Earlier Fatigue Research Articles

Acute oral digoxin in healthy adults hastens fatigue and increases plasma K+ during intense exercise, despite preserved skeletal muscle Na+,K+-ATPase.

We investigated acute effects of the Na+,K+-ATPase (NKA) inhibitor, digoxin, on muscle NKA content and isoforms, arterial plasma [K+] ([K+]a) and fatigue with intense exercise. In a randomised, crossover, double-blind design, 10 healthy adults ingested 0.50mg digoxin (DIG) or placebo (CON) 60min before cycling for 1min at 60% then at 95% until fatigue. Pre- and post-exercise muscle biopsies were analysed for [3H]-ouabain binding site content without (OB-Fab) and after incubation in digoxin antibody (OB+Fab) and NKA α1-2 and β1-2 isoform proteins. In DIG, pre-exercise serum [digoxin] reached 3.36 (0.80) nM [mean (SD)] and muscle NKA-digoxin occupancy was 8.2%. Muscle OB-Fab did not differ between trials, whereas OB+Fab was higher in DIG than CON (8.1%, treatment main effect, P=0.001), whilst muscle NKA α1-2 and β1-2 abundances were unchanged by digoxin. Fatigue occurred earlier in DIG than CON [-7.7%, 2.90 (0.77) vs. 3.14 (0.86) min, respectively; P=0.037]. [K+]a increased during exercise until 1min post-exercise (P=0.001), and fell below baseline at 3-10 (P=0.001) and 20min post-exercise (P=0.022, time main effect). In DIG, [K+]a (P=0.035, treatment effect) and [K+]a rise pre-fatigue were greater [1.64 (0.73) vs. 1.55 (0.73), P=0.016], with lesser post-exercise [K+]a decline than CON [-2.55 (0.71) vs. -2.74 (0.62) mM, respectively, P=0.003]. Preserved muscle OB-Fab with digoxin, yet increased OB+Fab with unchanged NKA isoforms, suggests a rapid regulatory assembly of existing NKA α and β subunits exists to preserve muscle NKA capacity. Nonetheless, functional protection against digoxin was incomplete, with earlier fatigue and perturbed [K+]a with exercise. KEY POINTS: Intense exercise causes marked potassium (K+) shifts out of contracting muscle cells, which may contribute to muscle fatigue. Muscle and systemic K+ perturbations with exercise are largely regulated by increased activity of Na+,K+-ATPase in muscle, which can be specifically inhibited by the cardiac glycoside, digoxin. We found that acute oral digoxin in healthy adults reduced time to fatigue during intense exercise, elevated the rise in arterial plasma K+ concentration during exercise and slowed K+ concentration decline post-exercise. Muscle functional Na+,K+-ATPase content was not reduced by acute digoxin, despite an 8.2% digoxin occupancy, and was unchanged at fatigue. Muscle Na+,K+-ATPase isoform protein abundances were unchanged by digoxin or fatigue. These suggest possible rapid assembly of existing subunits into functional pumps. Thus, acute digoxin impaired performance and exacerbated plasma K+ disturbances with intense, fatiguing exercise in healthy participants. These occurred despite the preservation of functional Na+,K+-ATPase in muscle.

Neuromuscular and mean force changes during a fatiguing bout of exercise with and without blood flow restriction

Surface electromyography (EMG) and mean force can be used to identify motor unit excitation and fatigue. Low-load resistance training with blood flow restriction (LL+BFR) may result in earlier fatigue and maximal muscle fibre recruitment compared to low-load resistance training (LL). The purpose of this investigation was to examine EMG and force responses during LL versus LL+BFR. Thirteen males (mean ± standard deviation = 24±4 years) completed a bout (1×30) of leg extension muscle actions at 30% of their 1 repetition maximum LL and LL+BFR while force, EMG amplitude, and EMG mean power frequency (EMG MPF) were recorded. EMG amplitude increased (74.2%) and EMG MPF decreased (22.6%) similarly during both conditions. There was no significant difference in mean force during the first 3 repetitions between LL+BFR (477.3±132.3 N) and LL (524.3±235.1 N) conditions, but mean force was lower during the last 3 repetitions for LL+BFR (459.7±179.3 N) compared to LL (605.4±276.4 N). The results of the present study indicated that a fatiguing bout of leg extension muscle actions performed LL and LL+BFR elicited similar neuromuscular responses. There was a significant difference in mean force during the last 3 repetitions (LL>LL+BFR) that may have been due to differences in the time spent near peak force.

Dynamic networks of psychological symptoms, impairment, substance use, and social support: The evolution of psychopathology among emerging adults.

Subthreshold/attenuated syndromes are established precursors of full-threshold mood and psychotic disorders. Less is known about the individual symptoms that may precede the development of subthreshold syndromes and associated social/functional outcomes among emerging adults. We modeled two dynamic Bayesian networks (DBN) to investigate associations among self-rated phenomenology and personal/lifestyle factors (role impairment, low social support, and alcohol and substance use) across the 19Up and 25Up waves of the Brisbane Longitudinal Twin Study. We examined whether symptoms and personal/lifestyle factors at 19Up were associated with (a) themselves or different items at 25Up, and (b) onset of a depression-like, hypo-manic-like, or psychotic-like subthreshold syndrome (STS) at 25Up. The first DBN identified 11 items that when endorsed at 19Up were more likely to be reendorsed at 25Up (e.g., hypersomnia, impaired concentration, impaired sleep quality) and seven items that when endorsed at 19Up were associated with different items being endorsed at 25Up (e.g., earlier fatigue and later role impairment; earlier anergia and later somatic pain). In the second DBN, no arcs met our a priori threshold for inclusion. In an exploratory model with no threshold, >20 items at 19Up were associated with progression to an STS at 25Up (with lower statistical confidence); the top five arcs were: feeling threatened by others and a later psychotic-like STS; increased activity and a later hypo-manic-like STS; and anergia, impaired sleep quality, and/or hypersomnia and a later depression-like STS. These probabilistic models identify symptoms and personal/lifestyle factors that might prove useful targets for indicated preventative strategies.

500 Late-Breaking: Heart Rate During Exercise Is Positively Correlated with State IV Mitochondrial Respiration in the Equine Skeletal Muscle

Abstract Mitochondria are critical for oxidative phosphorylation in skeletal muscle, especially in athletic species such as the horse. Mitochondrial respiration increases with physical exercise, but the relationship between mitochondrial respiration and cardiovascular functions are not well described in the horse. The objective of this study was to determine if there is a relationship between heart rate (HR) during and after submaximal exercise tests (SETs) and skeletal muscle mitochondrial respiration in polo ponies. We hypothesized that horses with greater maximum HR and average HR during the exercise tests would have greater mitochondrial respiration in skeletal muscle. Twelve fit polo ponies (14.8 ± 1.7 years old, 10 mares and 2 geldings) were equipped with Polar equine heart rate monitors (Polar Electro Inc., Lake Success, NY) and underwent 26-minute SETs designed to mimic a polo chukker followed by a 30-minute recovery period. Muscle biopsy samples from the semitendinosus muscle were taken 2 weeks prior to the SET to determine mitochondrial oxygen consumption using the Oroboros O2k high-resolution respirometer (Oroboros Instruments, Innsbruck, Austria). Data were analyzed using the PROC CORR procedure (SAS Inst. Inc., Cary, NC). Correlations were considered strong at r > 0.6 and significant at P < 0.05. Maximum HR during SET and state IV respiration were positively correlated (P = 0.02, r = 0.68). Average HR during SET and state IV respiration were also positively correlated (P = 0.01, r = 0.72). However, correlations between maximum and average HR and state III respiration were not as strong (P ≥ 0.05, r < 0.6). These data suggest that state IV mitochondrial respiration (proton leak) in equine skeletal muscle may impact cardiac responses to high-intensity exercise. Horses with higher HR during exercise may have less efficient oxidative phosphorylation, resulting in earlier fatigue and/or greater formation of reactive oxygen species resulting from proton leak.

Impaired Muscle Mitochondrial Function in Familial Partial Lipodystrophy.

Familial partial lipodystrophy (FPL), Dunnigan variety is characterized by skeletal muscle hypertrophy and insulin resistance besides fat loss from the extremities. The cause for the muscle hypertrophy and its functional consequences is not known. To compare muscle strength and endurance, besides muscle protein synthesis rate between subjects with FPL and matched controls (n = 6 in each group). In addition, we studied skeletal muscle mitochondrial function and gene expression pattern to help understand the mechanisms for the observed differences. Body composition by dual-energy X-ray absorptiometry, insulin sensitivity by minimal modelling, assessment of peak muscle strength and fatigue, skeletal muscle biopsy and calculation of muscle protein synthesis rate, mitochondrial respirometry, skeletal muscle transcriptome, proteome, and gene set enrichment analysis. Despite increased muscularity, FPL subjects did not demonstrate increased muscle strength but had earlier fatigue on chest press exercise. Decreased mitochondrial state 3 respiration in the presence of fatty acid substrate was noted, concurrent to elevated muscle lactate and decreased long-chain acylcarnitine. Based on gene transcriptome, there was significant downregulation of many critical metabolic pathways involved in mitochondrial biogenesis and function. Moreover, the overall pattern of gene expression was indicative of accelerated aging in FPL subjects. A lower muscle protein synthesis and downregulation of gene transcripts involved in muscle protein catabolism was observed. Increased muscularity in FPL is not due to increased muscle protein synthesis and is likely due to reduced muscle protein degradation. Impaired mitochondrial function and altered gene expression likely explain the metabolic abnormalities and skeletal muscle dysfunction in FPL subjects.

Safety, Fear and Neuromuscular Responses after a Resisted Knee Extension Performed to Failure in Patients with Severe Haemophilia.

Background: low–moderate intensity strength training to failure increases strength and muscle hypertrophy in healthy people. However, no study assessed the safety and neuromuscular response of training to failure in people with severe haemophilia (PWH). The purpose of the study was to analyse neuromuscular responses, fear of movement, and possible adverse effects in PWH, after knee extensions to failure. Methods: twelve severe PWH in prophylactic treatment performed knee extensions until failure at an intensity of five on the Borg CR10 scale. Normalised values of amplitude (nRMS) and neuromuscular fatigue were determined using surface electromyography for the rectus femoris, vastus medialis, and vastus lateralis. After the exercise, participants were asked about their perceived change in fear of movement, and to report any possible adverse effects. Results: Patients reported no adverse effects or increased fear. The nRMS was maximal for all the muscles before failure, the median frequency decreased, and wavelet index increased during the repetitions. The vastus lateralis demonstrated a higher maximum nRMS threshold and earlier fatigue, albeit with a lower and more progressive overall fatigue. Conclusions: severe PWH with adequate prophylactic treatment can perform knee extensions to task failure using a moderate intensity, without increasing fear of movement, or adverse effects.

Mechanisms of altered skeletal muscle action potentials in the R6/2 mouse model of Huntington's disease.

Huntington's disease (HD) patients suffer from progressive and debilitating motor dysfunction for which only palliative treatment is currently available. Previously, we discovered reduced skeletal muscle Cl- channel (ClC-1) and inwardly rectifying K+ channel (Kir) currents in R6/2 HD transgenic mice. To further investigate the role of ClC-1 and Kir currents in HD skeletal muscle pathology, we measured the effect of reduced ClC-1 and Kir currents on action potential (AP) repetitive firing in R6/2 mice using a two-electrode current clamp. We found that R6/2 APs had a significantly lower peak amplitude, depolarized maximum repolarization, and prolonged decay time compared with wild type (WT). Of these differences, only the maximum repolarization was accounted for by the reduction in ClC-1 and Kir currents, indicating the presence of additional ion channel defects. We found that both KV1.5 and KV3.4 mRNA levels were significantly reduced in R6/2 skeletal muscle compared with WT, which explains the prolonged decay time of R6/2 APs. Overall, we found that APs in WT and R6/2 muscle significantly and progressively change during activity to maintain peak amplitude despite buildup of Na+ channel inactivation. Even with this resilience, the persistently reduced peak amplitude of R6/2 APs is expected to result in earlier fatigue and may help explain the motor impersistence experienced by HD patients. This work lays the foundation to link electrical changes to force generation defects in R6/2 HD mice and to examine the regulatory events controlling APs in WT muscle.

The influence of peripheral arterial disease on lower limb surface myoelectric signals in patients living with type II diabetes mellitus

BackgroundThe aim of this study was to evaluate whether there are any significant differences in muscle activity between individuals living with type II diabetes mellitus (T2DM) and individuals living with T2DM and peripheral arterial disease (PAD), during gait at a self-selected speed. The influence of different stages of PAD on muscle activity during gait was also assessed with the use of surface electromyography (EMG). Research questionDoes PAD affect lower limb muscle activity during gait in the presence of T2DM? MethodsThis quantitative study involves a prospective, comparative, non-experimental subject design. Ninety participants were divided into three groups namely Group A (thirty participants living with T2DM), Group B(i) (thirty participants living with T2DM and mild PAD) and Group B(ii) (thirty participants living with T2DM and severe PAD). Surface electrode sensors were placed according to SENIAM guidelines, on six main lower limb muscles on both limbs. Muscle activity was recorded using a wireless system, where participants were instructed to walk at a self-selected speed on a 10-m walkway. Average Burst RMS was performed and the amplitude (mV) and the duration of muscle activation (s) was analysed. ResultsThere was a significant increase in muscle amplitude and duration of activation in the presence of lower limb ischaemia during gait. The largest significant difference (p = <0.05) in EMG amplitude and duration of activation when looking at the twelve muscles in general was found between participants living with T2DM and participants living with T2DM and severe PAD. SignificanceThe increase in muscle activity indicates that there are musculoskeletal and biomechanical changes in the lower limb musculature with increasing severity of PAD. Higher muscle exertion demands are required during gait which may result in earlier fatigue. EMG tests would be beneficial for detecting muscle dysfunction objectively and non-invasively in T2DM and PAD.

Skeletal Muscle Dysfunction and Metabolic Abnormalities in Individuals with Familial Partial Lipodystrophy Is Associated with Diminished Mitochondrial Fatty Acid Oxidation

Background: Familial Partial Lipodystrophy, Dunnigan variety (FPLD) is characterized by post-natal fat loss leading to severe insulin resistance. Affected individuals also display striking skeletal muscle hypertrophy, but there is limited information on muscle function and energy metabolism. We therefore systematically investigated muscle and mitochondrial function in 6 individuals with FPLD and 6 matched controls. Methods: Body composition and intramyocellular lipid content (IMCL) were assessed by DEXA and magnetic resonance spectroscopy, respectively. Maximal voluntary strength and fatigue were assessed for both recumbent leg press and seated chest press. Vastus lateralis muscle biopsies were obtained prior to and following a high fat (40%) mixed-meal. Oxygen consumption in isolated mitochondria was measured using substrates supporting carbohydrate or lipid-based respiration. Insulin Sensitivity Index (SI) was calculated by minimal modelling. Results: Individuals with FPLD had significantly lower SI, lower body fat content, and higher lean mass. Peak leg press and chest press force were not different, but FPLD individuals had earlier fatigue during chest press (number of repetitions: 15 ± 0.6 vs. 20 ± 0.3, p = 0.01). They also had a 50-60% decrease in state 3 respiration measured using substrates supporting lipid-based respiration (p = 0.04). Further, mitochondrial oxidative capacity showed a strong correlation with muscle fatigue (r = 0.76, p = 0.003), and inversely correlated with fasting and post-prandial lipemia and measures of insulin resistance. Conclusion: Individuals with FPLD have higher lean body mass and lower insulin sensitivity. Despite preserved peak muscle strength, they demonstrated earlier muscle fatigue. Decreased mitochondrial fatty acid oxidative capacity, likely related to elevated IMCL, may contribute to muscular and metabolic abnormalities. Disclosure V. Simha: None. I.R. Lanza: None. N. LeBrasseur: None. K. Klaus: None. J. Port: None. M.C. Laurenti: Other Relationship; Self; GlySens Incorporated. C. Cobelli: Research Support; Self; Sanofi-Aventis. Advisory Panel; Self; Novo Nordisk Inc.. K. Nair: None.

The impact of load carriage exercise on the etiology of neuromuscular fatigue

Purpose: The aim of this review is to highlight scientific evidence about the impact of prolonged load-carrying on the etiology of the neuromuscular (NM) fatigue. This is a big concern to prevent alteration of performance in repeated high intensity tasks during assault despite the earlier fatigue.

Submaximal oxygen cost during incremental exercise in children with developmental coordination disorder

There has been minimal evidence examining the differences in submaximal aerobic power between children with and without probable developmental coordination disorder (pDCD). This is important as most activities of daily living are performed at submaximal levels. The aim of this study was to examine the oxygen cost of work (VO2) performed during an incremental exercise protocol on a cycle ergometer. Subjects with pDCD (n=63) were matched for age and gender to 63 typically developing controls (12-13 years of age) using a nested case-control design. Motor coordination was assessed using the Movement Assessment Battery for Children. Children with pDCD had significantly lower VO2 peak values relative to controls (35.0 vs. 42.9 ml/kg/min, p<0.0001). At the submaximal level, mixed effects modeling demonstrated that, after controlling for relative body fat, and VO2 peak, children with pDCD had consistently greater oxygen cost (VO2 ml/kg/min) compared to controls at any given exercise intensity (p=0.0006). A significant interaction between pDCD and workload indicated that the difference in VO2 at higher workloads is greater than that at lower workloads (p=0.0004). Children with pDCD utilize more oxygen to sustain the same submaximal workload. The implication of these findings is that children with pDCD may experience earlier fatigue than well coordinated individuals when engaging in physical activity.

Physiological Responses and Stroke-Parameter Changes During Interval Swimming in Different Age-Group Female Swimmers

The purpose of the study was to examine the physiological responses, the stroke-parameter changes, and the ability to sustain a velocity corresponding to critical velocity (CV) during interval swimming on female swimmers of different age groups. Eight children (C; age: 10.4 ± 0.6 years), 11 young (Y; age: 13.1 ± 0.4 years), and 7 adults (A; age: 19.9 ± 4.6 years) swam all-out efforts of 50, 100, 200, 400 m for CV and critical stroke rate (CSR) calculation. Subsequently, the swimmers performed an interval training set of 5 × 300-m (C) and 5 × 400-m repetitions (Y and A) at a velocity corresponding to CV. The CV was higher in the Y and A compared with the C group (C: 0.962 ± 0.05, Y: 1.168 ± 0.09, A: 1.217 ± 0.05 m·s(-1), p < 0.05). The velocity of 5 × 300 and 5 × 400 m was not different compared with CV (C: 100 ± 2%, Y: 98 ± 3%, A: 98 ± 3% of CV, p > 0.05). The blood lactate concentration was similar between groups and was maintained steady within each group (C: 4.5 ± 1.4, Y: 4.9 ± 1.4, A: 3.9 ± 1.3 mmol·L(-1), p > 0.05). Heart rate was higher in the C and Y compared with the A group during the last 100 m of each repetition (p < 0.05). Stroke rate remained unchanged during the repetitions and was similar between groups and no different to the CSR (p > 0.05). Stroke length of the fifth repetition was 4.5 ± 4.0% shorter compared with the second repetition in the Y and 5.3 ± 2.0% shorter compared with the first repetition in the A group (p < 0.05). During the 28- to 31-minute duration intermittent swimming, children and young and adult female swimmers were able to sustain CV with a steady and similar blood lactate concentration. Decreased stroke length may indicate an earlier fatigue in young and adult swimmers.

Alveolar gas exchange and tissue deoxygenation during exercise in type 1 diabetes patients and healthy controls

We used near-infrared spectroscopy to investigate whether leg and arm skeletal muscle and cerebral deoxygenation differ during incremental cycling exercise in men with type 1 diabetes (T1D, n=10, mean±SD age 33±7 years) and healthy control men (matched by age, anthrometry, and self-reported physical activity, CON, n=10, 32±7 years) to seek an explanation for lower aerobic capacity (V˙O2peak) often reported in T1D. T1D had lower V˙O2peak (35±4mlkg−1min−1 vs. 43±8mlkg−1min−1, P<0.01) and peak work rate (219±33W vs. 290±44W, P<0.001) than CON. Leg muscle deoxygenation (↑ [deoxyhemoglobin]; ↓ tissue saturation index) was greater in T1D than CON at a given absolute submaximal work rate, but not at peak exercise, while arm muscle and cerebral deoxygenation were similar. Thus, in T1D compared with CON, faster leg muscle deoxygenation suggests limited circulatory ability to increase O2 delivery as a plausible explanation for lower V˙O2peak and earlier fatigue in T1D.

Muscle function, physical performance and body composition changes in men with prostate cancer undergoing androgen deprivation therapy

Prostate cancer (PCa) is the most common visceral malignancy in men with androgen deprivation therapy (ADT) the preferred therapy to suppress testosterone production and hence tumor growth. Despite its effectiveness in lowering testosterone, ADT is associated with side effects including loss of muscle mass, diminished muscle strength, decrements in physical performance, earlier fatigue and declining quality of life. This review reports a survey of the literature with a focus on changes in muscle strength, physical function and body composition, due to short-term and long-term ADT. Studies in these areas are sparse, especially well-controlled, prospective randomized trials. Cross-sectional and longitudinal data (up to 2 years) for men with PCa treated with ADT as well as patients with PCa not receiving ADT and age-matched healthy men are presented when available. Based on limited longitudinal data, the adverse effects of ADT on muscle function, physical performance and body composition occur shortly after the onset of ADT and tend to persist and worsen over time. Exercise training is a safe and effective intervention for mitigating these changes and initial guidelines for exercise program design for men with PCa have been published by the American College of Sports Medicine. Disparities in study duration, types of studies and other patient-specific variables such as time since diagnosis, cancer stage and comorbidities may all affect an understanding of the influence of ADT on health, physical performance and mortality.

Analysis of Time-to-Fatigue for Standing Jobs in Metal Stamping Industry

In metal stamping industry, almost all jobs are practically to be performed in standing position. Standing in a long period of time can lead to muscle fatigue. The objective of this study was to determine time-to-fatigue in the erector spinae, tibialis anterior, and gastrocnemius muscles of twenty production workers in a metal stamping company. The muscles activity was concurrently measured using surface electromyography (sEMG) during beginning, mid, and end of working sessions. Results of study found that gastrocnemius muscle fatigued earlier during all working sessions. In addition, working at the end of working session showed earlier fatigue than the beginning and mid of work days. The study concluded that standing in a long period of time is a cause to muscle fatigue experienced by the production workers.

Influence of Precorrosion on Fatigue Properties of Shot-Peened Aluminium 7075-T651

Abstract Pitting corrosion has a major influence on aging of structural elements made of high-strength aluminium alloys as corrosion pits lead to much earlier fatigue crack initiation under tensile dynamic loading. In order to improve material resistance to corrosion fatigue, it is necessary to reduce pit-tip stresses in the corroded pits areas. Shot peening (SP) is an important and well-known cold working process, having been used in industrial applications for a long time. Shot peening as intense plastic deformation in the thin surface layer affects cold surface hardening by primary inducing favorable residual compressive stresses. It is used in order to increase fatigue strength in operation and to improve fatigue resistance of precorroded material. The paper deals with the surface integrity of shot-peened high-strength 7075-T651 aluminium alloy. The paper describes the effects of SP treatment by presenting analyses of surface roughness measurement, residual stresses, material bending fatigue resistance, fractographic analysis of fatigued specimens, and electrochemical potentiodynamic testing.

Mechanisms of aerobic performance impairment with heat stress and dehydration

Environmental heat stress can challenge the limits of human cardiovascular and temperature regulation, body fluid balance, and thus aerobic performance. This minireview proposes that the cardiovascular adjustments accompanying high skin temperatures (T(sk)), alone or in combination with high core body temperatures (T(c)), provide a primary explanation for impaired aerobic exercise performance in warm-hot environments. The independent (T(sk)) and combined (T(sk) + T(c)) effects of hyperthermia reduce maximal oxygen uptake (Vo(2max)), which leads to higher relative exercise intensity and an exponential decline in aerobic performance at any given exercise workload. Greater relative exercise intensity increases cardiovascular strain, which is a prominent mediator of rated perceived exertion. As a consequence, incremental or constant-rate exercise is more difficult to sustain (earlier fatigue) or requires a slowing of self-paced exercise to achieve a similar sensation of effort. It is proposed that high T(sk) and T(c) impair aerobic performance in tandem primarily through elevated cardiovascular strain, rather than a deterioration in central nervous system (CNS) function or skeletal muscle metabolism. Evaporative sweating is the principal means of heat loss in warm-hot environments where sweat losses frequently exceed fluid intakes. When dehydration exceeds 3% of total body water (2% of body mass) then aerobic performance is consistently impaired independent and additive to heat stress. Dehydration augments hyperthermia and plasma volume reductions, which combine to accentuate cardiovascular strain and reduce Vo(2max). Importantly, the negative performance consequences of dehydration worsen as T(sk) increases.

Residual Stress Prediction and Relaxation in Welded Tubular Joints under Constant Cyclic Loading

In this paper three-dimensional welding simulations were carried out in FE software ANSYS in order to predict transient temperatures and the residual stresses in a three pass welded tubular joints. The thermal analysis and the moving heat source were verified with temperature measurements and the computed residual stresses were verified with hole drilling measurements. Then residual stress relaxation analyses were carried out on the tubular structure, with similar load cases as in earlier fatigue testing on the same tubular joint structures.

Effect of anterior cruciate ligament deficiency on economy of walking and jogging.

The metabolic cost of walking and jogging following injury to the anterior cruciate ligament is unknown. Economy of motion refers to the oxygen consumption for a submaximal work rate. The purpose of this study was to compare the economy of walking and jogging of an anterior cruciate ligament-deficient population with that of a control population without orthopaedic abnormalities. Steady-state oxygen consumption was measured in 30 patients and 98 controls while they were on a treadmill at various speeds. Deficiency of the anterior cruciate ligament was diagnosed arthroscopically. The patients also were tested for isokinetic knee extension-flexion strength, hip flexion, and abduction and adduction strength and underwent arthrometric measurement of anterior tibial displacement. The patients had a statistically significant increase in oxygen consumption when jogging at 160.9 m/min (p = 0.007); however, there was no significant effect of anterior cruciate ligament deficiency on economy at the other speeds tested. The patients had significant deficits in strength of all muscle groups tested. Steady-state oxygen consumption at 160.9 m/min tended to be inversely related to the deficit of strength of knee flexion (r = -0.44, p = 0.07). Arthrometric measurements and chronicity of injury were unrelated to steady-state oxygen consumption. These data indicate that anterior cruciate ligament deficiency increases oxygen consumption during jogging. In long-distance running, this decreased economy translates into significant additional caloric requirements, which may result in earlier fatigue.

Studies on laser- and plasma-welded titanium

In recent years, titanium has become a material of major interest in prosthetic dentistry. Due to its chemical properties, titanium has to be processed differently from conventional alloys. In this paper, two different methods of welding were investigated. Specimens machined from pure titanium rods were fused either by laser welding or plasma welding. Hardness profiles and light microscopy images were taken in the region of the weld. The mechanical properties were tested by alternating bending fatigue tests up to 3 million cycles. Light microscopy images and hardness profiles showed a larger heat-affected zone after plasma welding compared to laser welding. No significant differences comparing fatigue strength could be found between the two methods of welding. However, extreme loads led to earlier fatigue in the plasma-welded specimens. SEM images of the laser-welded joints showed fractures in the welding zone, while the plasma-welded specimens fractured mostly beyond the heat-affected zone. From these results, it can be assumed that both methods are suitable for welding titanium. At the moment, laser welding is the more suitable technique in dentistry because of its lower thermal alteration of the workpieces.