Middle-distance runners utilize the full continuum of energy systems throughout training, and given the infinite competition tactical scenarios, this event group is highly complex from a performance intervention point of view. However, this complexity results in numerous potential periodized nutrition interventions to optimize middle-distance training adaptation and competition performance. Middle-distance race intensity is extreme, with 800- to 5,000-m races being at ∼95% to 130% of VO2max. Accordingly, elite middle-distance runners have primarily Type IIa/IIx fiber morphology and rely almost exclusively on carbohydrate (primarily muscle glycogen) metabolic pathways for producing adenosine triphosphate. Consequently, the principle nutritional interventions that should be emphasized are those that optimize muscle glycogen contents to support high glycolytic flux (resulting in very high lactate values, of >20 mmol/L in some athletes) with appropriate buffering capabilities, while optimizing power to weight ratios, all in a macro- and microperiodized manner. From youth to elite level, middle-distance athletes have arduous racing schedules (10–25 races/year), coupled with excessive global travel, which can take a physical and emotional toll. Accordingly, proactive and integrated nutrition planning can have a profound recovery effect over a long race season, as well as optimizing recovery during rounds of championship racing. Finally, with evidence-based implementation and an appropriate risk/reward assessment, several ergogenic aids may have an adaptive and/or performance-enhancing effect in the middle-distance athlete. Given that elite middle-distance athletes undertake ∼400 to 800 training sessions with 10–25 races/year, there are countless opportunities to implement various periodized acute and chronic nutrition-based interventions to optimize performance.
Trent Stellingwerff, Ingvill Måkestad Bovim, and Jamie Whitfield
Alexander S.D. Gamble, Jessica L. Bigg, Tyler F. Vermeulen, Stephanie M. Boville, Greg S. Eskedjian, Sebastian Jannas-Vela, Jamie Whitfield, Matthew S. Palmer, and Lawrence L. Spriet
Several previous studies have reported performance decrements in team sport athletes who dehydrated approximately 1.5–2% of their body mass (BM) through sweating. This study measured on-ice sweat loss, fluid intake, sodium balance, and carbohydrate (CHO) intake of 77 major junior (JR; 19 ± 1 years), 60 American Hockey League (AHL; 24 ± 4 years), and 77 National Hockey League (NHL; 27 ± 5 years) players. Sweat loss was calculated from pre- to post-exercise BM plus fluid intake minus urine loss. AHL (2.03 ± 0.62 L/hr) and NHL (2.02 ± 0.74 L/hr) players had higher sweat rates (p < .05) than JR players (1.63 ± 0.58 L/hr). AHL (1.23 ± 0.69%; p = .006) and NHL (1.29% ± 0.63%; p < .001) players had ∼30% greater BM losses than JR players (0.89% ± 0.57%). There was no difference in fluid intake between groups (p > .05). Sodium deficits (sodium loss − intake) were greater (p < .05) in AHL (1.68 ± 0.74 g/hr) and NHL (1.56 ± 0.84 g/hr) players compared with JR players (1.01 ± 0.50 g/hr). CHO intake was similar between groups (14–20 g CHO/hr), with 29%, 32%, and 40% of JR, AHL, and NHL players consuming no CHO, respectively. In summary, sweat rates were high in all players, but the majority of players (74/77, 54/60, and 68/77 of JR, AHL, and NHL, respectively) avoided mild dehydration (>2% BM) during 60 min of practice. However, ∼15%, 41%, and 48% of the JR, AHL, and NHL players, respectively, may have reached mild dehydration and increased risk of performance decrements in a 90-min practice.
Alannah K.A. McKay, Peter Peeling, David B. Pyne, Nicolin Tee, Marijke Welveart, Ida A. Heikura, Avish P. Sharma, Jamie Whitfield, Megan L. Ross, Rachel P.L. van Swelm, Coby M. Laarakkers, and Louise M. Burke
This study implemented a 2-week high carbohydrate (CHO) diet intended to maximize CHO oxidation rates and examined the iron-regulatory response to a 26-km race walking effort. Twenty international-level, male race walkers were assigned to either a novel high CHO diet (MAX = 10 g/kg body mass CHO daily) inclusive of gut-training strategies, or a moderate CHO control diet (CON = 6 g/kg body mass CHO daily) for a 2-week training period. The athletes completed a 26-km race walking test protocol before and after the dietary intervention. Venous blood samples were collected pre-, post-, and 3 hr postexercise and measured for serum ferritin, interleukin-6, and hepcidin-25 concentrations. Similar decreases in serum ferritin (17–23%) occurred postintervention in MAX and CON. At the baseline, CON had a greater postexercise increase in interleukin-6 levels after 26 km of walking (20.1-fold, 95% CI [9.2, 35.7]) compared with MAX (10.2-fold, 95% CI [3.7, 18.7]). A similar finding was evident for hepcidin levels 3 hr postexercise (CON = 10.8-fold, 95% CI [4.8, 21.2]; MAX = 8.8-fold, 95% CI [3.9, 16.4]). Postintervention, there were no substantial differences in the interleukin-6 response (CON = 13.6-fold, 95% CI [9.2, 20.5]; MAX = 11.2-fold, 95% CI [6.5, 21.3]) or hepcidin levels (CON = 7.1-fold, 95% CI [2.1, 15.4]; MAX = 6.3-fold, 95% CI [1.8, 14.6]) between the dietary groups. Higher resting serum ferritin (p = .004) and hotter trial ambient temperatures (p = .014) were associated with greater hepcidin levels 3 hr postexercise. Very high CHO diets employed by endurance athletes to increase CHO oxidation have little impact on iron regulation in elite athletes. It appears that variations in serum ferritin concentration and ambient temperature, rather than dietary CHO, are associated with increased hepcidin concentrations 3 hr postexercise.