Title: Comparing hydration practices of long-distance runners during intended training, an intended event, and an actual event during COVID-19. Context: Prior studies on long-distance runners have yet to compare hydration practices intended in training to an actual event. Optimal hydration strategies and knowledge of EAH was assessed. Objective: The purpose of this research was to assess and compare the self-reported hydration practices of long-distance runners during an intended training run, an intended event, and during an event. Design: Cross-sectional online survey design Setting: 2020 Hyannis, Massachusetts Marathon; Connecticut trail races; online. Participants: There were 46 participants in the Hyannis, 26 participants in the Connecticut trail races, and 203 participants in the long-distance running studies. Main outcome Measure(s): Survey questions addressed hydration practices, including hydration strategies, and volumes consumed before and during a run. Additional data included demographics, training experience, sources of hydration information, and knowledge of EAH. Results: When comparing volumes consumed, higher correlations were found when comparing intended events in all three studies. In other words, runners intended to drink the same in an intended training run and an intended event. More variation was found when comparing intended volumes to actual volumes. All studies showed strong agreement in the selected hydration strategies between the scenarios and most were statistically significant. The “drinking to thirst hydration strategy”, was selected on average 17% of the time for Hyannis marathoners, 30% of the time for Connecticut trail runners, and 23% of the time for long-distance runners. This hydration strategy is recommended to decrease the risk of EAH in lieu of a personalized hydration plan. EAH awareness among runners was reported between 50-59% of the time in all studies. However, there was inconsistency in recognizing contributing and preventive EAH factors. Conclusion: There were differences in hydration practices when comparing an intended training run, an intended event, and an event. This indicates a need for ongoing education on hydration practices and EAH. If runners mimic appropriate hydration practices during training when running in an event, the risk of EAH may be decreased. The limitation of this research is the self-reported nature of historical data.

京都大学 / 0048 / 新制・課程博士 / 博士(農学) / 甲第21133号 / 農博第2259号 / 新制||農||1057(附属図書館) / 学位論文||H30||N5107(農学部図書室) / 京都大学大学院農学研究科食品生物科学専攻 / (主査)教授 保川 清, 教授 金本 龍平, 准教授 井上 和生 / 学位規則第4条第1項該当 / Doctor of Agricultural Science / Kyoto University / DFAM

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This study investigated the assessment of muscular endurance using the Universal Gym. Subjects included 19 women and 151 men (18-30 years). Measures of muscular endurance were evaluated at various percentages of 1 RM on twelve exercise stations and it appears that a percentage of 1 RM ranging from .7 for the arms, .5 to .9 for the legs, and ,5 to .8 for the trunk is required to produce fatigue state in the necessary repetition range.

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<p> In order to investigate possible negative effects of endurance training on muscle strength and power, 10 healthy young men underwent 10 weeks of endurance training. Subjects trained unilaterally on a cycle ergometer so that their opposite leg served as a control. Training consisted of 30 min per day for 3 days per week and progressed to 60 min per day for 5 days per week by the seventh week of training. This volume of endurance training exceeds the upper limits of that normally performed by athletes who compete in power sports. The exercise intensity was initially ~75% of pre-training maximum power output and was increased over time to maintain a training heart rate of 140-160 beats per minute. Endurance, strength, and power variables were assessed in each leg before and after the training period. Measurements included electrically stimulated twitch characteristics of the quadriceps, single-leg V̇O2peak and lactate threshold (Tlac), single-leg take-off vertical jump power indices from a force platform, and maximal leg press strength at a low-(60°/s) and high-velocity (300°/s). Needle biopsies were taken from the quadriceps femoris before and after the training period, and analyzed for fibre-type proportions, fibre area, oxidative enzyme activity and capillary density. Post-training, subjects increased leg V̇O2peak (7%) and Tlac in the trained leg. Leg press strength was unaffected by training. Vertical jump power was not impaired nor were evoked twitches. Following training, there was a decrease in % type IIb and an increase in % type IIa fibres (p<0.05). There were no significant changes in fibre area. Percent fibre area increased for type I and IIa and decreased for type IIb fibres in the trained leg (p<0.05). These data indicate that a 10-week endurance-training program increases aerobic power but does not impair muscle strength or power.</p> / Thesis / Master of Science (MSc)

Endurance exercise has been shown to both raise and lower leucine oxidation in studies in rodents. We studied the effects of a 38 d endurance exercise training program upon leucine turnover during a 90 min exercise bout at 60 % VO_2peak in 6 males and 6 females. Subjects were studied at both the same absolute (ABS) and relative (REL) exercise intensities post-training. Pre (PRE)- and post-training measurements were taken for analysis of: L-[1-^13C]leucine turnover, muscle branched-chain oxoacid dehydrogenase activity (BCOAD), muscle glycogen, phosphocreatine and ATP utilization, and resting enzyme activity of citrate synthase (CS) and NADH-cytochrome c-oxidoreductase (complex I-III). We also determined total substrate oxidation by indirect calorimetry, and plasma lactate, glucose, and insulin concentrations. The exercise training resulted in a significant increase in both CS (P < 0.001) and complex I- III (P < 0.05) activities. Leucine oxidation increased during exercise for the pre-training trial (P < 0.001), however, there was no increase for either the post-training ABS or REL trial. Leucine oxidation was significantly lower for females at all time points (P < 0.01). Total BCOAD activity was also significantly increased when comparing the PRE to both ABS and REL trials (P < 0.001). The % activation of BCOAD was significantly increased from t=0 to t=90 in both the PRE and REL exercise trials with the increase in PRE being greater (P < 0.001 (PRE), and P < 0.05 (REL)). Exercise RER was lower for females vs. males (P< 0.05). In addition, the ABS trial was significantly lower than PRE and REL (P < 0.01). Plasma lactate was significantly lower at all time points for ABS vs. PRE (P < 0.001) and REL vs. PRE at t=30 min of exercise (P < 0.001). Resting muscle glycogen was higher for both ABS and REL vs. PRE (P < 0.001). In conclusion, we found that 38 d of endurance exercise training significantly attenuated both leucine oxidation and BCOAD activation during 90 min of endurance exercise at 60 % VO_2peak for both absolute and relative exercise intensities. In addition, females were also shown to oxidize a greater proportion of energy from lipid and a lesser amount from carbohydrates and proteins during exercise. / Thesis / Master of Science (MS)

Exercise is known to induce changes in the gut, typically referred to as the ‘forgotten organ’, and changes in gut microbiota can also occur with exercise possibly imparting systemic benefits. The question remains whether or not microbiota from an exercised animal can independently affect skeletal muscle morphology. Our first objective was to examine whether an endurance exercise program could modify the microbiota in donor mice. Second, we aimed to elucidate if such an endurance-trained microbiota could be transferred to germ-free mice via fecal inoculation. Finally, we sought to determine how the morphology and functional characteristics of skeletal muscle were influenced as a result of fecal inoculation. We hypothesized that germ-free mice recipients inoculated with the microbiota from endurance trained donors would undergo morphological changes in muscle fibre type composition and physiological changes in skeletal muscle function associated with a more oxidative phenotype. Eight-week-old male C57BL/6NCrl donor mice (n = 20) were randomized into two groups: one group completed an endurance exercise training protocol on a treadmill machine 3x/week for 11 weeks (n = 10) while one group remained cage-bound (n = 10). Ten-week-old male (n = 7) and female (n = 9) germ-free mice were colonized with the cecal microbiota of the donor mice in that, equal numbers of germ-free mice were inoculated with exercised-microbiota as sedentary-microbiota. Glucose metabolism and performance measures were evaluated in the donors as well as the recipients post-inoculation. Muscle tissue was extracted for immunohistochemistry and mitochondrial assays. During the intra-peritoneal glucose tolerance test (IPGTT), significant differences in blood glucose were found at 30min between exercise-inoculated and sedentary-inoculated (23.4 ± 2.2; 29.0 ± 1.9 mmol/L, p<0.05).and change in blood glucose relative to baseline (12.04 ± 2.4; 18.3 ± 1.9 mmol/L, p<0.01). There were significant sex-based differences in the blood glucose response in inoculated animals such that there were significant differences in blood glucose between the exercise-inoculated females and sedentary-inoculated females at 15mins (28.4 ± 2.4; 30.6 ± 1.1 mmol/L, p<0.05) and 30mins (24.7 ± 3.6; 29.9 ± 2.4 mmol/L, p<0.01), however no differences between exercise-inoculated males and sedentary-inoculated males. In addition, there were significant differences in the change in blood glucose relative to baseline between the exercise-inoculated females and sedentary-inoculated females at 15mins (12.3 ± 1.9; 20.6 ± 0.8 mmol/L, p<0.01) and 30mins (10.2 ± 2.6; 19.9 ± 2.1 mmol/L, p<0.001). This novel characterization of a link between gut microbiota and skeletal muscle suggests a transmissible capacity of microbiota to impart properties of ‘healthy’ muscle into compromised populations. / Thesis / Master of Science (MSc) / The gut microbiome or microbiota describes the composition of the human gut – remarkably, over 100 trillion bacterial cells live in symbiosis with the cells of the human body. Research from the past decade has elucidated the salient nature of the human gut microbiome on immunity, metabolic homeostasis, and overall health and disease. Transformative research in the field has demonstrated the ability to transfer these bacterial colonies from one individual to another and elicit change, such as altering body mass and adiposity, respective to their donor. The interaction between gut microbiota and other organ systems i.e. brain, liver, adipose tissue has been the focus of several recent investigations, suggesting that lifestyle changes such as diet and exercise can influence communication between the gut and various other organs and contribute to changes in function. Skeletal muscle is the largest muscle in the human body accounting for 40% of total mass and although the main role of skeletal muscle is locomotion and postural stabilization, it is integral for the regulation of blood glucose as well as a reservoir for other macronutrients. Acute and chronic physical exercise cause a myriad of adaptive responses throughout the human body including in skeletal muscle and the gut. Therefore, the existence and influence of a gut-muscle link or ‘axis’ on human health cannot be ignored. What is unclear exactly, is if exercise-induced adaptations in the gut of an individual can be transferred to elicit change in the gut of a recipient and further induce adaptations at the level of the skeletal muscle.

Duchenne muscular dystrophy (DMD) is a fatal, x-linked disease that causes progressive muscle weakness and susceptibility to damage. DMD is caused by a lack of dystrophin, a large muscle protein that performs both structural and signaling functions. A promising treatment currently in clinical trials is microdystrophin gene therapy, which delivers a truncated version of dystrophin to muscle via a viral vector. Preclinical studies have established efficacy of microdystrophin to improve muscle quality and function. With clinical success of this treatment, patients affected by DMD could become more physically active. However, the effect of exercise on both dystrophic and gene therapy-treated muscles is unclear. Recently, we demonstrated that microdystrophin gene therapy with and without 21 weeks of voluntary wheel running (VWR) improved treadmill time to fatigue and in vivo plantarflexor torque output in young mdx mice, a mouse model of DMD. Although treated mice could run well, diaphragm force and power output were blunted by VWR. A subsequent study tested longevity of two different microdystrophin gene therapy constructs in combination with VWR. Versions of each construct are being tested in clinical trials. Construct 1 contained the nNOS-binding site found in full-length dystrophin, which localizes nNOS to the sarcolemma and reduces functional ischemia of exercising limb muscles, while construct 2 lacked the nNOS-binding site and was the same microdystrophin used in the previous study. Gene- therapy treated mice that were sedentary or performed 52 weeks of VWR demonstrated similar outcomes including increased plantarflexor torque and exceptional treadmill endurance capacity. However, ex vivo diaphragm and soleus force, as well as metabolic enzyme and mitochondrial respiration assays were differentially improved, revealing unique physiological adaptations to each microdystrophin construct. Together, the data demonstrated that response to exercise after gene therapy treatment was variable and dependent on age, microdystrophin construct, and muscle type. / Doctor of Philosophy / Duchenne muscular dystrophy (DMD) is a rare, fatal muscle disease that causes progressive muscle weakness and cardiorespiratory failure. Available treatments, such as corticosteroids, slow progression of the disease but do not address the underlying genetic cause. DMD is caused by a genetic mutation that results in the loss of the muscle protein dystrophin. Microdystrophin gene therapy aims to address the genetic cause of the disease by using a non-pathogenic virus to deliver microdystrophin, a small, functional version of dystrophin, to muscle. This gene therapy is in clinical trials, and, if it is successful, treated patients will likely want to engage in more physical activity than previously possible due to muscle weakness. However, the effects of physical activity on muscles treated with gene therapy are unclear. Therefore, we conducted two studies to test the effects of voluntary wheel running on microdystrophin gene therapy in the mdx mouse, a model of DMD. The first study demonstrated that voluntary wheel running was beneficial to whole-body muscle function in mice treated with microdystrophin gene therapy. However, adaptations to the gene therapy and voluntary wheel running were variable in individual muscles. In the second study, we tested two microdystrophin constructs, which each contain different structural components of full-length dystrophin. In addition, mice ran for 52 weeks, more than twice as long as the first study. The results of the second study found that adaptations in individual muscles depended on microdystrophin construct and activity level. Additionally, we confirmed that voluntary wheel running was beneficial to whole-body function of microdystrophin–treated muscles. Together, these studies demonstrated that adaptations of gene therapy-treated muscles were dependent on microdystrophin structure, activity level, and age.