Effect of diathermy on muscle temperature, electromyography, and mechanomyography.

This study examined the effects of pulsed shortwave diathermy on intramuscular temperature, surface electromyography (EMG), and mechanomyography (MMG) of the vastus lateralis. Thirty-five men were assigned to diathermy (n = 13), sham-diathermy (n = 12), or control (n = 10) groups. Each subject performed isometric maximal voluntary contractions (MVCs) and incremental ramp contractions (10%-90% MVC) before and after treatment. Torque, intramuscular temperature, EMG, and MMG were recorded. Temperature for the diathermy group increased (P

Surface electromyographic amplitude-to-work ratios during isokinetic and isotonic muscle actions.

CONTEXT: Isokinetic and isotonic resistance training exercises are commonly used to increase strength during musculoskeletal rehabilitation programs. Our study was designed to examine the efficacy of isokinetic and isotonic muscle actions using surface electromyographic (EMG) amplitude-to-work ratios (EMG/WK) and to extend previous findings to include a range of isokinetic velocities and isotonic loads. OBJECTIVE: To examine work (WK), surface EMG amplitude, and EMG/WK during concentric-only maximal isokinetic muscle actions at 60, 120, 180, 240, and 300 degrees /s and isotonic muscle actions at 10%, 20%, 30%, 40%, and 50% of the maximal voluntary isometric contraction (MVIC) torque during leg extension exercises. DESIGN: A randomized, counterbalanced, cross-sectional, repeated-measures design. SETTING: A university-based human muscle physiology research laboratory. PATIENTS OR OTHER PARTICIPANTS: Ten women (mean age = 22.0 +/- 2.6 years) and 10 men (mean age = 20.8 +/- 1.7 years) who were apparently healthy and recreationally active. INTERVENTION(S): Using the dominant leg, each participant performed 5 maximal voluntary concentric isokinetic leg extension exercises at randomly ordered angular velocities of 60, 120, 180, 240, and 300 degrees /s and 5 concentric isotonic leg extension exercises at randomly ordered loads of 10%, 20%, 30%, 40%, and 50% of the isometric MVIC. MAIN OUTCOME MEASURE(S): Work was recorded by a Biodex System 3 dynamometer, and surface EMG was recorded from the superficial quadriceps femoris muscles (vastus lateralis, rectus femoris, and vastus medialis) during the testing and was normalized to the MVIC. The EMG/WK ratios were calculated as the quotient of EMG amplitude (muVrms) and WK (J) during the concentric phase of each exercise. RESULTS: Isotonic EMG/WK remained unchanged ( P > .05) from 10% to 50% MVIC, but isokinetic EMG/WK increased ( P < .05) from 60 to 300 degrees /s. Isotonic EMG/WK was greater ( P < .05) than isokinetic EMG/WK for 50% MVIC versus 60 degrees /s, 40% MVIC versus 120 degrees /s, and 30% MVIC versus 180 degrees /s; however, no differences were noted ( P > .05) between 20% MVIC versus 240 degrees /s or 10% MVIC versus 300 degrees /s. An 18% decrease in active range of motion was seen for the isotonic muscle actions, from 10% to 50% MVIC, and a 3% increase in range of motion for the isokinetic muscle actions from 60 to 300 degrees /s was also observed. Furthermore, the peak angular velocities for the isotonic muscle actions ranged from 272.9 to 483.0 degrees /s for 50% and 10% MVIC, respectively. CONCLUSIONS: When considering EMG/WK, peak angular velocity, and range of motion together, our data indicate that maximal isokinetic muscle actions at 240 degrees /s or controlled-velocity isotonic muscle actions at 10%, 20%, or 30% MVIC may maximize the amount of muscle activation per unit of WK done during the early stages of musculoskeletal rehabilitation. These results may be useful to allied health professionals who incorporate open-chain resistance training exercises during the early phases of rehabilitation and researchers who use isotonic or isokinetic modes of resistance exercise to examine muscle function.

Acute Effects of Static and Proprioceptive Neuromuscular Facilitation Stretching on Muscle Strength and Power Output.

Context: Stretching is commonly used as a technique for injury prevention in the clinical setting. Our findings may improve the understanding of the neuromuscular responses to stretching and help clinicians make decisions for rehabilitation progression and return to play.Objective: To examine the short-term effects of static and proprioceptive neuromuscular facilitation stretching on peak torque (PT), mean power output (MP), active range of motion (AROM), passive range of motion (PROM), electromyographic (EMG) amplitude, and mechanomyographic (MMG) amplitude of the vastus lateralis and rectus femoris muscles during voluntary maximal concentric isokinetic leg extensions at 60 and 300 degrees .s.Design: A randomized, counterbalanced, cross-sectional, repeated-measures design.Setting: A university human research laboratory.Patients or Other Participants: Ten female (age, 23 +/- 3 years) and 9 male (age, 21 +/- 3 years) apparently healthy and recreationally active volunteers.Intervention(s): Four static or proprioceptive neuromuscular facilitation stretching exercises to stretch the leg extensor muscles of the dominant limb during 2 separate, randomly ordered laboratory visits.Main Outcome Measure(s): The PT and MP were measured at 60 and 300 degrees .s, EMG and MMG signals were recorded, and AROM and PROM were measured at the knee joint before and after the stretching exercises.Results: Static and proprioceptive neuromuscular facilitation stretching reduced PT (P = .051), MP (P = .041), and EMG amplitude (P = .013) from prestretching to poststretching at 60 and 300 degrees .s (P < .05). The AROM (P < .001) and PROM (P = .001) increased as a result of the static and proprioceptive neuromuscular facilitation stretching. The MMG amplitude increased in the rectus femoris muscle in response to the static stretching at 60 degrees .s (P = .031), but no other changes in MMG amplitude were observed (P > .05).Conclusions: Both static and proprioceptive neuromuscular facilitation stretching caused similar deficits in strength, power output, and muscle activation at both slow (60 degrees .s) and fast (300 degrees .s) velocities. The effect sizes, however, corresponding to these stretching-induced changes were small, which suggests the need for practitioners to consider a risk-to-benefit ratio when incorporating static or proprioceptive neuromuscular facilitation stretching.

Intraoperative Arthroscopic Cold Irrigation Solution Does Not Affect Postoperative Pain and Swelling.

OBJECTIVE: To determine what effect using a cold irrigating solution during arthroscopic knee surgery would have on postoperative pain intensity, pain-medicine consumption, and knee joint swelling. DESIGN AND SETTING: We employed a randomized, controlled trial design. Subjects were randomly assigned to either the cold (4 degrees C) irrigating saline group or room-temperature (18 degrees C) irrigating saline (control) group. Subjects were blinded to group assignment. All surgeries were performed at the same hospital by the same surgeon. SUBJECTS: The sample was 93 physically active patients (32 women, 61 men, mean age = 47.4 +/- 15.1 years) who had knee injuries requiring surgery. Those with cold sensitivities or contraindications to the use of cold were excluded. MEASUREMENTS: A 10-cm horizontal visual analog scale was used to measure postoperative pain intensity. Postoperative pain-medicine consumption was recorded using a daily log. Knee joint swelling (girth) was measured at midpatella and 2 in (5.08 cm) above midpatella. Pain and swelling measures were collected before and after surgery. RESULTS: No statistical or clinical differences were found between the cold-saline and control groups for pain, pain-medicine consumption, and postoperative swelling across the first 4 postoperative days. CONCLUSIONS: Our results suggest that using intra-articular cold saline to irrigate the knee joint during arthroscopic surgery had no statistically or clinically significant effect on postoperative pain, medication usage, or swelling in the first 4 postoperative days.

Peripheral neuropathy in workers exposed to nitromethane.

BACKGROUND: Two workers from a headlight subassembly plant developed severe peripheral neuropathy. These workers had extensive, but brief (1-2 months) dermal and inhalational exposure to nitromethane, a solvent. METHODS: Environmental sampling was performed for nitromethane and ethyl cyanoacrylate. Medical records, including electrodiagnostic studies, were reviewed. Literature on nitromethane, ethyl cyanoacrylate, and other exposures in the workplace was reviewed. RESULTS: Electromyography and nerve conduction studies performed on these patients were consistent with a severe, axonal neuropathy. No etiology was discovered despite an extensive medical evaluation. Environmental sampling revealed exposure to nitromethane at the threshold limit value. CONCLUSIONS: The history of acute onset of severe peripheral neuropathy temporally associated with exposure to nitromethane is suggestive of a toxic neuropathy. While it cannot be definitively concluded that these two workers developed peripheral neuropathy secondary to exposures at work, occupational exposure to nitromethane appears to be the most likely etiology.

Revision anterior cruciate ligament reconstruction using the lateral third of the ipsilateral patellar tendon after failure of a central-third graft: a preliminary report on 10 patients.

Long-term outcomes were reported for 10 (77%) of 13 cases of revision anterior cruciate ligament (ACL) reconstruction using the lateral third of the ipsilateral patellar tendon as a graft. All primary ACL reconstructions were ipsilateral central-third bone-patellar tendon-bone graft procedures. Mean age at follow-up was 30.7 years, and mean time from revision ACL surgery to follow-up was 42.9 months. At follow-up, average KT-1000 difference between knees was 2.4 mm. All patients had a negative pivot shift, extension within 5 degrees of the contralateral knee, and flexion within 15 degrees. Mean bilateral comparison ratios for isokinetic strength and hop testing were: extension, 83.5%; flexion, 96%; and single-leg hop 96.9%. No patella fractures or tendon ruptures had occurred. All patients had returned to their previous work level, and 8 of the 10 patients could participate in at least "moderate" sports activities (e.g., skiing and tennis). The results were comparable to published outcome reports for both primary and revision ACL reconstruction. The lateral third of the ipsilateral patellar tendon is a good graft option for revision ACL reconstruction.

Sustained ethanol inhibition of native AMPA receptors on medial septum/diagonal band (MS/DB) neurons.

The direct impact of ethanol on native, non-NMDA glutamate receptors was examined in acutely isolated MS/DB neurons from rat. The impact of ethanol functional tolerance and physical dependence on non-NMDA receptor function was also determined. Non-NMDA receptors were defined pharmacologically as predominantly the AMPA subtype, because both AMPA- or kainate-activated currents were blocked by GYKI 52466, a selective AMPA receptor antagonist. The relative magnitude of potentiation of AMPA-activated currents by 10 or 100 microM cyclothiazide was consistent with recombinant AMPA flop-subtype receptors. Finally, the selective kainate receptor agonist, SYM 8021, induced little current in MS/DB neurons. AMPA receptor currents when activated by kainate were sensitive to ethanol, showing inhibition of approximately 5 - 50% when 10 - 300 mM ethanol and kainate were briefly co-applied (3 s). Ethanol (100 mM) also inhibited both the initial transient peak and sustained currents activated by AMPA. Inhibition was sustained during continuous ethanol superfusions of 5 min, suggesting a lack of acute tolerance to ethanol-induced AMPA receptor blockade. Rapid application of 3 - 3000 microM kainate activated concentration-dependent currents in MS/DB neurons from Control and Ethanol Dependent animals that were not significantly different. Also, direct ethanol inhibition (300 mM) of kainate-activated currents was not reduced by ethanol dependence, suggesting a lack of functional tolerance. These results suggest that native AMPA receptors on MS/DB neurons are inhibited by pharmacologically-relevant concentrations of ethanol. However, these receptors, unlike NMDA receptors, do not undergo adaptation with sustained ethanol exposure sufficient to induce physical dependence. British Journal of Pharmacology (2000) 129, 87 - 94

Sensitivity of postsynaptic GABAB receptors on hippocampal CA1 and CA3 pyramidal neurons to ethanol.

Baclofen-induced hyperpolarization of hippocampal CA1 and CA3 pyramidal neurons was examined to assess the impact of ethanol on postsynaptic GABAB receptors. These receptors activate outward K+ currents via a pertussis toxin-sensitive G protein cascade to reduce membrane potential during the slow inhibitory postsynaptic potential. This inhibitory action may play a role in ethanol intoxication and withdrawal excitability. In both types of pyramidal neurons, baclofen applied consecutively in increasing concentrations caused concentration dependent hyperpolarization. There were no significant differences in resting membrane potential, input resistance, maximum baclofen-induced hyperpolarization or EC50 between CA1 and CA3 neurons, although slope values were significantly smaller in the former neurons. These parameters were not significantly changed in the presence of ethanol 10-100 mM. Chronic ethanol treatment (12 days) sufficient to induce physical dependence also did not shift sensitivity or maximum response to baclofen in CA1 neurons. These results suggest that GABAB receptors in this model are essentially insensitive to ethanol and do not confirm our earlier preliminary observation of a possible down-regulation of postsynaptic GABAB receptor function by chronic ethanol treatment.

Lanthanum and zinc sensitivity of GABAA-activated currents in adult medial septum/diagonal band neurons from ethanol dependent rats.

The impact of chronic ethanol treatment, sufficient to induce tolerance and physical dependence, on GABAA receptor function was studied in acutely isolated neurons from the medial septum/nucleus diagonal band (MS/nDB) of adult rats using whole cell, patch-clamp recordings. In ethanol-naive Controls, GABA (0.3-300 microM) induced concentration-dependent increases in Cl- current with a threshold of 0.3-1 microM, a mean maximal current of 7645 +/- 2148 pA at 100-300 microM, an EC50 of 11.3 +/- 1.3 microM and a slope of 1.53 +/- 0.07. GABA-activated currents in neurons from animals receiving two weeks of ethanol liquid diet treatment did not differ significantly on any of these measures. The rate of GABAA receptor desensitization (t1/2 = 6.49 +/- 1.19 s) estimated as the time required for loss of 50% of peak current during sustained application of 10 microM GABA, as well as the residual steady state current remaining following complete desensitization for controls was unchanged by chronic ethanol. The impact of chronic ethanol treatment on the GABAA receptor modulation by lanthanum and zinc which act as positive and negative allosteric modulators, respectively, was also evaluated. Test pulses of 3 microM GABA in control neurons showed maximal potentiation by 141 +/- 30% at approximately 1000 microM lanthanum with an EC50 of 107 +/- 34 microM and a slope of approximately 1. Lanthanum potentiation remained the same following chronic ethanol treatment. Initial estimates based on fitted concentration response curves suggested that maximal inhibition of 3 microM GABA responses by zinc at the level of 70.2 +/- 8.5% in control cells was significantly increased by chronic ethanol treatment to 95.3 +/- 2.5%, although the IC50 of 60.2 +/- 25 microM was not changed. However, this difference was not supported by direct tests of maximal 3-10 mM zinc concentrations. These results suggest that chronic ethanol treatment, sufficient to induce tolerance and physical dependence, probably does not lead to readily detectible changes in GABAA receptor function in MS/nDB neurons.

Use of computer-based instruction in athletic training education.

Computer-based instruction is being widely used in the education programs of many allied health professions. However, there has been little, if any, documentation of computer-based instruction use in athletic training education. The primary purpose of this study was to determine what percentage of undergraduate and graduate NATA-approved athletic training education programs are using some form of computer-based instruction (ie, computer-assisted instruction or interactive video). We also addressed the following research questions: 1) What athletic training educational software is currently being used by athletic training students and educators? 2) What factors currently impede the use of computer-based instruction in athletic training education? 3) What instructional methods are commonly used to incorporate computer-based instruction into the athletic training curricula? and 4) What are the attitudes of athletic training program directors toward the use of computer-based instruction in athletic training education? Surveys were mailed to the program directors (n = 97) of all graduate and undergraduate NATA-approved athletic training education programs. Eighty-six (87.7%) usable surveys were returned. Forty-eight (55.8%) of the respondents reported using some form of computer-based instruction in their athletic training education program; 47 (54.7%) used computer-assisted instruction and 9 (10.6%) used interactive video. Respondents also identified the educational software they use and their method for implementing this software. Software was used most often to supplement traditional instructional methods. A lack of funds was reported to be the primary impeding factor for those programs not using computer-based instruction. Respondents reported an overall positive attitude toward computer-based instruction use in athletic training education and indicated the need for increased development of athletic training/sports medicine software.

Acute exertional rhabdomyolysis and its relationship to sickle cell trait.

Exertional rhabdomyolysis, a syndrome characterized by skeletal muscle degeneration and muscle enzyme leakage, has been shown to occur in normal, healthy individuals following strenuous exercise. In severe cases, this syndrome can result in renal failure and sudden death. Although anyone who performs strenuous exercise may be at risk for developing exertional rhabdomyolysis, some individuals may be more susceptible than others. A number of case reports of exertional rhabdomyolysis involve persons with sickle-cell trait, leading to the theory that these individuals might be at greater risk for developing the syndrome than those without this trait. This article discusses the etiology of exertional rhabdomyolysis, the associated risk factors for persons with sickle-cell trait, and the recommended preventive measures. Additionally, several case studies of exertional rhabdomyolysis are reviewed.

Acute ethanol dependence or long-term ethanol treatment and abstinence do not reduce hippocampal responses to carbachol.

In the hippocampus of human alcoholics, prolonged ethanol treatment reduces the number of muscarinic ligand binding sites present at autopsy suggesting a decrease in functional muscarinic receptors. Whether these changes are due to alcohol-induced brain damage or ethanol dependence and represent a reduced level of cholinergic function is unknown. The present studies tested the impact of ethanol dependence or long-term ethanol treatment and subsequent withdrawal on the function of pre- and postsynaptic muscarinic receptors in the CA1 region of the rat hippocampus. Field excitatory postsynaptic potentials (EPSPs) were inhibited in a concentration-dependent manner by 0.1-100 microM carbachol. This presynaptic inhibitory action of carbachol involving muscarinic receptors was not significantly reduced either by ethanol treatment (12 days), causing physical dependence, or by long-term ethanol treatment (97-120 days) and abstinence (3-6 months). Postspike after hyperpolarizations (AHPs) were inhibited in a concentration-dependent manner by carbachol (6-2000 nM). This postsynaptic excitatory action of muscarinic receptors also was not significantly reduced either by 12-day ethanol treatment or by long-term ethanol treatment. Taken together, these results suggest that neither pre- nor postsynaptic muscarinic receptor function measured electrophysiologically is reduced by either ethanol dependence or long-term ethanol consumption and abstinence in the rat as suggested by reduced muscarinic ligand binding in the hippocampus of human alcoholics.

Use of the otoscope in the evaluation of common injuries and illnesses of the ear.

Ear injuries and/or illnesses make up only a small percentage of the total injuries seen by the athletic trainer. However, if these conditions are left undetected or untreated, permanent ear damage could result. Many ear injuries involve structures that can only be viewed through the use of an otoscope. Although more athletic trainers are using the otoscope to evaluate the ear, there is little documentation available in athletic training literature regarding its proper use. This article describes the proper use of the otoscope in evaluating the ear and discusses the common pathological conditions that might confront the athletic trainer. This article will provide a resource that can be used in conjunction with the guidance of your team physician to help you develop the knowledge and skills required for performing an otoscopic examination.

Interaction of ethanol and allosteric modulators with GABAA-activated currents in adult medial septum/diagonal band neurons.

Behavioral and electrophysiological studies suggest that neurons in the medial septum may express ethanol sensitive GABAA receptors. In the present study, patch-clamp recordings of whole-cell currents were used to directly characterize the ethanol sensitivity of GABAA receptors on acutely dissociated neurons, isolated from the medial septum/nucleus of the diagonal band (MS/nDB) of the adult rat brains. MS/nDB neurons displayed inward currents in response to GABA applied rapidly with a large-bore dual pipette system. The currents were mediated by the activation of GABAA receptors, since they reversed near the calculated reversal potential for chloride and were completely blocked by bicuculline. GABA responses were concentration dependent with an EC50 of 8.7 microM GABA and a slope of 1.35 suggesting cooperativity. Pharmacologically relevant concentrations of ethanol (3-300 mM) neither significantly increased nor decreased mean responses to GABA in neurons from Sprague Dawley or High Alcohol Sensitivity (HAS) rats. Mean GABA currents were significantly increased by 300 mM ethanol in neurons from 'ethanol sensitive' Fischer 344, ACI and Wistar Kyoto inbred rats. In subsets of neurons, 12.5 to 57.1% of those tested from these 5 rats strains, ethanol (30-300 mM) significantly increased GABA currents by > or = 20%. An additional, 10 percent of cells from Sprague Dawley rats showed ethanol-induced inhibition of GABA-activated current by < or = 20%. Allosteric modulators pentobarbital (10 microM), midazolam (1 microM) and lanthanum (300 microM), enhanced, while zinc (30 microM) decreased GABA-activated currents in all neurons, consistent with the well-known actions of these agents. These results suggest that GABAA receptors on MS/dDB neurons are pharmacologically similar to those on other neurons with respect to regulation by allosteric modulators. On the other hand, ethanol sensitivity of GABAA receptors varies considerably from cell to cell ranging from significant enhancement to inhibition of GABA-activated current.

Comparison of contractile responses of the guinea pig ileum longitudinal muscle to ethanol and GABAA agonists.

The guinea pig ileum myenteric plexus contains GABAA receptors linked to chloride ion channels which are pharmacologically similar to those in the central nervous system. The present study examined the reported ability of acute ethanol treatment to directly activate GABAA receptors or to increase GABAA agonist-mediated activation of the GABAA receptor in the myenteric plexus. Direct addition of ethanol to preparations of the guinea pig ileum longitudinal muscle had two effects. Immediately after ethanol (10-300 mM) was added to the tissue bath a concentration-related contractile response was observed which became maximal within 10 sec and then decayed over the next 60 sec. Contractile responses to higher concentrations of ethanol (greater than 100 mM) also were followed by a sustained reduction of longitudinal muscle tone. Contractions evoked by gamma-aminobutyric acid (GABA) and GABAA agonists, 3-aminopropane sulfonic acid (APSA) (3-100 microM) or muscimol (0.3-30 microM) developed maximally and decayed within 20 sec. Acetylcholine (0.01-10 microM) induced contractions were sustained over several minutes. Preincubation of tissue strips in ethanol (30 mM) for 1 min did not alter concentration relationships for GABA, muscimol or APSA contractile responses. Furthermore, addition of ethanol (10-100 mM) simultaneously with APSA, or 0.5, 2 or 5 min before the addition of APSA, also failed to consistently enhance contractile responses. Ethanol (30 mM) also did not alter desensitization-induced reductions in contractile responses to muscimol (3 microM) caused by preincubation of tissues with muscimol (1 microM). Finally, contractile responses to ethanol and APSA were completely blocked by atropine (0.1 microM) and tetrodotoxin (0.1 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of ethanol on gamma-vinyl GABA-induced GABA accumulation in the substantia nigra and on synaptosomal GABA content in six rat brain regions.

Two recently developed methods for estimating changes in presynaptic gamma-aminobutyric acid (GABA) homeostasis were used for the first time to evaluate the effects of acute and chronic ethanol treatments on GABA utilization. GABA accumulation in the left substantia nigra zona reticulata (SNR) following unilateral microinjection of gamma-vinyl GABA (GVG; 5 micrograms) was linear for at least 180 min while GABA concentrations in the uninjected right SNR did not change over this period. Net GABA accumulation (left minus right SNR) also increased linearly over this interval. Intraperitoneal (i.p.) administration of ethanol (0.3, 1 or 3 g/kg) 15 min after GVG microinjection did not significantly change either the rate of GABA accumulation in left SNR, the net GABA accumulated or the concentration of GABA in the uninjected right SNR relative to saline injected controls over the 45-min test interval. Likewise, GABA accumulation in the left SNR or steady-state GABA concentrations in the right SNR of chronically intoxicated rats or physically dependent animals withdrawn from ethanol for 12 h did not change significantly from that dextrose-fed controls. In a separate study, the effects of acute and chronic ethanol treatments on the concentration of GABA in synaptosomes isolated from the frontal cortex, hippocampus, tectum, striatum, cerebellum or brainstem were determined. Thirty min after acute treatment with ethanol (0.5, 1, 2 or 4 g/kg, i.p.) the concentration of GABA in synaptosomes from any of these brain regions was not significantly altered. Furthermore, chronic ethanol treatment sufficient to induce physical dependence and a severe ethanol withdrawal syndrome also did not significantly modify synaptosomal GABA concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)