No description available.

No description available.

Abstract Isokinetic normative data can be invaluable in identifying an individual’s strengths and weaknesses, and thus lead to a more effective use of the individual’s time to minimise or overcome his weaknesses while maintaining or improving existing strength. However, visual feedback (VF) may significantly affect the result of isokinetic testing, resulting in erroneous conclusions if not accounted for. Additionally, the previous use of VF to obtain increased strength values has resulted in inconsistent findings. The purpose of this study was to examine the effect of VF on concentric and eccentric knee extensor peak torque. Twenty-two sedentary, college-aged male and female volunteers were assigned to either Group 1 (n = 11) or Group 2 (n = 11) to either perform knee extensor concentric-eccentric (con-ecc) isokinetic testing with VF or without VF (no-VF) using a crossover method. After a one-week rest, the two groups underwent knee extensor con-ecc isokinetic testing using the alternative testing condition. Each test consisted of five maximal knee extensor con-ecc isokinetic testing contractions at 60° per second on the Cybex Norm system. The data indicated significant (p < 0.05) differences in the concentric peak torque of Group 1, Group 2 and Combined Group following VF when compared to no-VF. The eccentric peak torque of Group 1, Group 2 and Combined Group was found not to be significantly different following VF when compared to no-VF. Further, no significant interaction effect as a result of the different groups was found. Visual feedback of torque output can improve maximum voluntary concentric contraction in isokinetic dynamometry, but not maximum voluntary eccentric contraction. It is thus recommended that VF should be consistently provided during isokinetic testing, since it can also be used to help detect and correct errors in performance as well as derive reinforcement from correct performances.

No description available.

published_or_final_version / Zoology / Doctoral / Doctor of Philosophy

published_or_final_version / Zoology / Doctoral / Doctor of Philosophy

No description available.

No description available.

Muscle strain injuries affect a wide range of physically active people around the world and are reaching epidemic proportions. Despite the variety of treatment options available in rehabilitation, there are no clear guidelines for electrical stimulation that provide effective reproducible results that address the underlying cause of these injuries. For instance, electrotherapy is inefficient at stimulating muscles, because of imprecise parameters and an ability to target particular muscles. The difference between this study and previous research is the precise delivery of electrical stimulation (intramuscular) at two different frequencies (2 Hz and 50 Hz) and comparing it a control group. Objective: To determine the difference on muscle strength and functional status between three treatments modalities for sub acute and chronic hamstring strains. Design: A randomized experimental design was used to compare the effects of low (2 Hz), high (50 Hz) and no-electrical (control) intramuscular stimulation on muscle strength and mental and functional status (AMSMC HEALTH STATUS INDEX). Each group consisted of 18 subjects. Main Outcome: The difference in treatment modalities was evaluated by comparing the muscle strength test (Biodex Dynamometer) results and the AMSMC HEALTH STATUS INDEX results in pretest and post-test conditions. Results: The AMSMC HEALTH STATUS INDEX, but not muscle strength test (Biodex), changed significantly after 2-Hz electrical intramuscular stimulation (pre-test µ = 66.56, Std= 11.92, post-test µ= 92.89, Std= 6.25), whereas no statistically significant changes in health status index and muscle strength test occurred with 50-Hz (pre-test = 69.22, Std= 11.31, post-test µ= 70.22, Std= 12.27)) and no-electrical stimulation groups (pre-test µ= 69.11, post-test µ= 73.39, Std= 13.18).

Statins are the mainstay of cholesterol-lowering therapy and are taken by millions of people worldwide. These drugs are generally well-tolerated but can cause myopathy ranging from mild muscle pain to fatal rhabdomyolysis. The mechanism of statin-induced myopathy (SIM) is not fully understood and there is currently no convenient and reliable marker of SIM, but mitochondrial dysfunction has been implicated. We sought to investigate the effect of statins on mitochondrial DNA (mtDNA) levels in order to gain information on the mechanism of SIM and to explore the possibility of utilizing changing mtDNA levels as a marker of SIM. Several approaches were used. First, mtDNA levels were quantified in skeletal muscle biopsies collected from a previously published 8-week clinical trial of high-dose simvastatin or atorvastatin versus placebo. Forty-eight hypercholesterolemic subjects were randomly assigned to receive placebo (N=16), high dose atorvastatin 40mg/day (N=16), or high dose simvastatin 80mg/day (N=16) for 8 weeks. Muscle mtDNA content was assessed by real-time PCR atbaseline and after 8-weeks on statin treatment and found to be significantly reduced in the groupreceiving simvastatin (P=0.005) but not the other two. In addition, a significant positive correlation was observed between mtDNA and muscle ubiquinone in all groups (R=0.63, P<0.01), with the strongest association found in the simvastatin-treated subjects (R=0.75, P=0.002). Next, in an attempt to determine whether statin-induced muscle pain may be associated with muscle mtDNA depletion, archived muscle biopsies collected from statin users with muscle complaints were sought through a review of a muscle biopsy database and possible study samples were identified; however, this was put on hold as too much information was missing from the pathology reports. Third, a series of cell culture experiments were carried out in which human skeletal muscle myotubes were exposed to various concentrations of simvastatin or atorvastatin, in order to determine an appropriate dose range for subsequent mitochondrial toxicity experiments. Lastly, mtDNA content and expression was quantified in skeletal muscle biopsies collected from 10 patients with statin-induced rhabdomyolysis (SIR) and compared to 8 healthy controls to investigate whether muscle mtDNA is altered in rhabdomyolysis. No differences in mtDNA content or expression were observed between the two study groups, but this may have been be due to the SIR subjects' marked heterogeneity. Statin therapy can be associated with considerable alterations in mtDNA content, which may play a role in the aetiology of SIM. MtDNA levels alterations with statin exposure should be investigated further to explore the involvement of mitochondrial alterations in the mechanism of SIM, and determine whether these may represent a useful clinical tool for assessing statin-induced muscle toxicity.