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.

Effectiveness of powered hospital bed movers for reducing physiological strain and back muscle activation

Battery powered bed movers are becoming increasingly common within the hospital setting. The use of powered bed movers is believed to result in reduced physical efforts required by health care workers, which may be associated with a decreased risk of occupation related injuries. However, little work has been conducted assessing how powered bed movers impact on levels of physiological strain and muscle activation for the user. The muscular efforts associated with moving hospital beds using three different methods; manual pushing, StaminaLift Bed Mover (SBM) and Gzunda Bed Mover (GBM)were measured on six male subjects. Fourteen muscles were assessed moving a weighted hospital bed along a standardized route in an Australian hospital environment. Trunk inclination and upper spine acceleration were also quantified. Powered bed movers exhibited significantly lower muscle activation levels than manual pushing for the majority of muscles. When using the SBM, users adopted a more upright posture which was maintained while performing different tasks (e.g. turning a corner, entering a lift), while trunk inclination varied considerably for manual pushing and the GBM. The reduction in lower back muscular activation levels and the load reducing effect of a more upright posture may result in lower incidence of lower back injury.

Improving posture and decreasing pain with novel shoe insoles

A single subject longevity study is presented as a case study for the Medical Device Partnering Program (MDPP). The MDPP supports the development of cutting-edge medical devices and assistive technologies, through unique collaborations between researchers, industry, clinical end-users and government. The study aimed to identify what effect the innersole has on specific muscles that may influence stability and whether the innersole had any influence on gait. Three tests were conducted; a standard gait test, dynamic balance test and a standing balance test. Results from the kinematic analysis showed reduced variability in post testing results when compared to pre testing results. Reductions in muscle activation levels were also found across all tests. Further testing with a larger sample size is required to determine if these effects are due to the innersole.

Towards an accurate biomechanical model of the ankle

When compared with similar joint arthroplasties, the prognosis of Total Ankle Replacement (TAR) is not satisfactory although it shows promising results post surgery. To date, most models do not provide the full anatomical functionality and biomechanical range of motion of the healthy ankle joint. This has sparked additional research and evaluation of clinical outcomes in order to enhance ankle prosthesis design. However, the limited biomechanical data that exist in literature are based upon two-dimensional, discrete and outdated techniques1 and may be inaccurate. Since accurate force estimations are crucial to prosthesis design, a paper based on a new biomechanical modeling approach, providing three dimensional forces acting on the ankle joint and the surrounding tissues was published recently, but the identified forces were suspected of being under-estimated, while muscles were . The present paper reports an attempt to improve the accuracy of the analysis by means of novel methods for kinematic processing of gait data, provided in release 4.1 of the AnyBody Modeling System (AnyBody Technology, Aalborg, Denmark) Results from the new method are shown and remaining issues are discussed.

A simulation to describe the effects of in-shoe orthoses

The subtalar joint has been presumed to account for most of the pathologic motion in the foot and ankle, but research has shown that motion at other foot joints is greater than traditionally expected. Although recent research demonstrates the complexity of the kinematic variables in the foot and ankle, it still fails to expand our knowledge of the role of the musculotendinous structures in the biomechanics of the foot and ankle and how this is affected by in-shoe orthoses. The aim of this study was to simulate the effect of in-shoe foot orthoses by manipulation of the ground reaction force (GRF) components and centre of pressure (CoP) to demonstrate the resultant effect on muscle force in selected muscles during both the rearfoot loading response and stance phase of the gait cycle. We found that any medial wedge increases ankle joint load during gait cycle, while a lateral wedge decreases the joint load during the stance phase.

Effects of whole-body cryotherapy (-110 degrees C) on proprioception and indices of muscle damage

The purpose of this study was to investigate the effects of whole-body cryotherapy (WBC) on proprioceptive function, muscle force recovery following eccentric muscle contractions and tympanic temperature (TTY). Thirty-six subjects were randomly assigned to a group receiving two 3-min treatments of −110 ± 3 °C or 15 ± 3 °C. Knee joint position sense (JPS), maximal voluntary isometric contraction (MVIC) of the knee extensors, force proprioception and TTY were recorded before, immediately after the exposure and again 15 min later. A convenience sample of 18 subjects also underwent an eccentric exercise protocol on their contralateral left leg 24 h before exposure. MVIC (left knee), peak power output (PPO) during a repeated sprint on a cycle ergometer and muscles soreness were measured pre-, 24, 48 and 72 h post-treatment. WBC reduced TTY, by 0.3 °C, when compared with the control group (P<0.001). However, JPS, MVIC or force proprioception was not affected. Similarly, WBC did not effect MVIC, PPO or muscle soreness following eccentric exercise. WBC, administered 24 h after eccentric exercise, is ineffective in alleviating muscle soreness or enhancing muscle force recovery. The results of this study also indicate no increased risk of proprioceptive-related injury following WBC.

Use of Bayesian MUNE to show differing rate of loss of motor units in subgroups of ALS

Objectives To evaluate differences among patients with different clinical features of ALS, we used our Bayesian method of motor unit number estimation (MUNE). Methods We performed serial MUNE studies on 42 subjects who fulfilled the diagnostic criteria for ALS during the course of their illness. Subjects were classified into three subgroups according to whether they had typical ALS (with upper and lower motor neurone signs) or had predominantly upper motor neurone weakness with only minor LMN signs, or predominantly lower motor neurone weakness with only minor UMN signs. In all subjects we calculated the half life of MUs, defined as the expected time for the number of MUs to halve, in one or more of the abductor digiti minimi (ADM), abductor pollicis brevis (APB) and extensor digitorum brevis (EDB) muscles. Results The mean half life of MUs was less in subjects who had typical ALS with both upper and lower motor neurone signs than in those with predominantly upper motor neurone weakness or predominantly lower motor neurone weakness. In 18 subjects we analysed the estimated size of the MUs and demonstrated the appearance of large MUs in subjects with upper or lower motor neurone predominant weakness. We found that the appearance of large MUs was correlated with the half life of MUs. Conclusions Patients with different clinical features of ALS have different rates of loss and different sizes of MUs. Significance: These findings could indicate differences in disease pathogenesis.

The relationship between Bayesian motor unit number estimation and histological measurements of motor neurons in wild-type and SOD1 G93A mice

Objective: To assess the relationship between Bayesian MUNE and histological motor neuron counts in wild-type mice and in an animal model of ALS. Methods: We performed Bayesian MUNE paired with histological counts of motor neurons in the lumbar spinal cord of wild-type mice and transgenic SOD1 G93A mice that show progressive weakness over time. We evaluated the number of acetylcholine endplates that were innervated by a presynaptic nerve. Results: In wild-type mice, the motor unit number in the gastrocnemius muscle estimated by Bayesian MUNE was approximately half the number of motor neurons in the region of the spinal cord that contains the cell bodies of the motor neurons supplying the hindlimb crural flexor muscles. In SOD1 G93A mice, motor neuron numbers declined over time. This was associated with motor endplate denervation at the end-stage of disease. Conclusion: The number of motor neurons in the spinal cord of wild-type mice is proportional to the number of motor units estimated by Bayesian MUNE. In SOD1 G93A mice, there is a lower number of estimated motor units compared to the number of spinal cord motor neurons at the end-stage of disease, and this is associated with disruption of the neuromuscular junction. Significance: Our finding that the Bayesian MUNE method gives estimates of motor unit numbers that are proportional to the numbers of motor neurons in the spinal cord supports the clinical use of Bayesian MUNE in monitoring motor unit loss in ALS patients. © 2012 International Federation of Clinical Neurophysiology.

Quantitative studies of lower motor neuron degeneration in amyotrophic lateral sclerosis : Evidence for exponential decay of motor unit numbers and greatest rate of loss at the site of onset

Objective: To use our Bayesian method of motor unit number estimation (MUNE) to evaluate lower motor neuron degeneration in ALS. Methods: In subjects with ALS we performed serial MUNE studies. We examined the repeatability of the test and then determined whether the loss of MUs was fitted by an exponential or Weibull distribution. Results: The decline in motor unit (MU) numbers was well-fitted by an exponential decay curve. We calculated the half life of MUs in the abductor digiti minimi (ADM), abductor pollicis brevis (APB) and/or extensor digitorum brevis (EDB) muscles. The mean half life of the MUs of ADM muscle was greater than those of the APB or EDB muscles. The half-life of MUs was less in the ADM muscle of subjects with upper limb than in those with lower limb onset. Conclusions: The rate of loss of lower motor neurons in ALS is exponential, the motor units of the APB decay more quickly than those of the ADM muscle and the rate of loss of motor units is greater at the site of onset of disease. Significance: This shows that the Bayesian MUNE method is useful in following the course and exploring the clinical features of ALS. 2012 International Federation of Clinical Neurophysiology.

Leucocytes, cytokines and satellite cells : what role do they play in muscle damage and regeneration following eccentric exercise?

Exercise-induced muscle damage is an important topic in exercise physiology. However several aspects of our understanding of how muscles respond to highly stressful exercise remain unclear In the first section of this review we address the evidence that exercise can cause muscle damage and inflammation in otherwise healthy human skeletal muscles. We approach this concept by comparing changes in muscle function (i.e., the force-generating capacity) with the degree of leucocyte accumulation in muscle following exercise. In the second section, we explore the cytokine response to 'muscle-damaging exercise', primarily eccentric exercise. We review the evidence for the notion that the degree of muscle damage is related to the magnitude of the cytokine response. In the third and final section, we look at the satellite cell response to a single bout of eccentric exercise, as well as the role of the cyclooxygenase enzymes (COX1 and 2). In summary, we propose that muscle damage as evaluated by changes in muscle function is related to leucocyte accumulation in the exercised muscles. 'Extreme' exercise protocols, encompassing unaccustomed maximal eccentric exercise across a large range of motion, generally inflict severe muscle damage, inflammation and prolonged recovery (> 1 week). By contrast, exercise resembling regular athletic training (resistance exercise and downhill running) typically causes mild muscle damage (myofibrillar disruptions) and full recovery normally occurs within a few days. Large variation in individual responses to a given exercise should, however be expected. The link between cytokine and satellite cell responses and exercise-induced muscle damage is not so clear The systemic cytokine response may be linked more closely to the metabolic demands of exercise rather than muscle damage. With the exception of IL-6, the sources of systemic cytokines following exercise remain unclear The satellite cell response to severe muscle damage is related to regeneration, whereas the biological significance of satellite cell proliferation after mild damage or non-damaging exercise remains uncertain. The COX enzymes regulate satellite cell activity, as demonstrated in animal models; however the roles of the COX enzymes in human skeletal muscle need further investigation. We suggest using the term 'muscle damage' with care. Comparisons between studies and individuals must consider changes in and recovery of muscle force-generating capacity.

Bicep femoris voluntary activation deficits contribute to eccentric knee flexor weakness following intermittent running

INTRODUCTION: Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Eccentric hamstring muscle weakness following intermittent running has been implicated within the aetiology of HSI. This weakness following intermittent running is often greater eccentrically than concentrically, however the cause of this unique, contraction mode specific phenomenon is unknown. AIM: To determine if this preferential eccentric decline in strength is caused by declines in voluntary hamstring muscle activation. METHODS: Fifteen recreationally active males completed 18 × 20m overground sprints. Maximal strength (concentric and eccentric knee flexor and concentric knee extensor) was determined isokinetically at the velocities of ±1800.s-1 and ±600.s- while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. RESULTS: Overground intermittent running caused greater eccentric (27.2 Nm; 95% CI = 11.2 to 43.3; p=0.0001) than concentric knee flexor weakness (9.3 Nm; 95% CI = -6.7 to 25.3; P=0.6361). Following the overground running, voluntary activation levels of the lateral hamstrings showed a significant decline (0.08%; 95% CI = 0.045 to 0.120; P<0.0001). In comparison, medial hamstring activation showed no change following intermittent running. CONCLUSION: Eccentric hamstring strength is decreased significantly following intermittent overground running. Voluntary activation deficits in the biceps femoris muscle are responsible for some portion of this weakness. The implications of this finding are significant because the biceps femoris muscle is the most frequently strained of all the hamstring muscles and because fatigue appears to play an important part in injury occurrence.

The impact of fatigue caused by sprint running on the median power frequency of the hamstring muscle group

Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Intermittent running has been shown to result in preferential reductions in eccentric hamstring strength, which increase the risk of sustaining a HSI. The eccentric specific nature of this decline in hamstring function implicates central mechanisms, as peripheral fatigue mechanisms tend to impact upon both concentric and eccentric contractions modes. However, neural function of the hamstrings, such as the median power frequency (MPF) of the surface electromyography signal has yet to be examined in the fatigued hamstring following intermittent sprint running. AIM: To determine the impact of fatigue induced by intermittent sprinting on the MPF of the medial and lateral hamstring muscles. METHODS: Fifteen recreationally active males completed 18 × 20m overground sprints. Maximal strength (concentric and eccentric knee flexor and concentric knee extensor) was determined isokinetically at the velocities of ±180.s-1 and ±60.s- while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. RESULTS: Overground intermittent running caused a significant reduction in eccentric knee flexor strength (27.2 Nm; 95% CI = 11.2 to 43.3; p=0.0001) but not concentric strength (9.3 Nm; 95% CI = -6.7 to 25.3; P=0.6361). Following the overground running, MPF of the lateral hamstrings showed a significant decline eccentrically (0.86; 95% CI = 0.59 to 1.54; P=0.038) and concentrically (0.76; 95%CI = 0.66 to 0.83; P=0.039). Similar declines in MPF were also noted in the medial hamstrings eccentrically (1.54; 95% CI = 0.59 to 7.9; P=0.005) and concentrically (1.18; 95% CI = 0.44 to 6.8; P=0.040). CONCLUSION: Whilst sprint running induced fatigue led to a eccentric specific reduction in knee flexor torque, MPF was suppressed across both contraction modes. This would indicate that factors associated with the decline in MPF do not appear to explain the contraction mode-specific loss of strength after intermittent sprints. This would implicate other central mechanisms, such as declines in voluntary activation, in explaining the eccentric specific decline in strength seen following sprint running.

Do voluntary activation deficits contribute to eccentric weakness following intermittent running?

Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Eccentric hamstring muscle weakness following intermittent running has been implicated within the aetiology of HSI. This weakness following intermittent running is often greater eccentrically than concentrically, however the cause of this unique, contraction mode specific phenomenon is unknown. PURPOSE: To determine if this preferential eccentric decline in strength is caused by declines in voluntary hamstring muscle activation. METHODS: Fifteen recreationally active males completed 18 × 20m overground sprints. Maximal strength (concentric and eccentric knee flexor and concentric knee extensor) was determined isokinetically at the velocities of ±1800.s-1 and ±600.s- while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. RESULTS: Overground intermittent running caused greater eccentric (27.2 Nm; 95% CI = 11.2 to 43.3; p=0.0001) than concentric knee flexor weakness (9.3 Nm; 95% CI = -6.7 to 25.3; P=0.6361). Following the overground running, voluntary activation levels of the lateral hamstrings showed a significant decline (0.08%; 95% CI = 0.045 to 0.120; P<0.0001). In comparison, medial hamstring activation showed an increased level of activation following intermittent running (0.12%; 95% CI = 0.049 to 0.030; P = 0.0102). CONCLUSION: Eccentric hamstring strength is decreased significantly following intermittent overground running. Voluntary activation deficits in the biceps femoris muscle are responsible for some portion of this weakness. The implications of this finding are significant because the biceps femoris muscle is the most frequently strained of all the hamstring muscles and because fatigue appears to play an important part in injury occurrence.

Declines in eccentric knee flexor weakness following repeat sprint running are related to declines in biceps femoris voluntary activation

Introduction: Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Eccentric hamstring muscle weakness following intermittent running has been implicated within the aetiology of HSI. This weakness following intermittent running is sometimes greater eccentrically than concentrically, however the cause of this unique, contraction mode specific phenomenon is unknown. The purpose of this research was to determine whether declines in knee flexor strength following overground repeat sprints are caused by declines in voluntary activation of the hamstring muscles. Methods: Seventeen recreationally active males completed 3 sets of 6 by 20m overground sprints. Maximal isokinetic concentric and eccentric knee flexor and concentric knee extensor strength was determined at ±1800.s-1 and ±600.s-1 while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. Results: Overground repeat sprint running resulted in a significant decline in eccentric knee flexor strength (31.1 Nm; 95% CI = 21.8 to 40.3 Nm; p < 0.001). However, concentric knee flexor strength was not significantly altered (11.1 Nm; 95% CI= -2.8 to 24.9; p=0.2294). Biceps femoris voluntary activation levels displayed a significant decline eccentrically (0.067; 95% CI=0.002 to 0.063; p=0.0325). However, there was no significant decline concentrically (0.025; 95% CI=-0.018 to 0.043; p=0.4243) following sprinting. Furthermore, declines in average peak torque at -1800.s-1 could be explained by changes in hamstring activation (R2 = 0.70). Moreover, it was change in the lateral hamstring muscle activity that was related to the decrease in knee flexor torque (p = 0.0144). In comparison, medial hamstring voluntary activation showed no change for either eccentric (0.06; 95% CI = -0.033 to 0.102; p=0.298) or concentric (0.09; 95% CI = -0.03 to 0.16; p=0.298) muscle actions following repeat sprinting. Discussion: Eccentric hamstring strength is decreased significantly following overground repeat sprinting. Voluntary activation deficits in the biceps femoris muscle explain a large portion of this weakness. The implications of these findings are significant as the biceps femoris muscle is the most frequently strained of the knee flexors and fatigue is implicated in the aetiology of this injury.

Knee extensor strength differences in obese and healthy-weight 10-13 year olds

The purpose of this study was to investigate if obese children have reduced knee extensor (KE) strength and to explore the relationship between adiposity and KE strength. An observational case-control study was conducted in three Australian states, recruiting obese [n=107 (51 female, 56 male)] and healthy-weight [n=132 (56 female, 76 male)] 10–13 year old children. Body mass index, body composition (dual energy X-ray absorptiometry), isokinetic/isometric peak KE torques (dynamometry) and physical activity (accelerometry) were assessed. Results revealed that compared with their healthy-weight peers, obese children had higher absolute KE torques (P≤0.005), equivocal KE torques when allometrically normalized for fat-free mass (FFM) (P≥0.448) but lower relative KE torques when allometrically normalized for body mass (P≤0.008). Adjustments for maternal education, income and accelerometry had little impact on group differences, except for isometric KE torques relative to body mass which were no longer significantly lower in obese children (P≥0.013, not significant after controlling for multiple comparisons). Percent body fat was inversely related to KE torques relative to body mass (r= -0.22 to -0.35, P≤0.002), irrespective of maternal education, income or accelerometry. In conclusion, while obese children have higher absolute KE strength and FFM, they have less functional KE strength (relative to mass) available for weight-bearing activities than healthy-weight children. The finding that FFM-normalized KE torques did not differ suggests that the intrinsic contractile properties of the KE muscles are unaffected by obesity. Future research is needed to see if deficits in KE strength relative to mass translate into functional limitations in weight-bearing activities.