The effect of whole body vibration on oxygen uptake and electromyographic signal of the rectus femoris muscle during static and dynamic squat

Whole Body Vibrations consist of a vibration stimulus mechanically transferred to the body. The impact of vibration treatment on specific muscular activity, neuromuscular, and postural control has been widely studied. We investigated whole body vibration (WBV) effect on oxygen uptake and electromyographic signal of the rectus femoris muscle during static and dynamic squat. Fourteen healthy subjects performed a static and dynamic squat with and without vibration. During the vibration exercises, a significant increase was found in oxygen uptake (P=0.05), which increased by 44% during the static squat and 29.4% during the dynamic squat. Vibration increased heart rate by 11.1 ± 9.1 beats.min-1 during the static squat and 7.9 ± 8.3 beats.min-1 during the dynamic squat. No significant changes were observed in rate of perceived exertion between the exercises with and without vibration. The results indicate that the static squat with WBV produced higher neuromuscular and cardiorespiratory system activation for exercise duration ?60 sec. Otherwise, if the single bout duration was higher than 60 sec, the greater cardiorespiratory system activation was achieved during the dynamic squat with WBV while higher neuromuscular activation was still obtained with the static exercise.

A novel, dynamic, in vivo, non-contact method of measuring oxygen depletion rate of the anterior eye

Despite the importance of oxygen measurements, techniques have been limited by their invasive nature and small corneal area of assessment. The aim of this study was to assess a non-contact way of measuring oxygen uptake of the whole anterior eye.

Contact lenses and sport

Contact lenses seem to be the ideal method of vision correction for ametropic people who participate in sporting activities. This thesis sets out to evaluate the viewpoint of the optometric professional and that of the patient on the use of contact lenses in sport and to establish if education is needed within this area. It also aims to provide some scientific evidence on the effect of exercise on the physiology of the cornea with and without contact lenses. Silicone hydrogel contact lenses have previously been suggested to impede heat dissipation from the cornea compared to mid water hydrogels. This was further demonstrated with exercise. The physiological integrity of the cornea is dependant on the amount of oxygen available to its surfaces. Contact lenses can disrupt the diffusion of oxygen to the cornea. Previous methods of measuring the oxygen consumption of the cornea have been limited by their invasive nature and assessment of only a small surface area of the cornea. They are not suitable to measure corneal oxygen consumption during exercise with and without contact lenses. A new method needed to be established. This was achieved by designing a novel method by the use of an oxygen sensor inside an airtight goggle using dynamic quenching of luminescence method. This established a non-contact way of measuring the effect oxygen uptake with and without contact lenses in vivo, allowing the contact lens to be undisturbed in their natural environment. The new method differentiated between the closed-eye and the open-eye condition with a good within-visit repeatability. It also illustrated that the cornea utilises oxygen at a faster rate during controlled aerobic exercise at moderate intensity. New contact lenses are available specifically for sport, these claim to reduce glare and increase contrast for daylight outdoor sports. However, visual benefits of these types of contact lenses cannot be measured easily in an indoor clinical environment, such as the optometric practice. To demonstrate any potential benefits of these lenses emulation of them should be conducted outdoors.

Reactive oxygen and nitrogen species production in cardiomyoblasts during hypoxia and reoxygenation

Hypoxia is a stress condition in which tissues are deprived of an adequate O2 supply; this may trigger cell death with pathological consequences in cardiovascular or neurodegenerative disease. Reperfusion is the restoration of an oxygenated blood supply to hypoxic tissue and can cause more cell injury. The kinetics and consequences of reactive oxygen and nitrogen species (ROS/RNS) production in cardiomyoblasts are poorly understood. The present study describes the systematic characterization of the kinetics of ROS/RNS production and their roles in cell survival and associated protection during hypoxia and hypoxia/reperfusion. H9C2 cells showed a significant loss of viability under 2% O2 for 30min hypoxia and cell death; associated with an increase in protein oxidation. After 4h, apoptosis induction under 2% O2 and 10% O2 was dependent on the production of mitochondrial superoxide (O2-•) and nitric oxide (•NO), partly from nitric oxide synthase (NOS). Both apoptotic and necrotic cell death during 2% O2 for 4h could be rescued by the mitochondrial complex I inhibitor; rotenone and NOS inhibitor; L-NAME. Both L-NAME and the NOX (NADPH oxidase) inhibitor; apocynin reduced apoptosis under 10% O2 for 4h hypoxia. The mitochondrial uncoupler; FCCP significantly reduced cell death via a O2-• dependent mechanism during 2% O2, 30min hypoxia. During hypoxia (2% O2, 4h)/ reperfusion (21% O2, 2h), metabolic activity was significantly reduced with increased production of O2-• and •NO, during hypoxia but, partially restored during reperfusion. O2-• generation during hypoxia/reperfusion was mitochondrial and NOX- dependent, whereas •NO generation depended on both NOS and non-enzymatic sources. Inhibition of NOS worsened metabolic activity during reperfusion, but did not effect this during sustained hypoxia. Nrf2 activation during 2% O2, a sustained hypoxia and reperfusion was O2-•/•NO dependent. Inhibition of NF-?B activation aggravated metabolic activity during 2% O2, 4h hypoxia. In conclusion, mitochondrial O2-•, but, not ATP depletion is the major cause of apoptotic and necrotic cell death in cardiomyoblasts under 2% O2, 4h hypoxia, whereas apoptotic cell death under 10% O2, 4h, is due to NOS-dependent •NO. The management of ROS/RNS rather than ATP is required for improved survival during hypoxia. O2-• production from mitochondria and NOS is cardiotoxic during hypoxia/reperfusion. NF-?B activation during hypoxia and NOS activation during reperfusion is cardiomyoblast protective.