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Typescript (photocopy). / Digitized by Kansas Correctional Industries

Call number: LD2668 .T4 1978 K536 / Master of Science

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published_or_final_version / Sports Science / Master / Master of Science in Sports Science

The present study was designed to investigate the effects of exercise on vitamin B-6 metabolism. Four groups of subjects (intermittent, college, untrained, and high school) consisting of nineteen male and two female individuals, participated in the study. The subjects exercised either on a bicycle ergometer, by running three 1500 meter intervals, or both. Blood samples drawn prior to exercise (pre), after exercise (post), and 30 minutes after exercise (30 minute post), were analyzed for plasma pyridoxal 5'-phosphate (PLP), plasma B-6 (PB6), glucose, hemoglobin and hematocrit. A 24-hr urine collection the day before and the day of exercise was analyzed for urinary B-6 (UB6), 4-pyridoxic acid (4PA), creatinine, and urea nitrogen. The dietary intake of the four groups was greater than the RDA in vitamin B-6, riboflavin, thiamin, niacin, vitamins A and C, calcium and iron. The B-6/protein ratios of the college and untrained groups were adequate while the high school group's ratios were considered inadequate. The bicycle ergometer had a significant effect on the plasma PLP levels of the college and untrained groups (P< 0.005) and PB6 levels of the college group following exercise (P< 0.005). The 30 minute post plasma PLP levels were significantly lower for the college group (P< 0.005). During the run, the college group had significantly higher post exercise levels of plasma PLP (P< 0.005) and PBS (P< 0.005} as compared to the pre exercise sample. The high school group also had significantly higher levels of plasma PLP following, exercise for all three runs (P< 0.005, P< 0.025, and P< 0.01, respectively) as well as higher PB6 levels (P< 0.025, P< 0.01, and P< 0.025, respectively). The college athletes had a greater percent change in plasma PLP (P < 0.01) from the pre to post sample during the run as compared to the high school athletes. Urinary B-6 and 4PA were not significantly altered during either exercise suggesting a shift in PLP and the unphosphorylated forms of vitamin B-6 from one compartment to another. The significantly higher levels of plasma PLP and PB6 following exercise were attributed to an increased utilization of glycogen phosphorylase in the skeletal muscle with a subsequent release of PLP. / Graduation date: 1982

The objectives of this study were a) to determine if pyridoxine (PN) supplementation increases the rate at which plasma urea and ammonia return to basal levels, following exercise, b) to determine, by open circuit calorimetry, the utilization of carbohydrates, and c) to further understand vitamin B-6 metabolism during and following strenuous exercise. Six male athletes (age 26 ± 5 years and VO₂ max 66.4 ± 6.9 ml/kg/min) exercised for 1 hour on a cycle ergometer at 72% VO₂ max at two points during a 17 day study. For the first 8 days subjects received daily a placebo solution, while during the next half they received a PN dose (20 mg). Subjects consumed a constant diet the day before, day of, and day after the exercise test. Blood samples were taken the day of the exercise test at fasting (Fl), pre-exercise (PE), during exercise (DE), 1 min post exercise (I'P), 6 hour post exercise (6hP), and the day after the exercise test at fasting (F2). Plasma was analyzed for ammonia, urea, and pyridoxal 5'-phosphate (PLP). ANOVA showed no significant difference between treatments for either plasma ammonia or urea. While there was a significant increase (p<0.001) in plasma ammonia levels over time with the placebo, with supplementation the increase over time was not significant. With PN supplementation, plasma PLP levels were significantly correlated (p<0.05) with plasma ammonia levels at I'P. A slight decrease in plasma urea concentration was observed with the PN treatment at PE, DE, I'P, and 6hP. It was concluded that PN may reduce adverse consequences of plasma ammonia and urea seen with exercise. On the other hand, pyridoxine supplementation may produced a shift in the utilization of substrates of the subjects. Metabolic rate results showed that the contribution of carbohydrates as a energy source increased from 43.5 ± 13.7% with the placebo, to 52.0 ± 6.7% with the PN treatment (not significantly different). This observation lead to the conclusion that PN supplementation decreases glycogen stores compared to the glycogen stores without supplementation. Since the findings from this study suggest slightly more rapid plasma ammonia and urea restoration but decreased glycogen stores, they do not provide evidence for or against an increased need for vitamin B-6 in persons that are involved in strenuous exercises of medium duration. / Graduation date: 1988

A series of five studies were conducted to examine the effect of exercise on selected pulmonary function measurements. Studies I and II determined the effect of an acute bout of exercise on various lung volumes immediately post-exercise and over a 24-hour post-exercise period. There were significant mean increases of 210 ml (20.6%) and 260 ml (20.8%) in the 5-minute post-exercise residual volume (RV) measurement for studies I and II, respectively. There also were significant mean increases of 170 ml (3.4%) and 190 ml (2.7%) in the 5-minute post-exercise total lung capacity (TLC) for studies I and II, respectively, while vital capacity (VC) remained unchanged. RV and TLC remained significantly increased over the pre-exercise values through 30 and 15 minutes of recovery, respectively. Studies III through V were undertaken to determine the physiological mechanism underlying the responses reported in studies I and II. In study III, transthoracic electrical impedance (TEI) was significantly decreased below the pre-exercise value through 30-minutes of recovery, indicating that there was an increase in thoracic fluid volume following exercise. However, TEI measurements alone cannot separate between intra- and extravascular fluid shifts. Therefore, studies IV and V attempted to identify whether the decrease in TEI and increase in RV reported in study III were due to intra- or extravascular fluid shifts. Study IV examined the TEI, RV, and TLC responses before and following exercise, as central blood volume (CBV) was experimentally increased via G-suit inflation, and decreased via venous occlusion tourniquets. The results suggest that RV is relatively insensitive to intravascular volume shifts within the thorax. Study V determined and followed the effect of an acute bout of exercise on lung diffusion capacity (D(,Lco)). D(,Lco)/V(,A) did not increase significantly following exercise, suggesting that the decrease in TEI following exercise is the result of extravascular fluid accumulation. It was concluded that a sub-clinical pulmonary edema occurs following exercise. A logical sequence of events based on the results of studies I through V was proposed as a possible explanation for the responses of RV and TLC following exercise.

In order to achieve a better understanding of the impact of exercise on the concentration of serum free fatty acids (FFA) during post-exercise recovery, the purposes of this study were: (1) to determine the relationships between exercise intensity, total exercise energy expenditure, and the concentration of serum FFA during post-exercise recovery; (2) to examine the effects of exoge- nous glucose on post-exercise serum FFA and hormones controlling the FFA response; and (3) to examine the impact of acute exercise on hunger. Untrained, 12-h fasted, college-age males performed cycle ergometer exercise at exercise intensities ranging from 29 to 59% peak ‘VO₂ for total energy expenditures ranging from 162 to 320 kcal. Blood samples, hunger ratings, and metabolic indices were collected or measured before, during, and for 3 h post-exercise. In response to exercise of approximately 300 kcal, FFA was elevated for 3 h post-exercise. The FFA response was a function of total exercise energy expenditure, rather than exercise intensity, or combined effects of these factors. The response was associated with low insulin concentration but no changes were observed in blood glucose, glucagon, growth hormone, or cortisol. Glucose ingestion and infusion studies demonstrated that possible mechanisms con- tributing to the post-exercise FFA response included decreases in FFA re-esterification, increases in triglyceride hydrolysis, and decreases in sympathetic input to adipose tissue. Exercise caused a suppression of hunger for 2 h post-exercise which was a function of the combined effects of exercise intensity and total energy expenditure. An increase in core temperature may have contributed to the anorexigenic effect of exercise. In conclusion, exercise, performed in and followed by a period of fasting caused an elevation of FFA for 3 h during post-exercise recovery. The post-exercise recovery period should be considered an important phase in the physiological impact of exercise on the storage and utilization of fat.