Graduation date: 1995

Access to abstract permanently restricted to Ball State community only / Access to thesis permanently restricted to Ball State community only / School of Physical Education, Sport, and Exercise Science

Previous investigations have utilized extremes of diet and exercise during the week prior to a performance to raise muscle glycogen levels to 220 mmoles/kg wet tissue. This investigation was designed to determine if muscle glycogen levels can be supercompensated utilizing a combination of a depletion-taper sequence and diets of 15% carbohydrate (CHO, LC), 50% CHO (M), and 70% CHO (HC) in 3,000 kcal. Each depletion-taper sequence was conducted on a treadmill at 73% V02max and consisted of runs of 90, 40, 40, 20, 20 minutes and a day of rest on the six days prior to a 13 mile performance run. Trial C consisted of 3 days LC and 3 days HC; Trial B, consisted of 3 days M and 3 days HC; and Trial C, 6 days M. Muscle biopsies were obtained from the gastrocnemius prior to loading (day 4) and before and after the performance run. Trials A, B and C elevated muscle glycogen to 207, 203 and 160 mmoles/ kg wet tissue, respectively. Trials A and B resulted in significantly more glycogen utilization (105 and 107 mmoles/kg wet tissue, respectively) than did Trial C (65 mmoles/kg wet tissue). The times during the performance runs were not significantly different between the Trials. It is concluded that: 1. muscle glycogen levels can be supercompensated to levels comparable to previous investigations by employing a depletion-tapering sequence and less severe alteration in diet prior to competition; 2. carbohydrate loading is not necessary for trained runners preparing for a race of 13 miles.Supported by the National Dairy Council and the Ball State University Graduate Student Research Fund, 1980.Ball State UniversityMuncie, IN 47306

Serum lactage dehydrogenase and creatine phosphokinase level were studied in sixty male Sprague-Dawley rats weighing 400 to 680 grams. Five groups of ten rats each ran forty-five minutes (16 m/min) with variable percentages of the total bout consisting of downhill running (16° incline): Group I- 0%, Group II- 22%, Group III- 50%, Group IV- 78%, Group V- 100% downhill. Group VI consisted of ten sedentary controls. Serial blood samples were obtained immediately after exercise, 12, 24, 36, 48, and 60 hours found to exist between a non-trained rat’s weight and its ability to finish the exercise bout and live beyond 48 hours.Each exercise group, except Group V, showed s significant decrease in the CPK activity at 24 and/or 36 hours post-exercise. Group V showed a significant elevation (P<0.05) in LDH and CPK activity at 12 hours. With the total exercise time remaining the same, a linear relationship was suggested between duration of downhill running and LDH activity at 12 and 24 hours post-exercise, r=0.5880 (n=26) and r=0.4490 (n=28), respectively.Ball State UniversityMuncie, IN 47306

The purpose of this investigation was to quantify the acute pressor response to caffeine at rest and during exercise, and to compare responses for different reportings of caffeine consumption and sensitivity. Eight young men with high use (HU) consumption patterns (<600 mg/day) and eight with low use (LU) patterns (<90 mg/day) participated. Caffeine (C) (4.5 mg/kg fat free mass) and placebo (P) were administered, double-blind and counterbalanced. Systolic (SBP), diastolic blood pressure (DBP) and heart rate (HR) were monitored during baseline, 40 minutes of absorption and graded treadmill walking. Oxygen consumption (V02) and rating of perceived exertion (RPE) were monitored during exercise. No significant differences were found for the responses to C between HU and LU nor between sensitive and not sensitive groups. Following a 12 hour abstinence, caffeine significantly increase SBP and DBP at absorption compared to P (11/9 mm Hg). The increase was additive with exercise for SBP but not DBP. Caffeine significantly increased VO2 compared to P. No significant differences were found for HR nor RPE between C and P trials. The present data indicate chronic caffeine consumption does not build tolerance to the acute pressor response to caffeine ingestion, the resting pressor response is additive with the pressor response to exercise for SBP, and individual perceptions of caffeine sensitivity are not accurate predictors of pressor responses. / School of Physical Education

The purpose of this study was to analyze specific biomechanical and physiological variables in disabled swimmers performing a functional backcrawl. The effect of selectively placed flotation devices on the body position, exercise heart rate, and perceived exertion of the swimmer was compared to swimming with no flotation. The participants in the study included eight able-bodied males 21.5 (+2.51) yrs. and four disabled males 29.25 (+2.22) yrs. Each subject performed the backcrawl for 3 consecutive lengths of a 25 meter pool under four separate trial conditions: free swimming, swimming with the hip flotation device, the knee flotation device, and the ankle flotation device. Immediately following each trial a post-exercise heart rate was taken and the subject was asked to rate perceived exertion. Full recovery was allowed after each trial. Trials were video taped and digitized to determine the mean angles at the neck, trunk, hip, and knee during one complete stroke cycle. The investigator recognizes that this generalization presents the possibility for a bias in the data and that further study would warrant the utilization of the different phases of the stroke for determination of body angles. The results of the study demonstrated that a significant difference did exist between the disabled and able-bodied hip angle during free swimming. Within the disabled group, no significant differences were evident when comparing the body angles during free swimming to the same angles while swimming with each of the flotation devices. Correlations between heart rate and ratings of perceived exertion for all subjects (n=12) were significant in each of the four trial conditions. / School of Physical Education

FGF21 is a stress-inducible hormone predominantly secreted from the liver. FGF21 acts as a downstream target gene of hepatic transcription factor PPARα that plays an obligatory role in mediating metabolic adaptation responses to prolonged fasting. However, the physiological roles of FGF21 in regulating glucose homeostasis during adaptive starvation responses and its underlying mechanisms remain unknown. Furthermore, FGF21 is induced by both acute and chronic exercise training in both rodents and human. The physiological significances and the underlying mechanisms for exercise-induced FGF21 production have not been explored so far. Therefore, this study aims to investigate: 1) the mechanisms whereby FGF21 mediates the role of PPARα activation in modulating hepatic gluconeogenesis in response to prolonged fasting; 2) the physiological roles and mechanisms whereby FGF21 regulates exercise capacity and insulin sensitivity via its actions in the muscle during exercise; 3) the roles of FGF receptor-1 (FGFR1) and co-receptor βKlotho in mediating the metabolic effects of FGF21 during fasting and exercise. Our results show thatFGF21 is induced by fasting in the liver and enters into the brain. Both FGF21knockout (KO) mice and PPARα KO mice exhibit severe hypoglycemia and defective hepatic gluconeogenesis during prolonged fasting, and these changes are accompanied by impaired activation of the hypothalamic-pituitary-adrenal (HPA)axis and blunted release of corticosterone from adrenalgland. Moreover, intracerebroventricular injection of recombinant FGF21 reverses fasting hypoglycemia and impairment in hepatic gluconeogenesis by restoring corticosterone production in both FGF21 KO and PPARα KO mice. These effects are abrogated by blockage of hypothalamic FGFR1or by pharmacological inhibition of ERK1/2in the hypothalamus. In addition,FGF21 acts directly on the hypothalamic neurons to activate FGFR1/βKlotho-ERK1/2-CREBsignaling pathway, thereby leading to the transcriptional activation of corticotropin-releasing hormone (CRH) and subsequent activation of the HPA axis. FGF21 is also induced in the liver by exercise and FGF21 KO mice have decreased exercise capacity associated with lower mitochondrial content and thus lower insulin sensitivity compared to wildtype (WT)mice after exercise training.AMPK-PGC-1α signaling pathway is impaired in the muscle of FGF21 KO mice during exercise.FGF21treatmentincreasesmitochondrial content in myotubes, while inhibition of AMPK and knockdown of FGFR1, βKlotho and PGC-1αblocksthis effect. Moreover, FGF21 regulates genes and proteins involved in different steps of the autophagy process and these alterations are mediated by FGFR1/βKlotho-PGC-1α signaling cascade. Furthermore, replenishment of FGF21 reverses the reduced mitochondrial content and insulin sensitivity by restoring PGC-1α expression and subsequent increase in mitochondrial biogenesis and suppression of autophagy in the muscle of FGF21 KO mice. In conclusion, our results identify FGF21 as a critical hormonal regulator of glucose homeostasis during prolonged fasting, by coupling hepatic PPARα activation to corticosterone release via stimulation of the HPA axis in the brain. Moreover, FGF21 acts in the muscle through two distinctive mechanism to maintain mitochondrial homeostasis during exercise training, involving both biogenesis of new mitochondria and decreased clearance of stressed mitochondria and thus to mediate the beneficial effects of exercise on lipid and glucose metabolism. / published_or_final_version / Medicine / Doctoral / Doctor of Philosophy

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