Background: It has been reported that dancers are at greater risk of developing low bone mineral density (BMD) compared to general population; however, some published studies also highlight the positive effects of dance training on bone metabolism. Given the existing controversy, the aim of the current work was a) to investigate bone health status of professional ballet dancers and vocational dance students, and b) to investigate associated factors and mechanisms involved in dancers’ bone health. Design Cross-sectional, longitudinal analysis (2-yrs follow-up) and genetic association studies were conducted on a population which consisted of professional ballet dancers, vocational dance students and controls. Methods: The total of 58 professional ballet dancers (66 sex- aged-matched controls), and 152 vocational dance students (96 aged- and sex-matched controls) were screened for BMD status at impact [femoral neck (FN); lumbar spine (LS)] and non-impact sites (forearm). Tanner staging, age at menarche and menstrual status were assessed via questionnaires. Bone mass, nutrition, peak height velocity estimation, energy availability, insulin-like growth factor I (IGF-1), oestrogens, growth hormone, and sclerostin serum concentrations were longitudinally measured in a sub-sample of 101 vocational dance students and age- and sex-matched controls. Association between polymorphisms of the Wnt/β-catenin and ER signalling pathways with low BMD were further investigated. Results: Female vocational dance students were more likely to display low BMD at the forearm and LS than controls (OR= 0.1; p < 0.05 and OR=0.2; p < 0.05, respectively); the prevalence of low BMD at the forearm was significantly higher in female professional ballet dancers than controls (37.5% vs. 17.4%, p < 0.001). During the follow-up, both female and male vocational dancers revealed significantly lower BMD at impact and non-impact sites (p < 0.001) compared to controls. Serum IGF-1 concentrations were significantly increased in vocational dancers compared to controls at 2yrs follow-up (p < 0.05), as well as serum sclerostin (p < 0.05). Genetic variants at the Wnt/β-catenin and ER signalling pathways were identified as risk factors for low BMD at both impact and non-impact sites. Conclusion: Professional dancers and vocational dance students have lower bone health compared to controls. Genetic mechanisms seem to be determinant. It is recommend that dancers performing at elite level should be referred for bone densitometry.

The foot forms the dynamic base upon which a sprinter functions. The actions that occur within the foot are of critical importance to the task of sprint running, since they influence the functional mechanisms of the entire body and especially the lower extremity. The aim of this research was to evaluate how foot function may contribute to sprinting performance and the interaction between the mechanical properties of sprinting footwear and performance, with a focus on the role of the metatarsophalangeal joint (MPJ). Currently, little is known about the effect of footwear upon the normal biomechanical function of the MPJ during sprinting, as this joint has often been neglected in previous biomechanical studies of lower limb energetics. A series of empirical and theoretical investigations were therefore undertaken to advance the understanding in this area. The initial study revealed the importance of two important methodological issues on the analysis of MPJ function during sprinting. Appropriate MPJ axes representation and appropriate data processing procedures are vital to ensure the accurate assessment of joint kinetics. Empirical investigations on eight trained sprinters performing maximal sprint trials, both in barefoot and sprint spike conditions determined normal patterns of foot behaviour and the role of the MPJ during sprinting. Several aspects of foot function, including kinematic, kinetic and pressure characteristics, were determined. Sprint spikes reduced MPJ range of motion and dorsiflexion velocity but increased total energy generated during the push-off phase, biomechanical measures which may be linked to sprinting performance. To investigate whether manipulations in the mechanical properties of sprinting footwear may influence sprinting performance and MPJ function, sprint spikes with insoles of varying stiffness's were manufactured and mechanically tested. For a group of sprinters increasing the sprint spike stiffness did not elicit an improved sprinting performance. Due to the high variability between athletes and highly individualised responses to perturbations in footwear a single- subject analyses was undertaken. This study demonstrated that individual sprinting performance may be improved by implementation of relevant shoe mechanical characteristics. Whilst varying the mechanical characteristics of sprint spikes clearly showed controlling influences over the natural motion of the MPJ, the relatively minimal effect on the resultant MPJ energetics, potentially suggests that sprint spikes do not minimise energy loss during sprinting. The combined empirical and theoretical understanding therefore highlighted several aspects of MPJ function which could be altered by footwear in an attempt to improve sprint running performance.

Aerobic power (VOzma) and cardiac output decrease in both sexes with age. Endurance exercise is known to affect cardiac structures and function, and could therefore attenuate the effects of ageing. However, recent studies have suggested that men and women of similar ages adapt differently to exercise training, including adaptations in cardiac function. In younger men and women, training modality is also an important determinant of improvements in cardiac function, but the full effects of exercise training need to be determined both centrally and peripherally. Cardiac power output (CPO) incorporates measurements of both blood flow (Q) and mean blood pressure (MAP), and is the most comprehensive .method of measuring overall cardiac function. In preliminary studies we elucidated the reliability and reproducibility of the C02 rebreathing technique used to determine Q, and the potential effects of caffeine ingestion on CPO. Then older men and women participated in 30 weeks of training, with step-wise increments in exercise intensity. This programme increased aerobic p~wer and increased the extraction of oxygen in the peripheries, but with no discernable effects on the heart's maximum pumping or reserve capacities. Six week endurance training (interval and continuous) of young men produced similar results. However using proteomics, interval training induced greater expressions of some contractile proteins, creatine kinase-M and heat shock protein 70 kDa, in the vastus lateralis muscle, suggesting possible conversion towards a faster muscle phenotype, but only in men. We conclude that endurance training with exercise intensities < 75 % HRR induces increases in VOZmax and peripheral adaptations in older people, but intensities >75 % HRR are needed to induce changes in cardiac function. We also found no discemable cardiovascular sex-specific differences in either young or older people after either interval or continuous exercise training. However, skeletal muscle exhibited contractile and metabolic adaptations to these training regimes, and these were sex-specific.

Increasing physical activity (PA) and reducing the time spent sedentary can favourably impact health in youth. Active video games discourage sedentary behaviour by incorporating PA into video gaming, and have the potential for increasing opportunities for, and the promotion of, PA. The aims of this thesis were to a) compare adolescents' energy expenditure (EE) whilst playing sedentary and active video games; b) to examine the contribution of upper limb and total body movement to adolescents' EE whilst playing non-ambulatory active video games; c) to compare the physiological cost and enjoyment of active video gaming with sedentary video gaming and aerobic exercise in adolescents, and young and older adults; and, d) to evaluate the short-term (12 weeks) effects of a home-based active video gaming intervention on children's habitual PA and sedentary time, behaviour preferences, and, body composition, with a mid-test analysis incorporated at 6 weeks. The first three studies were cross-sectional. They revealed that active video games significantly increased PA and EE compared with sedentary video games in adolescents. These increases were typically of insufficient intensity though to contribute towards recommendations for daily PA in youth, and were less than those observed for authentic sports and brisk treadmill walking and treadmill jogging. Nevertheless, active video games encouraged PA and discouraged sedentary behaviour compared to sedentary equivalents. Further, similar physiological responses observed between adolescents and adults in study three provided support for the promotion of active rather than sedentary video gaming throughout the lifecourse. Greater enjoyment of active video games compared to a sedentary video game and brisk treadmill walking and treadmill jogging suggested that active video games may be an enjoyable mode of entertainment for young people and adults. The methodologically-focused study two revealed that the best single measure for explaining the variance in EE during active video gaming was a hip-mounted accelerometer. This was congruent with current recommendations for measuring habitual PA using accelerometers. Interestingly, using combined PA data from accelerometers placed on the hip and wrist similarly explained the variance in EE during active gaming compared to combined HR and activity monitoring. This provided support for the assessment of upper limb movements during non-ambulatory activities in adolescents. The intervention study revealed that a targeted increase in active video gaming and decrease in sedentary video gaming at 6 weeks did not positively affect children's PA relative to an age-matched comparison group. An increase in total video gaming was observed at 6 and 12 weeks relative to the comparison group, and this was accompanied by non-significant but detrimental changes in PA compared to the comparison group. These findings may suggest that an increase in time spent playing video games may be detrimental to PA in children. Rather than simply enabling PA by providing active video gaming equipment, interventions that consider the wide range of PA and sedentary behaviour opportunities available to young people in the home environment may be necessary to benefit PA and health. Further, the novelty effect observed for active video game use supports the call for the production of new active video games that attract children and sustain their interest.

It is well documented that regular endurance exercise induces skeletal muscle mitochondrial biogenesis. However, the optimal training stimulus and nutritional intervention for which to maximize mitochondrial adaptations to endurance exercise is not well known. Developments in molecular techniques now permit the examination of the cell signalling responses to acute exercise therefore increasing our understanding of how manipulation of the training protocol and nutrient availability may enhance the training stimulus to a given bout of exercise. The primary aim of this thesis is to therefore characterise the skeletal muscle cell signalling responses thought to regulate mitochondrial biogenesis following an acute bout of high-intensity interval exercise and moderate- intensity continuous exercise. A secondary aim is to subsequently examine how manipulation of carbohydrate (CHa) availability may enhance the activation of key regulatory cell signalling pathways. The aim of the first study (Chapter 4) was to develop two exercise protocols of varied activity profile, which induced comparable total oxygen consumption and energy expenditure after being matched for average intensity, duration and distance ran. In a repeated measures and randomised design, eight active males performed an acute bout of high-intensity interval (HIT) running (6 x 3 min at 90 % V02max interspersed with 6 x 3 min at 50 % V02max also performed with a 7-min warm up and cool down at 70 % V02max) and an acute bout of moderate-intensity continuous (CaNT) running (50-m in continuous running at 70 % V02max). As a result of average intensity (70 % V02max) duration (50-min) and distance ran (9843 ± 176) being equal between protocols, total oxygen consumption (HIT; 162 ± 6, CaNT; 166 ± 10 L) and energy expenditure (HIT; 811 ± 30, CaNT; 832 ± 48 kcal) were matched between protocols (P > 0.05). Despite higher ratings of perceived exertion in HIT compared with CaNT (HIT; 14 ± 0.5, caNT; 13 ± 0.4 AU, P < 0.05), subjects reported greater ratings of perceived enjoyment in the HIT protocol (HIT; 87 ± 2, CaNT; 61 ± 4 AU, P < 0.05) according to the Physical Activity Enjoyment scale. By matching these two protocols for work done, these data therefore provided an appropriate framework for which to examine the molecular signalling responses of human skeletal muscle to acute HIT and CaNT. The aim of the second study (Chapter 5) was to characterise the skeletal muscle cell signalling responses associated with the regulation mitochondrial biogenesis following HIT and CaNT. In a repeated measures and randomised design, muscle biopsies (vastus lateralis) were obtained pre-, post- and 3 h post-exercise from ten active males who performed the HIT and CaNT protocols developed in Chapter 4. Despite the obvious difference in activity profiles between protocols, muscle glycogen (HIT; 116 ± 11, CaNT; 111 ± 17 mmol/kg dry wt) decreased similarly between protocols (P < 0.05), and phosphorylation (P-) of AMPK (HIT; 1.5 ± 0.3, CaNT; 1.5 ± 0.1) and p38MAPK (HIT; 1.9 ± 0.1, CaNT; 1.5 ± 0.2) increased immediately post-exercise before returning to baseline 3 h post exercise. P-p53 (HIT; 2.7 ± 0.8, CaNT; 2.1 ± 0.8) and expression of PGC-1a mRNA (HIT; 4.2 ± 1.7, CaNT; 4.5 ± 0.9) increased 3 h post-exercise in both HIT and CaNT though there were no difference between protocols (P > 0.05). Data therefore demonstrate comparable cell signalling responses between HIT and CaNT when matched for work done, average intensity, duration and distance ran. Furthermore, this is the first time exercise is shown to up-regulate p53 phosphorylation in human skeletal muscle therefore highlighting an additional pathway by which exercise may regulate mitochondrial biogenesis. Progressing from the role of the exercise stimulus in initiating mitochondrial biogenesis, the aim of the third study (Chapter 6) was to examine the effects of reduced CHO availability on modulating the exercise-induced activation of the cell signalling pathways as characterised in Chapter 5. Although HIT and CaNT protocols resulted in comparable signalling in Chapter 5, we chose HIT as our chosen exercise model given that it is perceived as more enjoyable than CaNT, has application for improving both human health and performance and also because of its relevance as a training modality for elite athletes in team and endurance sports. In a repeated measures and randomised design, muscle biopsies (vastus lateralis) were obtained from eight active males pre-, post and 3 h after performing an acute bout of high-intensity interval running with either high (HIGH) or low CHO availability (LOW). In LOW, subjects performed a bout of glycogen depleting exercise the night before and reported to the laboratory on the subsequent morning in a fasted state as well as restricting CHO before, during and after exercise. Subjects in HIGH CHO loaded for 24 h before reporting to the laboratory to perform HIT with CHO consumed before, during and after exercise. Resting muscle glycogen (HIGH, 467 ± 19; LOW, 103 ± 9 rnmol.kq" dw) and utilisation (HIGH, 142 ± 34; LOW, and 30 ± 12) was greater in HIGH compared with LOW (P < 0.05). Phosphorylation (P-) of ACCSer79 (HIGH, 1.4 ± 0.4; LOW, 2.9 ± 0.9), a marker for AMPK activity, and p53ser15 (HIGH, 0.9 ± 0.4; LOW, 2.6 ± 0.8) was higher in LOW immediately post- and 3 h post-exercise, respectively (P < 0.05). Before and 3 h post-exercise, mRNA content of PDK4, Tfam, COXIVand PGC-1a were greater in LOW compared with HIGH (P < 0.05) whereas CPT1 showed trend towards significance (P = 0.09). However, only PGC-1a expression was increased by exercise (P < 0.05) where 3-fold increases occurred independent of CHO availability. Data demonstrate that low CHO availability enhances p53 phosphorylation in a manner that may be related to upstream signalling through AMPK. Given the emergence of p53 as a potential molecular regulator of mitochondrial biogenesis, such nutritional modulation of contraction-induced p53 activation may have implications for both athletic and clinical populations. In summary, the work undertaken from the studies in this thesis provides novel information in relation to the regulation of exercise-induced cell signalling responses associated with mitochondrial biogenesis. Specifically, this is first report to examine cell-signalling responses to running exercise where comparable signalling between HIT and CaNT was observed when protocols are matched for average intensity and duration. Furthermore, these data provide the first report of an exercise-induced increase in p53 phosphorylation in which data demonstrate low CHO availability augments the exercise-induced increase in p53 signalling which may be related to upstream signalling through AMPK. Further studies would now benefit from addressing the nuclear and mitochondrial abundance of p53 in response to an acute exercise challenge as well as comprehensively examining how training status, exercise intensity and CHO availability affects p53 regulation and downstream target genes.

No description available.

Delayed onset muscle soreness (DOMS) is a muscle strain injury that presents as tender or aching muscles, often felt during palpation or movement. DOMS is associated with unaccustomed, high-force muscular work and is most pronounced if the work involves a significant eccentric component. Despite substantial research into DOMS its aetiology is still unresolved. There have been recent suggestions that reactive oxygen species (ROS) may be involved in the aetiology of DOMS, however the evidence for this association is equivocal. Therefore, the aims of this thesis were to investigate the effects of unaccustomed exercise (downhill running) on DOMS, specifically investigating the role of ROS in its aetiology. Once this had been established, the effects of dietary intervention and antioxidant supplementation on DOMS and ROS were also investigated. Study 1 demonstrated that downhill running, which resulted in DOMS, also induced the production of ROS, detected by ESR spectroscopy as well as an increases in serum malondialdehyde (MDA) concentration. It was noted that this increase in ROS occurred -72 h post exercise and was therefore likely to be a result of increased phagocyte activity. Furthermore, the increase in ROS occurred after peak DOMS and when muscle function (as determined by losses of muscle torque assessed by isokinetic dynamometry) was returning to pre-exercise levels, suggesting a temporal dissociation between ROS production and DOMS following downhill running. Circulating levels of ROS were still increasing 72 h post exercise so this study was unable to map the full time-course of ROS production following downhill running. Study 2 investigated the effects of dietary CHO intake on DOMS, ROS and muscle function. It was found that pre-exercise CHO status had no effect on ROS production, DOMS or losses of muscle function following downhill running. The study demonstrated a bi-phasic increase in creatine kinase (CK), with the second increase corresponding with the post-exercise ROS production. The study extended the postexercise sampling period to 96 h, however, ROS were still increasing at this time and therefore this study was also unable to conclude a definitive tune course of ROS production following downhill running. Study 3 demonstrated that prolonged ascorbic acid supplementation attenuated the post-exercise increase in ROS production compared to placebo. This attenuation in ROS prevented the secondary peak in CK activity, however it had no effect on DOMS. Interestingly, supplementation with ascorbic acid resulted in more prolonged losses of muscle function. ROS peaked at 96 h post exercise and therefore the time course ofROS production following downhill running was established. From these studies it was concluded that downhill running did result in post-exercise ROS production. This post-exercise ROS production was associated with secondary muscle damage as measured by plasma CK activity although it had no effect on DOMS. Since supplementation with ascorbic acid attenuated ROS production and prolonged the losses of muscle function, it was suggested that ROS produced by phagocytes m the days following muscle-damaging exercise have a positive role in assisting in the recovery from the trauma.

Polycystic ovarian syndrome (PCOS) is a highly prevalent heterogeneous syndrome associated with abdominal obesity, insulin resistance and the metabolic syndrome. This clustering of risk factors could translate into an adverse cardiovascular disease (CVD) risk profile. Endothelial dysfunction, an early barometer of CVD, has been exhibited by women with PCOS; however, it remains unclear whether endothelial dysfunction is independent of CVD risk factors in this population. Exercise training has been found to enhance conduit artery and cutaneous microvessel endothelial function in various populations. Nevertheless, limited research exists regarding the cardiovascular effects of exercise in PCOS, and its impact on endothelial function in conduit arteries and cutaneous microvessels, has not been explored. The primary aim of this thesis was to examine nitric oxide (NO)-mediated endothelial function at different levels of the vascular tree in women with PCOS and to establish whether supervised exercise training induces a therapeutic effect on endothelial function. A systematic review of published studies comparing FMD in PCOS and control women was conducted. Twenty-one published studies were identified for inclusion (pCOS n=908; controls n=566). Differences in FMD between PCOS and controls were synthesised and meta-regressed against BMI and age. The pooled mean FMD was 3.5% lower (95% CI=3.4, 3.7%; P < 0.001) in women with PCOS compared with controls; and the PCOS-mediated reduction in FMD was most evident in studies involving less obese women. PCOS [n=35, 28y (95% CI=26, 30), 31kg/m2 (95% CI=27, 35)] and control women [n=16, 32y (95% CI=30, 35), 30kg/m2 (95% CI=25, 32)] were recruited. Brachial artery endothelial function was assessed using flow-mediated dilation (FMD). Internal adipose tissue (lAT), subcutaneous (SAT), visceral (VAT) and abdominal SAT was quantified using whole body magnetic resonance imaging and IH magnetic resonance spectroscopy quantified liver and skeletal muscle fat. Cardiorespiratory fitness, glycaemic control, reproductive hormone and lipid profiles were also assessed. FMD was impaired in PCOS when compared with control women [-4.5% (95% CI=-6.3, -2.8), P < O.OOl]. When FMD was adjusted for individual differences in IAT [-4.3% (95% CI=-6.l, -2.4), P < O.OOl], VAT [-4.4% (95% CI=-6.3, -2.5), P < O.OOl] and insulin resistance [-3.9% (95% CI=-5.6, -2.1), P < O.OO 1], the difference in FMD between groups remained. Ten women with PCOS [27y (95% CI=23, 32), 31 kg/rrr' (95% CI=28, 34)] completed a 16-week supervised exercise programme while 7 women with PCOS [29y (95% CI=24, 35), 35kg/m2 (95%CI=31, 40)] opted for conventional care and followed simple lifestyle advice. Exercise training improved FMD to a greater degree than conventional care [3.4% (95% CI=1.8, 5.1), P > 0.0005] and in parallel greater improvements in cardiorespiratory fitness were observed with exercise [4.7ml/kg/min (95% CI=1.4, 7.9), P=0.005]. These changes with exercise occurred independently of changes in VAT, SAT or insulin resistance. NO-mediated vasodilation in the cutaneous microvessels was examined in 11 PCOS [29y (95% CI=25, 34), 34kg/m2 (95% CI=30, 38)] and 6 control women [29y (95% CI=21, 37), 34kg/m2 (95% CI=28, 39)] using laser Doppler flowmetry combined with intra-dermal microdialysis of L-NG-monomethyl arginine to assay the NO dilator system in response to incremental local heating of the forearm. Six women with PCOS [30y (95% CI=22, 37), 31kg/m2 (95% CI=25, 37)] then undertook a 16-week exercise-training programme. Nitric oxide contribution was attenuated in women with PCOS at peak heating [-16.0CVCmax (95% CI=-32.5, 0.6), P=0.05] and during prolonged maximal heating [-15.4CVCmax (95% CI=- 29.6, -1.3), P=0.04], compared with control women. Cardiorespiratory fitness improved by 5.0ml/kg/min (95% CI=0.9, 9.2) following exercise training (P=0.03). This was accompanied by increased NO contribution to cutaneous blood flow between 36.5-42°C (P < 0.05), at peak heating [19.6CVCmax (95% CI=4.3, 34.9), P=0.02] and during prolonged maximal heating [17.1CVCmax (95% CI=2.2, 32.2), P=0.03]. The findings from this thesis suggest that endothelial dysfunction is an intrinsic characteristic of PCOS and that supervised exercise training enhances endothelial function in both conduit vessels and cutaneous microvessels, independent of adiposity or traditional CVD risk factors. The direct impact of exercise training on the vasculature of women with PCOS may decrease the risk of CVD morbidities, such as hypertension, and consequently reduce cardiovascular mortality in post-menopausal years.

No description available.

No description available.