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.

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.

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.

Respiratory symptoms and inflammatory responses to Difflam throat-spray intervention in half-marathon runners: a randomised controlled trial.

OBJECTIVE: In this study, the effects of Difflam Forte Anti-inflammatory Throat Spray on the incidence of upper respiratory symptoms (URS) and inflammatory responses after a half-marathon race were investigated. DESIGN AND SETTING: Double-blind placebo-controlled randomised trial conducted in association with a half-marathon event. PARTICIPANTS: 45 well-trained half-marathon runners. INTERVENTIONS: Difflam (n = 25) or placebo (n = 20) throat sprays were self-administered three times daily for 1 week before and 2 weeks after the race. MAIN OUTCOME MEASURES: Self-reported respiratory symptoms; plasma prostaglandin E(2), myeloperoxidase, interleukin (IL) 6, IL8, IL10 and IL1 receptor antagonist (IL1ra) concentrations; and salivary myeloperoxidase and IL6 concentrations. RESULTS: All subjects completed the intervention without reporting any adverse events. The proportion of athletes reporting URS was not substantially different between Difflam (52%) and placebo (56%) groups (p = 0.82). However, symptom severity scores were approximately 29% lower during Difflam treatment (4.7 (7.4) vs 6.6 (9.6)) AU). Post-exercise responses in plasma inflammatory markers did not differ substantially between Difflam and placebo groups. Post-race increases in salivary myeloperoxidase ( approximately 63%; trivial to moderate difference; p = 0.13) and salivary IL6 ( approximately 50%; trivial to moderate difference; p = 0.25) were greater in the Difflam group. CONCLUSIONS: Prophylactic use of the Difflam reduced the severity, but not the frequency, of URS among half-marathon runners. Post-race increases in systemic inflammatory markers were not altered by Difflam use, but markers of local inflammation (salivary myeloperoxidase and IL6) were augmented in the Difflam compared with the placebo group.

Oral administration of the probiotic Lactobacillus fermentum VRI-003 and mucosal immunity in endurance athletes.

OBJECTIVE: To evaluate the ability of a probiotic Lactobacillus fermentum VRI-003 (PCC) to enhance the mucosal immune system of elite athletes. DESIGN AND SETTING: A double-blind, placebo-controlled, crossover trial was conducted over a 4-month period of winter training. PARTICIPANTS; 20 healthy elite male distance runners. INTERVENTIONS: PCC was given at a daily dose of 1.26 x 10(10) as a freeze-dried powder in gelatin capsules. Placebo capsules contained an inert excipient. MAIN OUTCOME MEASURES: Treadmill performance (monthly), mucosal and systemic immunity (monthly), training (daily) and illness (daily) were assessed. Serum cytokine levels, salivary IgA levels and incidence, duration and severity of respiratory tract infections were measured. RESULTS: Subjects reported less than half the number of days of respiratory symptoms during PCC treatment (30 days) compared with placebo (72 days, p<0.001). Illness severity was also lower for episodes occurring during the PCC treatment (p = 0.06). There were no significant differences in the mean change in salivary IgA and IgA1 levels, or in interleukin (IL)4 and IL12 levels, between treatments. However, PCC treatment elicited a twofold (p = 0.07) greater change in whole-blood culture interferon gamma (IFNgamma) compared with placebo. No substantial changes in running performance measures were seen over the study period. CONCLUSIONS: Prophylactic administration of PCC was associated with a substantial reduction in the number of days and severity of respiratory illness in a cohort of highly trained distance runners. Maintenance of IFNgamma levels may be one mechanism underpinning the positive clinical outcomes.

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.

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.

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.

No effect of mild heat stress on the regulation of carbohydrate metabolism at the onset of exercise.

To investigate the influence of heat stress on the regulation of skeletal muscle carbohydrate metabolism, six active, but not specifically trained, men performed 5 min of cycling at a power output eliciting 70% maximal O2 uptake in either 20 degrees C (Con) or 40 degrees C (Heat) after 20 min of passive exposure to either environmental condition. Although muscle temperature (T(mu)) was similar at rest when comparing trials, 20 min of passive exposure and 5 min of exercise increased (P < 0.05) T(mu) in Heat compared with Con (37.5 +/- 0.1 vs. 36.9 +/- 0.1 degrees C at 5 min for Heat and Con, respectively). Rectal temperature and plasma epinephrine were not different at rest, preexercise, or 5 min of exercise between trials. Although intramuscular glycogen phosphorylase and pyruvate dehydrogenase activity increased (P < 0.05) at the onset of exercise, there were no differences in the activities of these regulatory enzymes when comparing Heat with Con. Accordingly, glycogen use in the first 5 min of exercise was not different when comparing Heat with Con. Similarly, no differences in intramuscular concentrations of glucose 6-phosphate, lactate, pyruvate, acetyl-CoA, creatine, phosphocreatine, or ATP were observed at any time point when comparing Heat with Con. These results demonstrate that, whereas mild heat stress results in a small difference in contracting T(mu), it does not alter the activities of the key regulatory enzymes for carbohydrate metabolism or glycogen use at the onset of exercise, when plasma epinephrine levels are unaltered.