The purpose of this thesis was to investigate the effects of nutritional supplementation following resistance exercise on protein metabolism, muscle glycogen resynthesis rate, hormonal responses and training status through two unique investigations. The purpose of the first investigation was to determine the effect of post-resistance exercise glucose supplementation upon skeletal muscle fractional synthetic rate (FSR), urinary urea excretion, and whole body and myofibrillar protein degradation (WBPD and MPD, respectively). Eight healthy young males performed unilateral knee extensor resistance exercise(8sets/~1 0reps/~85% 1 RM) such that the non-exercised limb served as a control. They received a carbohydrate (CHO) supplement (1g/kg) or placebo (PL) immediately (t=Oh) and 1 h (t=+1 h) following exercise. FSR was determined for both exercised (EX) and control (CON) limbs by incremental L-[1-13C]leucine enrichment of biopsy samples of vastus lateralis over -10 hours post-exercise. Plasma insulin and glucose were determined at t= -1.5, 0, 0.25, 0.5, 0.75, 1, 1.25, 1.5, 1.75, 2, 2.25, 2.5, -10, and -10.5h post-exercise. MPD and WBPD were estimated from 24 hr urinary 3-methylhistidine (3-MH) and L-[1-13C]leucine flux, respectively, and whole body net protein balance was estimated from 24 hr urinary urea excretion. Plasma insulin concentration was greater (p<0.01) at 0.5, 0.75, 1.25, 1.5, 1.75 and 2 h in the CHO compared to PL condition, as was plasma glucose at 0.5 and 0. 75 h (p<0.05). FSR was 36.1% greater in the CHO/EX leg than in the CHO/CON leg (p=N.S.) and 6.3% greater in the PUEX leg than in the PUCON leg(p=N.S.). 3-MH excretion was lower in the CHO (110.43 ± 3.62 J μmol/g creatinine) than PL condition (120.14 ± 5.82)(p<0.05) as was urinary urea nitrogen(8.60 ± 0.66 g/g creat vs. 12.28 ± 1.84)(p<0.05). These findings suggest that CHO supplementation (1g/kg) immediately and 1h following resistance exercise can significantly decrease myofibrillar protein breakdown and urinary urea excretion, thus resulting in a more positive muscle and whole body protein balance. The purpose of the second investigation was to determine the effect of various nutritional supplements upon whole body protein synthesis, urinary urea excretion, and whole body and myofibrillar protein degradation (WBPD and MPD respectively). Ten healthy young male resistance athletes performed a whole body circuit set workout (9 exercises/3 sets/80% 1 Repitition Maximum). Exercises for the legs were performed unilaterally so that the non-exercised leg served as a control They received a carbohydrate (CHO) supplement (1g/kg), a mixed CHO/PRO/FAT supplement (isoenergetic to CHO supplement)(68% CHO, 22% PRO, 10% FAT) or placebo (PL) immediately (t=Oh) and 1 h (t=+1h) following exercise. Immediately following exercise muscle glycogen was significantly lower (p<0.05) in vastus lateralis of the exercised leg than in the control leg immediately post-exercise in all three conditions. Both the CHO and CHO/PRO/FAT supplements resulted in significantly greater increases (p<0.05) in plasma insulin and glucose post-exercise than PL. The CHO and CHO/PRO/FAT also resulted in significantly greater(p<0.05) rates of muscle glycogen resynthesis vs. Placebo. No significant differences were observed between the three conditions for plasma testosterone and cortisol concentration post-exercise. Similarly, no differences were observed between the three conditions for urinary creatinine, and 3-MH and urea nitrogen excretion. Thus, nutritional supplements do not appear to decrease myofibrillar protein degradation as indicated by 3-MH and urea nitrogen excretion in highly trained resistance athletes. Taken together, the two studies suggest that highly trained resistance athletes and untrained individuals both benefit from nutritional supplementation following resistance exercise, but may do so through different mechanisms. / Thesis / Master of Science (MS)

Ten subjects were randomly assigned to train one arm with ballistic movements (BT), whereas the other arm trained with ballistic and heavy resistance movements (BT+HRT). The training program consisted of three training sessions per week, over a ten week period. The BT arm executed ten sets of six maximal ballistic elbow extension actions (10% MVC), whereas the BT+HRT arm executed five sets of six repetitions of maximal ballistic actions followed by five sets of five to eight repetitions of heavy resistance elbow extension actions. After training, evoked twitch contractile properties, ballistic, 1 RM, and isometric MVC measures were analyzed. Incorporated with all performance measures were EMG recordings of the agonist (AG) triceps and antagonist (ANT) biceps. Muscle biopsies of triceps were also taken to determine muscle fibre type composition, and fibre area. The BT+HRT arm demonstrated a significant decrease in the percent population of type IIb fibres (22% to 18. 8%). Furthermore, the BT+HRT arm produced hypertrophy, type IIa (6184 to 7086 μm²) and IIb (5714 to 6734 μm²) fibre areas increased, whereas type I fibre areas (3503 to 3828 μm²) did not significantly increase, after training. In contrast, the BT arm and control arm did not display fibre transformation or hypertrophy after training. Triceps evoked twitch peak torque increased for only the BT+HRT arm (12.5 to 13.8 N·m). Furthermore, the 1 RM increased significantly in the BT+HRT arm (~24%) but did not change significantly in the BT arm. However, ballistic and isometric MVC PT values increased similarly in both the BT (19.6 to 23.5 N·m; 45.4 to 52.6 N·m) and the BT+HRT (19.6 to 23.6 N·m; 49.6 to 56.0 N·m) arms. The EMG results corresponded to the performance results in that triceps AEMG in the 1 RM test tended to increased more after HRT (0.71 to 1.01 mV) than only BT (0.72 to 0.81 mV), but in the ballistic (HRT= 0.63 to 0.79 mV; BT= 0. 62 to 0. 73 mV) and isometric MVC performance measures (HRT= 0.80 to 0.84 mV; BT= 0.80 to 0.87 mV), the AEMG results were similar. Supplementary HRT caused muscle hypertrophy, particularly of the type II fibres, but did not promote improvement in ballistic performance with loads equal to or less than 10% of maximal isometric force. / Thesis / Master of Science (MS)

This thesis is missing page 222, the other copies of this thesis are missing the page as well. -Digitization Centre / N/A / Thesis / Master of Science (MS)

Athletes use a wide range of interventions to promote recovery from strenuous exercise, but few data are available regarding the efficacy of such practices. OBJECTIVE: To examine the effectiveness of commonly used interventions [Rest, light exercise (AR), contrast therapy (CT) and cryotherapy (CR)] during recovery between bouts of intense exercise. We tested the hypothesis that hydrotherapy interventions (CT and CR) would induce favorable physiological and/or psychological alterations such that performance would be improved versus AR and Rest. METHODS: In Study I, 12 active men (25-35 yrs; VO2peak = 46±3 ml·kg-1·min-1; mean±SD) performed 5 consecutive days of HI exercise (4-6 bouts x 30 sec 'all out' Wingate Tests, with 4-min recovery, each day). After each training session, subjects either rested for 20 min (CON, n=6) or completed a CT protocol (n=6) that consisted of alternating cold (10°C) and hot (40°C) tubs using a 4x2:3 min ratio. Performance measures [Peak (Wmax) and mean (Wmean) power, VO2peak, and a 250 kJ Time Trial (TT)] were assessed before and after the HIT. In Study II, 9 active men (29±6 yr, VO2peak = 44±8 ml·kg-1·min-1) performed 3 exercise trials separated by 1 wk. Each trial consisted of 3 x 50 KJ time trials(~100-120%VO2peak) with a different 20-min recovery period [CON, AR (cycling@ SOW) or CR (cold tub@ 10°C)] between rides each week. Venous blood samples were obtained after each recovery period, and analyzed for lactate, interleukin-6, neutrophils, and lymphocytes. Questionnaires designed to assess exercise preparedness were also completed daily in both studies. RESULTS: In Study I, Wmax and TT performance improved after 5 d of HI exercise (time effect, P<0.05), but there were no differences between groups (Wmax-CT: Post: 1310±45 vs Pre: 1215±86; CON: Post: 1343±54 vs Pre: 1220±74 W: TT-CT: Post: 15.8±0.6 vs Pre: 16.7±0.7; Rest: Post: 18.1±1.0 vs Pre: 18.8±1.2 min, means±SEM). In Study II, TT performance averaged 118±10 sec for bout 1 and was 8% and 14% slower during bouts 2 (128±11 sec) and 3 (134±11 sec), respectively, with no difference between treatments (Time effect, P≤0.05). Blood lactate was lower after AR compared to CR and Rest, and neutrophils and lymphocytes were higher and lower respectively (P≤0.05), after CR (8.7±1.3 and 1.4±0.2 x 109cells/L) versus AR (7.1±1.0 and 1.6±0.1) and Rest (6.7±0.7 and 1.6±0.1). With respect to the psychological measurements, the CT and CR groups in both studies reported feeling more revitalized after each treatment session and greater preparedness for subsequent exercise (Treatment effect, P≤.05). CONCLUSIONS: Exercise performance during repeated bouts of intense cycling was not influenced by the type of recovery intervention employed, either during a single session or over the course of a 5 d training session. CR caused greater perturbations in blood immune markers and most notably, hydrotherapy interventions created the perception that subjects were better prepared for subsequent exercise. / Thesis / Master of Science (MS)

Doctor of Philosophy / Department of Anatomy and Physiology / Thomas J. Barstow / The primary aim of this dissertation was to evaluate the factors that contribute to the cardiorespiratory and vascular responses following exercise conditioning and microgravity deconditioning. The first study of this dissertation (Chapter 2) revealed that exercise training in the head down tilt posture, which places increases central blood volume compared to upright, results in cardiorespiratory adaptations in both upright and head down tilt postures which are not completely expressed with exercise training in the upright posture. These findings suggest that augmentation of the ventricular volume load during exercise training may result in adaptations that transfer across multiple body positions. In the second and third studies measurements of blood velocity and flow were performed via Doppler ultrasound. In Chapter 3 we observed that in the brachial and femoral arteries blood moves with a slightly blunted parabolic velocity profile that is very stable across a range of mean arterial pressures and downstream limb resistances. We concluded that these findings support the current calculations of shear rate based on the assumptions of laminar flow. With these assumptions confirmed, the investigation in Chapter 4 could be performed. We observed that acute exposure to a sustained antegrade shear rate, via unilateral forearm heating, increased measurements of flow-mediated dilation and the overall rate of adjustment for forearm blood flow and vascular conductance during dynamic handgrip exercise. These findings suggest that one potential stimulus for improvements in vascular function and health following exercise conditioning may be exposure to elevations in antegrade shear. Lastly in Chapter 5 we changed focus to the cardiorespiratory deconditioning following long-duration microgravity exposure. We retrospectively reviewed and analyzed previous investigations of microgravity deconditioning and demonstrated that the decrease in maximal O2 consumption ( O2max) occurs as a function of duration of exposure and that both convective and diffusive O2 transport pathways substantially contribute to this decline. In addition we reviewed the current literature and highlighted potential mechanisms, across several organ systems, which may contribute to this decline in O2max. Collectively, these studies revealed the breath of plasticity for cardiorespiratory adaptations to a variety of stressors.

Ghrelin is an appetite-stimulating hormone produced mainly in the stomach and duodenum. Poor ghrelin control is often caused by obesity-related hyperinsulinemia, which fails to suppress ghrelin and results in excess appetite and higher body fat storage that perpetuates even greater fat accumulation. High intensity exercise has been shown to acutely decrease plasma acylated ghrelin concentrations in healthy weight individuals. However, the evidence for how exercise affects ghrelin in obese individuals is currently lacking. PURPOSE: To compare the effects of high intensity interval exercise on acute plasma acylated ghrelin levels in obese and non-obese males. METHODS: Eighteen subjects with a mean age of 29.8 yr. (± 7.6) were assessed for body fat percent (BF%), acylated ghrelin and hunger. Subjects included 9 non- obese men (BF% mean= 13.7 ± 3.6) and 9 obese men (BF% mean = 31.7 ± 4.7) who agreed to participate in this study. Using a crossover design, participants were randomly assigned to an exercise or control condition, with each subject acting as their own control. The exercise trial consisted of participants cycling at high intensity intervals for 20 minutes (not including the 5 minute warmup and cool down) at a rate of 65% to 85% of their heart rate reserve on a cycle ergometer followed by 60 minutes of rest. The control trial consisted of 90 minutes of rest. Blood samples (3-4ml) were collected at baseline, 0.5, 1, and 1.5 hours post-intervention. Acylated ghrelin concentrations were determined from plasma. Hunger was assessed using a 10-point Likert-type scale while blood samples were being drawn. Group means for plasma ghrelin concentrations between groups were analyzed using an independent t-test. The effect of exercise on ghrelin was analyzed using paired t-test. The relationship between perceived hunger and ghrelin was assessed using Pearson correlations. RESULTS: Baseline plasma ghrelin levels were significantly higher in the non-obese group when compared to the obese group (t = 3.43, p = .036). While exercise was effective in reducing plasma acylated ghrelin levels in the non-obese group (t = 2.34, p = .047), no significant changes were found in acylated ghrelin in the obese group between baseline or any time point following the exercise intervention. CONCLUSIONS: The low resting levels of plasma ghrelin concentrations exhibited by the obese subjects, when compared to non-obese subjects, may result in long fasting periods that lead to hypoglycemia and a hyperinsulinemic response at the next eating opportunity. Furthermore, the lack of reduction in ghrelin following exercise may result in an overconsumption of energy. Both the sustained ghrelin with associated excess energy intake and the hyperinsulinemia may result in sustained or increased fat storage in obese individuals.

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

Recent studies in men have shown plasma levels of vitamin B-6 and pyridoxal 5'-phosphate (PLP), the active form of vitamin B-6, to increase with exercise. It was hypothesized that muscle glycogen phosphorylase might be the source of these increases as this enzyme has been shown to increase with increasing vitamin B-6 (B6) intake in the rat, seemingly to store PLP. The investigation was designed to study the effects of diet-altered glycogen stores and B6 supplements on B6 metabolism during controlled strenuous exercise. The effect of exercise (EX) on the excretion of 4-pyridoxic acid (4PA), the major B6 urinary metabolite, was also studied. The study consisted of three experimental weeks during which carbohydrate (CHO)-modified diets were fed and six EX tests were administered (one each Wednesday and Saturday). Four trained male cyclists (20-23 years) served as subjects. Week 1 a normal CHO diet was fed (NC diet, 40% of total kilocalories as CHO). During week 2, which began 7 days after week 1, a low CHO diet was fed Sunday through Tuesday (LC diet, 11% CHO) to deplete muscle glycogen. In the same week, the LC diet was followed by a high CHO diet (HC diet, 71% CHO). The HC diet was fed Wednesday through Saturday to replete, or load, glycogen stores. The NC, LC, and HC diets contained 1.64, 1.55, and 1.82 mg of B6, respectively. Week 3, beginning 14 days after week 2, was identical to week 2, but with the daily addition of an 8 mg supplement of pyridoxine. Daily exercise was encouraged Sunday through Tuesday to facilitate glycogen depletion. The EX test consisted of 50 min of continuous bicycle ergometer exercise (30 min at 60% HRmax (maximal heart rate), 15 min at 80% HRmax, and 5 min at 90% HRmax). Blood samples were drawn prior to the exercise test (pre), 2 min prior to the 90% HR max interval (during), immediately post EX (post), 30 min post, and 60 min post EX. Plasma samples were analyzed for PLP, PB6, creatine kinase (a muscle enzyme), and hematocrit and hemoglobin. Urine was collected in 24 hour aliquots and analyzed for 4PA and creatinine. The HC diet was associated with significantly lower pre exercise PB6 and PLP levels than LC diet. This was attributed to the high CHO content of HC. Increased plasma PLP and PB6 levels (pre versus post) were seen for all EX tests. This was significant for PB6 levels of all EX tests. Exercise following LC resulted in smaller pre to post increases in PB6 and PLP than other unsupplemented EX tests, but this was significant only for EX following LC versus NC(Wed). Supplementation resulted in greater pre to post increases in PLP and PB6 than EX following unsupplemented diets, but this was significant only for LC versus LC+B6. Plasma PLP and PB6 levels dropped throughout the 60 min post EX period. The 60 min post PLP levels were significantly below pre for the EX tests following diets NC(Wed), LC, HC+B6. Neither plasma volume percent (%) changes (calculated from hematocrit) nor creatine kinase % changes correlated significantly with % changes in PB6 and PLP. Urinary 4PA was elevated on all EX test days as compared to non-test days, except for EX following LC. Tissue redistribution of B6 appears to be occurring with exercise. With the LC diet, more B6 is needed for increased amino acid catabolism in the liver. In this situation tissue redistribution was not associated with increased conversion of B6 to 4PA. Greater increases in PLP with EX following supplementation suggests increased storage may have occurred. These findings are supportive of the hypothesis that increased PLP levels with exercise may originate from PLP bound to phosphorylase. The need for supplemental B6 for the athlete was not established, as status was adequate with normal intakes. / Graduation date: 1983

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