Energy availability (EA) is the difference between energy intake and exercise energy expenditure relative to an individual’s fat-free mass (FFM).

LEA is a state in which energy intake is insufficient to cover the costs of both exercise and basic physiological functions, resulting in acute endocrine and metabolic disturbances, and — when sustained over the long term — adverse health and functional outcomes.^[1]

The effects of short-term low energy availability

LH=luteinizing hormone, FSH= follicle-stimulating hormone, GH = growth hormone, T₃ = triiodothyronine, E₂ = estrogen, β-HOB=beta-hydroxybutyrate. Adapted from Areta et al., 2021, Eur J Appl Physiol.

Note that EA is related to energy balance but is fundamentally different.^[1] Energy balance accounts for all components of energy expenditure (resting metabolic rate, energy expenditure during exercise and nonexercise activities, and dietary-induced thermogenesis) and is typically focused on changes in body weight and composition, whereas EA considers only exercise energy expenditure and is concerned with whether the amount of energy left over is sufficient to support exercise recovery and adaptations, as well as general health.

Consequently, LEA isn’t always associated with weight loss (although they are strongly correlated), and an individual can be weight stable and not have excessively low body fat but still experience adverse physiological effects induced by LEA.^[2] Alternatively, it’s possible to be in negative energy balance but have sufficient EA to avoid symptoms of LEA.

Energy balance vs. energy availability

Adapted from Areta et al., 2021, Eur J Appl Physiol.

In women, the threshold for LEA is well defined, with the available evidence indicating that exposure to an EA of 30 kcal/kgFFM/d or less for 3–6 days typically induces symptoms of LEA, although there is notable variation among individuals.^[3] However, a general rule of thumb for LEA has yet to be established in men, only that the threshold appears to be lower than that of women.^[4]^[5]

The results of the summarized study lend support to this idea because there were no significant differences between LEA1 (a value which has been associated with physiological disturbances in women^[6]^[7]) and AEA.

On the other hand, it was found that an EA of 15 kcal/kgFFM/d was sufficient to produce symptoms of LEA. Specifically, LEA2 decreased total testosterone, a finding that disagrees with the results of previous studies.

One study in recreationally trained men reported that 4 days of LEA at 15 kcal/kgFFM/d did not affect testosterone.^[8] Another study in well-trained male endurance athletes that involved 10 days of LEA at an average of 8.8 kcal/kgFFM/d did not find a statistically significant decrease in testosterone,^[9] but it bears mentioning that LEA was achieved solely by increasing exercise energy expenditure (i.e., energy intake was not decreased), which is an atypical protocol and thus the results may have limited generalizability. A third study found that 3 days of LEA at approximately 18.9 kcal/kgFFM/d reduced testosterone, but the change was not statistically significant compared to AEA.^[10]

In addition to these findings, neither the summarized study nor any of the abovementioned studies found a significant effect of LEA on the anabolic hormone IGF-1.

The lack of effect of LEA on markers of bone turnover reported in the summarized study is in agreement with the results of a separate study in recreationally trained men that involved 5 days of LEA at 15 kcal/kgFFM/d.^[5] In contrast, this same EA for 5–6 days was found to negatively affect markers of bone turnover in elite race walkers and recreationally trained men.^[11]^[12]

The mixed results are likely influenced by the small sample sizes in these studies. A small sample size is a limitation because there is notable variation between individuals in the response to a given suboptimal EA,^[3] and a small number of participants means that the data from each participant becomes that much more influential to the results. Consequently, the mixed results may be a product of the particular sample of participants studied, and the results might have been more consistent if larger samples were studied.

All in all, although the summarized study is a notable contribution to the research pertaining to LEA in men, further research is needed to determine a specific threshold value for LEA. The evidence suggests that an EA of approximately 15 kcal/kgFFM/d can lead to one or more symptoms of LEA in men, but this finding is inconsistent and based on a small number of studies with small sample sizes.

It’s important to keep in mind the short duration of randomized controlled trials that evaluated LEA. In these cases, only early endocrine perturbations were evaluated, which are not necessarily indicative of the long-term effects of a given EA. The lack of an effect of 3–5 days of LEA on certain physiological markers doesn’t mean that those same markers wouldn’t meaningfully change over a longer duration of exposure. Given the limitations of the available randomized controlled trials, it should be kept in mind that there is a robust amount of evidence from observational studies in male athletes demonstrating an association between suboptimal EA and an increased risk of low bone mineral density and low testosterone.^[13]

Finding the threshold for low energy availability in men Original paper