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Trevor L. Gillum, Charles L. Dumke and Brent C. Ruby

Purpose:

To describe the degrees of muscle-glycogen depletion and resynthesis in response to a half Ironman triathlon.

Methods:

One male subject (38 years of age) completed the Grand Columbian half Ironman triathlon (1.9-km swim, 90-km bike, 21.1-km run, Coulee City, Wash). Three muscle biopsies were obtained from his right vastus lateralis (prerace, immediately postrace, and 4 hours postrace). Prerace and postrace body weight were recorded, in addition to macronutrient consumption before, during, and after the race. Energy expenditure and whole-body substrate oxidation were estimated from linear regression established from laboratory trials (watts and run pace relative to VO2 and VCO2).

Results:

Body weight decreased 3.8 kg from prerace to postrace. Estimated CHO energy expenditure was 10,003 kJ for the bike segment and 5759 kJ for the run segment of the race. The athlete consumed 308 g of exogenous CHO (liquid and gel; 1.21 g CHO/min) during the race. Muscle glycogen decreased from 227.1 prerace to 38.6 mmol · kg wet weight−1 · h−1 postrace. During the 4 hours postrace, the athlete consumed a mixed diet (471 g CHO, 15 g fat, 64 g protein), which included liquid CHO sources and a meal. The calculated rate of muscle-glycogen resynthesis was 4.1 mmol · kg wet weight−1 · h−1.

Conclusion:

Completing a half Ironman triathlon depends on a high rate of muscle glycogenolysis, which demonstrates the importance of exogenous carbohydrate intake during the race. In addition, rates of muscle-glycogen resynthesis might be dampened by the eccentric damage resulting from the run portion of the race.

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Carla Cox, Steven Gaskill, Brent Ruby and Sharon Uhlig

The purpose of the present case study was threefold: (a) to estimate intake and expenditure of a dog driver (musher) while participating in the Iditarod, (b) to determine the hydration status of the musher at the completion of the event, and (c) to evaluate training related changes in aerobic capacity and body composition of a long-distance dog sled driver in preparation for and following completion of a 1049-mile (1692-km) sled dog race. Actual energy intake during the Iditarod Sled Dog Race was estimated at 8,921 kilojoules (kJ) per day. Nutrient intake expressed as percentage kJ of total energy (14%, 44% and 42% for protein, carbohydrates, and fat, respectively). Weight loss of .72 kg of body weight indicated an energy deficit of 1819 kJ per day during the race. Total energy needs per day were calculated to be 10,740 kJ/day. An increase in hematocrit and hemoglobin during the race may indicate dehydration during the event. There was an improvement in aerobic fitness during on-snow training as determined by ventilatory threshold and VO2peak data. Fat-free mass was maintained during training (46.4 kg), with a concomitant decrease in fat (2.4 kg). Fat-free mass was also maintained during the 12-day race.

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Robert A. Robergs, Susie B. McMinn, Cristine Mermier, Guy Leadbetter III, Brent Ruby and Chris Quinn

This study was conducted to compare blood glucose and glucoregulatory hormone responses to the ingestion of solid and liquid carbohydrate (CHO) during prolonged cycling, followed by 30 min of isokinetic cycling. Eight male cyclists randomly completed three cycling trials (LC = liquid CHO, SCE = solid CHO with water equal to LC, SCA = solid CHO + ad libitum water). Each subject cycled for 120 min at 65% of VO2max with CHO ingestion (0.6 g CHO/kg/hr) at 0, 30, 60, 90, and 120 min. Subjects then completed a 30-min maximal isokinetic ride at 90 rpm. There was no significant (p < .05) difference between the trials for plasma glucose, insulin, glucagon, glycerol, lactate, RER, HR, VO2 RPE, and total work performed during the isokinetic ride. However, serum glucose was significantly lower in the SCE and SCA trials compared to LC at 80 min. The ingestion of a solid food containing CHO. protein, and fat with added water produced similar blood glucose, metabolic, glucoregulatory hormone, and exercise performance responses to those seen with the ingestion of liquid CHO.

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Michael J. Cramer, Charles L. Dumke, Walter S. Hailes, John S. Cuddy and Brent C. Ruby

A variety of dietary choices are marketed to enhance glycogen recovery after physical activity. Past research informs recommendations regarding the timing, dose, and nutrient compositions to facilitate glycogen recovery. This study examined the effects of isoenergetic sport supplements (SS) vs. fast food (FF) on glycogen recovery and exercise performance. Eleven males completed two experimental trials in a randomized, counterbalanced order. Each trial included a 90-min glycogen depletion ride followed by a 4-hr recovery period. Absolute amounts of macronutrients (1.54 ± 0.27 g·kg-1 carbohydrate, 0.24 ± 0.04 g·kg fat-1, and 0.18 ± 0.03g·kg protein-1) as either SS or FF were provided at 0 and 2 hr. Muscle biopsies were collected from the vastus lateralis at 0 and 4 hr post exercise. Blood samples were analyzed at 0, 30, 60, 120, 150, 180, and 240 min post exercise for insulin and glucose, with blood lipids analyzed at 0 and 240 min. A 20k time-trial (TT) was completed following the final muscle biopsy. There were no differences in the blood glucose and insulin responses. Similarly, rates of glycogen recovery were not different across the diets (6.9 ± 1.7 and 7.9 ± 2.4 mmol·kg wet weight- 1·hr-1 for SS and FF, respectively). There was also no difference across the diets for TT performance (34.1 ± 1.8 and 34.3 ± 1.7 min for SS and FF, respectively. These data indicate that short-term food options to initiate glycogen resynthesis can include dietary options not typically marketed as sports nutrition products such as fast food menu items.

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John S. Cuddy, Dustin R. Slivka, Walter S. Hailes, Charles L. Dumke and Brent C. Ruby

Purpose:

The purpose of this study was to determine the metabolic profile during the 2006 Ironman World Championship in Kailua-Kona, Hawaii.

Methods:

One recreational male triathlete completed the race in 10:40:16. Before the race, linear regression models were established from both laboratory and feld measures to estimate energy expenditure and substrate utilization. The subject was provided with an oral dose of 2H2 18O approximately 64 h before the race to calculate total energy expenditure (TEE) and water turnover with the doubly labeled water (DLW) technique. Body weight, blood sodium and hematocrit, and muscle glycogen (via muscle biopsy) were analyzed pre- and postrace.

Results:

The TEE from DLW and indirect calorimetry was similar: 37.3 MJ (8,926 kcal) and 37.8 MJ (9,029 kcal), respectively. Total body water turnover was 16.6 L, and body weight decreased 5.9 kg. Hematocrit increased from 46 to 51% PCV. Muscle glycogen decreased from 152 to 48 mmoL/kg wet weight pre- to postrace.

Conclusion:

These data demonstrate the unique physiological demands of the Ironman World Championship and should be considered by athletes and coaches to prepare sufficient nutritional and hydration plans.

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John Quindry, Lindsey Miller, Graham McGinnis, Brian Kliszczewiscz, Dustin Slivka, Charles Dumke, John Cuddy and Brent Ruby

Previous research findings indicate that environmental temperature can influence exercise-induced oxidative-stress responses, although the response to variable temperatures is unknown. The purpose of this study was to investigate the effect of warm, cold, and “neutral,” or room, environmental temperatures on the blood oxidative stress associated with exercise and recovery. Participants (N = 12, age 27 ± 5 yr, VO2max = 56.7 ± 5.8 ml · kg-1 · min-1, maximal cycle power output = 300 ± 39 W) completed 3 exercise sessions consisting of a 1-hr ride at 60% Wmax, at 40% relative humidity in warm (33 °C), cold (7 °C), and room-temperature environments (20 °C) in a randomized crossover fashion. Rectal core temperature was monitored continually as participants remained in the respective trial temperature throughout a 3-hr recovery. Blood was collected preexercise and immediately, 1 hr, and 3 hr postexercise and analyzed for oxidative-stress markers including ferric-reducing ability of plasma (FRAP), Trolox-equivalent antioxidant capacity (TEAC), lipid hydroperoxides, and protein carbonyls. Core temperature was significantly elevated by all exercise trials, but recovery core temperatures reflected the given environment. FRAP (p < .001), TEAC (p < .001), and lipid hydroperoxides (p < .001) were elevated after warm exercise while protein carbonyls were not altered (p > .05). These findings indicate that moderate-intensity exercise and associated recovery in a warm environment elicits a blood oxidative-stress response not observed at comparable exercise performed at lower temperatures.

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Graham McGinnis, Brian Kliszczewiscz, Matthew Barberio, Christopher Ballmann, Bridget Peters, Dustin Slivka, Charles Dumke, John Cuddy, Walter Hailes, Brent Ruby and John Quindry

Hypoxic exercise is characterized by workloads decrements. Because exercise and high altitude independently elicit redox perturbations, the study purpose was to examine hypoxic and normoxic steady-state exercise on blood oxidative stress. Active males (n = 11) completed graded cycle ergometry in normoxic (975 m) and hypoxic (3,000 m) simulated environments before programing subsequent matched intensity or workload steady-state trials. In a randomized counterbalanced crossover design, participants completed three 60-min exercise bouts to investigate the effects of hypoxia and exercise intensity on blood oxidative stress. Exercise conditions were paired as such; 60% normoxic VO2peak performed in a normoxic environment (normoxic intensity-normoxic environment, NI-NE), 60% hypoxic VO2peak performed in a normoxic environment (HI-NE), and 60% hypoxic VO2peak performed in a hypoxic environment (HI-HE). Blood plasma samples drawn pre (Pre), 0 (Post), 2 (2HR) and 4 (4HR) hr post exercise were analyzed for oxidative stress biomarkers including ferric reducing ability of plasma (FRAP), trolox equivalent antioxidant capacity (TEAC), lipid hydroperoxides (LOOH) and protein carbonyls (PCs). Repeated-measures ANOVA were performed, a priori significance of p ≤ .05. Oxygen saturation during the HI-HE trial was lower than NI-NE and HI-NE (p < .05). A Time × Trial interaction was present for LOOH (p = .013). In the HI-HE trial, LOOH were elevated for all time points post while PC (time; p = .001) decreased post exercise. As evidenced by the decrease in absolute workload during hypoxic VO2peak and LOOH increased during HI-HE versus normoxic exercise of equal absolute (HI-NE) and relative (NI-NE) intensities. Results suggest acute hypoxia elicits work decrements associated with post exercise oxidative stress.

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Lindsey E. Miller, Graham R. McGinnis, Brian Kliszczewicz, Dustin Slivka, Walter Hailes, John Cuddy, Charles Dumke, Brent Ruby and John C. Quindry

Oxidative stress occurs as a result of altitude-induced hypobaric hypoxia and physical exercise. The effect of exercise on oxidative stress under hypobaric hypoxia is not well understood.

Purpose:

To determine the effect of high-altitude exercise on blood oxidative stress. Nine male participants completed a 2-d trek up and down Mt Rainer, in North America, at a peak altitude of 4,393 m. Day 1 consisted of steady-pace climbing for 6.25 hr to a final elevation of 3,000 m. The 4,393-m summit was reached on Day 2 in approximately 5 hr. Climb–rest intervals varied but were consistent between participants, with approximately 14 hr of total time including rest periods. Blood samples were assayed for biomarkers of oxidative stress and antioxidant potential at the following time points: Pre (before the trek), 3Kup (at ascent to 3,000 m), 3Kdown (at 3,000 m on the descent), and Post (posttrek at base elevation). Blood serum variables included ferric-reducing antioxidant potential (FRAP), Trolox equivalent antioxidant capacity (TEAC), protein carbonyls (PC), and lipid hydroperoxides. Serum FRAP was elevated at 3Kup and 3Kdown compared with Pre and Post values (p = .004, 8% and 11% increase from Pre). Serum TEAC values were increased at 3Kdown and Post (p = .032, 10% and 18% increase from Pre). Serum PC were elevated at 3Kup and 3Kdown time points (p = .034, 194% and 138% increase from Pre), while lipid hydroperoxides were elevated Post only (p = .004, 257% increase from Pre).

Conclusions:

Findings indicate that high-altitude trekking is associated with increased blood oxidative stress.