Live high, train low - influence on resting and post-exercise hepcidin levels.

The post-exercise hepcidin response during prolonged (>2 weeks) hypoxic exposure is not well understood. We compared plasma hepcidin levels 3 h after exercise [6 × 1000 m at 90% of maximal aerobic running velocity (vVO2max )] performed in normoxia and normobaric hypoxia (3000 m simulate altitude) 1 week before, and during 14 days of normobaric hypoxia [196.2 ± 25.6 h (median: 200.8 h; range: 154.3-234.8 h) at 3000 m simulated altitude] in 10 well-trained distance runners (six males, four females). Venous blood was also analyzed for hepcidin after 2 days of normobaric hypoxia. Hemoglobin mass (Hbmass ) was measured via CO rebreathing 1 week before and after 14 days of hypoxia. Hepcidin was suppressed after 2 (Cohen's d = -2.3, 95% confidence interval: [-2.9, -1.6]) and 14 days of normobaric hypoxia (d = -1.6 [-2.6, -0.6]). Hepcidin increased from baseline, 3 h post-exercise in normoxia (d = 0.8 [0.2, 1.3]) and hypoxia (d = 0.6 [0.3, 1.0]), both before and after exposure (normoxia: d = 0.7 [0.3, 1.2]; hypoxia: d = 1.3 [0.4, 2.3]). In conclusion, 2 weeks of normobaric hypoxia suppressed resting hepcidin levels, but did not alter the post-exercise response in either normoxia or hypoxia, compared with the pre-exposure response.

The effects of injury and illness on haemoglobin mass.

This study sought to quantify the effects of reduced training, surgery and changes in body mass on haemoglobin mass (Hbmass) in athletes. Hbmass of 15 athletes (6 males, 9 females) was measured 9±6 (mean±SD) times over 162±198 days, during reduced training following injury or illness. Additionally, body mass (n=15 athletes) and episodes of altitude training (n=2), iron supplementation (n=5), or surgery (n=3) were documented. Training was recorded and compared with pre-injury levels. Analysis used linear mixed models for ln(Hbmass), with Sex, Altitude, Surgery, Iron, Training and log(Body Mass) as fixed effects, and Athlete as a fixed and random effect. Reduced training and surgery led to 2.3% (p=0.02) and 2.7% (p=0.04) decreases in Hbmass, respectively. Altitude and iron increased Hbmass by 2.4% (p=0.03) and 4.2% (p=0.05), respectively. The effect of changes in body mass on Hbmass was not statistically significant (p=0.435).The estimates for the effects of surgery and altitude on Hbmass should be confirmed by future research using a larger sample of athletes. These estimates could be used to inform the judgements of experts examining athlete biological passports, improving their interpretation of Hbmass perturbations, which athletes claim are related to injury, thereby protecting innocent athletes from unfair sanctioning.

No change in hemoglobin mass after 40 days of physical activity in previously untrained adults.

A high hemoglobin mass (Hb(mass)) is associated with a high maximum aerobic power (VO(2max)), however, the extent to which Hb(mass) is influenced by training is currently unclear. Accordingly, this study monitored changes in Hb(mass) and VO(2max) in 12 previously untrained adults (aged 18-25 years) following 40 days of regular physical activity. Hb(mass) and VO(2max) were assessed at the start and end of a 40-day physical activity program, which comprised of approximately 40 min of daily, moderate-intensity physical activity. Relative VO(2max) increased by 11.3%, yet there was no significant change in relative Hb(mass) (1.7%) and body mass (0.2%) during the 40-day period. There was a significant correlation between Hb(mass) and VO(2max) at the start of the study (r=0.58, P=0.05), but not between the change in relative VO(2max) and the change in relative Hb(mass) (r=-0.07, P=0.83). Our results support the concept of relative stability in Hb(mass) with approximately 1 month of moderate-intensity physical activity suggesting that Hb(mass) may be used for talent identification and possibly for anti-doping purposes.

Detraining decreases Hb(mass) of triathletes.

Haemoglobin mass (Hbmass) determination using CO rebreathing may assist to detect illegal blood doping practices, however variations in Hbmass with periods of intensive training and detraining must be quantified. This study aimed to determine the effect of a 30-day period of detraining on Hbmass in ultra-endurance triathletes. 9 male recreational triathletes (29-44 years) participated in the study. Hbmass was assessed using CO rebreathing 30 days and 10 days before an ultra-endurance triathlon and after ~10, 20 and 30 days of detraining following the race. V˙O2max was assessed 10 days before the race and also after the 30-day detraining period, which consisted of an 87% reduction in training hours. After 30-days of detraining there was a 3.1% decrease in mean Hbmass from 868±99 to 840±94 g, (p=0.03), and a 4.7% decrease in mean V˙O2max from 4.83±0.29 to 4.61±0.41 L/min as well as a 2.8% increase of body mass from 75.1±6.4 to 77.1±6.1 kg and a 28% increase in skinfold total from 43.9±14.2 to 55.1±14.0 mm. Individual decreases in Hbmass following detraining would need to be considered if using Hbmass for anti-doping purposes.

Spurious Hb mass increases following exercise.

Sensitivity of the Athlete Blood Passport for blood doping could be improved by including total haemoglobin mass (Hb(mass)), but this measure may be unreliable immediately following strenuous exercise. We examined the stability of Hb(mass) following ultra-endurance triathlon (3.8 km swim, 180 km bike, 42.2 km run). 26 male sub-elite triathletes, 18 Racers and 8 Controls, were tested for Hb(mass) using CO re-breathing, twice 1-5 days apart. Racers were measured before and 1-3 h after the triathlon. Controls did no vigorous exercise on either test day. Serum haptoglobin concentration and urine haemoglobin concentration were measured to assess intravascular haemolysis. There was a 3.2% (p<0.01) increase in Racers' Hb(mass) from pre-race (976 g ± 14.6%, mean ±% coefficient of variation) to post-race (1 007 g ± 13.8%), as opposed to a - 0.5% decrease in Controls (pre-race 900 g ± 13.9%, post-race 896 g ± 12.4%). Haptoglobin was - 67% (p<0.01) reduced in Racers (pre-race 0.48 g / L ± 150%, post-race 0.16 g / L ± 432%), compared to - 6% reduced in Controls (pre-race 1.08 g / L ± 37%, post-race 1.02 g / L ± 37%). Decreased serum haptoglobin concentration in Racers, which is suggestive of mild intravascular blood loss, was contrary to the apparent Hb(mass) increase post-race. Ultra-endurance triathlon racing may confound the accuracy of post-exercise Hb(mass) measures, possibly due to splenic contraction or an increased rate of CO diffusion to intramuscular myoglobin.

Detecting autologous blood transfusions: a comparison of three passport approaches and four blood markers.

Blood passport has been suggested as an indirect tool to detect various kinds of blood manipulations. Autologous blood transfusions are currently undetectable, and the objective of this study was to examine the sensitivities of different blood markers and blood passport approaches in order to determine the best approach to detect autologous blood transfusions. Twenty-nine subjects were transfused with either one (n=8) or three (n=21) bags of autologous blood. Hemoglobin concentration ([Hb]), percentage of reticulocytes (%ret) and hemoglobin mass (Hbmass) were measured 1 day before reinfusion and six times after reinfusion. The sensitivity and specificity of a novel marker, Hbmr (based on Hbmass and %ret), was evaluated together with [Hb], Hbmass and OFF-hr by different passport methods. Our novel Hbmr marker showed superior sensitivity in detecting the highest dosage of transfused blood, with OFF-hr showing equal or superior sensitivities at lower dosages. Hbmr and OFF-hr showed superior but equal sensitivities from 1 to 4 weeks after transfusion compared with [Hb] and Hbmass, with Hbmass being the only tenable prospect to detect acute transfusions. Because autologous blood transfusions can be an acute practice with blood withdrawal and reinfusion within a few days, Hbmass seems to be the only option for revealing this practice.

Quality control technique to reduce the variability of longitudinal measurement of hemoglobin mass.

The sensitivity of the athlete blood passport to detect blood doping may be improved by the inclusion of total hemoglobin mass (Hb(mass)), but the comparability of Hb(mass) from different laboratories is unknown. To optimize detection sensitivity, the analytical variability associated with Hb(mass) measurement must be minimized. The aim of this study was to investigate the efficacy of using quality controls to minimize the variation in Hb(mass) between laboratories. Three simulated laboratories were set up in one location. Nine participants completed three carbon monoxide (CO) re-breathing tests in each laboratory. One participant completed two CO re-breathing tests in each laboratory. Simultaneously, quality controls containing Low (1-3%) and High (8-11%) concentrations of percent carboxyhemoglobin (%HbCO) were measured to compare hemoximeters in each laboratory. Linear mixed modeling was used to estimate the within-subject variation in Hb(mass), expressed as the coefficient of variation, and to estimate the effect of different laboratories. The analytic variation of Hb(mass) was 2.4% when tests were conducted in different laboratories, which reduced to 1.6% when the model accounted for between-laboratory differences. Adjustment of Hb(mass) values using quality controls achieved a comparable analytic variation of 1.7%. The majority of between-laboratory variation in Hb(mass) originated from the difference between hemoximeters, which could be eliminated using appropriate quality controls.

Time course of haemoglobin mass during 21 days live high:train low simulated altitude.

The aim of this study was to determine the time course of changes in haemoglobin mass (Hb(mass)) in well-trained cyclists in response to live high:train low (LHTL). Twelve well-trained male cyclists participated in a 3-week LHTL protocol comprising 3,000 m simulated altitude for ~14 h/day. Prior to LHTL duplicate baseline measurements were made of Hb(mass), maximal oxygen consumption (VO(2max)) and serum erythropoietin (sEPO). Hb(mass) was measured weekly during LHTL and twice in the week thereafter. There was a 3.3% increase in Hb(mass) and no change in VO(2max) after LHTL. The mean Hb(mass) increased at a rate of ~1% per week and this was maintained in the week after cessation of LHTL. The sEPO concentration peaked after two nights of LHTL but there was only a trivial correlation (r = 0.04, P = 0.89) between the increase in sEPO and the increase in Hb(mass). Athletes seeking to gain erythropoietic benefits from moderate altitude need to spend >12 h/day in hypoxia.

Improved running economy and increased hemoglobin mass in elite runners after extended moderate altitude exposure.

There is conflicting evidence whether hypoxia improves running economy (RE), maximal O(2) uptake (V(O)(2max)), haemoglobin mass (Hb(mass)) and performance, and what total accumulated dose is necessary for effective adaptation. The aim of this study was to determine the effect of an extended hypoxic exposure on these physiological and performance measures. Nine elite middle distance runners were randomly assigned to a live high-train low simulated altitude group (ALT) and spent 46+/-8 nights (mean+/-S.D.) at 2860+/-41m. A matched control group (CON, n=9) lived and trained near sea level ( approximately 600m). ALT decreased submaximal V(O)(2) (Lmin(-1)) (-3.2%, 90% confidence intervals, -1.0% to -5.2%, p=0.02), increased Hb(mass) (4.9%, 2.3-7.6%, p=0.01), decreased submaximal heart rate (-3.1%, -1.8% to -4.4%, p=0.00) and had a trivial increase in V(O)(2max) (1.5%, -1.6 to 4.8; p=0.41) compared with CON. There was a trivial correlation between change in Hb(mass) and change in V(O)(2max) (r=0.04, p=0.93). Hypoxic exposure of approximately 400h was sufficient to improve Hb(mass), a response not observed with shorter exposures. Although total O(2) carrying capacity was improved, the mechanism(s) to explain the lack of proportionate increase in V(O)(2max) were not identified.

Live and/or sleep high:train low, using normobaric hypoxia.

The increase in oxygen transport elicited by several weeks of exposure to moderate to high altitude is used to increase physical performance when returning to sea level. However, many studies have shown that aerobic performance may not increase at sea level after a training block at high altitude. Subsequently, the concept of living high and training low was introduced in the early 1990s and was further modified to include simulated altitude using hypobaric or normobaric hypoxia. Review is given of the main studies that have used this procedure. Hematological changes are limited to insignificant or moderate increase in red cell mass, depending on the "dose" of hypoxia. Maximal aerobic performance is increased when the exposure to hypoxia is at least over 18 days. Submaximal performance and running economy have been found increased in several, but not all, studies. The tolerance (fatigue, sleep, immunological status, cardiac function) is good when the altitude or simulated altitude is not higher than 3000 m. Virtually no data are available about the effect of this procedure upon anaerobic performance. The wide spread of these techniques deserves further investigations.

Preparation for football competition at moderate to high altitude.

Analysis of approximately 100 years of home-and-away South American World Cup matches illustrate that football competition at moderate/high altitude (>2000 m) favors the home team, although this is more than compensated by the likelihood of sea-level teams winning at home against the same opponents who have descended from altitude. Nevertheless, the home team advantage at altitudes above approximately 2000 m may reflect that traditionally, teams from sea level or low altitude have not spent 1-2 weeks acclimatizing at altitude. Despite large differences between individuals, in the first few days at high altitude (e.g. La Paz, 3600 m) some players experience symptoms of acute mountain sickness (AMS) such as headache and disrupted sleep, and their maximum aerobic power (VO2max) is approximately 25% reduced while their ventilation, heart rate and blood lactate during submaximal exercise are elevated. Simulated altitude for a few weeks before competition at altitude can be used to attain partial ventilatory acclimation and ameliorated symptoms of AMS. The variety of simulated altitude exposures usually created with enriched nitrogen mixtures of air include resting or exercising for a few hours per day or sleeping approximately 8 h/night in hypoxia. Preparation for competition at moderate/high altitude by training at altitude is probably superior to simulated exposure; however, the optimal duration at moderate/high altitude is unclear. Preparing for 1-2 weeks at moderate/high altitude is a reasonable compromise between the benefits associated with overcoming AMS and partial restoration of VO2max vs the likelihood of detraining.

The effect of acute simulated moderate altitude on power, performance and pacing strategies in well-trained cyclists.

Athletes regularly compete at 2,000-3,000 m altitude where peak oxygen consumption (VO2peak) declines approximately 10-20%. Factors other than VO2peak including gross efficiency (GE), power output, and pacing are all important for cycling performance. It is therefore imperative to understand how all these factors and not just VO2peak are affected by acute hypobaric hypoxia to select athletes who can compete successfully at these altitudes. Ten well-trained, non-altitude-acclimatised male cyclists and triathletes completed cycling tests at four simulated altitudes (200, 1,200, 2,200, 3,200 m) in a randomised, counter-balanced order. The exercise protocol comprised 5 x 5-min submaximal efforts (50, 100, 150, 200 and 250 W) to determine submaximal VO2 and GE and, after 10-min rest, a 5-min maximal time-trial (5-minTT) to determine VO2peak and mean power output (5-minTT(power)). VO2peak declined 8.2 +/- 2.0, 13.9 +/- 2.9 and 22.5 +/- 3.8% at 1,200, 2,200 and 3,200 m compared with 200 m, respectively, P < 0.05. The corresponding decreases in 5-minTT(power) were 5.8 +/- 2.9, 10.3 +/- 4.3 and 19.8 +/- 3.5% (P < 0.05). GE during the 5-minTT was not different across the four altitudes. There was no change in submaximal VO2 at any of the simulated altitudes, however, submaximal efficiency decreased at 3,200 m compared with both 200 and 1,200 m. Despite substantially reduced power at simulated altitude, there was no difference in pacing at the four altitudes for athletes whose first trial was at 200 or 1,200 m; whereas athletes whose first trial was at 2,200 or 3,200 m tended to mis-pace that effort. In conclusion, during the 5-minTT there was a dose-response effect of hypoxia on both VO2peak and 5-minTT(power) but no effect on GE.

Acute weight loss followed by an aggressive nutritional recovery strategy has little impact on on-water rowing performance.

OBJECTIVES: To assess the influence of moderate, acute weight loss on on-water rowing performance when aggressive nutritional recovery strategies were used in the two hours between weigh in and racing. METHODS: Competitive rowers (n = 17) undertook three on-water 1800 m time trials under cool conditions (mean (SD) temperature 8.4 (2.0) degrees C), each separated by 48 hours. No weight limit was imposed for the first time trial--that is, unrestricted body mass (UNR1). However, one of the remaining two trials followed a 4% loss in body mass in the previous 24 hours (WT(-4%)). No weight limit was imposed for the other trial (UNR2). Aggressive nutritional recovery strategies (WT(-4%), 2.3 g/kg carbohydrate, 34 mg/kg Na+, and 28.4 ml/kg fluid; UNR, ad libitum) were used in the first 90 minutes of the two hours between weigh in and performance trials. RESULTS: WT(-4%) had only a small and statistically non-significant effect on the on-water time trial performance (mean 1.0 second, 95% confidence interval (CI) -0.9 to 2.8; p = 0.29) compared with UNR. This was despite a significant decrease in plasma volume at the time of weigh in for WT(-4%) compared with UNR (-9.2%, 95% CI -12.8% to -5.6%; p<0.001). CONCLUSIONS: Acute weight loss of up to 4% over 24 hours, when combined with aggressive nutritional recovery strategies, can be undertaken with minimal impact on on-water rowing performance, at least in cool conditions.

Chronic intermittent hypoxia and incremental cycling exercise independently depress muscle in vitro maximal Na+-K+-ATPase activity in well-trained athletes.

Athletes commonly attempt to enhance performance by training in normoxia but sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia reduces muscle Na(+)-K(+)-ATPase content, whereas fatiguing contractions reduce Na(+)-K(+)-ATPase activity, which each may impair performance. We examined whether LHTL and intense exercise would decrease muscle Na(+)-K(+)-ATPase activity and whether these effects would be additive and sufficient to impair performance or plasma K(+) regulation. Thirteen subjects were randomly assigned to two fitness-matched groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate altitude (3,000 m, inspired O(2) fraction = 15.48%) for 23 nights and lived and trained by day under normoxic conditions in Canberra (altitude approximately 600 m). Con lived, trained, and slept in normoxia. A standardized incremental exercise test was conducted before and after LHTL. A vastus lateralis muscle biopsy was taken at rest and after exercise, before and after LHTL or Con, and analyzed for maximal Na(+)-K(+)-ATPase activity [K(+)-stimulated 3-O-methylfluorescein phosphatase (3-O-MFPase)] and Na(+)-K(+)-ATPase content ([(3)H]ouabain binding sites). 3-O-MFPase activity was decreased by -2.9 +/- 2.6% in LHTL (P < 0.05) and was depressed immediately after exercise (P < 0.05) similarly in Con and LHTL (-13.0 +/- 3.2 and -11.8 +/- 1.5%, respectively). Plasma K(+) concentration during exercise was unchanged by LHTL; [(3)H]ouabain binding was unchanged with LHTL or exercise. Peak oxygen consumption was reduced in LHTL (P < 0.05) but not in Con, whereas exercise work was unchanged in either group. Thus LHTL had a minor effect on, and incremental exercise reduced, Na(+)-K(+)-ATPase activity. However, the small LHTL-induced depression of 3-O-MFPase activity was insufficient to adversely affect either K(+) regulation or total work performed.

Sleep in athletes undertaking protocols of exposure to nocturnal simulated altitude at 2650 m.

A popular method to attempt to enhance performance is for athletes to sleep at natural or simulated moderate altitude (SMA) when training daily near sea level. Based on our previous observation of periodic breathing in athletes sleeping at SMA, we hypothesised that athletes' sleep quality would also suffer with hypoxia. Using two typical protocols of nocturnal SMA (2650 m), we examined the effect on the sleep physiology of 14 male endurance-trained athletes. The selected protocols were Consecutive (15 successive exposure nights) and Intermittent (3x 5 successive exposure nights, interspersed with 2 normoxic nights) and athletes were randomly assigned to follow either one. We monitored sleep for two successive nights under baseline conditions (B; normoxia, 600 m) and then at weekly intervals (nights 1, 8 and 15 (N1, N8 and N15, respectively)) of the protocols. Since there was no significant difference in response between the protocols being followed (based on n=7, for each group) we are unable to support a preference for either one, although the likelihood of a Type II error must be acknowledged. For all athletes (n=14), respiratory disturbance and arousal responses between B and N1, although large in magnitude, were highly individual and not statistically significant. However, SpO2 decreased at N1 versus B (p<0.001) and remained lower on N8 (p<0.001) and N15 (p<0.001), not returning to baseline level. Compared to B, arousals were more frequent on N8 (p=0.02) and N15 (p=0.01). The percent of rapid eye movement sleep (REM) increased from N1 to N8 (p=0.03) and N15 (p=0.01). Overall, sleeping at 2650 m causes sleep disturbance in susceptible athletes, yet there was some improvement in REM sleep over the study duration.

Effects of body composition and fat distribution on ventilatory function in adults.

Clinically, gross obesity is associated with disturbances of ventilatory function, but less severe obesity is not generally thought to have a significant effect on ventilatory function. The purpose of this report was to examine cross-sectional data to determine the effects of body composition and fat distribution on ventilatory function in 1235 adults (621 men and 614 women). Forced vital capacity (FVC) was used as a measure of ventilatory function and was adjusted for age, height, smoking, and bronchial symptoms in separate models for men and women. Body fat and fat-free mass were estimated from skinfold-thickness measurements. Adjusted FVC was not significantly associated with body mass or body mass index, but was negatively associated with percentage body fat in men (P = 0.0003) and women (P = 0.043) and positively associated with fat-free mass in men (P = 0.018) and women (P = 0.0001). Handgrip strength was positively associated with adjusted FVC in both sexes (P < 0.02), suggesting that the effect of fat-free mass may be mediated by muscular strength. Adjusted FVC was negatively associated with subscapular-skinfold thickness in both sexes (P < 0.0003) and with waist circumference (P = 0.01) and waist-to-hip ratio (P = 0.03) in men. Previous reports that considered only body mass index or body mass failed to distinguish the opposing effects of fat-free mass and fat mass on FVC.

Retest reliability of recall measures of leisure-time physical activity in Australian adults.

BACKGROUND: Several studies have reported that short-term recall measures of physical activity participation have acceptable repeatability, but in most cases employed convenience samples and did not use optimal statistics. In this Australian study repeatability was assessed on participants recall of activity over two different time periods and over the same time period. METHODS: Two 14-day recall measures of physical activity participation were administered in two studies to randomly selected population samples of adults in Adelaide, South Australia. Intraclass correlation coefficients (ICC), 80% and 95% limits of agreement and the kappa statistic were calculated. RESULTS: For a continuous measure of energy expenditure the ICC was 0.86 using recall of the same 2-week period (N = 115), and was 0.58 for activity recalled over different 2-week period (N = 116). For categorized energy expenditure (inactive, low, Moderate and Vigorous categories), kappa was 0.76 for recall of the same period and was 0.36 for different recall periods. Similar results were observed for continuous and categorical forms of a measure of physical activity that recorded frequency of participation in vigorous and moderate activities and walking. The 80% limits of agreement were markedly smaller than 95% limits of agreement, but were still large. CONCLUSIONS: These data suggest that the variation in repeatability coefficients between recall of the same 2-week time period and activity recalled over different 2-week periods was due to actual variation in physical activity participation over different time periods, and not to poor recall or to poor measurement characteristics. The recall measures appear to have good repeatability for most respondents, but repeatability is poor for a substantial minority of the population.

Effect of exercise intensity and duration on postexercise metabolism.

Data are reported on the net recovery O2 consumption (VO2) for nine male subjects (mean age 21.9 yr, VO2max 63.0 ml.kg-1.min-1, body fat 10.6%) used in a 3 (independent variables: intensities of 30, 50, and 70% VO2max) x 3 (independent variables: durations of 20, 50, and 80 min) repeated measures design (P less than or equal to 0.05). The 8-h mean excess postexercise O2 consumptions (EPOCs) for the 20-, 50-, and 80-min bouts, respectively, were 1.01, 1.43, and 1.04 liters at 30% VO2max (6.8 km/h); 3.14, 5.19, and 6.10 liters at 50% VO2max (9.5 km/h); and 5.68, 10.04, and 14.59 liters at 70% VO2max (13.4 km/h). The mean net total O2 costs (NTOC = net exercise VO2 + EPOC) for the 20-, 50-, and 80-min bouts, respectively, were 20.48, 53.20, and 84.23 liters at 30% VO2max; 38.95, 100.46, and 160.59 liters at 50% VO2max; and 58.30, 147.48, and 237.17 liters at 70% VO2max. The nine EPOCs ranged only from 1.0 to 8.9% of the NTOC (mean 4.8%) of the exercise. These data, therefore, indicate that in well-trained subjects the 8-h EPOC per se comprises a very small percentage of the NTOC of exercise.

Comparison of energy expenditure elevations after submaximal and supramaximal running.

Although exercise intensity has been identified as a major determinant of the excess postexercise oxygen consumption (EPOC), no studies have compared the EPOC after submaximal continuous running and supramaximal interval running. Eight male middle-distance runners [age = 2.1 +/- 3.1 (SD) yr; mass = 67.8 +/- 5.1 kg; maximal oxygen consumption (VO2max) = 69.2 +/- 4.0 ml.kg-1.min-1] therefore completed two equated treatments of treadmill running (continuous running: 30 min at 70% VO2max; interval running: 20 x 1-min intervals at 105% VO2max with intervening 2-min rest periods) and a control session (no exercise) in a counter-balanced research design. The 9-h EPOC values were 6.9 +/- 3.8 and 15.0 +/- 3.3 liters (t-test:P = 0.001) for the submaximal and supramaximal treatments, respectively. These values represent 7.1 and 13.8% of the net total oxygen cost of both treatments. Notwithstanding the higher EPOC for supramaximal interval running compared with submaximal continuous running, the major contribution of both to weight loss is therefore via the energy expended during the actual exercise.

Impaired interval exercise responses in elite female cyclists at moderate simulated altitude.

The effect of hypoxia on the response to interval exercise was determined in eight elite female cyclists during two interval sessions: a sustained 3 x 10-min endurance set (5-min recovery) and a repeat sprint session comprising three sets of 6 x 15-s sprints (work-to-relief ratios were 1:3, 1:2, and 1:1 for the 1st, 2nd, and 3rd sets, respectively, with 3 min between each set). During exercise, cyclists selected their maximum power output and breathed either atmospheric air (normoxia, 20.93% O(2)) or a hypoxic gas mix (hypoxia, 17.42% O(2)). Power output was lower in hypoxia vs. normoxia throughout the endurance set (244+/-18 vs. 226+/-17, 234+/-18 vs. 221+/-25, and 235+/-18 vs. 221+/-25 W for 1st, 2nd, and 3rd sets, respectively; P< 0.05) but was lower only in the latter stages of the second and third sets of the sprints (452+/-56 vs. 429+/-49 and 403+/-54 vs. 373+/- 43 W, respectively; P<0.05). Hypoxia lowered blood O(2) saturation during the endurance set (92.9+/-2.9 vs. 95.4+/-1.5%; P<0.05) but not during repeat sprints. We conclude that, when elite cyclists select their maximum exercise intensity, both sustained (10 min) and short-term (15 s) power are impaired during hypoxia, which simulated moderate ( approximately 2,100 m) altitude.