Model-order selection in Zernike polynomial expansion of corneal surfaces using the efficient detection criterion

Corneal-height data are typically measured with videokeratoscopes and modeled using a set of orthogonal Zernike polynomials. We address the estimation of the number of Zernike polynomials, which is formalized as a model-order selection problem in linear regression. Classical information-theoretic criteria tend to overestimate the corneal surface due to the weakness of their penalty functions, while bootstrap-based techniques tend to underestimate the surface or require extensive processing. In this paper, we propose to use the efficient detection criterion (EDC), which has the same general form of information-theoretic-based criteria, as an alternative to estimating the optimal number of Zernike polynomials. We first show, via simulations, that the EDC outperforms a large number of information-theoretic criteria and resampling-based techniques. We then illustrate that using the EDC for real corneas results in models that are in closer agreement with clinical expectations and provides means for distinguishing normal corneal surfaces from astigmatic and keratoconic surfaces.

Using complex network metrics to predict the persistence of metapopulations with asymmetric connectivity patterns

Almost all metapopulation modelling assumes that connectivity between patches is only a function of distance, and is therefore symmetric. However, connectivity will not depend only on the distance between the patches, as some paths are easy to traverse, while others are difficult. When colonising organisms interact with the heterogeneous landscape between patches, connectivity patterns will invariably be asymmetric. There have been few attempts to theoretically assess the effects of asymmetric connectivity patterns on the dynamics of metapopulations. In this paper, we use the framework of complex networks to investigate whether metapopulation dynamics can be determined by directly analysing the asymmetric connectivity patterns that link the patches. Our analyses focus on “patch occupancy” metapopulation models, which only consider whether a patch is occupied or not. We propose three easily calculated network metrics: the “asymmetry” and “average path strength” of the connectivity pattern, and the “centrality” of each patch. Together, these metrics can be used to predict the length of time a metapopulation is expected to persist, and the relative contribution of each patch to a metapopulation’s viability. Our results clearly demonstrate the negative effect that asymmetry has on metapopulation persistence. Complex network analyses represent a useful new tool for understanding the dynamics of species existing in fragmented landscapes, particularly those existing in large metapopulations.

Higher-Order spectra of nonlinear polynomial models for Chua's circuit

Polynomial models are shown to simulate accurately the quadratic and cubic nonlinear interactions (e.g. higher-order spectra) of time series of voltages measured in Chua's circuit. For circuit parameters resulting in a spiral attractor, bispectra and trispectra of the polynomial model are similar to those from the measured time series, suggesting that the individual interactions between triads and quartets of Fourier components that govern the process dynamics are modeled accurately. For parameters that produce the double-scroll attractor, both measured and modeled time series have small bispectra, but nonzero trispectra, consistent with higher-than-second order nonlinearities dominating the chaos.

The acute adaptations of normal and pathological human Achilles tendons to eccentric and concentric exercise

Eccentric exercise is the conservative treatment of choice for mid-portion Achilles tendinopathy. While there is a growing body of evidence supporting the medium to long term efficacy of eccentric exercise in Achilles tendinopathy treatment, very few studies have investigated the short term response of the tendon to eccentric exercise. Moreover, the mechanisms through which tendinopathy symptom resolution occurs remain to be established. The primary purpose of this thesis was to investigate the acute adaptations of the Achilles tendon to, and the biomechanical characteristics of, the eccentric exercise protocol used for Achilles tendinopathy rehabilitation and a concentric equivalent. The research was conducted with an orientation towards exploring potential mechanisms through which eccentric exercise may bring about a resolution of tendinopathy symptoms. Specifically, the morphology of tendinopathic and normal Achilles tendons was monitored using high resolution sonography prior to and following eccentric and concentric exercise, to facilitate comparison between the treatment of choice and a similar alternative. To date, the only proposed mechanism through which eccentric exercise is thought to result in symptom resolution is the increased variability in motor output force observed during eccentric exercise. This thesis expanded upon prior work by investigating the variability in motor output force recorded during eccentric and concentric exercises, when performed at two different knee joint angles, by limbs with and without symptomatic tendinopathy. The methodological phase of the research focused on establishing the reliability of measures of tendon thickness, tendon echogenicity, electromyography (EMG) of the Triceps Surae and the standard deviation (SD) and power spectral density (PSD) of the vertical ground reaction force (VGRF). These analyses facilitated comparison between the error in the measurements and experimental differences identified as statistically significant, so that the importance and meaning of the experimental differences could be established. One potential limitation of monitoring the morphological response of the Achilles tendon to exercise loading is that the Achilles tendon is continually exposed to additional loading as participants complete the walking required to carry out their necessary daily tasks. The specific purpose of the last experiment in the methodological phase was to evaluate the effect of incidental walking activity on Achilles tendon morphology. The results of this study indicated that walking activity could decrease Achilles tendon thickness (negative diametral strain) and that the decrease in thickness was dependent on both the amount of walking completed and the proximity of walking activity to the sonographic examination. Thus, incidental walking activity was identified as a potentially confounding factor for future experiments which endeavoured to monitor changes in tendon thickness with exercise loading. In the experimental phase of this thesis the thickness of Achilles tendons was monitored prior to and following isolated eccentric and concentric exercise. The initial pilot study demonstrated that eccentric exercise resulted in a greater acute decrease in Achilles tendon thickness (greater diametral strain) compared to an equivalent concentric exercise, in participants with no history of Achilles tendon pain. This experiment was then expanded to incorporate participants with unilateral Achilles tendinopathy. The major finding of this experiment was that the acute decrease in Achilles tendon thickness observed following eccentric exercise was modified by the presence of tendinopathy, with a smaller decrease (less diametral strain) noted for tendinopathic compared to healthy control tendon. Based on in vitro evidence a decrease in tendon thickness is believed to reflect extrusion of fluid from the tendon with loading. This process would appear to be limited by the presence of pathology and is hypothesised to be a result of the changes in tendon structure associated with tendinopathy. Load induced fluid movement may be important to the maintenance of tendon homeostasis and structure as it has the potential to enhance molecular movement and stimulate tendon remodelling. On this basis eccentric exercise may be more beneficial to the tendon than concentric exercise. Finally, EMG and motor output force variability (SD and PSD of VGRF) were investigated while participants with and without tendinopathy performed the eccentric and concentric exercises. Although between condition differences were identified as statistically significant for a number of force variability parameters, the differences were not greater than the limits of agreement for repeated measures. Consequently the meaning and importance of these findings were questioned. Interestingly, the EMG amplitude of all three Triceps Surae muscles did not vary with knee joint angle during the performance of eccentric exercise. This raises questions pertaining to the functional importance of performing the eccentric exercise protocol at each of the two knee joint angles as it is currently prescribed. EMG amplitude was significantly greater during concentric compared to eccentric muscle actions. Differences in the muscle activation patterns may result in different stress distributions within the tendon and be related to the different diametral strain responses observed for eccentric and concentric muscle actions.

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.

Rate of torque and electromyographic development during anticipated eccentric contraction is lower in previously strained hamstrings

Background: Hamstring strain injuries are prevalent in sport and re-injury rates have been high for many years. Whilst much focus has centred on the impact of previous hamstring strain injury on maximal eccentric strength, high rates of torque development is also of interest, given the important role of the hamstrings during the terminal swing phase of running. The impact of prior strain injury on myoelectrical activity of the hamstrings during tasks requiring high rates of torque development has received little attention. Purpose: To determine if recreational athletes with a history of unilateral hamstring strain injury, who have returned to training and competition, will exhibit lower levels of myoelectrical activity during eccentric contraction, rate of torque development and impulse 30, 50 and 100ms after the onset of myoelectrical activity or torque development in the previously injured limb compared to the uninjured limb. Study design: Case-control study Methods: Twenty-six recreational athletes were recruited. Of these, 13 athletes had a history of unilateral hamstring strain injury (all confined to biceps femoris long head) and 13 had no history of hamstring strain injury. Following familiarisation, all athletes undertook isokinetic dynamometry testing and surface electromyography assessment of the biceps femoris long head and medial hamstrings during eccentric contractions at -60 and -1800.s-1. Results: In the injured limb of the injured group, compared to the contralateral uninjured limb rate of torque development and impulse was lower during -600.s-1 eccentric contractions at 50 (RTD, injured limb = 312.27 ± 191.78Nm.s-1 vs. uninjured limb = 518.54 ± 172.81Nm.s-1, p=0.008; IMP, injured limb = 0.73 ± 0.30 Nm.s vs. uninjured limb = 0.97 ± 0.23 Nm.s, p=0.005) and 100ms (RTD, injured limb = 280.03 ± 131.42Nm.s-1 vs. uninjured limb = 460.54.54 ± 152.94Nm.s-1,p=0.001; IMP, injured limb = 2.15 ± 0.89 Nm.s vs. uninjured limb = 3.07 ± 0.63 Nm.s, p<0.001) after the onset of contraction. Biceps femoris long head muscle activation was lower at 100ms at both contraction speeds (-600.s-1, normalised iEMG activity (x1000), injured limb = 26.25 ± 10.11 vs. uninjured limb 33.57 ± 8.29, p=0.009; -1800.s-1, normalised iEMG activity (x1000), injured limb = 31.16 ± 10.01 vs. uninjured limb 39.64 ± 8.36, p=0.009). Medial hamstring activation did not differ between limbs in the injured group. Comparisons in the uninjured group showed no significant between limbs difference for any variables. Conclusion: Previously injured hamstrings displayed lower rate of torque development and impulse during slow maximal eccentric contraction compared to the contralateral uninjured limb. Lower myoelectrical activity was confined to the biceps femoris long head. Regardless of whether these deficits are the cause of or the result of injury, these findings could have important implications for hamstring strain injury and re-injury. Particularly, given the importance of high levels of muscle activity to bring about specific muscular adaptations, lower levels of myoelectrical activity may limit the adaptive response to rehabilitation interventions and suggest greater attention be given to neural function of the knee flexors following hamstring strain injury.

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.

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.