Hamstring strain injuries : factors that lead to injury and re-injury

Hamstring strain injuries (HSIs) are common in a number of sports and incidence rates have not declined in recent times. Additionally, the high rate of recurrent injuries suggests that our current understanding of HSI and re-injury risk is incomplete. Whilst the multifactoral nature of HSIs is agreed upon by many, often individual risk factors and/or causes of injury are examined in isolation. This review aims to bring together the causes, risk factors and interventions associated with HSIs to better understand why HSIs are so prevalent. Running is often identified as the primary activity type for HSIs and given the high eccentric forces and moderate muscle strain placed on the hamstrings during running these factors are considered to be part of the aetiology of HSIs. However, the exact causes of HSIs remain unknown and whilst eccentric contraction and muscle strain purportedly play a role, accumulated muscle damage and/or a single injurious event may also contribute. Potentially, all of these factors interact to varying degrees depending on the injurious activity type (i.e. running, kicking). Furthermore, anatomical factors, such as the biarticular organization, the dual innervations of biceps femoris (BF), fibre type distribution, muscle architecture and the degree of anterior pelvic tilt, have all been implicated. Each of these variables impact upon HSI risk via a number of different mechanisms that include increasing hamstring muscle strain and altering the susceptibility of the hamstrings to muscle damage. Reported risk factors for HSIs include age, previous injury, ethnicity, strength imbalances, flexibility and fatigue. Of these, little is known, definitively, about why previous injury increases the risk of future HSIs. Nevertheless, interventions put in place to reduce the incidence of HSIs by addressing modifiable risk factors have focused primarily on increasing eccentric strength, correcting strength imbalances and improving flexibility. The response to these intervention programmes has been mixed with varied levels of success reported. A conceptual framework is presented suggesting that neuromuscular inhibition following HSIs may impede the rehabilitation process and subsequently lead to maladaptation of hamstring muscle structure and function, including preferentially eccentric weakness, atrophy of the previously injured muscles and alterations in the angle of peak knee flexor torque. This remains an area for future research and practitioners need to remain aware of the multifactoral nature of HSIs if injury rates are to decline.

A novel device using the Nordic hamstring exercise to assess eccentric knee flexors strength : a reliability and retrospective injury study

STUDY DESIGN: Reliability and case-control injury study. OBJECTIVES: 1) To determine if a novel device, designed to measure eccentric knee flexors strength via the Nordic hamstring exercise (NHE), displays acceptable test-retest reliability; 2) to determine normative values for eccentric knee flexors strength derived from the device in individuals without a history of hamstring strain injury (HSI) and; 3) to determine if the device could detect weakness in elite athletes with a previous history of unilateral HSI. BACKGROUND: HSIs and reinjuries are the most common cause of lost playing time in a number of sports. Eccentric knee flexors weakness is a major modifiable risk factor for future HSIs, however there is a lack of easily accessible equipment to assess this strength quality. METHODS: Thirty recreationally active males without a history of HSI completed NHEs on the device on 2 separate occasions. Intraclass correlation coefficients (ICCs), typical error (TE), typical error as a co-efficient of variation (%TE), and minimum detectable change at a 95% confidence interval (MDC95) were calculated. Normative strength data were determined using the most reliable measurement. An additional 20 elite athletes with a unilateral history of HSI within the previous 12 months performed NHEs on the device to determine if residual eccentric muscle weakness existed in the previously injured limb. RESULTS: The device displayed high to moderate reliability (ICC = 0.83 to 0.90; TE = 21.7 N to 27.5 N; %TE = 5.8 to 8.5; MDC95 = 76.2 to 60.1 N). Mean±SD normative eccentric flexors strength, based on the uninjured group, was 344.7 ± 61.1 N for the left and 361.2 ± 65.1 N for the right side. The previously injured limbs were 15% weaker than the contralateral uninjured limbs (mean difference = 50.3 N; 95% CI = 25.7 to 74.9N; P < .01), 15% weaker than the normative left limb data (mean difference = 50.0 N; 95% CI = 1.4 to 98.5 N; P = .04) and 18% weaker than the normative right limb data (mean difference = 66.5 N; 95% CI = 18.0 to 115.1 N; P < .01). CONCLUSIONS: The experimental device offers a reliable method to determine eccentric knee flexors strength and strength asymmetry and revealed residual weakness in previously injured elite athletes.

Neuromuscular hamstring function in response to intermittent running and previous injury

This thesis examined the impact of previous hamstring injury and fatigue on the function of the hamstring muscles and their neural control. The work established the role of neuromuscular inhibition after hamstring injury and involved the development of a new field testing device for eccentric hamstring strength, which is now in high demand in elite sport worldwide. David has four peer-reviewed publications from this doctoral work.

Increased tubulointerstitial recruitment of human CD141(hi) CLEC9A(+) and CD1c(+) myeloid dendritic cell subsets in renal fibrosis and chronic kidney disease

Dendritic cells (DCs) play critical roles in immune-mediated kidney diseases. Little is known, however, about DC subsets in human chronic kidney disease, with previous studies restricted to a limited set of pathologies and to using immunohistochemical methods. In this study, we developed novel protocols for extracting renal DC subsets from diseased human kidneys and identified, enumerated, and phenotyped them by multicolor flow cytometry. We detected significantly greater numbers of total DCs as well as CD141(hi) and CD1c(+) myeloid DC (mDCs) subsets in diseased biopsies with interstitial fibrosis than diseased biopsies without fibrosis or healthy kidney tissue. In contrast, plasmacytoid DC numbers were significantly higher in the fibrotic group compared with healthy tissue only. Numbers of all DC subsets correlated with loss of kidney function, recorded as estimated glomerular filtration rate. CD141(hi) DCs expressed C-type lectin domain family 9 member A (CLEC9A), whereas the majority of CD1c(+) DCs lacked the expression of CD1a and DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN), suggesting these mDC subsets may be circulating CD141(hi) and CD1c(+) blood DCs infiltrating kidney tissue. Our analysis revealed CLEC9A(+) and CD1c(+) cells were restricted to the tubulointerstitium. Notably, DC expression of the costimulatory and maturation molecule CD86 was significantly increased in both diseased cohorts compared with healthy tissue. Transforming growth factor-β levels in dissociated tissue supernatants were significantly elevated in diseased biopsies with fibrosis compared with nonfibrotic biopsies, with mDCs identified as a major source of this profibrotic cytokine. Collectively, our data indicate that activated mDC subsets, likely recruited into the tubulointerstitium, are positioned to play a role in the development of fibrosis and, thus, progression to chronic kidney disease.

Eccentric hamstring strength and hamstring injury risk in Australian footballers

Purpose Is eccentric hamstring strength and between limb imbalance in eccentric strength, measured during the Nordic hamstring exercise, a risk factor for hamstring strain injury (HSI)? Methods Elite Australian footballers (n=210) from five different teams participated. Eccentric hamstring strength during the Nordic was taken at the commencement and conclusion of preseason training and in season. Injury history and demographic data were also collected. Reports on prospectively occurring HSIs were completed by team medical staff. Relative risk (RR) was determined for univariate data and logistic regression was employed for multivariate data. Results Twenty-eight HSIs were recorded. Eccentric hamstring strength below 256N at the start of preseason and 279N at the end of preseason increased risk of future HSI 2.7 (relative risk, 2.7; 95% confidence interval, 1.3 to 5.5; p = 0.006) and 4.3 fold (relative risk, 4.3; 95% confidence interval, 1.7 to 11.0; p = 0.002) respectively. Between limb imbalance in strength of greater than 10% did not increase the risk of future HSI. Univariate analysis did not reveal a significantly greater relative risk for future HSI in athletes who had sustained a lower limb injury of any kind within the last 12 months. Logistic regression revealed interactions between both athlete age and history of HSI with eccentric hamstring strength, whereby the likelihood of future HSI in older athletes or athletes with a history of HSI was reduced if an athlete had high levels of eccentric strength. Conclusion Low levels of eccentric hamstring strength increased the risk of future HSI. Interaction effects suggest that the additional risk of future HSI associated with advancing age or previous injury was mitigated by higher levels of eccentric hamstring strength.

Biceps femoris long-head architecture: A reliability and retrospective injury study

Purpose: To determine i) the reliability of two-dimensional ultrasonography for the assessment of biceps femoris long head (BFlh) architectural characteristics; ii) if limbs with a history of strain injury in the BFlh display different architecture and eccentric strength compared to uninjured limbs. Methods: This case-control study (control [n=20], injured group [n=16], males) assessed the BFlh architecture at rest and during graded isometric contractions using two-dimensional ultrasonography. The control group were assessed three times (>24hrs apart) to determine reliability. Previously injured individuals were evaluated once. Results The assessment of BFlh architecture was highly reliable (intraclass correlations >0.90). Fascicle length (p<0.001; d range: 0.67 to 1.34) and fascicle length relative to muscle thickness (p<0.001; d range: 0.58 to 0.85) of the previously injured BFlh were significantly less than the contralateral uninjured BFlh at all intensities. Pennation angle of the previously injured BFlh was significantly greater (p<0.001; d range: 0.62 to 0.88) than the contralateral uninjured BFlh at all intensities. Eccentric strength in the previously injured limb was significantly lower than the contralateral limb (-15.4%; -52.5N; 95% CI=-28.45 to -76.23; p<0.001, d=0.56). Conclusion These data indicate that two-dimensional ultrasonography is reliable for assessing BFlh architecture at rest and during graded isometric contractions. Fascicle length, fascicle length relative to muscle thickness and pennation angle are significantly different in previously injured BFlh compared to an uninjured contralateral BFlh. Eccentric strength of the previously injured limb is also significantly lower than the uninjured contralateral limb. These findings have implications for rehabilitation and injury prevention practices which should consider altered architectural characteristics.

Glutathione transferase activities in renal carcinomas and adjacent normal renal tissues : factors influencing renal carcinogenesis induced by xenobiotics

In general, the biological activation of nephrocarcinogenic chlorinated hydrocarbons proceeds via conjugatiton with glutathione. It has mostly been assamed that the main site of initial conjugation is the liver, followed by a mandatory transfer of intermediates to the kidney. It was therefore of interest to study the enzyme activities of subgroups of glutathione transferases (GSTs) in renal cancers and the surrounding normal renal tissues of the same individuals (n = 21). For genotyping the individuals with respect to known polymorphic GST isozymes the following substrates with differential specificity were used: 1-chloro-2,4-dinitrobenzene for overall GST activity (except GST θ); 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole for GST α; 1,2-dichloro-4-nitro-benzene for GST μ; ethacrynic acid and 4-vinylpyridine for GST π; and methyl chloride for GST θ. In general, the normal tissues were able to metabolize the test substrates. A general decrease in individual GST enzyme activities was apparent in the course of cancerization, and in some (exceptional) cases individual activities, expressed in the normal renal tissue, were lost in the tumour tissue. The GST enzyme activities in tumours were independent of tumour stage, or the age and gender of the patients. There was little influence of known polymorphisms of GSTM1, GSTM3 and GSTP1 upon the activities towards the test substrates, whereas the influence of GSTT1 polymorphism on the activity towads methyl chloride was straightforward. In general, the present findings support the concept that the initial GST-dependent bioactivation step of nephrocarcinogenic chlorinated hydrocarbons may take place in the kidney itself. This should be a consideration in toxicokinetic modelling.

Is there evidence to support the use of the angle of peak torque as a marker of hamstring injury and re-injury risk?

Hamstring strain injuries are the predominant injury in many sports, costing athletes and clubs a significant financial and performance burden. Therefore the ability to identify and intervene with individuals who are considered at a high risk of injury is important. One measure which has grown in popularity as an outcome variable following hamstring intervention/prevention studies and rehabilitation is the angle of peak knee flexor torque. This current opinion article will firstly introduce the measure and the processes behind it. Secondly, this article will summarise how the angle of peak knee flexor torque has been suggested to measure hamstring strain injury risk. Finally various limitations will be presented and outlined as to how they may influence the measure. These include the lack of muscle specificity, the common concentric contraction mode of assessment, reliability of the measure, various neural contributions (such as rate of force development and neuromuscular inhibition) as well as the lack of prospective data showing any predictive value in the measure.

Bcl-2 genes and growth factors in the pathology of ischaemic acute renal failure

For the past decade, an attempt has been made by many research groups to define the roles of the growing number of Bcl-2 gene family proteins in the apoptotic process. The Bcl-2 family consists of pro-apoptotic (or cell death) and anti-apoptotic (or cell survival) genes and it is the balance in expression between these gene lineages that may determine the death or survival of a cell. The majority of studies have analysed the role/s of the Bcl-2 genes in cancer development. Equally important is their role in normal tissue development, homeostasis and non-cancer disease states. Bcl-2 is crucial for normal development in the kidney, with a deficiency in Bcl-2 producing such malformation that renal failure and death result. As a corollary, its role in renal disease states in the adult has been sought. Ischaemia is one of the most common causes of both acute and chronic renal failure. The section of the kidney that is most susceptible to ischaemic damage is the outer zone of the outer medulla. Within this zone the proximal tubules are most sensitive and often die by necrosis or desquamate. In the distal nephron, apoptosis is the more common form of cell death. Recent results from our laboratory have indicated that ischaemia-induced acute renal failure is associated with up-regulation of two anti-apoptotic Bcl-2 proteins (Bcl-2 and Bcl-XL) in the damaged distal tubule and occasional up-regulation of Bax in the proximal tubule. The distal tubule is a known reservoir for several growth factors important to renal growth and repair, such as insulin-like growth factor-1 (IGF-1) and epidermal growth factor (EGF). One of the likely possibilities for the anti-cell death action of the Bcl-2 genes is that the protected distal cells may be able to produce growth factors that have a further reparative or protective role via an autocrine mechanism in the distal segment and a paracrine mechanism in the proximal cells. Both EGF and IGF-1 are also up-regulated in the surviving distal tubules and are detected in the surviving proximal tubules, where these growth factors are not usually synthesized. As a result, we have been using in vitro methods to test: (i) the relative sensitivities of renal distal and proximal epithelial cell populations to injury caused by mechanisms known to act in ischaemia-reperfusion; (ii) whether a Bcl-2 anti-apoptotic mechanism acts in these cells; and (iii) whether an autocrine and/or paracrine growth factor mechanism is initiated. The following review discusses the background to these studies as well as some of our preliminary results.

Bcl-X(L) translocation in renal tubular epithelial cells in vitro protects distal cells from oxidative stress

BACKGROUND: The molecular pathogenesis of different sensitivities of the renal proximal and distal tubular cell populations to ischemic injury, including ischemia-reperfusion (IR)-induced oxidative stress, is not well-defined. An in vitro model of oxidative stress was used to compare the survival of distal [Madin-Darby canine kidney (MDCK)] and proximal [human kidney-2 (HK-2)] renal tubular epithelial cells, and to analyze for links between induced cell death and expression and localization of selected members of the Bcl-2 gene family (anti-apoptotic Bcl-2 and Bcl-X(L), pro-apoptotic Bax and Bad). METHODS: Cells were treated with 1 mmol/L hydrogen peroxide (H2O2) or were grown in control medium for 24 hours. Cell death (apoptosis) was quantitated using defined morphological criteria. DNA gel electrophoresis was used for biochemical identification. Protein expression levels and cellular localization of the selected Bcl-2 family proteins were analyzed (Western immunoblots, densitometry, immunoelectron microscopy). RESULTS: Apoptosis was minimal in control cultures and was greatest in treated proximal cell cultures (16.93 +/- 4.18% apoptosis) compared with treated distal cell cultures (2.28 +/- 0.85% apoptosis, P < 0.001). Endogenous expression of Bcl-X(L) and Bax, but not Bcl-2 or Bad, was identified in control distal cells. Bcl-X(L) and Bax had nonsignificant increases (P> 0.05) in these cells. Bcl-2, Bax, and Bcl-X(L), but not Bad, were endogenously expressed in control proximal cells. Bcl-X(L) was significantly decreased in treated proximal cultures (P < 0.05), with Bax and Bcl-2 having nonsignificant increases (P> 0.05). Immunoelectron microscopy localization indicated that control and treated but surviving proximal cells had similar cytosolic and membrane localization of the Bcl-2 proteins. In comparison, surviving cells in the treated distal cultures showed translocation of Bcl-X(L) from cytosol to the mitochondria after treatment with H2O2, a result that was confirmed using cell fractionation and analysis of Bcl-X(L) expression levels of the membrane and cytosol proteins. Bax remained distributed evenly throughout the surviving distal cells, without particular attachment to any cellular organelle. CONCLUSION: The results indicate that in this in vitro model, the increased survival of distal compared with proximal tubular cells after oxidative stress is best explained by the decreased expression of anti-apoptotic Bcl-X(L) in proximal cells, as well as translocation of Bcl-X(L) protein to mitochondria within the surviving distal cells.

Renal and genitourinary emergencies

Genitourinary (GU) problems are a common complaint in the community and to the emergency department (ED). Urinary tract infections (UTIs) are the second most common bacterial disease. UTIs rank as the sixteenth most frequently reported problem to general practitioners in Australia1 and between 10% and 20% of women will experience at least one UTI in their lifetime. Over 1,000,000 Australians are currently suffering with nephrolithiasis (renal calculi) and it is hy-pothesised that Australia’s hot, dry climate causes more stone formation than many other coun-tries in the world. Acute kidney injury (AKI) is a common complication of any trauma. Hypovol-aemia results in severe hypotension and this precipitates the development of acute tubular necrosis and subsequent AKI. The incidence of chronic kidney disease (CKD) is rising across the world. CKD is classified into five stages with those in stage 5 being classified as being in end stage kidney disease (ESKD). It is estimated that there are over 1.5 million people in Australia with CKD and there were over 16,000 Australians and over 2900 individuals in New Zealand with ESKD.2 Indigenous populations from both countries (Aboriginals, Torres Strait Islanders, Maoris, and Pacific Islanders) are over-represented in the number of people with all stages of CKD in both countries. Patients with compromised renal function often require the assistance of paramedics and will arrive at the ED with life-threatening fluid and electrolyte imbalances. Spe-cific GU emergencies discussed in this chapter are acute renal failure, rhabdomyolysis, chronic kidney disease, UTIs, acute urinary retention, urinary calculi, testicular torsion, epididymitis, and priapism. Refer to Chapter 31 for discussion of sexually transmitted infections (STIs) in women and to Chapter X for discussion of genitourinary trauma.

Determination of urinary thymidine glycol using affinity chromatography, HPLC and post-column reaction detection : a biomarker of oxidative DNA damage upon kidney transplantation

Reactive oxygen species are generated during ischaemia-reperfusion of tissue. Oxidation of thymidine by hydroxyl radicals (HO) leads to the formation of 5,6-dihydroxy-5,6-dihydrothymidine (thymidine glycol). Thymidine glycol is excreted in urine and can be used as biomarker of oxidative DNA damage. Time dependent changes in urinary excretion rates of thymidine glycol were determined in six patients after kidney transplantation and in six healthy controls. A new analytical method was developed involving affinity chromatography and subsequent reverse-phase high-performance liquid chromatography (RP-HPLC) with a post-column chemical reaction detector and endpoint fluorescence detection. The detection limit of this fluorimetric assay was 1.6 ng thymidine glycol per ml urine, which corresponds to about half of the physiological excretion level in healthy control persons. After kidney transplantation the urinary excretion rate of thymidine glycol increased gradually reaching a maximum around 48 h. The excretion rate remained elevated until the end of the observation period of 10 days. Severe proteinuria with an excretion rate of up to 7.2 g of total protein per mmol creatinine was also observed immediately after transplantation and declined within the first 24 h of allograft function (0.35 + 0.26 g/mmol creatinine). The protein excretion pattern, based on separation of urinary proteins on sodium dodecyl sulphate-polyacrylamide gel electrophorosis (SDS-PAGE), as well as excretion of individual biomarker proteins, indicated nonselective glomerular and tubular damage. The increased excretion of thymidine glycol after kidney transplantation may be explained by ischaemia-reperfusion induced oxidative DNA damage of the transplanted kidney.

Teachers’ understanding of school connectedness : implications for the development and implementation of school based injury prevention strategies

Aim: Worldwide, injury is the leading cause of death and disability for young people. Injuries among young people are commonly associated with risk taking behaviour, including violence and transport risks, which often occur in the context of alcohol use. The school environment has been identified as having a significant role in shaping adolescent behaviour. In particular, school connectedness, the degree to which adolescents feel that they belong and are accepted at school, has been shown to be an important protective factor. Strategies for increasing school connectedness may therefore be effective in reducing risk taking and associated injury. Prior to developing connectedness strategies, it is important to understand the perspectives of those in the school regarding the construct and how it is realised in the school context. The aim of this research was to understand teachers’ perspectives of school connectedness, the strategies they employ to connect with students, and their perceptions of school connectedness as a strategy for risk taking and injury prevention. Method: In depth interviews of approximately 45 minutes duration were conducted with 13 Health and PE teachers and support staff from 2 high schools in Southeast Queensland, Australia. Additionally, 6 focus group workshop discussions were held with 35 Education department employees (5-6 per group), including teachers from 15 Southeast Queensland high schools. Results: Participants were found to place strong importance on the development of connectedness among students, including those at risk for problem behaviour. Strategies used to promote connectedness included building trust, taking an interest in each student and being available to talk to, and finding something positive for students to succeed at. Teachers identified strategies as being related to decreased risk taking behavior. Teacher training on school connectedness was perceived as an important and useful inclusion in a school based injury prevention program. Conclusions: The established link between increased school connectedness and decreased problem behaviour has implications for school based strategies designed to decrease adolescent risk taking behaviour and associated injury. Targeting school connectedness as a point of intervention, in conjunction with individual attitude and behaviour change programs, may be an effective injury prevention strategy.