This case study examines the impact of low serum ferritin (sFe) on physiological assessment measures and performance in a young female 1500-m runner undertaking approximately 95–130 km/wk training. The study spans 4 race seasons and an Olympic Games. During this period, 25 venous blood samples were analyzed for sFe and hemoglobin (Hb); running economy, VO2max, and lactate threshold were measured on 6 occasions separated by 8–10 mo. Training was carefully monitored including 65 monitored treadmill training runs (targeting an intensity associated with the onset of blood lactate accumulation) using blood lactate and heart rate. Performances at competitive track events were recorded. All data were compared longitudinally. Mean sFe was 24.5 ± 7.6 μg/L (range 10–47), appearing to be in gradual decline with the exception of 2 data points (37 and 47 μg/L) after parenteral iron injections before championships, when the lowest values tended to occur, coinciding with peak training volumes. Each season, 1500-m performance improved, from 4:12.8 in year 1 to 4:03.5 in year 4. VO2max (69.8 ± 2.0 mL · kg−1 · min−1) and running economy (%VO2max at a fixed speed of 16 km/h; max 87.8%, min 80.3%) were stable across time and lactate threshold improved (from 14 to 15.5 km/h). Evidence of anemia (Hb <12 g/dL) was absent. These unique data demonstrate that in 1 endurance athlete, performance can continue to improve despite an apparent iron deficiency. Raising training volume may have caused increased iron utilization; however, the effect of this on performance is unknown. Iron injections were effective in raising sFe in the short term but did not appear to affect the long-term pattern.
Charles R. Pedlar, Gregory P. Whyte, Richard Burden, Brian Moore, Gill Horgan and Noel Pollock
Nathan A. Lewis, Ann Redgrave, Mark Homer, Richard Burden, Wendy Martinson, Brian Moore and Charles R. Pedlar
Purpose: To examine a diagnosis of unexplained underperformance syndrome (UUPS, or overtraining syndrome) in an international rower describing a full recovery and return to elite competition the same year. Methods: On diagnosis and 4 and 14 mo postdiagnosis, detailed assessments including physiological, nutritional, and biomarkers were made. Results: Clinical examination and laboratory results for hematology, biochemistry, thyroid function, immunology, vitamins, and minerals were unremarkable and did not explain the presentation and diagnosis. Redox biomarkers including hydroperoxides, plasma antioxidant capacity, red blood cell glutathione, superoxide dismutase, coenzyme Q10, vitamin E (α- and γ-tocopherol), and carotenoids (lutein, α-carotene, β-carotene) provided evidence of altered redox homeostasis. The recovery strategy began with 12 d of training abstinence and nutritional interventions, followed by 6 wk of modified training. At 4 mo postintervention, performance had recovered strongly, resulting in the athlete’s becoming European champion that same year. Further improvements in physiological and performance indices were observed at 14 mo postintervention. Physiologically relevant increases in concentrations of carotenoids were achieved at each postintervention time point, exceeding the reported critical-difference values. Conclusions: Increasing athlete phytonutrient intake may enhance recovery and tolerance of training and environmental stressors, reducing the risk of unexplained UUPS. Alterations in redox homeostasis should be considered as part of the medical management in UUPS. This is the first reported case study of an elite athlete with alterations in redox homeostasis in conjunction with a diagnosis of UUPS.
Nathan A. Lewis, Andrew J. Simpkin, Sarah Moseley, Gareth Turner, Mark Homer, Ann Redgrave, Charles R. Pedlar and Richard Burden
Background: Identifying strategies that reduce the risk of illness and injury is an objective of sports science and medicine teams. No studies have examined the relationship between oxidative stress (OS) and illness or injury in international athletes undergoing periods of intensified training and competition. Purpose: The authors aimed to identify relationships between illness, injury, and OS. Methods: A longitudinal, observational study of elite male rowers (n = 10) was conducted over 18 weeks, leading into World Championships. Following a recovery day and a 12-hour fast, hydroperoxides (free oxygen radicals test) and total antioxidant capacity (free oxygen radicals defense) were measured in venous blood, with the ratio calculated as the oxidative stress index (OSI). At all study time points, athletes were independently dichotomized as ill or not ill, injured or not injured. OS data were compared between groups using independent t tests. A Cox proportional hazard model was used to assess the association of OS with injury and illness while adjusting for age and body mass index. Results: Free oxygen radicals defense was lower (P < .02) and OSI was higher (P < .001) with illness than without illness. Free oxygen radicals test and OSI were higher with injury than without injury (P < .001). A 0.5 mmol·L−1 increase in free oxygen radicals defense was associated with a 30.6% illness risk reduction (95% confidence interval, 7%–48%, P = .014), whereas 0.5 unit increase in OSI was related to a 11.3% increased illness risk (95% confidence interval, 1%–23%, P = .036). Conclusions: OS is increased in injured and ill athletes. Monitoring OS may be advantageous in assessing recovery from and in reducing injury and illness risk given the association.