Publications by authors named "Aimee Morabito"

Purpose: We investigated short-term (9 d) exposure to low energy availability (LEA) in elite endurance athletes during a block of intensified training on self-reported well-being, body composition, and performance.

Methods: Twenty-three highly trained race walkers undertook an ~3-wk research-embedded training camp during which they undertook baseline testing and 6 d of high energy/carbohydrate (HCHO) availability (40 kcal·kg FFM -1 ·d -1 ) before being allocated to 9 d continuation of this diet ( n = 10 M, 2 F) or a significant decrease in energy availability to 15 kcal·kg FFM -1 ·d -1 (LEA: n = 10 M, 1 F). A real-world 10,000-m race walking event was undertaken before (baseline) and after (adaptation) these phases, with races being preceded by standardized carbohydrate fueling (8 g·kg body mass [BM] -1 for 24 h and 2 g·kg BM -1 prerace meal).

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Introduction: Although an acute exercise session typically increases bone turnover markers (BTM), the impact of subsequent sessions and the interaction with preexercise calcium intake remain unclear despite the application to the "real-life" training of many competitive athletes.

Methods: Using a randomized crossover design, elite male rowers ( n = 16) completed two trials, a week apart, consisting of two 90-min rowing ergometer sessions (EX1, EX2) separated by 150 min. Before each trial, participants consumed a high (CAL; ~1000 mg) or isocaloric low (CON; <10 mg) calcium meal.

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Previous research investigating single bouts of exercise have identified baseline iron status and circulating concentrations of interleukin-6 (IL-6) as contributors to the magnitude of postexercise hepcidin increase. The current study examined the effects of repeated training bouts in close succession on IL-6 and hepcidin responses. In a randomized, crossover design, 16 elite male rowers completed two trials, a week apart, with either high (1,000 mg) or low (<50 mg) calcium pre-exercise meals.

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Chronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a catabolic environment. Healthy young adults (N = 13; seven male, six female) were subjected to one night of total sleep deprivation (DEP) and normal sleep (CON) in a randomized cross-over design.

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