and right feet, head, shoulders, and chest during ball juggling manouvers, whilst calling the rhythm to the kids may have been the crucial factor to overcome the dysfunctional brain induced pain - muscle inco-ordination cycle, which I was in. Additionally, I was cycling which allowed me to focus on motor drive into the affected.limb. However, work by Lorrimer Moseley on CRPS has established that 'brain laterality' must be established before commencing trans-cortical rehabilitation techniques. Lorrimer's clinical interventions use 'mirror imaging' techniques which are only effective once the patient is able to discriminate the left and right sides of the affected body parts, presented visually, in various twists and angles.   Alternatively, the altered pain state can result in a hostage like situation, whereby the pain takes control. Similar to the 'Stockholm Syndrome' where the hostage begins to sympathise with their captors, so do some peoples brain states, where it begin to sympathise with the pain, creating an intractable bondage and dysfunctional state. One screening question which may reflect commitment to the process of rehabilitatation is to question whether they were able to resist the cookie jar when they were a child? Or were they committed to any sporting endeavours as a child? This may give some indication for the presence of motor engrams which can be used to overcome dysfunctional pain induced muscle synergies (neurotags), but also indicate an ability to be self disciplined, as well as being able to reconcile and identify goal oriented objectives, in spite of the cognitive pain processes? Remember that neurons that fire together, wire together. Uploaded : 18 October 2017 Read More
  • Thu 03 Aug 2017

    Sickle Cell Trait and Acute Low Back Pain

    Researchers believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to the uncommon paraspinal compartment syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, they believe that SCT may represent an additional risk factor for LPSMN. Accordingly, they presented six cases of LPSMN in elite African American football players with SCT. See link below Read More
  • Thu 03 Aug 2017

    Ibuprofen, Resistance Training, Bone Density

    Taking Ibuprofen immediately after resistance training has a deleterious effect on bone mineral content at the distal radius, whereas taking Ibuprofen or undertaking resistance training individually prevented bone mineral loss. Read More
  • Tue 11 Jul 2017

    Mitochondrial Health and Sarcopenia

    The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living. Published 11 July 2017 Read More
  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) by Martin Krause When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups. In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. An interesting case of EDS and it's affect on post concussion syndrome can be read elsewhere on this site. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 17 October 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More

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Updated : 10 May 2014

No responsibility is assumed by Back in Business Physiotherapy for any injury and/or damage to persons or property as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material in this and it's related websites. Because of rapid advances in the medical sciences, the author recommends that there should be independent verification of diagnoses and exercise prescription. The information provided on Back in Business Physiotherapy is designed to support, not replace, the relationship that exists between a patient/site visitor and their treating health professional.

Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected