Study design and participants
The participants and methods used in this cross-sectional study have earlier been described in detail,18 but briefly 67 male cyclists, triathletes and long-distance runners were recruited to the study through local sport clubs and social media in three phases (figure 1). The reason for dividing the athletes into three different cohorts were mainly due to limited access to the laboratory and test personnel. In addition, we aimed for including the athletes in their postcompetition period that differed between the cyclists and the long-distance runners. Inclusion criteria were male, 18–50 years old, competing in a demanding endurance sport, maximal oxygen uptake (VO2max) >55 mL/kg/min, training frequency ≥four sessions/week the previous year and competing at a regional or national level. Since these athletes were part of an intervention study, they also had to be disease and injury free. Thirteen participants were excluded leaving a total of 53 subjects (16 runners, 32 cyclists and 5 triathletes) in the final data analysis (figure 1). All subjects were categorised as well trained19 or at performance level four.20
Figure 1Flow chart showing the recruitment process and exclusion of participants. EI, energy intake.
All subjects gave their verbal and written informed consent before study participation.
Measures
The data collection was performed during four non-consecutive days, followed by three or four consecutive days of food and exercise registration. The participants were told to arrive in a fasted state on days 2–4, refrain from using products containing tobacco and caffeine, not to engage in more than 1 hour of low intensity exercise the day before testing and strength training was prohibited.
On day 1, body height (Seca Optima, Seca, UK) and body weight (InBody 720, Biospace, Seoul, Korea) were measured, and the participants performed an incremental test to exhaustion to determine VO2max. On day 2, RMR was measured, and the participants received instructions on how to record their energy intake and expenditure and they completed questionnaires. On day 3 and 4, blood samples were drawn, and body composition was assessed using Dual-energy X-ray absorptiometry (GE- Lunar Prodigy, Madison, Wisconsin, USA).
Exercise and eating behaviour
The Exercise Dependence Scale (EXDS) was used to assess symptoms of EXD.21 This 21-item scale operationalises EXD based on the Diagnostic and Statistical Manual of Mental Disorder IV22 criteria for substance dependence and consists of the subscales tolerance, withdrawal, intention effect, lack of control, time, reduction in other activities and continuance. Each question is ranged on a 6-point Likert scale from ‘newer’ to ‘always’. Since this was a group of healthy athletes with absence of disease and injuries, and with fewer participants compared with previous studies using EXDS,21 23 we did not expect to find a sufficient number of ‘at risk’ subjects to be able to group them based on the cut-off suggested by Hausenblas and Downs.21 Therefore, the subjects were divided into ‘lower EXDS score’ or ‘higher EXDS score’ based on the mean EXDS total score for the group.
ED symptoms were assessed using the Eating Disorder Examination Questionnaire (EDE-Q),24 a 28-item measure of ED psychopathology ranged on a 6-point Likert scale. The EDE-Q assesses the frequency or severity of core ED symptoms and related behaviours and beliefs over the past 28 days. The instrument comprises four subscales: restraint, eating concern, shape concern and weight concern. In the present study, a mean total EDE-Q score of 2.3 or more indicated ED pathology, as recommended by Müller et al.5 The EDE-Q was only distributed to the athletes included in cohorts II and III, where 34 athletes answered the EDE-Q satisfactorily.
Resting metabolic rate
RMR was measured by ventilated hood (Oxycon Pro, Eric Jeager, Germany) according to standardised laboratory proceedings18 and assessed using the Weir equation25: (3.94 (VO2)+1.1 (VCO2))×1.44. To calculate the ratio between measured RMR and predicted RMR, the Cunningham equation26 was used. Subjects with an RMRratio<0.90 were categorised as having low RMR.27
Energy availability (EA), energy intake and energy expenditure
Participants registered their energy intake using a digital kitchen scale during a period of 3 or 4 days in their home environment mirroring their typical food patterns and training regime and logged their food records using software from Dietist Net (Dietist Net, Kost och Näringsdata, Bromma, Sweden). For measurements of EEE, the subjects recorded all training sessions with their heart rate monitor (Polar M400/V800) during the same period as energy intake was registered. The records were obtained as epochs of 5 s during every training session. EEE was calculated from such recordings, using the validated equations described by Crouter et al
28: EEE (kcal/kg/min)=((5.95*HRaS) + (0.23*age) + (84*1)–134)/4186.8 where HRaS=Heart rate (HR) above sleeping HR (beats/min) and age in years. Sleeping HR was estimated from a resting supine measurement of HR during the RMR measurement, as previously reported28 and defined as: sleep HR=0.83 * supine HR.
EA was calculated by subtracting EEE from the daily energy intake, calculated relative to fat free mass (FFM).29 In order not to underestimate EA, EEE only represented the energy attributable to training. RMR was therefore subtracted from EEE before being used in the equation for EA. LEA was defined as EA <30 kcal/kg FFM/day, since this cut-off has previously been used for male athletes.14
Blood sampling
Fasting blood samples were taken according to standardised laboratorial procedures drawn by a qualified biotechnician. Blood samples from cohort I were analysed at Hormonlabor C831, Bern, Switzerland, and blood samples from cohorts II and III were analysed at Sørlandets Hospital in Kristiansand and Aker Hormonlab in Oslo, Norway. Reference values were defined based on the Norwegian laboratories standards: cortisol (138–690 mmol/L); testosterone (18–40 years: 7.2–24 nmol/L; >41 years: 4.6–24 nmol/L); T3 (1.2–2.7 nmol/L); IGF-1 (19–30 years: 17–63 nmol/L; 31–54 years: 11–40 nmol/L); insulin (<160 pmol/L); and glucose (4–6 mmol/L).