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Aim: To highlight energy availability status, resting metabolic rate measures, dietary protein intake, and testosterone concentration in 4 elite male track cycling athletes (mean [SD]: age: 20.8 [1.5] y, body mass: 76.3 [3.6] kg, height: 181.8 [2.9] cm). Method: A cross-sectional observation included measures of energy availability (energy intake minus exercise energy expenditure, divided by fat-free mass), resting metabolic rate from indirect calorimetry, dietary protein intake from food records, blood analysis to assess sex hormone status, and performance markers. Results: Midrange testosterone (16.9–19.8 nmol/L), lowered resting metabolic rate ratio (0.76–0.98), varied luteinizing hormone (4–10 U/L), and suboptimal energy availability (26–41 kcal/kg fat-free mass/d, range) were observed in the male track cyclists. Protein intakes ranged from 2.0 g to 2.8 g protein/kg/d. Conclusion: The current cohort may have within-day energy deficiency, putting them in a catabolic state.

This article explores the socio-cultural dimensions of elite sportswomen’s experiences of low energy availability (LEA), focusing particularly on elite track cyclists. With a multidisciplinary research team (two sport scientists and a feminist sociologist), the project began with a suite of quantitative measures that identified five of eight women track cycling athletes categorized with LEA and three athletes categorized with sub-optimal energy availability. This was then followed by semi-structured interviews that revealed the athletes’ complex relationships with body image, menstruation, and nutrition practices, and varied experiences of LEA. Bringing the qualitative data into dialogue with the previously collated physiological data, however, helped us acknowledge the silences and deflection strategies among those with more severe cases of LEA. Ultimately, this article offers original insights both into elite track cyclists’ understandings of body image, menstruation, and nutrition as associated with LEA, and important reflections on the challenges of doing interviews with sportswomen on sensitive topics in high-performance sporting environments.

Most of the low energy availability (LEA) research has been conducted in female populations. The occurrence of LEA in male athletes is not well known, even with an understanding of the components involved in and contributing to LEA. Cycling is a major risk factor for LEA due to inherent sports characteristics: low impact, high energy demands, and a common perception that leanness is a performance advantage. The purpose of this review is to discuss the cycling-specific studies that have documented components of RED-S. The review demonstrates male cyclists (1) experience energy deficits daily, weekly and throughout a season; (2) exhibit lower bone mineral density at the spine compared to the hip, and low bone mineral density correlating with LEA and; (3) demonstrate downregulation of the endocrine system with elevated cortisol, reduced testosterone and insulin-like growth factor 1. The complexity of LEA is further explored by the socio-psychological contribution that may impact eating behaviours, and therefore increase the risk of developing LEA. Future research directions include applying multifaceted research methods to gain a greater understanding of this syndrome and the effect of LEA on male cyclists.

New findings What is the topic of this review? We review the issues with using predicted resting metabolic rate equations in athletic populations. What advances does it highlight? The use of dated predicted resting metabolic rate equations is not appropriate for athletic populations until more studies have been conducted among these unique populations. Abstract Resting metabolic rate (RMR) is the amount of energy the body uses at rest. A suppressed RMR has been correlated with low energy availability and therefore used as an indicator of an individual's energy state. Furthermore, confounding identification of low energy availability within an athletic population are the physiological measures required, which can be time consuming and require professional expertise. To negate the demands of laboratory protocols in measuring RMR, predicted RMR (p RMR) equations were developed. Caution should be exercised when applying the p RMR equations for determining low energy availability in athletes owing to the population used to develop the equations and the higher metabolic cost of fat-free mass, thus elevated RMR, associated with athletes. Moreover, a low ratio of measured RMR to p RMR is often used as an alternative marker for energy deficiency. Predictive equations should implement fat-free mass within the algorithm when estimating RMR in athletic populations. The purpose of this paper is to describe p RMR equation development and the issues associated with use of p RMR equations for athletic populations. As professional sport increases, validation of p RMR equations in the modern athlete population is needed to monitor energy availability for athletic health and performance.

Effects of resistance training and detraining on glucose and insulin responses to an oral glucose load, muscle fiber type, and muscular performance in the offspring of those with type 2 diabetes (familial insulin resistant (FIR)) were investigated.Six FIR participants and 10 controls (C) completed 9 wk of resistance training and 9 wk of detraining. Measures of strength and power, an oral glucose tolerance test, and a muscle biopsy to determine myosin heavy chain (MHC) fiber composition were taken at baseline (T1), after training (T2), and after detraining (T3).Three-repetition maximum increased (P ≤ 0.001) similarly in both groups in all strength measures, e.g., leg press (FIR T1, T2: 121 ± 34 kg, 186 ± 50 kg; C T1, T2: 137 ± 42 kg, 206 ± 64 kg, respectively (means ± SD)). Wingate peak power increased (FIR T1, T2: 505 ± 137 W, 523 ± 143 W; C T1, T2: 636 ± 211 W, 672 ± 223 W, respectively; P ≤ 0.005 (means ± SD)). Training reduced insulin area under the curve more (P = 0.050) in FIR (T1, T2: 1219 ± 734 pmol·L, 837 ± 284 pmol·L, respectively (means ± SD)) than that in C (T1, T2: 647 ± 268 pmol·L, 635 ± 258 pmol·L, respectively (means ± SD)). MHC distribution did not change with training. Strength (three-repetition maximum measures) decreased with detraining (P ≤ 0.001) although Wingate power did not. Detraining increased insulin area under the curve (P = 0.018) in FIR (T2, T3: 837 ± 285 pmol·L, 1040 ± 194 pmol·L, respectively (means ± SD)) but not in C (T2, T3: 635 ± 258 pmol·L, 625 ± 213 pmol·L, respectively (means ± SD)). MHC IIX fibers increased with detraining (P = 0.026).FIR appears to have exaggerated responses to resistance training and detraining, with a greater reduction in insulin release with glucose ingestion after training and increase when training ceases. Resistance training has a significant effect on insulin responses and may reduce future risk of type 2 diabetes mellitus among FIR.