Comparison of Power Output Between Rotor and Normal Cranks During a 16.1 KM Time Trial

Previous research has evaluated the Rotor crank system on indices of endurance performance (e.g. peak power output, VO2max, lactate threshold, onset of blood lactate accumulation, economy, delta, and gross efficiency) under laboratory conditions. However, previous research has not attempted to determine whether the use of the Rotor cranks can improve sustainable power output during a time trial. The purpose of this study was to investigate the effect of the Rotor crank system on 16.1km time trial performance in the field. Eleven recreationally trained cyclists (7 male, 4 female; age 21±2 yrs) volunteered to participate in the study. On two separate days, each subject performed two 16.1 km time trials (i.e. one Rotor crank (RC) and one normal crank (NC)) each day. Crank arm length was 175mm for both systems. Each time trial was preceded by a 15-minute familiarization period. The trial order was randomly selected and a crossover design was used. Thirty minutes separated each trial, which included a five minute active cool-down, ten minutes of bicycle preparation and fifteen minutes of cycling to familiarize the subjects with the new crank system. Mean power (watt), heart rate (HR), cadence, and time to completion (minutes) were recorded using the Cyclops PowerTap Pro (Madison, WI, USA). The data was averaged for each subject’s two RC and NC trials. A two-tailed dependent t-test was used to analyze differences between the RC and NC systems for the measured variables. There were no significant differences (p\u3c0.05) between the two crank systems. Finish times were 30.04 ± 1.5 and 29.77 ± 1.7 for the RC and NC, respectively. Similarly, mean power output was 226.63 ± 39.1 and 230.21 ± 37.3 for the RC and NC, respectively. There were also no significant differences in average cadence and HR for the trials. The theoretical improvement in cycling efficiency by eliminating the dead spot of the pedal stroke did not translate into an improvement in cycling performance during 16.1km time trial cycling

The Effects of 3-Weeks of Aerobic Exercise in Heat on Fitness and PGC1a in Females

The effects of exercise training in the heat are well documented in men. However, the effects of exercise training in the heat in women have not received as much attention. We have previously reported a blunted rise in PGC1α in men after acute aerobic exercise in the heat. Purpose: To determine the impact of three weeks of aerobic exercise training in the heat compared to training in room temperature on thermoregulation, PGC1α mRNA response, and aerobic capacity in women. Methods: Twenty-three untrained college aged females (24±4 yoa, 168±5 cm, and 67.3±11.2 kg) were randomly assigned to 3 weeks of aerobic exercise training in either 20°C (n=12) or 33°C (n=11). Results: VO2max in room temperature conditions increased with training (2.57±0.35 to 2.71±0.32 L·min-1, p=0.01), but independent of temperature condition (p=0.821). HR decreased with training (152±16 to 140±0.13 bpm, p\u3c0.001), but was independent of temperature condition (p=0.341). Sweat rate increased with training (0.655±0.192 to 0.775±0.212 L·hr-1, p=0.006) and was higher in 33°C (0.835±0.144 L·hr-1) than 20°C (0.605±0.132 L·hr-1, p\u3c0.001). PGC1α mRNA increased with an acute exercise bout before (1.01±0.10 to 4.96±2.08 fold, p\u3c0.001) and after training (1.07±0.10 to 3.21±1.39 fold, p\u3c0.001) and had a smaller response after training than before training (p=0.005), but there were no differences between temperature groups (p=0.661). Conclusions: Women can increase aerobic fitness and maintain their exercise induced PGC1α mRNA response in the heat equally to that of room temperature conditions. This response contrasts with the blunted PGC1α mRNA response and VO2 max alterations previously observed in men

Substrate Use and Biochemical Response to a 3,211-km Bicycle Tour in Trained Cyclists

The purpose of this study was to assess the physiological adaptations in physically fit individuals to a period of intensified training. Ten trained males cycled outdoors ~170 km day−1 on 19 out of 21 days. Expired gas was collected on days 1 and 21 during maximal graded exercise and used for the determination of gross efficiency and whole body substrate use. Muscle biopsies were obtained before and after exercise on days 2 and 22 for the determination of mtDNA/gDNA ratio, gene expression, metabolic enzyme activity and glycogen use. Muscle glycogen before and after exercise, fat oxidation, and gross efficiency increased, carbohydrate oxidation decreased (p \u3c 0.05), and VO2max did not change over the 21 days of training. Citrate synthase (CS), β-hydroxyacyl CoA dehydrogenase (β-HAD) and cytochrome c oxidase (COX) enzyme activity did not change with training. CS and β-HAD mRNA did not change with acute exercise or training. COX (subunit IV) mRNA increased with acute exercise (p \u3c 0.05) but did not change over the 21 days. PGC-1α mRNA increased with acute exercise, but did not increase to the same degree on day 22 as it did on day 2 (p \u3c 0.05). UCP3 mRNA decreased with training (p \u3c 0.05). Acute exercise caused an increase in mitofusin2 (MFN2) mRNA (p \u3c 0.05) and a trend for an increase in mtDNA/gDNA ratio (p = 0.057). However, training did not affect MFN2 mRNA or mtDNA/gDNA ratio. In response to 3,211 km of cycling, changes in substrate use and gross efficiency appear to be more profound than mitochondrial adaptations in trained individuals

Metabolic Profile of the Ironman World Championships: A Case Study

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 field measures to estimate energy expenditure and substrate utilization. The subject was provided with an oral dose of (2)H(2)(18)O 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

Skeletal Muscle Metabolic Gene Response to Carbohydrate Feeding During Exercise in the Heat

Background: Heat stress down-regulates mitochondrial function, while carbohydrate supplementation attenuates the exercise induced stimulation of mitochondrial biogenesis in humans. The effects of exogenous carbohydrate during exercise in the heat on metabolic mRNA have not been investigated in humans. The purpose of this study was to determine the impact of exercise with and without carbohydrate supplementation on skeletal muscle metabolic response in the heat. Methods: Eight recreationally active males (4.05 ± 0.2 L.min-1) completed 2 trials which included 1 hr of cycling at 70% workload max and 3 hr recovery in a hot environment. Both trials were conducted in a climate controlled environmental chamber (38°C and 40% RH). The trials differed by the consumption of either a 6% carbohydrate (CHO) containing beverage (8 ml.kg-1.hr-1) or placebo (P) during exercise in random order. Muscle biopsies were obtained from the vastus lateralis before exercise, immediately post-exercise and at the end of the 3 hr recovery period. Muscle was analyzed for muscle glycogen and mRNA related to metabolic and mitochondrial development (MFN2, PGC-1α, GLUT4, UCP3). Expired gases were measured to determine whole body substrate use during exercise. Results: Carbohydrate oxidation and muscle glycogen utilization did not differ between trials, whereas fat oxidation was elevated during exercise in P. Exercise caused an increase in PGC-1α, and GLUT4 (P \u3c 0.05) independent of exogenous carbohydrate provision. Carbohydrate consumption attenuated the mRNA response in UCP3 (P \u3c 0.05). Conclusions: This study indicates that the provision of exogenous carbohydrate attenuates the stimulation of mRNA expression of UCP3 following exercise in the heat

Effects on Oxygen Consumption and Metabolic Gene Expression when Determining Experimental Exercise Intensity Based on Exercise Capacity Tests Conducted in Hypoxic and Normoxic Environments

Abstract: Exercise intensity can be set relative to VO2 max measured during hypoxic or control conditions in studies investigating exercise in hypoxic environments. It currently is not clear which is the most appropriate method. Objective: The objective of this brief report is to determine the response to 1 hour of cycling at 60% of peak power when measured in either normoxic or hypoxic conditions. Methods: Eleven recreationally active male participants (24 ± 4 yrs, 173 ± 20 cm, 82 ± 12 kg, 15.2 ± 7.1% fat, 4.0 ± 0.6 L x min-1 VO2 max) completed two 1 hour cycling exercise trials at 60% of peak power followed by 4 hours of recovery in ambient environmental conditions (975 m) and at normobaric hypoxic conditions simulating 3000 m in a randomized counter balanced order. Results: VO2 max was not different between trials in relative (p=0.272) or absolute terms (p=0.105) but peak power at VO2 max was higher in the 975 m trial (288 ± 17 watts) than the 3000 m trial (262 ± 12 watts, p=0.003) corresponding to differences at 60% of VO2 max power. Gene expression of HIF-1α, COX, PGC-1α, HK, and PFK increased with exercise (p\u3c0.05) but did not differ between trials. There was a trend (p=0.072) toward increased muscle glycogen use in 975m. Conclusions: Although there were not statistical differences for muscle markers in the current study, these data should be considered when determining exercise intensity in hypoxia related research

Independent Effects of Hypoxia and Altitude on Human Physiology

PURPOSE: Decreased fraction of inspired oxygen (FiO2) is often used to simulate the atmospheric partial pressure of oxygen decreases experienced during high altitude sojourns. Therefore, we aimed to independently investigate hypoxia and altitude by isolating oxygen concentration and barometric pressure. METHODS: 18 subjects completed 3 trials (sea level, hypoxia, altitude). 90-minute duration and intensity matched hypoxic stimuli were induced via decreased FiO2 or 4,200 m ascent. Relative tissue oxygenation change and cardiovascular variables were measured during rest and a 3-minute step-test. RESULTS: Muscle oxygenated hemoglobin (O2Hb) and muscle deoxygenated hemoglobin (HHb) were not different across environments during rest or exercise (p\u3e0.339) with alterations noted during rest to exercise transitions (p2Hb at hypoxia and altitude were lower than sea level (p2Hb was lower at altitude than sea level (p=0.007) similarly trending compared to hypoxia (p=0.066). Exercising brain O2Hb was not different between hypoxia and sea level (p=0.158). Brain HHb at hypoxia and altitude were higher than sea level (p-1) and altitude (141±3 beats·min-1) were lower than sea level (127±44 beats·min- 1, p0.208). Exercise stroke volume at altitude (109.6±4.1 mL) was higher than hypoxia (97.8±3.3 mL) and sea level (99.8±3.9 mL, pCONCLUSIONS: During acute hypoxic stimuli, skeletal muscle maintains oxygenation while the brain does not. Tissue oxygenation may be mediated by environmentally driven cardiovascular compensation. FiO2 decreases may not satisfactorily simulate all physiological outcomes experienced during altitude induced barometric pressure decreases

Blood oxidative-stress markers during a high-altitude trek

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