Long-term daily vibration exposure alters current perception threshold (CPT) sensitivity and myelinated axons in a rat-tail model of vibration-induced injury.

Repeated exposure to hand-transmitted vibration through the use of powered hand tools may result in pain and progressive reductions in tactile sensitivity. The goal of the present study was to use an established animal model of vibration-induced injury to characterize changes in sensory nerve function and cellular mechanisms associated with these alterations. Sensory nerve function was assessed weekly using the current perception threshold test and tail-flick analgesia test in male Sprague-Dawley rats exposed to 28 d of tail vibration. After 28 d of exposure, Aß fiber sensitivity was reduced. This reduction in sensitivity was partly attributed to structural disruption of myelin. In addition, the decrease in sensitivity was also associated with a reduction in myelin basic protein and 2',3'- cyclic nucleotide phosphodiasterase (CNPase) staining in tail nerves, and an increase in circulating calcitonin gene-related peptide (CGRP) concentrations. Changes in Aß fiber sensitivity and CGRP concentrations may serve as early markers of vibration-induced injury in peripheral nerves. It is conceivable that these markers may be utilized to monitor sensorineural alterations in workers exposed to vibration to potentially prevent additional injury.

Recovery of vascular function after exposure to a single bout of segmental vibration.

Work rotation schedules may be used to reduce the negative effects of vibration on vascular function. This study determined how long it takes vascular function to recover after a single exposure to vibration in rats (125 Hz, acceleration 5 g). The responsiveness of rat-tail arteries to the vasoconstricting factor UK14304, an α2C-adrenoreceptor agonist, and the vasodilating factor acetylcholine (ACh) were measured ex vivo 1, 2, 7, or 9 d after exposure to a single bout of vibration. Vasoconstriction induced by UK14304 returned to control levels after 1 d of recovery. However, re-dilation induced by ACh did not return to baseline until after 9 d of recovery. Exposure to vibration exerted prolonged effects on peripheral vascular function, and altered vascular responses to a subsequent exposure. To optimize the positive results of work rotation schedules, it is suggested that studies assessing recovery of vascular function after exposure to a single bout of vibration be performed in humans.

Acute effects of COREXIT EC9500A on cardiovascular functions in rats.

These studies characterized cardiovascular responses after an acute inhalation exposure to COREXIT EC9500A, the oil dispersant used in the Deepwater Horizon oil spill. Male Sprague-Dawley rats underwent a single 5-h inhalation exposure to COREXIT EC9500A (average exposure level 27.12 mg/m(3)) or air. On d 1 and 7 following the exposure, rats were implanted with indwelling catheters and changes in heart rate and blood pressure were assessed in response to increasing levels of adrenoreceptor agonists. A separate group of rats was euthanized at the same time points, ventral tail arteries were dissected, and vascular tone along with dose-dependent responses to vasoconstricting and dilating factors were assessed in vitro. Agonist-induced dose-dependent increases in heart rate and blood pressure were greater in COREXIT EC9500A-exposed than in air-exposed rats at 1 d but not 7 d after the exposure. COREXIT EC9500A exposure also induced a rise in basal tone and reduced responsiveness of tail arteries to acetylcholine-induced vasodilation at 1 d but not 7 d following the exposure. These findings demonstrate that an acute exposure to COREXIT EC9500A exerts transient effects on cardiovascular and peripheral vascular functions.

Control and quantitation of voluntary weight-lifting performance of rats.

The present paper describes an exercise model that produces a voluntary hindlimb weight-lifting response. Each rat was operantly conditioned to enter a vertical tube, insert its head into a weighted ring (either 70 g or 700 g), lift the ring until its nose interrupted an infrared detector, and then lower the ring. Load cells measured the external force generated, and displacement transducers measured the vertical displacement of the ring during each lifting and lowering movement. The apparatus and training procedures were computer automated. Peak force, velocity, work, and power were calculated for each movement. Rats in both groups easily acquired the task after 12-15 training sessions, on average, conducted 5 days/wk. Once rats were trained, the lifting patterns were quite stable during several more weeks of posttraining exercise; however, the lighter 70-g load gave rise to more variable performances across rats. Results demonstrate the utility of quantitating the biomechanics of volitional movements and suggest that the present model can establish and maintain controlled repetitive movements necessary for studies of adaptation and/or injury in muscles, tendon, and bone.

Volitional Weight-Lifting in Rats Promotes Adaptation via Performance and Muscle Morphology prior to Gains in Muscle Mass.

Investigation of volitional animal models of resistance training has been instrumental in our understanding of adaptive training. However, these studies have lacked reactive force measurements, a precise performance measure, and morphological analysis at a distinct phase of training - when initial strength gains precede muscle hypertrophy. Our aim was to expose rats to one month of training (70 or 700 g load) on a custom-designed weight-lifting apparatus for analysis of reactive forces and muscle morphology prior to muscle hypertrophy. Exclusively following 700 g load training, forces increased by 21% whereas muscle masses remained unaltered. For soleus (SOL) and tibialis anterior (TA) muscles, 700 g load training increased muscle fiber number per unit area by ∼20% and decreased muscle fiber area by ∼20%. Additionally, number of muscle fibers per section increased by 18% for SOL muscles. These results establish that distinct morphological alterations accompany early strength gains in a volitional animal model of load-dependent adaptive resistance training.

The effects of impact vibration on peripheral blood vessels and nerves.

Research regarding the risk of developing hand-arm vibration syndrome after exposure to impact vibration has produced conflicting results. This study used an established animal model of vibration-induced dysfunction to determine how exposure to impact vibration affects peripheral blood vessels and nerves. The tails of male rats were exposed to a single bout of impact vibration (15 min exposure, at a dominant frequency of 30 Hz and an unweighted acceleration of approximately 345 m/s(2)) generated by a riveting hammer. Responsiveness of the ventral tail artery to adrenoreceptor-mediated vasoconstriction and acetylcholine-mediated re-dilation was measured ex vivo. Ventral tail nerves and nerve endings in the skin were assessed using morphological and immunohistochemical techniques. Impact vibration did not alter vascular responsiveness to any factors or affect trunk nerves. However, 4 days following exposure there was an increase in protein-gene product (PGP) 9.5 staining around hair follicles. A single exposure to impact vibration, with the exposure characteristics described above, affects peripheral nerves but not blood vessels.

Characterization of frequency-dependent responses of the vascular system to repetitive vibration.

OBJECTIVE: Occupational exposure to hand-transmitted vibration can result in damage to nerves and sensory loss. The goal of this study was to assess the frequency-dependent effects of repeated bouts of vibration on sensory nerve function and associated changes in nerves. METHODS: The tails of rats were exposed to vibration at 62.5, 125, or 250 Hz (constant acceleration of 49 m/s2) for 10 days. The effects on sensory nerve function, nerve morphology, and transcript expression in ventral tail nerves were measured. RESULTS: Vibration at all frequencies had effects on nerve function and physiology. However, the effects tended to be more prominent with exposure at 250 Hz. CONCLUSION: Exposure to vibration has detrimental effects on sensory nerve function and physiology. However, many of these changes are more prominent at 250-Hz exposure than at lower frequencies.

Characterization of frequency-dependent responses of the vascular system to repetitive vibration.

OBJECTIVE: The current frequency weighting proposed in the International Standards Organization-5349 standard may underestimate the risk of injury associated with exposure to vibration >100 Hz. The goal of this study was to assess the frequency-dependent responses of the peripheral vascular system to repeated bouts of vibration. METHODS: The effects of exposure to vibration at 62.5, 125, or 250 Hz (constant acceleration of 49 m/s2) on vascular morphology, oxidative stress, inflammation, and gene expression were examined in the ventral tail artery of rats. RESULTS: Vascular responses indicative of dysfunction (eg, remodeling and oxidative activity) became more pronounced as the frequency of the exposure increased. CONCLUSION: Exposure to vibration frequencies that induce the greatest stress and strain on the tail (ie, >100 Hz) result in vascular changes indicative of dysfunction.