Influence of averaging method on muscle deoxygenation interpretation during repeated-sprint exercise.

Near-infrared spectroscopy (NIRS) is a common tool used to study oxygen availability and utilization during repeated-sprint exercise. However, there are inconsistent methods of smoothing and determining peaks and nadirs from the NIRS signal, which make interpretation and comparisons between studies difficult. To examine the effects of averaging method on deoxyhaemoglobin concentration ([HHb]) trends, nine males performed ten 10-s sprints, with 30 seconds of recovery, and six analysis methods were used for determining peaks and nadirs in the [HHb] signal. First, means were calculated over predetermined windows in the last 5 and 2 seconds of each sprint and recovery period. Second, moving 5-seconds and 2-seconds averages were also applied, and peaks/nadirs were determined for each 40-seconds sprint/recovery cycle. Third, a Butterworth filter was used to smooth the signal, and the resulting signal output was used to determine peaks and nadirs from predetermined time points and a rolling approach. Correlation and residual analysis showed that the Butterworth filter attenuated the "noise" in the signal, while maintaining the integrity of the raw data (r = .9892; mean standardized residual -9.71 × 103  ± 3.80). Means derived from predetermined windows, irrespective of length and data smoothing, underestimated the magnitude of peak and nadir [HHb] compared to a rolling mean approach. Consequently, sprint-induced metabolic changes (inferred from Δ[HHb]) were underestimated. Based on these results, we suggest using a digital filter to smooth NIRS data, rather than an arithmetic mean, and a rolling approach to determine peaks and nadirs for accurate interpretation of muscle oxygenation trends.

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.

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.

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.