Sequential Submaximal Training in Elite Male Rowers Does Not Result in Amplified Increases in Interleukin-6 or Hepcidin.

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. Each trial involved two, submaximal 90-min rowing ergometer sessions, 2.5 hr apart, with venous blood sampled at baseline; pre-exercise; and 0, 1, 2, and 3 hr after each session. Peak elevations in IL-6 (approximately 7.5-fold, p < .0001) and hepcidin (approximately threefold, p < .0001) concentrations relative to baseline were seen at 2 and 3 hr after the first session, respectively. Following the second session, concentrations of both IL-6 and hepcidin remained elevated above baseline, exhibiting a plateau rather than an additive increase (2 hr post first session vs. 2 hr post second session, p = 1.00). Pre-exercise calcium resulted in a slightly greater elevation in hepcidin across all time points compared with control (p = .0005); however, no effect on IL-6 was evident (p = .27). Performing multiple submaximal training sessions in close succession with adequate nutritional support does not result in an amplified increase in IL-6 or hepcidin concentrations following the second session in male elite rowers. Although effects of calcium intake require further investigation, athletes should continue to prioritize iron consumption around morning exercise prior to exercise-induced hepcidin elevations to maximize absorption.

Short Severe Energy Restriction with Refueling Reduces Body Mass without Altering Training-Associated Performance Improvement.

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). RESULTS: Dual-energy x-ray absorptiometry-assessed body composition showed BM loss (2.0 kg, P < 0.001), primarily due to a 1.6-kg fat mass reduction ( P < 0.001) in LEA, with smaller losses (BM = 0.9 kg, P = 0.008; fat mass = 0.9 kg, P < 0.001) in HCHO. The 76-item Recovery-Stress Questionnaire for Athletes, undertaken at the end of each dietary phase, showed significant diet-trial effects for overall stress ( P = 0.021), overall recovery ( P = 0.024), sport-specific stress ( P = 0.003), and sport-specific recovery ( P = 0.012). However, improvements in race performance were similar: 4.5% ± 4.1% and 3.5% ± 1.8% for HCHO and LEA, respectively ( P < 0.001). The relationship between changes in performance and prerace BM was not significant ( r = -0.08 [-0.49 to 0.35], P = 0.717). CONCLUSIONS: A series of strategically timed but brief phases of substantially restricted energy availability might achieve ideal race weight as part of a long-term periodization of physique by high-performance athletes, but the relationship between BM, training quality, and performance in weight-dependent endurance sports is complicated.

The Impact of Acute Calcium Intake on Bone Turnover Markers during a Training Day in Elite Male Rowers.

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. Biochemical markers including parathyroid hormone (PTH), serum ionized calcium (iCa) and BTMs (C-terminal telopeptide of type I collagen, osteocalcin) were monitored from baseline to 3 h after EX2. RESULTS: Although each session caused perturbances of serum iCa, CAL maintained calcium concentrations above those of CON for most time points, 4.5% and 2.4% higher after EX1 and EX2, respectively. The decrease in iCa in CON was associated with an elevation of blood PTH ( P < 0.05) and C-terminal telopeptide of type I collagen ( P < 0.0001) over this period of repeated training sessions and their recovery, particularly during and after EX2. Preexercise intake of calcium-rich foods lowered BTM over the course of a day with several training sessions. CONCLUSIONS: Preexercise intake of a calcium-rich meal before training sessions undertaken within the same day had a cumulative and prolonged effect on the stabilization of blood iCa during exercise. In turn, this reduced the postexercise PTH response, potentially attenuating the increase in markers of bone resorption. Such practical strategies may be integrated into the athlete's overall sports nutrition plan, with the potential to safeguard long-term bone health and reduce the risk of bone stress injuries.

The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment.

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. Anabolic and catabolic hormonal profiles were assessed across the following day. Postprandial muscle protein fractional synthesis rate (FSR) was assessed between 13:00 and 15:00 and gene markers of muscle protein degradation were assessed at 13:00. Acute sleep deprivation reduced muscle protein synthesis by 18% (CON: 0.072 ± 0.015% vs. DEP: 0.059 ± 0.014%·h-1 , p = .040). In addition, sleep deprivation increased plasma cortisol by 21% (p = .030) and decreased plasma testosterone by 24% (p = .029). No difference was found in the markers of protein degradation. A single night of total sleep deprivation is sufficient to induce anabolic resistance and a procatabolic environment. These acute changes may represent mechanistic precursors driving the metabolic dysfunction and body composition changes associated with chronic sleep deprivation.