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Biomedical subjects

C J Gore

Publications and source records attributed to C J Gore.

At least 19 recordsLinked to original sources
PubMed2006

Interspersed normoxia during live high, train low interventions reverses an early reduction in muscle Na+, K +ATPase activity in well-trained athletes.

Hypoxia and exercise each modulate muscle Na(+), K(+)ATPase activity. We investigated the effects on muscle Na(+), K(+)ATPase activity of only 5 nights of live high, train low hypoxia (LHTL), 20 nights consecutive (LHTLc) versus intermittent LHTL (LHTLi), and acute sprint exercise. Thirty-three athletes were assigned to control (CON, n = 11), 20-nights LHTLc (n = 12) or 20-nights LHTLi (4 x 5-nights LHTL interspersed with 2-nights CON, n = 10) groups. LHTLc and LHTLi slept at a simulated altitude of 2,650 m (F(I)O(2) 0.1627) and lived and trained by day under normoxic conditions; CON lived, trained, and slept in normoxia. A quadriceps muscle biopsy was taken at rest and immediately after standardised sprint exercise, before (Pre) and after 5-nights (d5) and 20-nights (Post) LHTL interventions and analysed for Na(+), K(+)ATPase maximal activity (3-O-MFPase) and content ([(3)H]-ouabain binding). After only 5-nights LHTLc, muscle 3-O-MFPase activity declined by 2% (P < 0.05). In LHTLc, 3-O-MFPase activity remained below Pre after 20 nights. In contrast, in LHTLi, this small initial decrease was reversed after 20 nights, with restoration of 3-O-MFPase activity to Pre-intervention levels. Plasma [K(+)] was unaltered by any LHTL. After acute sprint exercise 3-O-MFPase activity was reduced (12.9 +/- 4.0%, P < 0.05), but [(3)H]-ouabain binding was unchanged. In conclusion, maximal Na(+), K(+)ATPase activity declined after only 5-nights LHTL, but the inclusion of additional interspersed normoxic nights reversed this effect, despite athletes receiving the same amount of hypoxic exposure. There were no effects of consecutive or intermittent nightly LHTL on the acute decrease in Na(+), K(+)ATPase activity with sprint exercise effects or on plasma [K(+)] during exercise.

Adult↗
PubMed2006

Effects of exercise intensity and duration on the excess post-exercise oxygen consumption.

Recovery from a bout of exercise is associated with an elevation in metabolism referred to as the excess post-exercise oxygen consumption (EPOC). A number of investigators in the first half of the last century reported prolonged EPOC durations and that the EPOC was a major component of the thermic effect of activity. It was therefore thought that the EPOC was a major contributor to total daily energy expenditure and hence the maintenance of body mass. Investigations conducted over the last two or three decades have improved the experimental protocols used in the pioneering studies and therefore have more accurately characterized the EPOC. Evidence has accumulated to suggest an exponential relationship between exercise intensity and the magnitude of the EPOC for specific exercise durations. Furthermore, work at exercise intensities >or=50-60% VO2max stimulate a linear increase in EPOC as exercise duration increases. The existence of these relationships with resistance exercise at this stage remains unclear because of the limited number of studies and problems with quantification of work intensity for this type of exercise. Although the more recent studies do not support the extended EPOC durations reported by some of the pioneering investigators, it is now apparent that a prolonged EPOC (3-24 h) may result from an appropriate exercise stimulus (submaximal: >or=50 min at >or=70% VO2max; supramaximal: >or=6 min at >or=105% VO2max). However, even those studies incorporating exercise stimuli resulting in prolonged EPOC durations have identified that the EPOC comprises only 6-15% of the net total oxygen cost of the exercise. But this figure may need to be increased when studies utilizing intermittent work bouts are designed to allow the determination of rest interval EPOCs, which should logically contribute to the EPOC determined following the cessation of the last work bout. Notwithstanding the aforementioned, the earlier research optimism regarding an important role for the EPOC in weight loss is generally unfounded. This is further reinforced by acknowledging that the exercise stimuli required to promote a prolonged EPOC are unlikely to be tolerated by non-athletic individuals. The role of exercise in the maintenance of body mass is therefore predominantly mediated via the cumulative effect of the energy expenditure during the actual exercise.

Adaptation, Physiological↗
PubMed2006

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.

Adolescent↗
PubMed2005

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.

Adult↗
PubMed2004

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.

Adult↗
PubMed2003

Improved running economy in elite runners after 20 days of simulated moderate-altitude exposure.

To investigate the effect of altitude exposure on running economy (RE), 22 elite distance runners [maximal O(2) consumption (Vo(2)) 72.8 +/- 4.4 ml x kg(-1) x min(-1); training volume 128 +/- 27 km/wk], who were homogenous for maximal Vo(2) and training, were assigned to one of three groups: live high (simulated altitude of 2,000-3,100 m)-train low (LHTL; natural altitude of 600 m), live moderate-train moderate (LMTM; natural altitude of 1,500-2,000 m), or live low-train low (LLTL; natural altitude of 600 m) for a period of 20 days. RE was assessed during three submaximal treadmill runs at 14, 16, and 18 km/h before and at the completion of each intervention. Vo(2), minute ventilation (Ve), respiratory exchange ratio, heart rate, and blood lactate concentration were determined during the final 60 s of each run, whereas hemoglobin mass (Hb(mass)) was measured on a separate occasion. All testing was performed under normoxic conditions at approximately 600 m. Vo(2) (l/min) averaged across the three submaximal running speeds was 3.3% lower (P = 0.005) after LHTL compared with either LMTM or LLTL. Ve, respiratory exchange ratio, heart rate, and Hb(mass) were not significantly different after the three interventions. There was no evidence of an increase in lactate concentration after the LHTL intervention, suggesting that the lower aerobic cost of running was not attributable to an increased anaerobic energy contribution. Furthermore, the improved RE could not be explained by a decrease in Ve or by preferential use of carbohydrate as a metabolic substrate, nor was it related to any change in Hb(mass). We conclude that 20 days of LHTL at simulated altitude improved the RE of elite distance runners.

Acclimatization↗
PubMed2003

Sleep quality responses to atmospheric variation: case studies of two elite female cyclists.

Strategies applied during sleep to potentially enhance athlete performance use different atmospheric conditions. High altitude conditions are known to affect sleep adversely but the effects of mild-moderate altitude and O2 enrichment at mild altitude are uncertain. We performed case studies using two elite female road cyclists (mass and maximal aerobic power of 62 kg, 65.8 ml x kg(-1) x min(-1); 57 kg, 62.7 ml x kg(-1) x min(-1)) to examine changes in sleep for different atmospheric conditions applied throughout the preparation for, and during, an International Stage race. Conditions were: i) normoxia (600 m), ii) simulated moderate altitude (2650 m), iii) natural mild altitude (1380 m) and iv) O2 enrichment at mild altitude (30% O2@ 1300-1500 m). We measured respiratory disturbances, arousals, number of awakenings, blood oxygen saturation (SpO2), heart rate (HR), rapid eye movement sleep (REM) and deep sleep. Respiratory disturbances, SpO2 and HR responses were similar for both cyclists for all conditions. Compared with normoxia, both cyclists had somewhat reduced REM at natural mild altitude and moderate simulated altitude but differed in their REM and deep sleep responses to O2 enrichment. Compared with mild altitude, both showed increased awakenings and deep sleep with O2 enrichment. Only one cyclist clearly increased her REM sleep with O2 enrichment compared to mild altitude. Our data highlight two different sleep quality responses to atmospheric variation.

Altitude↗
PubMed2002

Changes in performance, maximal oxygen uptake and maximal accumulated oxygen deficit after 5, 10 and 15 days of live high:train low altitude exposure.

Nineteen well-trained cyclists (14 males and 5 females, mean initial .VO(2max) 62.3 ml kg(-1 )min(-1)) completed a multistage cycle ergometer test to determine maximal mean power output in 4 min (MMPO(4min)), maximal oxygen uptake (.VO(2max)) and maximal accumulated oxygen deficit (MAOD). The athletes were divided into three groups, each of which completed 5, 10 or 15 days of both a control condition (C) and live high:train low altitude exposure (LHTL). The C groups lived and trained at the ambient altitude of 610 m. The LHTL groups spent 8-10 h night(-1) in normobaric hypoxia at a simulated altitude of 2,650 m, and trained at the ambient altitude of 610 m. The changes to MMPO(4min), .VO(2max) and MAOD in response to LHTL altitude exposure were not significantly different for the 5-, 10- and 15-day treatment periods. For the pooled data from all three treatment periods, there were significant increases in MMPO(4min) [mean (SD) 5.15 (0.83) W kg(-1) vs 5.34 (0.78) W kg(-1)] and MAOD [50.1 (14.2) ml kg(-1) vs 54.9 (13.1) ml kg(-1)] in the LHTL athletes between pre- and post-altitude exposure. There were no significant changes in MMPO(4min) [5.09 (0.76) W kg(-1) vs 5.16 (0.86) W kg(-1)] or MAOD [50.5 (14.1) ml kg(-1) vs 49.1 (13.0) ml kg(-1)] in the C athletes over the corresponding period. There were significant increases in .VO(2max) in the athletes during both the LHTL [63.2 (9.0) ml kg(-1 )min(-1) vs 64.1 (9.0) ml kg(-1 )min(-1)] and C [62.0 (8.6) ml kg(-1 )min(-1) vs 63.4 (9.2) ml kg(-1 )min(-1)] conditions. In these athletes, there was no difference in the impact of 5, 10 or 15 days of LHTL on the increases observed in MMPO(4min), .VO(2max) or MAOD; and LHTL increased MMPO(4min) and MAOD more than training at low altitude alone.

Adult↗
PubMed2002

Expression of CD94 and 56(bright) on natural killer lymphocytes - the influence of exercise.

This study was undertaken to determine the effects of acute intense exercise on the cell membrane-bound glycoprotein designated cluster of differentiation (CD) 94. This marker on natural killer (NK) lymphocytes contributes to control of cell function. CD94 was measured on natural killer lymphocytes from 11 adult (average 25 yrs), well-trained male subjects, (Vdot;O 2 peak mean, 5.01 L x min -1) before and immediately after a final, 4 min all-out, cycle ergometry test. Using flow cytometry, lymphocyte populations were distinguished as either having (CD94 +) or lacking (CD94 -) the cell marker. The absolute number of CD94 + and CD94 - natural killer cells increased with exercise but the mean fluorescence intensity (MFI) for CD94 decreased from pre 131, to post 117 (p = 0.01). The percentage of NK cells that were CD94 + did not change, but exercise did mobilise natural killer cells of greater MFI for the surface markers designated CD16/CD56 (pre 750 to post 1 050, p < 0.001). The latter suggests that some exercise-mobilised natural killer cells may have originated from the liver as CD56 +bright cells.

Adult↗
PubMed2001

An evaluation of the concept of living at moderate altitude and training at sea level.

Despite equivocal findings about the benefit of altitude training, current theory dictates that the best approach is to spend several weeks living at > or =2500 m but training near sea level. This paper summarizes six studies in which we used simulated altitude (normobaric hypoxia) to examine: (i) the assumption that moderate hypoxia compromises training intensity (two studies); and (ii) the nature of physiological adaptations to sleeping in moderate hypoxia (four studies). When submaximal exercise was >55% of sea level maximum oxygen uptake (VO2max), 1800 m simulated altitude significantly increased heart rate, blood lactate and perceived exertion of skiers. In addition, cyclists self-selected lower workloads during high-intensity exercise in hypoxia (2100 m) than in normoxia. Consequently, our findings partially confirm the rationale for 'living high, training low'. In the remaining four studies, serum erythropoietin increased 80% in the early stages of hypoxic exposure, but the reticulocyte response did not significantly exceed that of control subjects. There was no significant increase in haemoglobin mass (Hb(mass)) and VO2max tended to decrease. Performance in exercise tasks lasting approximately 4 min showed a non-significant trend toward improvement (1.0+/-0.4% vs. 0.1+/-0.4% for a control group; P=0.13 for group x time interaction). We conclude that sleeping in moderate hypoxia (2650-3000 m) for up to 23 days may offer practical benefit to elite athletes, but that any effect is not likely due to increased Hb(mass) or VO2max.

Adaptation, Physiological↗
PubMed2001

Associations of physical activity with body weight and fat in men and women.

OBJECTIVE: Increasing physical activity is strongly advocated as a key public health strategy for weight gain prevention. We investigated associations of leisure-time physical activity (LTPA) and occupational/domestic physical activity with body mass index (BMI) and a skinfold-derived index of body fat (sum of six skinfolds), among normal-weight and overweight men and women. DESIGN: Analyses of cross-sectional self-report and measured anthropometric data. SUBJECTS: A total of 1302 men and women, aged 18-78 y, who were part of a randomly selected sample and who agreed to participate in a physical health assessment. MEASUREMENTS: Self-report measures of physical activity, measured height and weight, and a skinfold-derived index of body fatness. RESULTS: Higher levels of LTPA were positively associated with the likelihood of being in the normal BMI and lower body fat range for women, but few or no associations were found for men. No associations were found between measures of occupational/domestic activity and BMI or body fat for men or women. CONCLUSION: By using a skinfold sum as a more direct measure of adiposity, this study extends and confirms the previous research that has shown an association between BMI and LTPA. Our results suggest gender differences in the relationship of leisure-time physical activity with body fatness. These findings, in conjunction with a better understanding of the causes of such differences, will have important public health implications for the development and targeting of weight gain prevention strategies.

Adipose Tissue↗
PubMed2001

Live high:train low increases muscle buffer capacity and submaximal cycling efficiency.

This study investigated whether hypoxic exposure increased muscle buffer capacity (beta(m)) and mechanical efficiency during exercise in male athletes. A control (CON, n=7) and a live high:train low group (LHTL, n=6) trained at near sea level (600 m), with the LHTL group sleeping for 23 nights in simulated moderate altitude (3000 m). Whole body oxygen consumption (VO2) was measured under normoxia before, during and after 23 nights of sleeping in hypoxia, during cycle ergometry comprising 4 x 4-min submaximal stages, 2-min at 5.6 +/- 0.4 W kg(-1), and 2-min 'all-out' to determine total work and VO(2peak). A vastus lateralis muscle biopsy was taken at rest and after a standardized 2-min 5.6 +/- 0.4 W kg(-1) bout, before and after LHTL, and analysed for beta(m) and metabolites. After LHTL, beta(m) was increased (18%, P < 0.05). Although work was maintained, VO(2peak) fell after LHTL (7%, P < 0.05). Submaximal VO2 was reduced (4.4%, P < 0.05) and efficiency improved (0.8%, P < 0.05) after LHTL probably because of a shift in fuel utilization. This is the first study to show that hypoxic exposure, per se, increases muscle buffer capacity. Further, reduced VO2 during normoxic exercise after LHTL suggests that improved exercise efficiency is a fundamental adaptation to LHTL.

Adaptation, Physiological↗
PubMed2001

A comparison of the physiological response to simulated altitude exposure and r-HuEpo administration.

Concerns have been raised about the morality of using simulated altitude facilities in an attempt to improve athletic performance. One assumption that has been influential in this debate is the belief that altitude houses simply mimic the physiological effects of illegal recombinant human erythropoietin (r-HuEpo) doping. To test the validity of this assumption, the haematological and physiological responses of 23 well-trained athletes exposed to a simulated altitude of 2650-3000 m for 11-23 nights were contrasted with those of healthy volunteers receiving a low dose (150 IU x kg(-1) per week) of r-HuEpo for 25 days. Serial blood samples were analysed for serum erythropoietin and percent reticulocytes; maximal oxygen uptake (VO2max) was assessed before and after r-HuEpo administration or simulated altitude exposure. The group mean increase in serum erythropoietin (422% for r-HuEpo vs 59% for simulated altitude), percent reticulocytes (89% vs 30%) and VO2max (6.6% vs -2.0%) indicated that simulated altitude did not induce the changes obtained with r-HuEpo administration. Based on the disparity of these responses, we conclude that simulated altitude facilities should not be considered unethical based solely on the tenet that they provide an alternative means of obtaining the benefits sought by illegal r-HuEpo doping.

Adult↗
PubMed2001

The effect of altitude on cycling performance: a challenge to traditional concepts.

Acute exposure to moderate altitude is likely to enhance cycling performance on flat terrain because the benefit of reduced aerodynamic drag outweighs the decrease in maximum aerobic power [maximal oxygen uptake (VO2max)]. In contrast, when the course is mountainous, cycling performance will be reduced at moderate altitude. Living and training at altitude, or living in an hypoxic environment (approximately 2500 m) but training near sea level, are popular practices among elite cyclists seeking enhanced performance at sea level. In an attempt to confirm or refute the efficacy of these practices, we reviewed studies conducted on highly-trained athletes and, where possible, on elite cyclists. To ensure relevance of the information to the conditions likely to be encountered by cyclists, we concentrated our literature survey on studies that have used 2- to 4-week exposures to moderate altitude (1500 to 3000 m). With acclimatisation there is strong evidence of decreased production or increased clearance of lactate in the muscle, moderate evidence of enhanced muscle buffering capacity (beta m) and tenuous evidence of improved mechanical efficiency (ME) of cycling. Our analysis of the relevant literature indicates that, in contrast to the existing paradigm, adaptation to natural or simulated moderate altitude does not stimulate red cell production sufficiently to increase red cell volume (RCV) and haemoglobin mass (Hb(mass)). Hypoxia does increase serum erthyropoietin levels but the next step in the erythropoietic cascade is not clearly established; there is only weak evidence of an increase in young red blood cells (reticulocytes). Moreover, the collective evidence from studies of highly-trained athletes indicates that adaptation to hypoxia is unlikely to enhance sea level VO2max. Such enhancement would be expected if RCV and Hb(mass) were elevated. The accumulated results of 5 different research groups that have used controlled study designs indicate that continuous living and training at moderate altitude does not improve sea level performance of high level athletes. However, recent studies from 3 independent laboratories have consistently shown small improvements after living in hypoxia and training near sea level. While other research groups have attributed the improved performance to increased RCV and VO2max, we cite evidence that changes at the muscle level (beta m and ME) could be the fundamental mechanism. While living at altitude but training near sea level may be optimal for enhancing the performance of competitive cyclists, much further research is required to confirm its benefit. If this benefit does exist, it probably varies between individuals and averages little more than 1%.

2,3-Diphosphoglycerate↗
PubMed2001

Detection of recombinant human erythropoietin abuse in athletes utilizing markers of altered erythropoiesis.

BACKGROUND AND OBJECTIVES: The detection of recombinant human erythropoietin (r-HuEPO) abuse by athletes remains problematic. The main aim of this study was to demonstrate that the five indirect markers of altered erythropoiesis identified in our earlier work were reliable evidence of current or recently discontinued r-HuEPO use. A subsidiary aim was to refine weightings of the five markers in the initial model using a much larger data set than in the pilot study. A final aim was to verify that the hematologic response to r-HuEPO did not differ between Caucasian and Asiatic subjects. DESIGN AND METHODS: Recreational athletes resident in Sydney, Australia (Sydney, n = 49; 16 women, 33 men) or Beijing, China (Beijing, n=24; 12 women, 12 men) were randomly assigned to r-HuEPO or placebo groups prior to a 25 day administration phase. Injections of r-HuEPO (or saline) were administered double-blind at a dose of 50 IU/kg three times per week, with oral iron (105 mg) or placebo supplements taken daily by all subjects. Blood profiles were monitored during and for 4 weeks after drug administration for hematocrit (Hct), reticulocyte hematocrit (RetHct), percent macrocytes (%Macro), serum erythropoietin (EPO) and soluble transferrin receptor (sTfr), since we had previously shown that these five variables were indicative of r-HuEPO use. RESULTS: The changes in Hct, RetHct, %Macro, EPO and sTfr in the Sydney trial were qualitatively very similar to the changes noted in our previous administration trial involving recreational athletes of similar genetic origin. Statistical models developed from Fisher's discriminant analysis were able to categorize the user and placebo groups correctly. The same hematologic response was demonstrated in Beijing athletes also administered r-HuEPO. INTERPRETATION AND CONCLUSIONS: This paper confirms that r-HuEPO administration causes a predictable and reproducible hematologic response. These markers are disturbed both during and for several weeks following r-HuEPO administration. This work establishes an indirect blood test which offers a useful means of detecting and deterring r-HuEPO abuse. Ethnicity did not influence the markers identified as being able to detect athletes who abuse r-HuEPO.

Adult↗
PubMed2000

Simulated moderate altitude elevates serum erythropoietin but does not increase reticulocyte production in well-trained runners.

The purpose of this study was to investigate whether the modest increases in serum erythropoietin (sEpo) experienced after brief sojourns at simulated altitude are sufficient to stimulate reticulocyte production. Six well-trained middle-distance runners (HIGH, mean maximum oxygen uptake, VO2max = 70.2 ml x kg(-1) x min(-1) spent 8-11 h per night for 5 nights in a nitrogen house that simulated an altitude of 2650 m. Five squad members (CONTROL, mean VO2max= 68.9 ml x kg(-1) x min(-1) undertook the same training, which was conducted under near-sea-level conditions (600 m altitude), and slept in dormitory-style accommodation also at 600 m altitude. For both groups, this 5-night protocol was undertaken on three occasions, with a 3-night interim between successive exposures. Venous blood samples were measured for sEpo after 1 and 5 nights of hypoxia on each occasion. The percentage of reticulocytes was measured, along with a range of reticulocyte parameters that are sensitive to changes in erythropoiesis. Mean serum erythropoietin levels increased significantly (P < 0.01) above baseline values [mean (SD) 7.9 (2.4) mU x ml(-1)] in the HIGH group after the 1st night [11.8 (1.9) mU x ml(-1), 57%], and were also higher on the 5th night [10.7 (2.2) mU x ml(-1), 42%] compared with the CONTROL group, whose erythropoietin levels did not change. After athletes spent 3 nights at near sea level, the change in sEpo during subsequent hypoxic exposures was markedly attenuated (13% and -4% change during the second exposure; 26% and 14% change during the third exposure; 1st and 5th nights of each block, respectively). The increase in sEpo was insufficient to stimulate reticulocyte production at any time point. We conclude that when daily training loads are controlled, the modest increases in sEpo known to occur following brief exposure to a simulated altitude of 2650 m are insufficient to stimulate reticulocyte production.

Adult↗
PubMed2000

Arterial hypoxaemia in endurance athletes is greater during running than cycling.

The effect of both training discipline and exercise modality on exercise-induced hypoxaemia (EIH) was examined in seven runners and six cyclists during 5 min high intensity treadmill and cycle exercise. There were no significant interactions between training discipline, exercise modality and arterial P(O(2)) (Pa(O(2))) when subject groups were considered separately but when pooled there were significant differences between exercise modalities. After min 2 of exercise arterial hydrogen ion concentration, minute ventilation, alveolar P(O(2)) (PA(O(2))) and Pa(O(2)) were all lower with treadmill running with the largest differential for the latter occurring at min 5 (treadmill, 80.8+/-1.8; cycle, 90.2+/-2.5, mmHg, N=13, P< or = 0.05). At every min of exercise, the differences in Pa(O(2)) between the ergometers were strongly associated with similar differences in PA(O(2)) and alveolar to arterial P(O(2)) (PA(O(2))-Pa(O(2))). It is concluded that the greater EIH with treadmill running is a consequence of the combined effect of a reduced lactic acidosis-induced hyperventilation and greater ventilation-perfusion inequality with this exercise mode.

Acidosis, Lactic↗