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Breath-by-breath energy expenditure during open water swimming has not yet been explored in an ecological environment. This study aimed to investigate and compare energetics and kinematics of 5 km swimming, in both swimming pool and open water conditions. Through four independent studies, oxygen uptake ( $$\dot{V}\text{O}$$ 2) kinetics, heart rate (HR), blood lactate concentration ([La−]) and glucose level (BGL), metabolic power ( $$\dot{E}$$ ), energy cost (C) and kinematics were assessed during 5 km front crawl trials in a swimming pool and open water conditions. A total of 38 competitive open water swimmers aged 16–27 years volunteered for this four part investigation: Study A (pool, ten females, 11 males), Study B (pool, four females, six males), Study C (pool case study, one female) and Study D (open water, three females, four males). In the swimming pool, swimmers started with an above average swimming speed (v), losing efficiency along the 5 km, despite apparent homeostasis for [La−], BGL, $$\dot{V}\text{O}$$ 2, $$\dot{E}$$ and C. In open water, swimmers started the 5 km with a below average v, increasing the stroke rate (SR) in the last 1000 m. In open water, $$\dot{V}\text{O}$$ 2 kinetics parameters, HR, [La−], BGL, respiratory exchange ratio and C were affected by the v and SR fluctuations along the 5 km. Small fluctuations were observed for energetic variables in both conditions, but changes in C were lower in swimming pool than in open water. Coaches should adjust the training plan accordingly to the specificity of open water swimming.

Purpose: The extent to which hepcidin regulation after acute bouts of exercise is influenced by baseline (resting) concentrations of key iron parameters remains uncertain. This investigation explored the influence of selected iron parameters and 25-km race walk time on 3-h post-exercise hepcidin-25 levels in international-level race walkers. Methods: Twenty-four male race walkers completed a graded exercise test and a 25-km race-walk trial. Throughout the 25-km race-walk, venous blood samples were collected pre-exercise, immediately post-exercise, and at 3-h post-exercise. Blood was analysed for serum ferritin, serum iron, Interleukin-6 (IL-6), and hepcidin-25 concentration. Results: IL-6 and hepcidin-25 increased (7.6- and 7.5-fold, respectively) in response to the 25-km race-walk trial (both p < 0.01). Significant individual relationships were evident between 3-h post-exercise hepcidin-25, baseline serum ferritin and serum iron (r > 0.62; p < 0.05). Multiple regression analysis showed that these two iron parameters, in addition to post-exercise IL-6 concentration and 25-km race-walk time, accounted for ~77% of the variance in 3-h post-exercise hepcidin-25 (p < 0.01). A median split by the cohort’s baseline serum ferritin concentration (LOW: 58.0 vs. HIGH: 101.8 µg/L; p < 0.01) showed a significant between group difference in the 3-h post-exercise hepcidin-25 (LOW: 6.0 ± 3.6 vs. 11.3 ± 5.4 nM; p = 0.01), despite no differences in baseline serum iron, post-exercise IL-6, or 25-km race-walk time (all p > 0.05). Conclusion: Despite exercise activating numerous hepcidin regulators, baseline iron status appears to play a dominant role in the regulation of hepcidin-25 in elite-level athletes subsequent to endurance exercise.

Differences in the immune and inflammatory response to exercise between healthy and illness-prone athletes may be one explanation why some athletes experience a greater incidence of upper respiratory symptoms than others. The aim of this study was to compare the C-reactive protein (CRP) response to acute exercise between healthy and illness-prone trained distance runners. Runners were classified as healthy (or =2 episodes of upper respiratory symptoms per year; n = 10) or illness-prone (or =4 episodes per year; n = 8) and completed three treadmill running protocols. CRP concentrations were determined prior to and 24 h following each exercise protocol and responses compared between the two groups. Plasma concentrations of Interleukin (IL)-6, IL-8, IL-10 and the IL-1 receptor antagonist (IL-1ra) were also determined immediately, 1 h, 10 h and 24 h post-exercise. The CRP response at 24 h post-exercise was not substantially different between healthy and illness-prone athletes (approximately 2-10%). There were small to moderate correlations between resting CRP concentrations and the peak IL-6 (r = 0.28, P = 0.04), IL-8 (r = 0.31, P = 0.03), IL-10 (r = 0.28, P = 0.05) and IL-1ra (r = 0.30, P = 0.03) concentrations post-exercise. The CRP response to exercise was not useful in distinguishing between healthy and illness-prone athletes. The relationship between resting CRP concentrations and the peak pro- and anti-inflammatory responses to exercise supports the likely involvement of CRP in the complex network regulating exercise-induced inflammatory disturbance.

To expand our understanding of the overall anti-inflammatory nature of routine exercise; we compared resting blood values from adults who habitually undertake frequent, moderate levels of exercise to reference interval values assumed to reflect values largely from non-exercisers. This information would be useful for clinicians interpreting blood tests assessing inflammatory, immune and acute phase responses. Blood samples were collected from 119 community adult self-reported routine exercisers (61 males and 58 females aged 18–60 years). Samples were analysed for 20 cellular and non-cellular biomarkers which included 11 immunological and 9 acute phase reactants. These data were compared to reference intervals from the same hospital laboratory that performed the analyses on our participants’ samples. Individual analyte values were also compared with participants’ self-reported 150 day exercise patterns which included exercise frequency, intensity and duration. In general, mean values for routine exercise participants fell at the lower end of laboratory reference interval for most inflammatory analytes. More than 10 % of participants had numbers of CD19+, CD8+ and 16/56+ NK cells below the low end of the respective reference interval. More than 10 % of observed acute phase reactant values (for C3, haptoglobin and ferritin) were also below the low end of the reference interval. At rest IgM (r = −0.22) and IgG (r = −0.31) values correlated negatively (p

We compared changes in performance and total haemoglobin mass (tHb) of elite swimmers in the weeks following either Classic or Live High:Train Low (LHTL) altitude training. Twenty-six elite swimmers (15 male, 11 female, 21.4 ± 2.7 years; mean ± SD) were divided into two groups for 3 weeks of either Classic or LHTL altitude training. Swimming performances over 100 or 200 m were assessed before altitude, then 1, 7, 14 and 28 days after returning to sea-level. Total haemoglobin mass was measured twice before altitude, then 1 and 14 days after return to sea-level. Changes in swimming performance in the first week after Classic and LHTL were compared against those of Race Control (n = 11), a group of elite swimmers who did not complete altitude training. In addition, a season-long comparison of swimming performance between altitude and non-altitude groups was undertaken to compare the progression of performances over the course of a competitive season. Regardless of altitude training modality, swimming performances were substantially slower 1 day (Classic 1.4 ± 1.3% and LHTL 1.6 ± 1.6%; mean ± 90% confidence limits) and 7 days (0.9 ± 1.0% and 1.9 ± 1.1%) after altitude compared to Race Control. In both groups, performances 14 and 28 days after altitude were not different from pre-altitude. The season-long comparison indicated that no clear advantage was obtained by swimmers who completed altitude training. Both Classic and LHTL elicited ~4% increases in tHb. Although altitude training induced erythropoeisis, this physiological adaptation did not transfer directly into improved competitive performance in elite swimmers.

White cell counts at rest might be lower in athletes participating in selected endurance-type sports. Here, we analysed blood tests of elite athletes collected over a 10-year period. Reference ranges were established for 14 female and 14 male sports involving 3,679 samples from 937 females and 4,654 samples from 1,310 males. Total white blood cell counts and counts of neutrophils, lymphocytes and monocytes were quantified. Each sport was scaled (1-5) for its perceived metabolic stress (aerobic-anaerobic) and mechanical stress (concentric-eccentric) by 13 sports physiologists. Substantially lower total white cell and neutrophil counts were observed in aerobic sports of cycling and triathlon (~16% of test results below the normal reference range) compared with team or skill-based sports such as water polo, cricket and volleyball. Mechanical stress of sports had less effect on the distribution of cell counts. The lower white cell counts in athletes in aerobic sports probably represent an adaptive response, not underlying pathology.

Elite athletes often undertake altitude training to improve sea-level athletic performance, yet the optimal methodology has not been established. A combined approach of live high/train low plus train high (LH/TL+TH) may provide an additional training stimulus to enhance performance gains. Seventeen male and female middle-distance runners with maximal aerobic power (VO2max) of 65.5 +/- 7.3 mL kg(-1) min(-1) (mean +/- SD) trained on a treadmill in normobaric hypoxia for 3 weeks (2,200 m, 4 week(-1)). During this period, the train high (TH) group (n = 9) resided near sea-level (approximately 600 m) while the LH/TL+TH group (n = 8) stayed in normobaric hypoxia (3,000 m) for 14 hours day(-1). Changes in 3-km time trial performance and physiological measures including VO2max, running economy and haemoglobin mass (Hb(mass)) were assessed. The LH/TL+TH group substantially improved VO2max (4.8%; +/-2.8%, mean; +/-90% CL), Hb(mass) (3.6%; +/-2.4%) and 3-km time trial performance (-1.1%; +/-1.0%) immediately post-altitude. There was no substantial improvement in time trial performance 2 weeks later. The TH group substantially improved VO2max (2.2%; +/-1.8%), but had only trivial changes in Hb(mass) and 3-km time-trial performance. Compared with TH, combined LH/TL+TH substantially improved VO2max (2.6%; +/-3.2%), Hb(mass) (4.3%; +/-3.2%), and time trial performance (-0.9%; +/-1.4%) immediately post-altitude. LH/TL+TH elicited greater enhancements in physiological capacities compared with TH, however, the transfer of benefits to time-trial performance was more variable.

Measurement of IL-6 has been widely undertaken to examine inflammatory and immune responses to exercise. Use of salivary IL-6 offers an alternative to the invasive collection procedures required for IL-6 measurement in plasma samples. Rarely, however, has the degree of association between plasma and salivary IL-6 been reported. The aim of the current study was to investigate the relationship between resting salivary and plasma IL-6 concentrations in 45 trained distance runners (36 males, 9 females; age: 35.1 +/- 8.0 y, mean +/- SD). Plasma and saliva samples were collected from athletes under resting conditions. Plasma IL-6 concentrations were determined using a Bioplex suspension array system and commercially available reagents. Salivary IL-6 concentrations were determined using a commercially available high-sensitivity ELISA kit. At rest, the mean (+/- SD) plasma IL-6 concentration was 3.43 +/- 3.75 pg mL(-1) compared to a mean salivary IL-6 concentration of 1.80 +/- 4.25 pg mL(-1). IL-6 concentrations in plasma and saliva samples were not correlated (r = -0.031, p = 0.85). At rest, salivary IL-6 concentrations do not reflect plasma IL-6 concentrations. The potential for salivary IL-6 to act as a surrogate marker for plasma IL-6 responses when examining inflammatory and immune responses to exercise, therefore, appears unlikely.

An evaluation of the hand-held portable Lactate Pro Analyser (KDK) was undertaken to assess its accuracy, reliability and versatility. Capillary blood samples were drawn from elite athletes in both laboratory and field settings and analysed in parallel. Accuracy was determined in relation to three other lactate analysers: (1) the ABL 700 Series Acid-Base analyser (n = 172 cases), (2) the Accusport Lactate Meter (n = 118 cases), and (3) the YSI 2300 Stat lactate analyser (n = 22 cases). The level of agreement was determined over the range of 1-18 mM. The repeatability of results between two different Lactate Pro analysers was also determined over the same range. Versatility was assessed in the field, where the Lactate Pro was used with elite athletes under a range of outdoor and indoor testing conditions. The correlations between the Lactate Pro and the ABL 700 Series Acid-Base analyser, YSI 2300 and Accusport were r = 0.98, r = 0.99, r = 0.97. The correlation between the two Lactate Pro analysers on the same sample (n = 96 cases) was r = 0.99. The level of agreement between the Lactate Pro and other analysers was generally less than +/- 2.0 mM over the physiological range of 1.0-18.0 mM (range of mean difference: -0.06 mM to 0.52 mM). The Lactate Pro was easy to operate and successfully completed the sample analysis in 100% of the tests performed. In summary, the Lactate Pro is accurate, reliable and exhibits a high degree of agreement with other lactate analysers.