The need for an alternative method to determine intravascular volumes.

It is well described that numerous environmental factors, including exercise, modulate plasma volume (PV). These modulations prove problematic when a number of haematological markers are measured as a concentration in blood plasma. A primary example is haemoglobin concentration ([Hb]), a marker of erythropoiesis commonly used within medicine and also used to detect blood doping. Natural changes in PV can confound [Hb] values when a volume change is detected rather than a true change in haemoglobin mass (Hbmass) (e.g. volume expansion resulting in a [Hb] decrease and pseudo-anemia vs. Hbmass decline resulting in anaemia). Currently, there is no simple solution to correct for PV shifts, and this has proven problematic when monitoring volumetric health markers in clinical and anti-doping settings. This narrative review explores the influence that PV shifts have on volumetric biomarkers, such as [Hb]. The progressive expansion in PV observed during multi-day endurance events will be summarised, and the observed impact PV variance has on concentration-based markers will be quantified. From this, the need for alternative methods to correct [Hb] for volume fluctuations is highlighted. Available methods for calculating intravascular volumes are then discussed, with a focus on a recently developed approach using a panel of 'volume descriptive' biomarkers from a standard blood test. Finally, the practical applications of this novel PV blood test within both anti-doping and clinical settings will be examined.

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.

Training environment and Vitamin D status in athletes.

This study assessed the associations between gender, anthropometry, predominant training environment and Vitamin D status in 72 elite athletes. Additionally, any links between Vitamin D status and recent injury/health status, or sun protection practices were investigated. Athletes underwent an anthropometric assessment and provided venous blood samples for the determination of 25-hydroxyvitamin D (25(OH)D), the accepted biological marker of Vitamin D status. Finally, athletes completed a questionnaire relating to their recent training and injury history, and their sun protection practices. The athlete cohort were divided by predominant training environment as either indoor, outdoor, or mixed training environment athletes. The average ( ± SD) 25(OH)D levels of the group were 111 ± 37 nmol/L, with the indoor training group (90 ± 28 nmol/L) significantly lower than the outdoor (131 ± 35 nmol/L), and mixed (133 ± 29 nmol/L) training groups (p = 0.0001). Anthropometrical measures were positively associated with 25(OH)D levels; however, recent injury status or sun protection practice showed no association. Given the significant differences in 25(OH)D levels between the outdoor and indoor predominant training environments, coaches of indoor athletes may wish to monitor their athletes' Vitamin D levels throughout the year, in order to avoid any possibilities of a deficiency occurring.

Effects of a recovery swim on subsequent running performance.

The effects of a swimming-based recovery session implemented 10 h post high intensity interval running on subsequent run performance the next day was investigated. Nine well trained triathletes performed two high intensity interval running sessions (HIIS) (8x3 min at 85-90% VO(2peak) velocity), followed 10 h later by either a swim recovery session (SRS) (20x100 m at 90% of 1 km time trial speed), or a passive recovery session (PRS). Subsequently, a time to fatigue run (TTF) was completed 24 h post-HIIS. Venous blood samples were taken pre-HIIS and pre-TTF to determine the levels of circulating C-Reactive Protein (CRP). Subjects were also asked to rate their perceived recovery prior to commencing the TTF run. The SRS resulted in a significantly longer (830+/-198 s) TTF as compared to PRS (728+/-183 s) ( P=0.005). There was also a significant percentage change from baseline in the CRP levels 24 h post-HIIS (SRS=-23%, PRS=+/-5%, P=0.007). There were no significant differences in perceived recovery between two conditions ( P=0.40) . The findings of the present study showed that a swimming-based recovery session enhanced following day exercise performance, possibly due to the hydrostatic properties of water and its associated influence on inflammation.

Effect of swimming intensity on subsequent cycling and overall triathlon performance.

OBJECTIVES: To investigate the effects of different swimming intensities on subsequent cycling and overall triathlon performance. METHODS: Nine highly trained, male triathletes completed five separate laboratory sessions comprising one graded exercise test, a swim time trial (STT), and three sprint distance triathlons (TRI). The swimming velocities of the three TRI sessions were 80-85% (S80), 90-95% (S90), and 98-102% (S100) of the STT velocity. Subsequent cycling and running were performed at a perceived maximal intensity. Swimming stroke mechanics were measured during the swim. Plasma lactate concentration and ratings of perceived exertion were recorded at the conclusion of the swim and over the course of subsequent cycling and running. Oxygen consumption was recorded during the cycle. RESULTS: The S80 and S90 cycle times were faster than the S100 cycle time (p<0.05). The overall triathlon time of S80 was faster than that of S100 (p<0.05). The S100 swim was characterised by a greater stroke rate than S80 and S90 (p<0.05) and a greater plasma lactate concentration than S80 (p<0.01). CONCLUSION: A swimming intensity below that of a time trial effort significantly improves subsequent cycling and overall triathlon performance.