Riveting hammer vibration damages mechanosensory nerve endings.

Hand-arm vibration syndrome (HAVS) is an irreversible neurodegenerative, vasospastic, and musculoskeletal occupational disease of workers who use powered hand tools. The etiology is poorly understood. Neurological symptoms include numbness, tingling, and pain. This study examines impact hammer vibration-induced injury and recoverability of hair mechanosensory innervation. Rat tails were vibrated 12 min/d for 5 weeks followed by 5 week recovery with synchronous non-vibrated controls. Nerve fibers were PGP9.5 immunostained. Lanceolate complex innervation was compared quantitatively in vibrated vs sham. Vibration peak acceleration magnitudes were characterized by frequency power spectral analysis. Average magnitude (2515 m/s2 , root mean squared) in kHz frequencies was 109 times that (23 m/s2 ) in low Hz. Percentage of hairs innervated by lanceolate complexes was 69.1% in 5-week sham and 53.4% in 5-week vibration generating a denervation difference of 15.7% higher in vibration. Hair innervation was 76.9% in 5-weeks recovery sham and 62.0% in 5-week recovery vibration producing a denervation difference 14.9% higher in recovery vibration. Lanceolate number per complex (18.4 ± 0.2) after vibration remained near sham (19.3 ± 0.3), but 44.9% of lanceolate complexes were abnormal in 5 weeks vibrated compared to 18.8% in sham. The largest vibration energies are peak kHz accelerations (approximately 100 000 m/s2 ) from shock waves. The existing ISO 5349-1 standard excludes kHz vibrations, seriously underestimating vibration injury risk. The present study validates the rat tail, impact hammer vibration as a model for investigating irreversible nerve damage. Persistence of higher denervation difference after 5-week recovery suggests repeated vibration injury destroys the capability of lanceolate nerve endings to regenerate.

Use Of Ankle Immobilization In Evaluating Treatments To Promote Longitudinal Muscle Growth In Mice.

INTRODUCTION: Difficulty in modeling congenital contractures (deformities of muscle-tendon unit development that include shortened muscles and lengthened tendons) has limited research of new treatments. METHODS: Early immobilization of the ankle in prepuberal mice was used to produce deformities similar to congenital contractures. Stretch treatment, electrostimulation, and local intramuscular injection of a follistatin analog (FST-288) were assessed as therapeutic interventions for these deformities. RESULTS: Ankle immobilization at full plantarflexion and 90 ° created tendon lengthening and muscle shortening in the tibialis anterior and soleus. Stretch treatment produced minimal evidence for longitudinal muscle growth and electrostimulation provided no additional benefit. Stretch treatment with FST-288 produced greater longitudinal muscle growth and less tendon lengthening, constituting the best treatment response. DISCUSSION: Ankle immobilization recapitulates key morphologic features of congenital contracture, and these features can be mitigated by a combination of stretch and pharmacological approaches that may be useful in patients. Muscle Nerve 58: 718-725, 2018.

Stretch-activated signaling is modulated by stretch magnitude and contraction.

INTRODUCTION: Stretch therapy is commonly utilized to prevent shortening maladaptation of skeletal muscle. Stretch in combination with isometric contraction prevents shortening, but the signaling mechanisms are not understood. METHODS: Using a soleus tenotomy + stretch rat model, the phosphorylation-activation of mechanosensitive kinases (Akt, p70(S6K), p38 MAPK, and ERK1/2) were measured for various stretch magnitudes, set relative to optimal soleus length (Lo). RESULTS: The kinases were not activated by passive stretch until it exceeded the normal physiological range. Stretch + isometric contraction resulted in relatively strong phosphorylation, even at short lengths. CONCLUSIONS: Whereas passive stretch results in kinase phosphorylation only during extreme lengthening, isometric contraction generated pronounced phosphorylation of kinases at Lo and Lo + 25%, indicating stimulation of pathways that lead to the preservation or increase of muscle length. Understanding the effects of passive and active stretch with respect to Lo and contraction is essential for predicting therapeutic outcomes and influencing optimal muscle length.

Preserving sarcomere number after tenotomy requires stretch and contraction.

INTRODUCTION: Passive stretch therapy is utilized to improve the range of motion of chronically shortened muscles. However, human studies show conflicting results as whether passive stretch is clinically effective. METHODS: The soleus muscles of adult rats were tenotomized to induce muscle shortening adaptation. Muscles included were non-treated normal, subjected to daily static stretch, or lengthened and isometrically contracted for 20 min/day. Muscle fiber structure was analyzed histochemically. Sarcomeres per millimeter length were counted to assess the effect of treatment. RESULTS: Passive stretch significantly reduced central core lesion formation, but sarcomere loss was not prevented. The addition of isometric contraction during static stretch significantly (P < 0.001) reduced sarcomere loss. CONCLUSIONS: Passive stretch alone does not prevent shortening adaptation. Contraction is required in combination with stretch to preserve the number of sarcomeres in series. The combination of stretch and contraction is necessary to maintain proper muscle fiber length.

Stretch reduces central core lesions and calcium build-up in tenotomized soleus.

The incidence of skeletal muscle tendon rupture is increasing. The unloaded, shortened muscle undergoes rapid degeneration. Rehabilitation takes 10-12 weeks and includes stretch therapy. Outcomes may be improved by understanding the pathophysiological changes and stretch mechanisms. We investigated the effects of passive stretch on preventing central core lesions in a rat tenotomy model of simulated Achilles tendon rupture. Adult male rats were tenotomized bilaterally. At 7 days, 39% of the soleus fibers possessed central core lesions. Whole muscle calcium concentration progressively increased and plateaued by 4 days. Dantrolene, a calcium release blocker, injected daily for 7 days, reduced central core lesion formation and calcium build-up. Passive stretch, 20 min/day, inhibited central core lesion formation. Calcium increased at 4 days in mitochondria, and stretch prevented this increase. These findings indicate that stretch therapy reduces central core lesion occurrence by preventing calcium elevation in hypershortened muscles.

Comparison of continuous and intermittent vibration effects on rat-tail artery and nerve.

Hand-transmitted vibration from powered-tools can cause peripheral vasospasm and neuropathy. A rat-tail model was used to investigate whether the pattern of vibration influenced the type and severity of tissue damage. The tails of awake rats were vibrated continuously or intermittently for a total of 4 hours at 60 HZ, 49 m/s(2). Nerves and arteries were harvested immediately or 24 hours after treatment. Tails subjected to intermittent vibration showed transiently increased sensitivity to thermal stimuli. Intermittent vibration caused the most nerve injury immediately and 24 hours after vibration. Continuous vibration invoked a persistent reduction in vascular lumen size. Compared to epinephrine-induced transient vacuolation in vascular smooth muscle cells, both continuous and intermittent vibration caused greater persistence of vacuoles, indicating a vibration-induced pathological process. All vibration groups exhibited elevated nitrotyrosine immunoreactivity indicative of free-radical damage. Pattern of vibration exposure may exert a major influence on the type of vibration injury.

Effects of temperature on vibration-induced damage in nerves and arteries.

Vasospastic episodes in hand-arm vibration syndrome are more prevalent among power-tool workers in cold climates. To test whether cold enhances vibration-induced damage in arteries and nerves, tails of Sprague-Dawley rats were vibrated at room temperature (RT) or with tail cooling (<15 degrees C). Cold vibration resulted in a colder tail than either treatment alone. Vibration at both temperatures reduced arterial lumen size. RT vibration generated more vacuoles in arteries than cold vibration. Vibration and cold induced nitration of tyrosine residues in arteries, suggesting free-radical production. Vibration and cold generated similar percentages of myelinated axons with disrupted myelin. Cold with and without vibration caused intraneural edema and dilation of arterioles and venules with blood stasis, whereas vibration alone did not. The similarities, differences, and interactive effects of cold and vibration on nerve and artery damage indicate that temperature is involved mechanistically in the pathophysiology of hand-arm vibration syndrome.

Nifedipine pretreatment reduces vibration-induced vascular damage.

A rat-tail vibration model of hand-arm vibration was employed to test whether preemptive administration of nifedipine (5 mg/kg) to block vasoconstriction prevents vibration-induced arterial damage. The tails of vibrated and nifedipine-pretreated vibrated Sprague-Dawley rats were exposed continuously to 4 h of 60-HZ vibration at 49 m/s(2) rms. In nonvibrated anesthetized rats, the ventral tail arteries were bathed for 15 min in situ in 1 mM epinephrine or 1 mM norepinephrine to induce structural changes indicative of intense vasoconstriction. Arteries were processed for light and electron microscopy 45 min after treatment. Compared to sham control, 4-h vibration significantly (P < 0.01) reduced lumen size, generated endothelial disruption (7.0 +/- 2.6%), elevated nuclear factor of activated T cells c3 (NFATc3) expression in endothelial and smooth muscle cells, and increased smooth muscle cell vacuolization. The findings demonstrate that blockage of vibration-induced vasoconstriction with nifedipine prevents acute vascular damage. Smooth muscle and endothelial cells structurally altered by vasoconstriction are rendered susceptible to damage by vibration.

Evidence for frequency-dependent arterial damage in vibrated rat tails.

The effects of single 4-hr bouts of continuous 30, 60, 120, and 800 Hz tail vibration (49 m/sec2, root mean squared) were compared to assess frequency-amplitude-related structural damage of the ventral caudal artery. Amplitudes were 3.9, 0.98, 0.24, and 0.0055 mm, respectively. Vibrated, sham-vibrated, and normal arteries were processed for light and electron microscopy. The Curry rat tail model of hand-arm vibration (Curry et al. Muscle Nerve 2002;25:527-534) proved well-suited for testing multiple frequencies. NFATc3 immunostaining, an early marker of cell damage, increased in smooth muscle and endothelial cells after 30, 60, and 120 Hz but not 800 Hz. Increased vacuolization, which is indicative of smooth muscle contraction, occurred for all frequencies except 800 Hz. Vacuoles increased in both endothelial and smooth muscle cells after 60 and 120 Hz. Only 30 Hz showed pronounced smooth muscle cell vacuolization along the internal and external elastic membranes, suggesting stretch-mediated contraction from the large amplitude shear stress. Discontinuities in toluidine blue staining of the internal elastic membrane (IEM) increased for all frequencies, indicating vibration-induced structural weakening of this structure. Patches of missing IEM and overlying endothelium occurred in approximately 5% of arteries after 60, 120, and 800 Hz. The pattern of damage after 800 Hz suggests that the IEM is disrupted because it resonates at this frequency. Vibration acceleration stress and smooth muscle contraction appear to be the major contributors to arterial damage. The pattern of vibration-induced arterial damage of smooth muscle and endothelial cells is frequency-amplitude-dependent.

Vibration injury damages arterial endothelial cells.

Prolonged exposure to hand-transmitted vibration can cause debilitating neural and vascular dysfunction in humans. It is unclear whether the pathophysiology involves simultaneous or sequential injury of arteries and nerves. The mechanism of vibration injury was investigated in a rat tail model, containing arteries and nerves structurally similar to those in the human hand. Tails were selectively vibrated for 1 or 9 days with the remainder of the animal at rest. One vibration bout of 4 h/day, 60 HZ, 5 g (49 m/s(2)) acceleration, injured endothelial cells. Injury was signaled by elevated immunostaining for NFATc3 transcription factor. Electron microscopy revealed that vibration for 9 days produced loss and thinning of endothelial cells, with activated platelets coating the exposed subendothelial tissue. Endothelial cells and arterial smooth muscle cells contained double membrane-limited, swollen processes indicative of vasoconstriction-induced damage. Laser doppler surface recording demonstrated that 5 min of vibration significantly diminished tissue blood perfusion. These findings indicate that early injury involves vasoconstriction and denuding of the arterial endothelium.

Thin filament diversity and physiological properties of fast and slow fiber types in astronaut leg muscles.

Slow type I fibers in soleus and fast white (IIa/IIx, IIx), fast red (IIa), and slow red (I) fibers in gastrocnemius were examined electron microscopically and physiologically from pre- and postflight biopsies of four astronauts from the 17-day, Life and Microgravity Sciences Spacelab Shuttle Transport System-78 mission. At 2.5-microm sarcomere length, thick filament density is approximately 1,012 filaments/microm(2) in all fiber types and unchanged by spaceflight. In preflight aldehyde-fixed biopsies, gastrocnemius fibers possess higher percentages (approximately 23%) of short thin filaments than soleus (9%). In type I fibers, spaceflight increases short, thin filament content from 9 to 24% in soleus and from 26 to 31% in gastrocnemius. Thick and thin filament spacing is wider at short sarcomere lengths. The Z-band lattice is also expanded, except for soleus type I fibers with presumably stiffer Z bands. Thin filament packing density correlates directly with specific tension for gastrocnemius fibers but not soleus. Thin filament density is inversely related to shortening velocity in all fibers. Thin filament structural variation contributes to the functional diversity of normal and spaceflight-unloaded muscles.