This study investigated the influence of dehydration on urinary levels of pseudoephedrine (PSE) after prolonged repeated effort activity. Fourteen athletes performed a simulated team game circuit (STGC) outdoors over 120 min under three different hydration protocols: hydrated (HYD), dehydrated (DHY) and dehydrated + postexercise fluid bolus (BOL). In all trials, a 60 mg dose of PSE was administered 30 min before trial and at half time of the STGC. Urinary PSE levels were measured before drug administration and at 90 min postexercise. In addition, body mass (BM) changes and urinary specific gravity (USG), osmolality (OSM), creatinine (Cr), and pH values were recorded. No differences in PSE levels were found 90 min postexercise between conditions (HYD: 208.5 ± 116.5; DHY: 238.9 ± 93.5; BOL: 195.6 ± 107.3 μg·ml−1), although large variations were seen within and between participants across conditions (range: 33–475 μg·ml−1: ICC r = .03–0.16, p > .05). There were no differences between conditions in USG, OSM, pH or PSE/Cr ratio. In conclusion, hydration status did not influence urinary PSE levels after prolonged repeated effort activity, with ~70% of samples greater than the WADA limit (>150 μg.ml−1), and ~30% under. Due to the unpredictability of urinary PSE values, athletes should avoid taking any medications containing PSE during competition.
Daniel Jolley, Brian Dawson, Shane K. Maloney, James White, Carmel Goodman and Peter Peeling
Chelsie E. Winchcombe, Martyn J. Binnie, Matthew M. Doyle, Cruz Hogan and Peter Peeling
Purpose: To determine the reliability and validity of a power-prescribed on-water (OW) graded exercise test (GXT) for flat-water sprint kayak athletes. Methods: Nine well-trained sprint kayak athletes performed 3 GXTs in a repeated-measures design. The initial GXT was performed on a stationary kayak ergometer in the laboratory (LAB). The subsequent 2 GXTs were performed OW (OW1 and OW2) in an individual kayak. Power output (PWR), stroke rate, blood lactate, heart rate, oxygen consumption, and rating of perceived exertion were measured throughout each test. Results: Both PWR and oxygen consumption showed excellent test–retest reliability between OW1 and OW2 for all 7 stages (intraclass correlation coefficient > .90). The mean results from the 2 OW GXTs (OWAVE) were then compared with LAB, and no differences in oxygen consumption across stages were evident (P ≥ .159). PWR was higher for OWAVE than for LAB in all stages (P ≤ .021) except stage 7 (P = .070). Conversely, stroke rate was lower for OWAVE than for LAB in all stages (P < .010) except stage 2 (P = .120). Conclusions: The OW GXT appears to be a reliable test in well-trained sprint kayak athletes. Given the differences in PWR and stroke rate between the LAB and OW tests, an OW GXT may provide more specific outcomes for OW training.
Peter Peeling, Brian Dawson, Carmel Goodman, Grant Landers, Erwin T. Wiegerinck, Dorine W. Swinkels and Debbie Trinder
Urinary hepcidin, inflammation, and iron metabolism were examined during the 24 hr after exercise. Eight moderately trained athletes (6 men, 2 women) completed a 60-min running trial (15-min warm-up at 75–80% HRpeak + 45 min at 85–90% HRpeak) and a 60-min trial of seated rest in a randomized, crossover design. Venous blood and urine samples were collected pretrial, immediately posttrial, and at 3, 6, and 24 hr posttrial. Samples were analyzed for interleukin-6 (IL-6), C-reactive protein (CRP), serum iron, serum ferritin, and urinary hepcidin. The immediate postrun levels of IL-6 and 24-hr postrun levels of CRP were significantly increased from baseline (6.9 and 2.6 times greater, respectively) and when compared with the rest trial (p ≤ .05). Hepcidin levels in the run trial after 3, 6, and 24 hr of recovery were significantly greater (1.7–3.1 times) than the pre- and immediate postrun levels (p ≤ .05). This outcome was consistent in all participants, despite marked variation in the magnitude of rise. In addition, the 3-hr postrun levels of hepcidin were significantly greater than at 3 hr in the rest trial (3.0 times greater, p ≤ .05). Hepcidin levels continued to increase at 6 hr postrun but failed to significantly differ from the rest trial (p = .071), possibly because of diurnal influence. Finally, serum iron levels were significantly increased immediately postrun (1.3 times, p ≤ .05). The authors concluded that high-intensity exercise was responsible for a significant increase in hepcidin levels subsequent to a significant increase in IL-6 and serum iron.
Marc Sim, Brian Dawson, Grant Landers, Dorine W. Swinkels, Harold Tjalsma, Debbie Trinder and Peter Peeling
The effect of exercise modality and intensity on Interleukin-6 (IL-6), iron status, and hepcidin levels was investigated. Ten trained male triathletes performed 4 exercise trials including low-intensity continuous running (L-R), low-intensity continuous cycling (L-C), high-intensity interval running (H-R), and high-intensity interval cycling (H-C). Both L-R and L-C consisted of 40 min continuous exercise performed at 65% of peak running velocity (vVO2peak) and cycling power output (pVO2peak), while H-R and H-C consisted of 8 × 3-min intervals performed at 85% vVO2peak and pVO2peak. Venous blood samples were drawn pre-, post-, and 3 hr postexercise. Significant increases in postexercise IL-6 were seen within each trial (p < .05) and were significantly greater in H-R than L-R (p < .05). Hepcidin levels were significantly elevated at 3 hr postexercise within each trial (p < .05). Serum iron levels were significantly elevated (p < .05) immediately postexercise in all trials except L-C. These results suggest that, regardless of exercise mode or intensity, postexercise increases in IL-6 may be expected, likely influencing a subsequent elevation in hepcidin. Regardless, the lack of change in postexercise serum iron levels in L-C may indicate that reduced hemolysis occurs during weight-supported, low-intensity activity.
Peter Peeling, Tanya Blee, Carmel Goodman, Brian Dawson, Gary Claydon, John Beilby and Alex Prins
This investigation examined the effect of intramuscular iron injections on aerobic-exercise performance in iron-deficient women. Sixteen athletes performed a 10-min steady-state sub maximal economy test, a VO2max test, and a timed test to exhaustion at VO2max workload. Subjects were randomly assigned to an iron-supplemented group (IG) receiving intramuscular iron injections or to a placebo group (PG). Twenty days after the first injection, exercise and blood testing were repeated. A final blood test occurred on Day 28. Post supplementation, no differences were found between the groups’ sub maximal or maximal VO2, heart rate, or blood lactate (P > 0.05). Time to exhaustion was increased in the IG (P < 0.05) but was not greater than that of the PG (P > 0.05). The IG’s serum ferritin (SF) was significantly increased on Days 20 and 28 (mean ± standard error: 19 ± 3 to 65 ± 11 to 57 ± 12 µg/L; P < 0.01), with a percentage change from baseline significantly greater than in the PG (P < 0.01). It was concluded that intramuscular iron injections can effectively increase SF without enhancing sub maximal or maximal aerobic-exercise performance in iron-depleted female athletes.
Brian Dawson, Carmel Goodman, Tanya Blee, Gary Claydon, Peter Peeling, John Beilby and Alex Prins
Non-anemic, iron depleted women were randomly assigned to an injection group (IG) or oral group (OG) to assess which method is more efficient for increasing iron stores over a short time period. IG received a course of 5 × 2 mL intramuscular injections over 10 d, and OG received one tablet daily for 30 d. Fourteen, 21 and 28 d after commencing supplementation, ferritin concentration in OG significantly increased from baseline (means ± standard error: 27 ± 3 to 40 ± 5 to 41 ± 5 to 41 ± 5 µg/L; P < 0.01). Similarly, on days 15, 20, and 28 post the first injection, ferritin concentration in IG significantly increased from baseline (means ± standard error: 20 ± 2 to 71 ± 17 to 63 ± 11 to 63 ± 7 µg/L; P < 0.01), and was also significantly greater than OG at day 15 and 28 (P < 0.05). Iron injections are significantly more effective (both in time and degree of increase) in improving ferritin levels over 30 d than oral tablets.
Marcus J. Colby, Brian Dawson, Peter Peeling, Jarryd Heasman, Brent Rogalski, Michael K. Drew and Jordan Stares
Objectives: To assess the effect of multiple high-risk-scenario (HRS) exposures on noncontact injury prediction in elite Australian footballers. Design: Retrospective cohort study. Methods: Sessional workload data (session rating of perceived exertion, global positioning system–derived distance, sprint distance, and maximum velocity) from 1 club (N = 60 players) over 3 seasons were collated; several established HRSs were also defined. Accumulated HRS sessional exposures were calculated retrospectively (previous 1–8 wk). Noncontact injury data were documented. Univariate and multivariate Poisson regression models determined injury incidence rate ratios (IRRs) while accounting for moderating effects (preseason workload volume and playing experience). Model performance was evaluated using receiver operating characteristics (area under curve). Results: Very low (0–8 sessions: IRR = 5.76; 95% confidence interval [CI], 1.69–19.66) and very high (>15 sessions: IRR = 4.70; 95% CI, 1.49–14.87) exposures to >85% of an individual’s maximal velocity over the previous 8 wk were associated with greater injury risk compared with moderate exposures (11–12 sessions) and displayed the best model performance (area under curve = 0.64). A single session corresponding to a very low chronic load condition over the previous week for all workload variables was associated with increased injury risk, with sprint distance (IRR = 3.25; 95% CI, 1.95–5.40) providing the most accurate prediction model (area under curve = 0.63). Conclusions: Minimal exposure to high-velocity efforts (maximum speed exposure and sprint volume) was associated with the greatest injury risk. Being underloaded may be a mediator for noncontact injury in elite Australian football. Preseason workload and playing experience were not moderators of this effect.
Paul S.R. Goods, Brian T. Dawson, Grant J. Landers, Christopher J. Gore and Peter Peeling
This study aimed to assess the impact of 3 heights of simulated altitude exposure on repeat-sprint performance in teamsport athletes.
Ten trained male team-sport athletes completed 3 sets of repeated sprints (9 × 4 s) on a nonmotorized treadmill at sea level and at simulated altitudes of 2000, 3000, and 4000 m. Participants completed 4 trials in a random order over 4 wk, with mean power output (MPO), peak power output (PPO), blood lactate concentration (Bla), and oxygen saturation (SaO2) recorded after each set.
Each increase in simulated altitude corresponded with a significant decrease in SaO2. Total work across all sets was highest at sea level and correspondingly lower at each successive altitude (P < .05; sea level < 2000 m < 3000 m < 4000 m). In the first set, MPO was reduced only at 4000 m, but for subsequent sets, decreases in MPO were observed at all altitudes (P < .05; 2000 m < 3000 m < 4000 m). PPO was maintained in all sets except for set 3 at 4000 m (P < .05; vs sea level and 2000 m). BLa levels were highest at 4000 m and significantly greater (P < .05) than at sea level after all sets.
These results suggest that “higher may not be better,” as a simulated altitude of 4000 m may potentially blunt absolute training quality. Therefore, it is recommended that a moderate simulated altitude (2000–3000 m) be employed when implementing intermittent hypoxic repeat-sprint training for team-sport athletes.
Cruz Hogan, Martyn J. Binnie, Matthew Doyle, Leanne Lester and Peter Peeling
Purpose: To compare methods of monitoring and prescribing on-water exercise intensity (heart rate [HR], stroke rate [SR], and power output [PO]) during sprint kayak training. Methods: Twelve well-trained flat-water sprint kayak athletes completed a preliminary on-water 7 × 4-min graded exercise test and a 1000-m time trial to delineate individual training zones for PO, HR, and SR into a 5-zone model (T1–T5). Subsequently, athletes completed 2 repeated trials of an on-water training session, where intensity was prescribed based on individual PO zones. Times quantified for T1–T5 during the training session were then compared between PO, HR, and SR. Results: Total time spent in T1 was higher for HR (P < .01) compared with PO. Time spent in T2 was lower for HR (P < .001) and SR (P < .001) compared with PO. Time spent in T3 was not different between PO, SR, and HR (P > .05). Time spent in T4 was higher for HR (P < .001) and SR (P < .001) compared with PO. Time spent in T5 was higher for SR (P = .03) compared with PO. Differences were found between the prescribed and actual time spent in T1–T5 when using PO (P < .001). Conclusions: The measures of HR and SR misrepresented time quantified for T1–T5 as prescribed by PO. The stochastic nature of PO during on-water training may explain the discrepancies between prescribed and actual time quantified for power across these zones. For optimized prescription and monitoring of athlete training loads, coaches should consider the discrepancies between different measures of intensity and how they may influence intensity distribution.
Peter Peeling, Martyn J. Binnie, Paul S.R. Goods, Marc Sim and Louise M. Burke
A strong foundation in physical conditioning and sport-specific experience, in addition to a bespoke and periodized training and nutrition program, are essential for athlete development. Once these underpinning factors are accounted for, and the athlete reaches a training maturity and competition level where marginal gains determine success, a role may exist for the use of evidence-based performance supplements. However, it is important that any decisions surrounding performance supplements are made in consideration of robust information that suggests the use of a product is safe, legal, and effective. The following review focuses on the current evidence-base for a number of common (and emerging) performance supplements used in sport. The supplements discussed here are separated into three categories based on the level of evidence supporting their use for enhancing sports performance: (1) established (caffeine, creatine, nitrate, beta-alanine, bicarbonate); (2) equivocal (citrate, phosphate, carnitine); and (3) developing. Within each section, the relevant performance type, the potential mechanisms of action, and the most common protocols used in the supplement dosing schedule are summarized.