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Oxygen uptake ( O2) kinetics determine the magnitude of the O2 deficit and the degree of metabolic perturbation and is considered to be an important determinant of exercise tolerance; however, there is limited empirical evidence to demonstrate that O2 kinetics is a direct determinant of exercise tolerance. The purpose of this thesis was to investigate O2 kinetics as a determinant of exercise tolerance and to consider its potential interaction with the maximum O2 ( O2max) and the W′ (the curvature constant of the hyperbolic power-duration relationship) in setting the tolerable duration of exercise. Recreationally-active adult humans volunteered to participate in the investigations presented in this thesis. Pulmonary O2 kinetics was assessed on a breath-by-breath basis and exercise tolerance was assessed by a time-to-exhaustion trial, with exhaustion taken as the inability to maintain the required cadence. A period of repeated sprint training (RST) resulted in faster phase II O2 kinetics (Pre: 29 ± 5, Post: 23 ± 5 s), a reduced O2 slow component (Pre: 0.52 ± 0.19, Post: 0.40 ± 0.17 L•min-1), an increased O2max (Pre: 3.06 ± 0.62, Post: 3.29 ± 0.77 L•min-1) and a 53% improvement in severe exercise tolerance. A reduced O2 slow component and enhanced exercise tolerance was also observed following inspiratory muscle training (Pre: 0.60 ± 0.20, Post: 0.53 ± 0.24 L•min-1; Pre: 765 ± 249, Post: 1061 ± 304 s, respectively), L-arginine (ARG) administration (Placebo: 0.76 ± 0.29 L•min-1 vs. ARG: 0.58 ± 0.23; Placebo: 562 ± 145 s vs. ARG: 707 ± 232 s, respectively) and dietary nitrate supplementation administered as nitrate-rich beetroot juice (BR) (Placebo: 0.74 ± 0.24 vs. BR: 0.57 ± 0.20 L•min-1; Placebo: 583 ± 145 s vs. BR: 675 ± 203, respectively). However, compared to a control condition without prior exercise, the completion of a prior exercise bout at 70% Δ (70% of the difference between the work rate at the gas exchange threshold [GET] and the work rate at the O2max + the work rate at the GET) with 3 minutes recovery (70-3-80) speeded overall O2 kinetics by 41% (Control: 88 ± 22 s, 70-3-80: 52 ± 13 s), but impaired exercise tolerance by 16% (Control: 437 ± 79 s, 70-3-80: 368 ± 48 s) during a subsequent exercise bout. When the recovery duration was extended to 20 minutes (70-20-80) to allow a more complete replenishment of the W′, overall kinetics was speeded to a lesser extent (by 23%; 70-20-80: 68 ± 19 s) whereas exercise performance was enhanced by 15% (70-20-80: 567 ± 125 s) compared to the control condition. In addition, the faster O2 kinetics observed when exercise was initiated with a fast start (FS; 35 ± 6 s), compared to an even start (ES; 41 ± 10 s) and slow start (SS; 55 ± 14 s) pacing strategy, allowed the achievement of O2max in a 3 minute trial and exercise performance was enhanced. Exercise performance was unaffected in a 6 minute trial with a FS, despite faster O2 kinetics, as the O2max was attained in all the variously paced trials. Therefore, the results of this thesis demonstrate that changes in exercise performance cannot be accounted for, purely, by changes in O2 kinetics. Instead, enhanced exercise performance appears to be contingent on the interaction between the factors underpinning O2 kinetics, the O2max and the W′, in support of the proposed ‘triad model’ of exercise performance.

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The aim of these experiments was to investigate the influence that dietary manipulation has upon acid-base balance and substrate availability at rest and during high intensity exercise. It was hoped to identify some of the mechanisms that may control the utilisation of energy substrate and influence the onset of fatigue during high intensity exercise. A pattern of dietary and exercise manipulation intended to alter carbohydrate (CHO) and fat availability was undertaken during the first two experiments. In addition to influencing energy substrate availability, the diet and exercise regimen also significantly influenced resting acid-base balance and high intensity exercise capacity. The reduction in exercise performance afer administration of a low CHO, high fat, high protein diet may have been due to the diet-induced acidosis produced by this diet. However, it is also probable that glycogen availability was influencing exercise performance in this situation. A fixed period of exercise under the same experimental conditions indicates that a higher than normal muscle glycogen content may dictate the pattern of substrate utilisation during high intensity exercise. In a second series of experiments it was demonstrated that dietary manipulation alone will influence acid-base balance and exercise capacity. A high fat, high protein diet will produce a metabolic acidosis but will not influence total muscle glycogen content. In this situation, it is unlikely that a reduction in high intensity exercise performance can be attributed to the availability of muscle glycogen. It is possible that a change in fat availability, rather than muscle glycogen content, will influence the pattern of substrate utilisation during high intensity exercise. However, it is unlikely that a change in fat availability will be responsible for the reduction in exercise capacity recorded after a high fat, high protein diet. The reduction in exercise capacity may be the result of a diet-induced acidosis. Although it is unlikely that dietary acidosis will influence H+ efflux from muscle it may influence pre-exercise muscle buffering capacity. The resulting greater decline in muscle pH during exercise after a high fat, high protein diet may influence muscle function: firstly, by inhibiting the activation of muscle contraction which is due possibly to a reduction in the release of Ca2+ from the sarcoplasmic reticulum and a reduction in the affinity of the myofilaments to Ca2+. Secondly, by inhibiting muscle relaxation which is thought to result from a disruption in actin-myosin corss-bridge separation and a reduction in the rate of Ca2+ removal from the myofibril cytoplasm. Thirdly, by inhibiting muscle glycolysis at the point of PFK. Finally, there is some evidence to suggest that the rate of muscle lactate efflux and/or the metabolic fate of lactate produced during high intensity exercise are different from normal after a period of dietary manipulation.

Approved for public release; distribution is unlimited / Modeling fatigue, sleepiness, and performance is of significant interest to military leaders because military operations often provide limited sleep opportunities for many individuals. The ANAM Readiness Evaluation System (ARES) Commander Battery is under consideration as a quick, inexpensive method of testing a crewmember's level of functioning. This thesis analyzed data collected during a previous field fatigue study conducted at the Naval Officer Indoctrination School (OIS) in Newport, Rhode Island. Linear mixed-effects models were developed and ARES data were evaluated for how they vary across participants, testing sessions, and time of day. / Lieutenant, United States Navy Reserve

Cancer-related fatigue (CRF) is a subjective, distressing symptom for a majority of cancer patients and survivors. CRF is commonly an under-diagnosed, under-treated, and underreported symptom that negatively affects the lives of patients causing decreased quality of life,impairment, and negative socioeconomic consequences (NCCN, 2014; Weis & Horneber, 2015). The purpose of this study is to determine whether oncology providers are assessing for CRF utilizing an evidence-based tool and understanding their attitudes towards CRF assessment inpractice. The aim of this project is to evaluate and potentially improve the awareness and assessment of CRF in the cancer patient population by utilizing an evidence-based assessment tool. A survey was administered to oncology providers (Advanced Practice Registered Nurses(APRNs), MDs, DOs, and PAs) in the state of Arizona via emails and flyers. Data collected included demographics of participants, practice characteristics, CRF assessment and use of evidence-based tools, CRF assessment barriers, CRF interventions, and CRF assessment attitudes and beliefs. Data from 31 surveys were used for analysis. A majority of the respondentswere female (84%, n=26) and APRNs (76%, n=22). All of the providers surveyed reported assessing for CRF in practice; however, 62% (n=18) of providers did not utilize an evidence based tool for CRF assessment. Every provider agreed they felt comfortable assessing for CRF,that it was important, and their responsibility in practice. Sixty-two percent of providers (n=18)stated they were likely to research more information on CRF assessment for use in their practice after the survey. A Fisher's exact test was completed to determine if there was a relationship between the type of provider and use of an evidence-based CRF assessment tool. With the alpha set at 0.05 the p-value was 0.677, not significant, meaning there was no relationship between the type of provider and use of an evidence-based CRF assessment tool. After analysis of results, it was concluded that further education would be beneficial to enhance provider knowledge of evidence-based CRF tools and available clinical practice guidelines on CRF. The continued education would work to improve patient CRF assessment and treatment in cancer patients. Further research is also needed to improve knowledge of CRF evidence-based tools and barriers to their use in practice.