Biomedical subjects

William T Stauber

Publications and source records attributed to William T Stauber.

8 recordsLinked to original sources

PubMed2006

Transforming growth factor-beta following skeletal muscle strain injury in rats.

Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine implicated in inflammatory processes, wound healing, and fibrosis. In muscle diseases (i.e., dystrophy and inflammatory myopathy) and in animal models of muscle injury (i.e., produced by cardiotoxin, laceration, and eccentric contractions), increased TGF-beta was associated with muscle fibrosis and healing. Although TGF-beta transcript abundance was increased following injury, many studies presume that TGF-beta protein was also active as evident by increases in collagen transcript abundance. The purpose was to determine whether TGF-beta protein is present and active 48 h following injury. Using female rats, muscle strains were produced by stretching (50 stretches) the plantar flexor muscles. Forty-eight hours following injury, the medial gastrocnemius was removed and compartmentalized into five equal segments. Damaged myofibers with intracellular concanavalin A staining were counted. The percentage of damaged myofibers was significantly greater in the distal-most segment. TGF-beta was assessed by using immunohistochemistry, RT-PCR, and immunoblot analysis. Immunohistochemistry revealed the presence of TGF-beta1 in areas of myofiber injury, whereas TGF-beta2 was not detected. Increases in TGF-beta1 and TGF-beta2 transcript abundance following strain injury were documented by RT-PCR analysis. Increases in TGF-beta1 and TGF-beta2 precursor abundance were observed following strain injury by using immunoblot analysis but there was no change in active TGF-beta abundance. Although there was no correlation between the amount of cellular injury and TGF-beta transcript and protein abundance, elevated levels of TGF-beta1 and TGF-beta2 precursor proteins were present in strain-injured skeletal muscles 48 h after injury.

Animals↗

PubMed2005

Streptomycin and EDTA decrease the number of desmin-negative fibers following stretch injury.

Streptomycin and ethylene diamine tetraacetic acid (EDTA) were used to examine the role of extracellular calcium in stretch-induced muscle injury. Streptomycin was injected in one group of rats, three times daily for 8 days (S, 300 mg.kg(-1).day(-1) intraperitoneally). In another group, EDTA was administered (150 mg.kg(-1) IP) 20 min before and 24 h after the injury protocol. Untreated rats (C) served as controls. Muscle injury was produced by 40 stretches of active dorsiflexor muscles by ankle rotation from 80 degrees to 130 degrees (velocity 1.75 rad.s(-1)). Ten minutes after the injury protocols, all animals lost the same amount of isometric force at both low and high stimulation frequencies (20 HZ; S, 56 +/- 6%; EDTA, 47 +/- 7%; C, 55 +/- 4%) and 120 HZ; S, 11 +/- 3%, EDTA, 13 +/- 3%; C, 11 +/- 3%). Tibialis anterior (TA) muscles were removed after 48 h for morphometric analysis. In both streptomycin-and EDTA-treated rats, the percent of injured (i.e., desmin-negative) myofibers in TA was reduced compared to untreated, injured muscles (S, 0.35 +/- 0.08%; EDTA, 0.64 +/- 0.19%; C, 1.81 +/- 0.43%). Thus, streptomycin and EDTA treatment did not alter the development of muscle weakness (i.e., isometric force deficit), but almost abolished the histopathologic changes. This study shows that the mechanisms for muscle weakness and histopathologic changes (inflammation) following repeated muscle strains can largely be dissociated from each other and helps explain why there is no correlation between isometric force deficits and the number of pathologic cells.

Animals↗

PubMed2004

Factors involved in strain-induced injury in skeletal muscles and outcomes of prolonged exposures.

Repetitive motion disorders can involve lengthening of skeletal muscles to perform braking actions to decelerate limbs under load often resulting in muscle strains and injury. Injury is a loss of isometric force (weakness) requiring days to recover. The capacity of skeletal muscle to tolerate repeated strains is dependent on multiple factors including individual variation. The most important factors producing muscle strain injury are the magnitude of the resisting force (peak-stretch force) and the number of strains. Other factors such as muscle length and fiber type contribute to the susceptibility to injury as well, but to a lesser degree. Strain injury can also lead to inflammation and pain. Chronic exposure to repeated strains can result in fibrosis that is not completely reversed after months of rest. Long rest times appear to be the only factor reported to prevent inflammation in rats following repeated strain injury. Further understanding of the mechanism for prevention of histopathologic changes by long rest times should provide a rationale for prevention of negative outcomes.

Biomechanical Phenomena↗

PubMed2003

Attenuation of stretch-induced histopathologic changes of skeletal muscles by quinacrine.

Quinacrine is an inhibitor of phospholipase A(2), an enzyme thought to be involved in activity-related injury of skeletal muscles. Histopathologic changes after injury by stretches of activated plantar-flexor muscles were measured in untreated and quinacrine-treated rats. On day 4 of treatment (50 mg.kg(-1) intraperitoneally for 5 days), 30 stretches were induced by ankle rotation after muscles reached a maximal isometric force. During the stretch protocol, peak stretch forces and isometric force deficits after each stretch [total deficits 56.7 +/- 2.8% (untreated rats) and 59.6 +/- 1.7% (quinacrine-treated rats)] were similar for both groups (n = 6 each). Two days after the stretch protocol, histopathologic changes were evaluated using antibody staining on cross-sections of gastrocnemius medialis muscles. Swollen myofibers devoid of desmin were identified. Similar cells, but not all swollen myofibers, in adjacent sections stained for albumin. Quinacrine reduced the number of desmin-negative and albumin-positive cells by 88% (P < 0.05) and 84% (P < 0.05), indicating that it attenuated histopathologic changes that follow stretch injury of activated skeletal muscles. Histopathologic changes following muscle injury or myopathic disease may thus be reduced or even prevented by selective drug intervention, thereby reducing the risk of muscle fibrosis. Muscle Nerve 27: 65-71, 2003

Albumins↗

PubMed2002

Prevention of histopathologic changes from 30 repeated stretches of active rat skeletal muscles by long inter-stretch rest times.

This study was performed to examine the protective effect of a long rest between stretches of activated rat plantar flexor muscles on immediate functional and delayed structural signs of injury. Plantar flexor muscles activated by nerve stimulation by ankle rotation from 1.57 to 0.70 rad under anesthesia (brevital) were stretched 30 times. Three groups of female Sprague Dawley rats were tested: (1) long inter-stretch (180 s, S180), (2) short inter-stretch (40 s, S40), and (3) short inter-isometric contraction (40 s, IC40) times. Isometric and peak stretch forces during the stretch protocols and force-frequency relationships before and 1 h after the stretching protocols were measured. Histopathologic changes were evaluated in medial gastrocnemius muscle samples using antibodies to cellular (actin, desmin, dystrophin, fast myosin) and extracellular (laminin, albumin, complement C3) proteins and markers for neutrophils (W3/13) and macrophages (ED1). Both stretch protocols produced the same force deficits [mean (SEM)] [S40 56.7 (2.1)%, S180 51.3 (3.7)%] with little recovery within 1 h. After 2 days, histopathologic changes were present only in samples from the S40 protocol including desmin negative fibers [162 (32)] which stained for albumin, complement C3, laminin, actin and fast myosin. Many of the necrotic fibers also contained infiltrating neutrophils and macrophages. In summary, histopathologic changes in rat gastrocnemius muscle following repeated stretch injury was prevented by long inter-stretch rests.

Animals↗

PubMed2002

Force deficits by stretches of activated muscles with constant or increasing velocity.

PURPOSE: Force deficits produced by constant (CV) versus increasing velocity (IV) stretches of rat plantar flexor muscles at low and high levels of nerve activation were studied. METHODS: Twenty repeated stretches were imposed on isometric contractions by ankle rotation from 90 degrees to 40 degrees at 300 degrees.s(-1) and at 3000 degrees.s(-2) during 80-Hz (CV80 and IV80) and 20-Hz stimulation (CV20 and IV20). Rest periods between contractions were 3 min. Isometric and peak stretch forces during the stretch protocols and force-frequency relationships before and 1 h after the stretch protocols were measured. RESULTS: Peak stretch forces were similar for IV80-CV80 and for IV20-CV20 rats but were lower for IV20-CV20 than for IV80-CV80 rats throughout the stretch protocol. At the end of the stretch protocol, isometric force deficits were similar for IV80 (49.9 +/- 2.1%) and CV80 (54.5 +/- 2.5%) and for IV20 (16.4 +/- 2.8%) and CV20 (15.8 +/- 1.9%) but lower for IV20-CV20 rats. In contrast, for all groups, deficits in peak stretch force were similar at the end of the stretch protocol (IV80: 35.0 +/- 1.8%, CV80: 32.3 +/- 2.2%, IV20: 26.8 +/- 3.6%, CV20: 28.0 +/- 2.0%). After 1 h, isometric force deficits were similar for either IV80-CV80 or IV20-CV20 at 5, 10, 20, 40, 60, and 80 Hz stimulation but were lower for IV20-CV20. CONCLUSIONS: Variation in velocity of ankle rotation with similar peak stretch forces did not influence the amount of stretch-induced force deficits. High peak stretch forces produced greater isometric force deficits than low peak stretch forces, but the relative loss in peak stretch force was not force dependent. Different mechanisms may account for isometric force deficits and peak stretch force deficits caused by repeated stretches of activated skeletal muscles.

Acceleration↗

PubMed2002

Fatigue and recovery at long and short muscle lengths after eccentric training.

PURPOSE: To determine the effects of high-speed eccentric training of rat plantar flexor muscles on: 1) maximum (120 Hz) force at 90 degrees ankle position; 2) fatigue (40 concentric muscle actions, ROM 50 degrees) and recovery (6 concentric muscle actions) tested at short or long muscle lengths; and 3) low-frequency fatigue. METHODS: Training consisted of eccentric muscle actions from ankle positions of 140 degrees to 40 degrees (velocity approximately 400 degrees x s(-1)) followed by unresisted concentric muscle actions (5 x 10 repetitions, 5 d x wk(-1) for 6 wk). Fatigue was induced by concentric muscle actions with a rest of 12.5 s between muscle actions, and recovery consisted of equivalent concentric muscle actions performed every 5 min for 30 min. Low-frequency fatigue was measured 35 min after testing at 90 degrees ankle position by using the ratio of isometric force produced by 20- and 100-Hz stimulation frequencies. RESULTS: Eccentric training increased maximal isometric force per muscle weight by 22% whereas muscle weights were unchanged. In control muscles (C), isometric force immediately preceding each concentric muscle action decreased more at long lengths than at short lengths during the fatigue protocol; this length-dependent difference disappeared after 30 min of recovery. At short lengths, isometric force decreased less in trained muscles (T) (C: 78.4 +/- 3.6%; T: 59.6 +/- 4.4%) and recovered more during the following 30-min period (C: 84.7 +/- 2.5%; T: 95.4 +/- 2.8% of initial values). Changes in F20/F100 were smaller for trained muscles (C: 35.4 +/- 2.0%; T: 22.0 +/- 1.4%). CONCLUSIONS: High-speed eccentric training (5 d x wk(-1) for 6 wk) reduced fatigability and enhanced recovery mainly at long muscle lengths. It also reduced low-frequency fatigue, which may be attributed to alterations in intracellular calcium handling.

Adaptation, Physiological↗

PubMed2002

Effect of contraction history on torque deficits by stretches of active rat skeletal muscles.

Effects of contraction history on torque deficits by stretches of active skeletal muscles were examined. After three contractions using maximal and submaximal activation (80 and 20 Hz) at an ankle position of 40 degrees (i.e., long muscle length) and with maximal activation at 120 degrees (i.e., short muscle length), the isometric and stretch torques (15 stretches) of rat plantar flexor muscles (bout 1) were measured. Controls were unconditioned. Stretches (i.e., ankle rotation from 90 degrees to 40 degrees, velocity: 50 degrees. s-1) were imposed on maximal isometric contractions at 90 degrees (i.e., preloaded stretches). All groups performed a second bout following 2 hours of rest after bout 1. After maximal contractions at long muscle length, preload torque at 90 degrees and stretch torque at 40 degrees for stretch 1 of bout 1 were 25% and 18% lower than the other groups. However, for all groups, bout 1 ended and bout 2 began and ended with similar isometric and stretch torques. Stretches early in bout 2, with preloads similar to stretches in bout 1, had greater stretch torques resulting in larger torque deficits. Torque deficits, possibly caused by damage to muscle structures and excitation-contraction uncoupling, were not prevented by a history of isometric contractions. Different contraction histories can result in similar isometric torques but different stretch torques.

Animals↗