Cold water immersion is commonly used to alleviate the stress and damage that ensues following strenuous exercise. Alongside its purported performance and analgesic benefits recent literature highlights the positive impact it may have towards endurance adaptive responses, particularly on key markers of mitochondrial biogenesis. Despite these recent advances showing PGC-1α, the ‘master regulator’ of mitochondrial biogenesis, being augmented in its post-exercise response by cold water immersion, the precise controlling mechanisms remain to be determined. However, it has been suggested that local cooling effects on AMPK and p38 MAPK related signalling and/or increased systemic β-adrenergic stimulation are involved. Study 1 (Chapter 4) examined whether post-exercise cold-water immersion induced augmentation of PGC-1α mRNA is mediated through local or systemic mechanisms. Participants completed acute cycling followed by seated-rest (CON) or single-leg cold-water immersion (CWI; 10 min, 8°C) with muscle biopsies obtained pre-, post- and 3 h post-exercise from a single limb in the CON condition but from both limbs in CWI (thereby providing tissue from a CWI and non-immersed limb, NOT). Muscle temperature decreased following CWI (-5°C), with lesser changes observed in CON and NOT (-3°C; P<0.05). A significant interaction effect was present for AMPK phosphorylation (P=0.031). Exercise (CON) increased gene expression of PGC-1α 3 h post-exercise (~5-fold; P<0.001). Post-exercise CWI augmented PGC-1α expression above CON in immersed (CWI; ~9-fold; P=0.003) and NOT limbs (~12-fold; P=0.001). Plasma Normetanephrine concentration was higher in CWI vs. CON post-immersion (860 vs. 665 pmol·L-1; P=0.034). Data herein reports for the first time that local cooling of the immersed limb evokes transcriptional control of PGC1-α in the non-immersed limb, suggesting increased systemic β-adrenergic activation of AMPK may mediate, in part, post-exercise cold-induction of PGC-1α mRNA. Study 2 (Chapter 5) assessed the impact of combining a post-exercise cooling stimulus with prior low glycogen as both stressors are shown to separately enhance the post-exercise PGC-1α response. A single-leg depletion protocol and bi-lateral muscle biopsies with and without post-exercise CWI were utilised to give the following conditions: High glycogen control (HI CON), Low glycogen control (LO CON), High glycogen CWI (HI CWI) and Low glycogen CWI (LO CWI). HI limbs began the experimental day ~190 mmol·kg-1dry weight (dw) with low limbs at ~85 mmol·kg-1dw glycogen before undergoing the same relative exercise protocol as Chapter 4. PGC-1α mRNA was different between conditions (P = 0.039) with HI glycogen limbs showing greater expression than contralateral LO glycogen limbs (P < 0.05). PGC-1α mRNA increased to a greater extent in CWI HI vs. CON HI (ES 0.67 Large). Data herein supports previous research that shows post-exercise CWI is able to augment PGC-1α above the exercise response alone, however this response was not evident in heavily depleted limbs (~85 mmol·kg-1dw), suggesting a critical threshold may exist for the expected enhancement of PGC-1α to occur when exercise is commenced in a low glycogen state. Chapter 6 sought to examine the contribution of CWI (Chapter 4, Experiment 1) and/or low muscle glycogen (Chapter 5, Experiment 2) in the activation of PGC-1α via either the canonical (Exon 1a) or the alternative promoter (Exon 1b) regions. Data was obtained using muscle biopsy samples collected from the previous chapters (Chapter 4 and 5). Exercise increased the expression of promoter specific PGC-1α, with greater fold changes seen in Exon 1b. Experiment 1 (Chapter 4) showed PGC-1α Exon 1b expression closely matched the pattern of expression seen for total-PGC-1α, with large, systemic cold-induced increases in the non-immersed (NOT, 2344 fold change from Pre, P = 0.010) and immersed (CWI, 1860 fold change from Pre, P = 0.07), compared with the control limb (CON, 579 fold change from Pre). Results from experiment 2 (Chapter 5) saw PGC-1α Exon 1a and 1b gene expression increase post-exercise, with the Exon 1b response showing lower fold-changes at 3h post-exercise compared to those from Experiment 1 (chapter 4), despite the same exercise protocol being utilised (~200 fold increases in experiment 2 vs. ~2000 fold increases in experiment 1). The data suggests that depletion exercise in the days prior to the experimental day may have raised basal RNA levels, which may have therefore contributed to dampened fold-changes seen post-exercise when relativized to pre-exercise values. The lack of a cold augmentation in promoter specific PGC-1α gene expression in experiment 2 suggests this response may be extremely acute, and may not occur when cooling is undertaken on the third day of exercise. This thesis provides a novel insight into the influence of local, systemic and upstream activating mechanisms regulating the post-exercise, post-cooling and exercising in low glycogen states upon PGC-1α. These findings provide mechanistic application for future study designs and practical application in the support for the use of CWI when the intended target is an upregulation of the gene PGC-1α.

Traditional nutritional approaches for endurance training typically advise high carbohydrate (CHO) availability before, during and after each training session to suppor high training volume, intensity and recovery. However, during the last decade, accumulating data demonstrate that carefully scheduled periods of reduced CHO availability actually augment training-induced oxidative adaptations of skeletal muscle, the so-called train-low paradigm. In accordance with this movement there is also growing rationale ot consume protein before, during and/or after train-low sessions in an attempt to simultaneously promote mitochondrial biogenesis, muscle protein synthesis (MPS) and improve net muscle protein balance. The aim of this thesis was to assess the effects of reduced CHO but high protein availability on the regulation of molecular pathways associated with modulation of the aforementioned components of training adaptation. On the basis of characterising such molecular responses, a secondary aim was to formulate a nevel framework for which to practically apply train-low paradigms. Given the enhanced oxidative adaptatios observed when training in CHO restricted state is potentially regulated through free fatty acid (FFA)-mediated signalling, the aim of study 1 (chapter 4) was to test the hypothesis that leucine-enriched protein feeding before and during exercise does not impair FFA availability or whole body lipid oxidation during exercise. Here I utulised a novel leucine enriched protein gel and compaired this agains a whey drink or placebo gel in a repeated masures design. This study showed that despite the insulemic effects of protein provision, there was no imparment in FFA availability or whole body lipid oxidation during exercise. Therefore, suggesting that protein feeding does not hinder a key objective of train-low sessions. Building on the results from study 1, I next saught to characterise the effects of reduced CHO but high leucine availability on exercise capacity and cell-signalling responses associated with exercise-induced regulation of mitochondrial biogenesis and MPS. While low CHO availability inhibited exercise capacity, comparible mitochondrial signalling responces were seen at the point of fatigue despite participants performing significantly more work in high CHO condition. This demonstrated that training with low CHO is work-efficient in eliciting beneficial signals regulating mitochondrial biogenesis. Despite providing leucine rich protein before, during and after exercise, MPS related signalling could not be rescued during the CHO restriced post-exercise period in the low CHO condition. The data from this study suggest that although there are potential metabolic benefits associated with reduced pre-exercise CHO availability, the post-exercise meal should contain sufficient CHO to restore muscle glycogen to sufficient levels and/or provide the nexessary energy to support post-exercise remodelling process. Having identified the potential detrimental effects of low CHO recovery, the aim of study 3 (Chapter 6) was to examine the role of leucine availability in regulating post-exercise skeletal muscle remodelling processes in recovery from a train-low training session. Here I fed one of two protein types, a collagen (naturally low in leucine) or a whey (naturally high in leucine) protein during a low CHO training session, in a repeated measures design. When considered with study 2, the data from this study suggested that leucine is essential for reactivation of signalling mechanisms involved in protein translation, interestingly while low CHO training appeared to activate components of the system that selectively degrades malfunctional parts of the cell, leucine content had no effect on these processes. When taken together, the novel data presented in this thesis allude to a potential muscle glycogen threshold hypothesis surmising that reduced pre-exercise muscle glycogen may enhance the activation of those pathways regulating mitochondrial biogenesis but also suggest that keeping glycogen (and energy) at critically low levels may impair the regulation if post-exercise remodelling processes. From a practical perspective, data lend support for a potential “fuel for the work required” train-low paradigm in that athletes could strategically reduce CHO availability prior to completing pre-determined training workloads that can be redily performed with reduced CHO availability, thereby inducing a work efficient approach to training. Alternativly, when the goals of the training session are to complete the highest workload possible over more prolonged duration, then adequate CHO should be provided prior to and during the specific training session.

ACL injury is predominant in female footballers largely due to a combination of kinetic and neuromuscular risk factors. The majority of ACL injuries in football occur during an unanticipated cutting manoeuvre, and the risk of this injury is heightened during the final 30 minutes of each half of match-play. Due to an increased injury incidence towards the end of match-play, it is possible that fatigue might serve as a risk factor for ACL injury. However, there currently exists limited research examining the effects of fatigue on a variety of kinetic and electromyographic variables in female footballers during an unanticipated cutting manoeuvre. Neuromuscular training programmes have been utilised in injury prevention studies and proven effective in reducing injury incidence by improving certain kinetic and neuromuscular ACL injury risk factors. The overall aim of this thesis is to examine the effectiveness of neuromuscular training on the fatigue resistance of ACL injury risk factors in female footballers. Study one of this thesis examined the reliability of a combination of kinetic and electromyographic measures in female footballers performing an unanticipated cutting manoeuvre. There were no significant differences in mean values and large to nearly perfect correlations (ICC = 0.49 - 0.96) for all kinetic variables. The majority of kinetic variables displayed a CV of less than 10%, with the exception of loading rates and time to peak force (CV% = 17.33 - 24.51). In comparison to previous research, electromyographic variables displayed a greater range of typical error (CV% = 17.6 - 129.2); however, the majority of electromyographic variables displayed a large, very large or nearly perfect correlation (ICC = 0.26 – 0.91) and no significant differences in the mean score. In line with previous research, standards of reliability, and anticipated changes in response to acute fatigue, all kinetic and electromyographic variables were deemed acceptable to use in subsequent studies. Kinetic variables showed better reliability than electromyographic variables, which was to be expected due to electromyographic measures being a physiological measure. Previous research has established that 16 - 18 year old female footballers are at highest risk of ACL injury, and it is most commonly caused during performance of an unanticipated cutting manoeuvre. It has also been established that the majority of injuries in female football are sustained in the last 30 minutes of each half when fatigue is present. Therefore, acute fatigue appears to be an influential risk factor for ACL injury. Study two of this thesis examined the effects of acute fatigue on the electromyographic and kinetic ACL injury risk factors in 16 - 18 year old female footballers, when performing an unanticipated cutting manoeuvre. A modified SAFT90 protocol was used to mimic football match-play. Data showed that during the unanticipated cutting manoeuvre following the SAFT90, participants produced greater GRF (vGRF; possibly, apGRF very likely), lower GCT (very likely), increased background hamstring activation (0 - 30 ms; very likely) and increased short-latency feedback activation of the hamstrings (31 - 60 ms; likely and possibly). Results suggested that following a simulated match-play protocol, female footballers experienced greater force absorption while utilising a safer muscle recruitment strategy. Therefore, injury prevention training should seek to improve a player’s aility to tolerate ground reaction forces when experiencing acute fatigue, with a large emphasis on enhancing neuromuscular control within the hamstrings muscle group.

Objectives: To understand the experiences of physiotherapists as Extended Scope Practitioners (ESPs) working in acute NHS hospitals using the concepts of Institutional Entrepreneurs engaged in Institutional Work. Design: A qualitative study using an interpretative phenomenological framework. Methods: In depth, semi-structured interviews which were analysed thematically using the steps suggested by Van Manen (1992). Themes which emerged represented the experiences of all the participants. Once the themes were identified the concepts of Institutional Entrepreneurs and Institutional work were applied to provide an understanding of the ESPs` experiences. Participants: 12 ESPs from three acute hospitals from a variety of clinical specialties (2 gynaecology, 3 neurology, 2 orthopaedics, 2 paediatrics, 1 pain management, 1 cardiology, 1 respiratory). Results: The first theme identified the motivation of the participants to extend their remit and create opportunities for the new role. The impact of this, for some participants, was a confused professional identity not aligned with physiotherapy. They felt different to physiotherapists in the way they thought clinically and their methods of practice. This manifested itself in their refusal to wear a uniform. The second theme explored negotiation and agreements of clinical boundaries between the participants, consultants, managers and other clinical staff. The ESPs were proactive and astute basing their actions on both a professional and business logic. They knew when to propose or create an opportunity, when to consider alternatives and when not to act based on the professional relationships with other professions, NHS pressures or likelihood of success. The final theme identified the adaptive nature of ESP roles. The participants were sensitive, and felt vulnerable, to NHS change. They voiced concerns over the sustainability of such posts in terms of succession planning and a lack of framework to develop such roles in the future. Using the typography of Institutional Work provided an understanding of the ESPs` experiences. It identified successful and less successful types of work and enabled discussion on what can be achieved at the micro, individual level, what needs input from the macro, profession level and how the two can support each other. It also identified weaknesses to be addressed that would benefit the professions development. Conclusion: The results from this study address the dearth of literature on the experiences of ESPs and provides details which will have resonance with physiotherapists and insight for other professions. It is recommended that a more robust ESP professional network, to champion and diffuse new practice into the NHS, is needed. Secondly there is a need for a recognised and nationally validated education programme for extended practice. This study refines the institutional work concept and highlights the inter-relationships between diverse types of work. It challenges the assertion of a sequential order of institutional work and illustrates how individuals embedded in the institutions of the NHS and physiotherapy can stimulate change through strands of institutional work that are sympathetic to the workplace environment and culture. This study provides empirical evidence that institutional work is performed by ordinary individuals which can diffuse through a profession. In doing so it provides insight for physiotherapists and other professions as to ways and means this can be achieved.

Pre-participation cardiac screening (PCS) of the athlete has recently become mandatory by many national and international sporting governing bodies and aims to identify those at risk of sudden cardiac death (SCD) from an undiagnosed cardiac condition. The term athletes’ heart (AH) describes the physiological adaptation that occurs from chronic exposure to exercise training however, this process can mimic cardiac remodelling caused by pathological conditions such as cardiomyopathy. Transthoracic echocardiography (TTE) plays an integral role during PCS however, differentiation from inherited conditions is often based on a ‘one size fits all’ interpretation of echocardiographic derived measures. To improve the sensitivity and specificity of echocardiography in PCS it is pertinent to understand normal physiological cardiac adaptation in specific sporting disciplines. This thesis focuses on cardiac structure and function of the elite, male, rugby football league (RFL) athlete with the application of TTE including novel speckle tracking echocardiography (STE). The aims of this thesis were 1) to establish left ventricular (LV) structural and functional indices of the senior RFL athlete using TTE and STE and a mathematical model of the structural-functional relationship; 2) to determine structural and functional indices of the right heart of the senior RFL athlete using TTE and STE; 3) to provide a comparative and holistic, structural and functional assessment of the junior and senior RFL athletic heart using TTE and STE and 4) To assess variation in cardiac parameters across the competitive season in the senior RFL athlete using TTE and STE. A comprehensive cardiac assessment of the elite RFL athlete was established throughout this thesis. The LV has a predominance for normal LV geometry irrespective of age or seasonal time point. Mathematical modelling highlights the interaction of divergent effects of left ventricular cavity size (LVIDd) and mean wall thickness (MWT) on LV function to maintain a normal ejection fraction (EF). Significant regional variation in LV STE parameters was apparent including lower apical rotation and twist parameters in senior athletes compared to controls (8.2 ± 3.9 ̊ vs. 11.2 ± 4.6 ̊ and 14 ± 4.7 vs 16.1 ± 4.6 ̊ respectively) suggesting potential adaptive mechanisms to training. The right ventricle (RV) and right atrium (RA) are larger in athletes compared to controls even after scaling (proximal right ventricular outflow dimension in parasternal long axis (RVOTplax) (23 ± 3 vs. 20 ± 2 mm/(m2)0.5), proximal right ventricular outflow dimension in parasternal short axis (RVOT1) (24 ± 3 vs. 21 ± 3 mm/(m2)0.5) and RA volume (RAvol) (22 ± 5 vs. 16 ± 4 ml/(m2)1.5)). The RVOT and RA are also larger in senior compared to junior athletes (RVOTplax (23 ± 3 vs. 22 ± 3 mm/(m2)0.5, RVOT1 (24 ± 3 vs. 23 ± 3 mm/(m2)0.5 and RAvol (22 ± 5 vs. 21 ± 5 ml/(m2)1.5) suggesting that the right heart is more sensitive to chronic training. Despite significant structural remodelling, RV function in the RFL athlete is normal as assessed by TTE (right ventricular fractional area change (RVFAC) > 33% and STE RV strain (ɛ) < -21%), irrespective of age and time of season. Significant seasonal functional changes were observed with STE as apical rotation (pre-season, 9.8 ± 4 ̊; mid-season, 6.1 ± 2.8 ̊; end-season, 5.8 ± 3.2 ̊ and post-season break, 6.6 ± 3.1 ̊) and twist (pre-season, 16.6 ± 4.7o; mid-season, 12.6 ± 4o; end-season 12.1 ± 4.5o and post-season break, 12.4 ± 3.5 ̊) are higher at pre-season than at any other time-point, highlighting physiological variation during the RFL season. The use of standard and novel echocardiographic techniques have provided further understanding of the normal physiological adaptation of the AH in RFL athletes which may lead to improvements in PCS of this athlete group.

Congested activity schedules are common in soccer, with implications for impaired performance and increased injury risk. It has recently been suggested that valid soccer-specific exercise protocols (SSEP’s) may offer a unique opportunity to assess the physical demands associated with periods of fixture congestion. Fixture congestion in the current thesis is defined as a high frequency of soccer-specific activity performed with less than or equal to seventy-two hours of recovery interspersing successive bouts. Study one describes the development of a novel treadmill-based SSEP characterised by clusters of high intensity (HI) efforts. The SSEP was validated against the velocity profile and total distance (TD) covered, and elicited a physical response comparable to match-play. Study two utilised the same SSEP to consider the physical response associated with successive bouts of soccer-specific activity interspersed with either 48 or 72h recovery. There was no difference in the fatigue response associated with two soccer simulations, with 48 h sufficient for full recovery of the physiological and PlayerLoadTM data. The 48 h recovery was therefore applied in Study three, where three games in a week is typically the worst case scenario for fixture congestion. Study three quantified the cumulative and residual physiological and biomechanical response associated with the completion of three successive bouts of the SSEP, completed with 48 hrs recovery between each trial. Study three also assessed the physical response associated with successive bouts of different exercise modalities (continuous, repeat-sprint, and intermittent), specific to the demands of the SSEP. The physical response was specific to each activity modality, but the volume of work and number of HI efforts performed across the three SSEP’s elicited a mechanical and muscular emphasis with residual fatigue. Study four attempted to assess the effectiveness of an interchange rule on reducing the cumulative and residual physical fatigue response associated with the completion of the SSEP. The interchange rule appeared to elicit a positive effect on the physiological and perceptual response to, and rate of mechanical recovery following the completion of the SSEP. Study five focused on developing and assessing the effectiveness of a novel post-match active recovery protocol on aiding the rate of post-trial mechanical and perceptual recovery. The active recovery protocol had a positive effect on the eccentric knee flexor angle of peak torque data recorded at 300 deg·s-1. The current series of studies offers a mechanistic understanding of the physical response associated with periods of short-term fixture congestion in soccer. The current studies have implications for the design and micro management of training and competition schedules, and the contemporary use of biomechanical analyses to quantify markers of performance and injury.

By theoretically framing sportspeople’s drinking within a social identity perspective, this thesis aims to elucidate the social psychological processes underpinning the link between sport group membership and alcohol use. It is argued that focusing on these group-level processes provides theoretically grounded foundations for applied practice. The thesis utilised both quantitative and qualitative methods. Secondary data analyses in Study 1 indicate that athletic identification plays a significant role in shaping alcohol consumption in different sporting contexts. Study 2 examined longitudinally personal and group-based social identities. Results indicated that alcohol consumption increased sports group identification over time, and this identification positively related to wellbeing. In contrast, a personal athletic identity was weakly associated with alcohol behaviours, indicating that there may be utility in harnessing these dual identities when addressing health in sport. Qualitative explorations in Study 3 exposed sport-related drinking as strategic and functional practices that served to provide a positive sport experience at the group-level. To achieve this, the sports group exhibited self-monitoring and regulating influences, whereby members’ alcohol behaviours could both be encouraged or deterred by the wider group. Experimental manipulations in Study 4 sought to examine effects of alcohol consumption and social identity processes between sporting and non-sporting participants. Findings indicate that intoxication exaggerates in-group biases for those highly identified with their group, pointing to a hitherto unexamined interplay between the psychopharmacological effects of alcohol and intergroup behaviour. Overall, the thesis highlights the central role of sport-related identities in defining alcohol behaviours. Its contributions outline how a number of social identity processes (identification, wellbeing, self- and social control) may be drawn upon to address risky drinking among student sportspeople.

Cardiovascular adaptations to long-term high intensity causes physiological remodelling of the Right ventricle (RV) due to frequent exposure to elevated exercise intensity. Evidence suggests dynamic exercise training serves as the primarily stimulator for the RV adaptation. This cardiac adaption might exceed the cut off limit meeting structural criteria for arrhythmogenic right ventricular cardiomyopathy (ARVC) disease. Athlete pre-participation screening is focused on detecting pathological conditions like ARVC. Current issues include: indices that differentiated ARVC patients and healthy people; the impact of different levels of dynamic training exposure on the RV structure, function in elite male athletes; insight into the RV structural and functional in those athletes meet the structural TFC (MTFC) for ARVC and those that do not (NMTFC) via utilising 12-leads Electrocardiography (ECG) and echocardiography. Study one is a systematic review and meta-analysis technique that employed a case-control design sought to determine the extent of the RV structural and functional ranges in ARVC. In second study, athletes were grouped according to their sporting discipline using the Mitchell Classification as Low Dynamic (LD), Moderate Dynamic (MD) or High Dynamic (HD) and underwent through traditional and novel echocardiography techniques with a focused and comprehensive assessment of the RV. In study 3, athletes were grouped to MTFC for ARVC and those NMTFC. Study four, retrospective study looking at the 12-lead ECG for athletes in study MTFC compared to NMTFC. The key finding form the first study was a significant differences in a range of structural and functional echocardiographic parameters between ARVC patients and healthy control participants. Patients with ARVC had larger RV outflow tract (RVOT) diameter at short-axis view (mean ± SD; 34 vs. 28 mm P < 0.001) and RV end-diastolic area (23 vs. 18 cm2 P<0.001) compared to healthy controls. ARVC patients also had lower value on conventional and global RV strain (ε) parameters. HD and MD sport disciplines in second study had generally larger absolute and scaled RV structural indices than LD group. There were no between group differences in conventional RV functional indices as well as global RV ε (LD: -23.4 ± 3.1 vs MD: -22.7 ± 2.7 vs HD: -23.5 ± 2.6, %) and strain rate (P > 0.01). The base to apex ε gradient in the RV septum was lower in the MD athletes compared to HD and LD due to a lower apical septal ε which significantly correlated with absolute RV chamber size. In third study, MTFC had larger absolute and scaled RVOT diameter compared to NMTFC (P ˂0.05) but these athletes did not develop a proportional increase in the RV inflow dimensions. MTFC also had lower global RV ε, peak systolic and late diastolic tissue velocity compared to NMTFC. Study four, MTFC had generally normal ECG finding compared to NMTFC. The finding have important implication for cardiovascular screening of athletes.

Postural balance is one of the most important aspects of everyday movement, especially in complex movements such as jumping, kicking or movements involving overhead/arm motion. In sporting activities, players often need to complete goal-directed tasks of an end-effector (e.g. tennis racket), while also needing to control their balance, in order to produce a successful task. However, studying the interaction between postural balance and end-effector control, in a biomechanical context and particularly in the tennis serve is difficult and remains largely unexplored. Traditionally, to explore postural balance researchers have to observe the whole-body centre of mass (CoM) location. However, for marker-based motion capture systems, collecting and processing data is time-consuming. If the researchers are interested in examining the movements of only some parts of the body, then reductions in model complexity may be possible while still retaining an ability to track CoM location. Therefore, the first aim of this research was to find an appropriate biomechanical model to quantify accurate whole-body (X)CoM representation. The second aim was then to investigate the interaction between postural balance control and end-effector performance, during the tennis serve, within a single target location and between different serving locations. The first study of this thesis showed that anteroposterior and medio-lateral displacement profiles of the CoM representation, based on the lower limbs, trunk and upper limbs showed strong agreement with the full-body model, and this only slightly reduced for the lower limbs and trunk only. Representations based on the lower limbs only showed less agreement, particularly for the extrapolated CoM (XCoM) in kicking. Our results justified the use of some model reductions for specific needs, saving measurement effort whilst limiting the error of tracking (X)CoM trajectories in the context of whole-body balance investigation. The second study of this thesis demonstrated that there is no direct interaction between the XCoM displacement, the changes in arms/trunk angular momentum, and maximum racket velocity during the preparation, propulsion and forward swing phases of a tennis serve. Only in the forward swing phase, a significant relationship between trunk angular momentum and maximum racket velocity was found which means the trunk segmental acceleration may play a role in controlling balance when generating the maximum racket velocity during the serve towards this target location. The third and final study in this thesis focussed on only the forward swing phase, and indicated that only the change in arms angular momentum influenced the maximum racket velocity. This was found specifically when serving into the wider part of the advantage court. Furthermore, individual relationships were evident between serving conditions. The novel approach introduced in this thesis, and the key outcomes of the work, have the potential to give researchers, coaches and athletes, who are working and playing in relevant dynamic sporting tasks, an opportunity to better understand the interaction between how control of the end-effector adapts while maintaining postural stability during the serve. Moreover, the work also guides the choice of biomechanical marker sets to estimate the centre of mass during dynamic activity.

Ischaemic preconditioning (IPC) is an intervention whereby brief intermittent ischaemic episodes are induced in a limb (usually 4x5-minute arterial occlusion bouts, interspersed with 5-minutes of reperfusion) either at the site of interest (IPC), or at a distance from the site of interest (Remote; RIPC). Although originally linked to cardiology, recently studies have investigated the effects of IPC administered on a limb prior to exercise with some showing improvements in exercise performance. The overarching aim of the present thesis was to investigate how to optimise IPC to further enhance exercise performance. The optimal protocol of IPC on exercise performance was quantified by manipulating: 1. the number of cycles, 2. amount of muscle tissue, and 3. local vs Remote occlusion, which were applied in a randomized counterbalanced order in study 1 (Chapter 3). IPC dose, location and occlusion area differed prior to a 375 KJ time trial (TT) performance in 12 trained men. The traditional 4x5-min IPC stimulus resulted in the fastest TT time compared to SHAM [17 secs (90% CI: 0, 34 secs); P=0.097], but there was no benefit of applying a greater number of cycles [5 secs (-35, 26 secs); P=0.49] or employing unilateral IPC [18 secs (-11, 48 secs, P=0.29]. Local versus Remote cuff placement did not result in changes in TT time [0 secs (-16, 16 secs; P > 0.9]. Overall, regardless of location, the 4x5-minute dose seemed to provide the most benefit to exercise performance. The ability of IPC to enhance exercise capacity may be mediated through altering exercise-induced blood flow and/or vascular function. Study 2 (Chapter 4) investigated the blood flow response to exercise, using ultrasound, when exercise was preceded by a control (SHAM) condition, or either local or Remote (R)IPC in eighteen recreationally trained males. Vascular 4 function tests were also performed before SHAM and (R)IPC and at the end of exercise. IPC resulted in enlarged brachial artery diameter during exercise [0.016 cm (0.003 to 0.03 cm); P=0.016] compared to RIPC, but blood flow during exercise was similar between conditions. No changes in post-exercise vascular function were observed between conditions. Therefore, enhanced vasodilation following local (but not Remote) IPC, when performed prior to exercise, does not translate into increased blood flow during exercise nor impact post-exercise vascular function. IPC could alleviate deleterious muscle damage responses after exercise-induced muscle damage (EIMD; often lasting < 72 hours). Study 3 (Chapter 5) investigated whether IPC could negate eccentric exercise-induced reductions in torque production. Eleven recreationally trained males completed 200 repetitions of maximal eccentric contractions when preceded by IPC or SHAM performed in a randomized order, separated by a 9-week washout period. Muscle function tests were performed after IPC/SHAM prior to eccentric exercise and at 1-hour, 24-hours, 48-hours & 72-hours post-EIMD. Venous blood samples were taken at all time points. Greater maximal [15.2 N.m-1 (6.2 to 24.1); P=0.006] and mean [13.3 N.m-1 (5.3 to 21.3); P=0.007] torque production during a fixed angle voluntary maximal voluntary contraction (MVC) task and during a 60 deg·sec-1 [10.1 (4.9 to 15.3); P=0.002 & 9.8 N.m-1 (6.1 to 13.5; P < 0.005] isokinetic task were evident after IPC versus SHAM prior to eccentric exercise (EIMD). This was maintained throughout the (72-hour) muscle damage window. Lower cytokine (IL-6 and IL-1ra) were reported after IPC versus SHAM (P < 0.002, respectively). IPC resulted in greater overall HSP-27 & 32 levels (P < 0.01) whilst HSP-72 was lower (P=0.001) versus SHAM. Therefore, IPC can enhance maximal torque production during isokinetic dynamometry, before and after muscle damaging exercise and induce advantageous extracellular stress responses to EIMD in humans. 5 Study 4 employed IPC in a practical exercise-priming model, that aimed to maximise repeated sprint ability (RSA). Eleven trained cyclists performed 4 experimental visits in a repeated measures design. The "traditional" 4x5-minute local IPC (IPC) dose was compared to a SHAM condition (20 mmHg). IPC or SHAM were performed on two separate visits, each combined with either passive muscle heating (HEAT) on two visits, or thermoneutral (non-heated) insulation on two visits, prior to an "all out" repeated sprint task (10x6-second sprints with 24-seconds of recovery). There were no meaningful changes in 10x6-second average [12 (-7 to 31) watts; P=0.28] or peak [6 (-14 to 26) watts; P=0.62] power output following IPC versus SHAM. Additionally, no benefit was observed when muscle temperature was elevated in combination with IPC [5 (-14 to 19) watts; P=0.67], or separately to IPC [9 (-9 to 28); P=0.4] versus SHAM. Overall, it appears that IPC, nor (the combination of) muscle heating can positively impact RSA performance in trained cyclists versus a SHAM condition. The findings from this thesis suggest that using a "traditional" dose of 4x5-minute cycles, either on the legs or the arms, promote performance enhancements in aerobic tasks such as cycling TT performance. These potential performance improvements are likely not resultant from increased limb blood flow. IPC can also enhance muscle function following muscle damaging exercise and induce advantageous extracellular stress responses to EIMD. Nevertheless, IPC alone or when combined with local muscle heating likely has no meaningful enhancements in repeated sprint cycling performance. The findings from this thesis may help athletes to establish a better understanding of how IPC can be used prior to exercise.