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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.

Key points Brief (5–6 days) adaptation to a low carbohydrate high fat diet in elite athletes increased exercise fat oxidation to rates previously observed with medium (3–4 weeks) or chronic (>12 months) adherence to this diet, with metabolic changes being washed out in a similar time frame.Increased fat utilisation during exercise was associated with a 5–8% increase in oxygen cost at speeds related to Olympic Programme races.Acute restoration of endogenous carbohydrate (CHO) availability (24 h high CHO diet, pre‐race CHO) only partially restored substrate utilisation during a race warm‐up. Fat oxidation continued to be elevated above baseline values although it was lower than achieved by 5–6 days’ keto adaptation; CHO oxidation only reached 61% and 78% of values previously seen at exercise intensities related to race events.Acute restoration of CHO availability failed to overturn the impairment of high‐intensity endurance performance previously associated with low carbohydrate high fat adaptation, potentially due to the blunted capacity for CHO oxidation. Abstract We investigated substrate utilisation during exercise after brief (5–6 days) adaptation to a ketogenic low‐carbohydrate (CHO), high‐fat (LCHF) diet and similar washout period. Thirteen world‐class male race walkers completed economy testing, 25 km training and a 10,000 m race (Baseline), with high CHO availability (HCHO), repeating this (Adaptation) after 5–6 days’ LCHF (n = 7; CHO: 200%) increases in exercise fat oxidation occurred in the LCHF Adaptation economy and 25 km tests, reaching mean rates of ∼1.43 g min−1. However, relative V˙O2 (ml min−1 kg−1) was higher (P, Key points Brief (5–6 days) adaptation to a low carbohydrate high fat diet in elite athletes increased exercise fat oxidation to rates previously observed with medium (3–4 weeks) or chronic (>12 months) adherence to this diet, with metabolic changes being washed out in a similar time frame.Increased fat utilisation during exercise was associated with a 5–8% increase in oxygen cost at speeds related to Olympic Programme races.Acute restoration of endogenous carbohydrate (CHO) availability (24 h high CHO diet, pre‐race CHO) only partially restored substrate utilisation during a race warm‐up. Fat oxidation continued to be elevated above baseline values although it was lower than achieved by 5–6 days’ keto adaptation; CHO oxidation only reached 61% and 78% of values previously seen at exercise intensities related to race events.Acute restoration of CHO availability failed to overturn the impairment of high‐intensity endurance performance previously associated with low carbohydrate high fat adaptation, potentially due to the blunted capacity for CHO oxidation.

Objectives To examine iron stores, hemoglobin mass, and performance before, during and after intermittent altitude exposure in a professional male rugby player experiencing iron overload following blood transfusions for treatment for acute myeloid leukemia. Design Longitudinal, repeated measures, single case-study. Methods The player was followed prior to (control), and during (study), an in-season block of altitude training. During the control period two venesections were performed for a total of 750 mL of blood removal. Internal and external training load, match statistics, blood volume, plasma volume, haemoglobin mass, serum ferritin and reticulocyte count were monitored throughout. Results During the control period serum ferritin declined following the two venesections (∼51%) as did haemoglobin mass (∼2%), reticulocyte count remained stable. During the study period serum ferritin further declined (∼30%), however haemoglobin mass and reticulocyte count increased (∼4% and ∼14% respectively). Internal training load for the control and study period was similar, however external training load was lower in the study period. Match statistics were not favourable for the player during the control period, however they improved during the study period. Conclusions This case supports the theory that individuals with elevated iron availability are well placed to achieve increases in haemoglobin mass. Furthermore, although therapeutic venesections may still be required to manage iron overload, the addition of altitude exposure may be a method to assist in reducing total body iron by means of mobilising available (excessive) iron to incorporate into haemoglobin. Altitude exposure did not hinder the players’ performance. Further research is encouraged.

Introduction: We sought to determine the effect of low and moderate normobaric hypoxia on oxygen consumption and anaerobic contribution during interval running at different exercise intensities. Methods: Eight runners (age, 25 +/- 7 yr, V[spacing dot above]O2max: 72.1 +/- 5.6 mL[middle dot]kg-1[middle dot]min-1) completed three separate interval sessions at threshold (4 x 5 min, 2-min recovery), V[spacing dot above]O2max (8 x 90 s, 90-s recovery), and race pace (10 x 45 s, 1 min 45 s recovery) in each of; normoxia (elevation: 580 m, FiO2: 0.21), low (1400 m, 0.195) or moderate (2100 m, 0.18) normobaric hypoxia. The absolute running speed for each intensity was kept the same at each altitude to evaluate the effect of FiO2 on physiological responses. Expired gas was collected throughout each session, with total V[spacing dot above]O2 and accumulated oxygen deficit calculated. Data were compared using repeated-measures ANOVA. Results: There were significant differences between training sessions for peak and total V[spacing dot above]O2, and anaerobic contribution (P < 0.001, P = 0.01 respectively), with race pace sessions eliciting the lowest and highest responses respectively. Compared to 580 m, total V[spacing dot above]O2 at 2100 m was significantly lower (P < 0.05), and anaerobic contribution significantly higher (P < 0.05) during both threshold and V[spacing dot above]O2max sessions. No significant differences were observed between altitudes for race pace sessions. Conclusions: To maintain oxygen flux, completing acute exercise at threshold and V[spacing dot above]O2max intensity at 1400 m simulated altitude appears more beneficial compared with 2100 m. However, remaining at moderate altitude is a suitable when increasing the anaerobic contribution to exercise is a targeted response to training.

© Copyright 2017 by the American College of Sports Medicine. Purpose Independent heat and hypoxic exposure can enhance temperate endurance performance in trained athletes, although their combined effects remain unknown. This study examined whether the addition of heat interval training during "live high, train low" (LHTL) hypoxic exposure would result in enhanced performance and physiological adaptations as compared with heat or temperate training. Methods Twenty-six well-trained runners completed 3 wk of interval training assigned to one of three conditions: 1) LHTL hypoxic exposure plus heat training (H + H; 3000 m for 13 h·d -1, train at 33°C, 60% relative humidity [RH]), 2) heat training with no hypoxic exposure (HOT, live at

We investigated the effects of adaptation to a ketogenic low carbohydrate (CHO), high fat diet (LCHF) during 3 weeks of intensified training on metabolism and performance of world-class endurance athletes. We controlled three isoenergetic diets in elite race walkers: high CHO availability (g kg−1 day−1: 8.6 CHO, 2.1 protein, 1.2 fat) consumed before, during and after training (HCHO, n = 9); identical macronutrient intake, periodised within or between days to alternate between low and high CHO availability (PCHO, n = 10); LCHF (< 50 g day−1 CHO; 78% energy as fat; 2.1 g kg−1 day−1 protein; LCHF, n = 10). Post-intervention, ˙V O2peak during race walking increased in all groups (P < 0.001, 90% CI: 2.55, 5.20%). LCHF was associated with markedly increased rates of whole-body fat oxidation, attaining peak rates of 1.57±0.32 gmin−1 during 2 h of walking at 80% ˙V O2peak.However, LCHFalso increased the oxygen (O2) cost of race walking at velocities relevant to real-life race performance: O2 uptake (expressed as a percentage of new ˙V O2peak) at a speed approximating 20 km race pace was reduced in HCHO and PCHO (90% CI:−7.047,−2.55 and−5.18,−0.86, respectively), but was maintained at pre-intervention levels in LCHF. HCHO and PCHO groups improved times for 10 km race walk: 6.6% (90% CI: 4.1, 9.1%) and 5.3% (3.4, 7.2%), with no improvement (−1.6% (−8.5, 5.3%)) for the LCHF group. In contrast to training with diets providing chronic or periodised high-CHO availability, and despite a significant improvement in ˙V O2peak, adaptation to the topical LCHF diet negated performance benefits in elite endurance athletes, in part due to reduced exercise economy.

Objectives: To investigate diet-exercise interactions related to bone markers in elite endurance athletes after a 3.5-week ketogenic low-carbohydrate, high-fat (LCHF) diet and subsequent restoration of carbohydrate (CHO) feeding.Methods: World-class race walkers (25 male, 5 female) completed 3.5-weeks of energy-matched (220 kJ·kg·d−1) high CHO (HCHO; 8.6 g·kg·d−1 CHO, 2.1 g·kg·d−1 protein, 1.2 g·kg·d−1 fat) or LCHF (0.5 g·kg·d−1 CHO, 2.1 g·kg·d−1 protein, 75–80% of energy from fat) diet followed by acute CHO restoration. Serum markers of bone breakdown (cross-linked C-terminal telopeptide of type I collagen, CTX), formation (procollagen 1 N-terminal propeptide, P1NP) and metabolism (osteocalcin, OC) were assessed at rest (fasting and 2 h post meal) and after exercise (0 and 3 h) at Baseline, after the 3.5-week intervention (Adaptation) and after acute CHO feeding (Restoration).Results: After Adaptation, LCHF increased fasting CTX concentrations above Baseline (p = 0.007, Cohen's d = 0.69), while P1NP (p < 0.001, d = 0.99) and OC (p < 0.001, d = 1.39) levels decreased. Post-exercise, LCHF increased CTX concentrations above Baseline (p = 0.001, d = 1.67) and above HCHO (p < 0.001, d = 0.62), while P1NP (p < 0.001, d = 0.85) and OC concentrations decreased (p < 0.001, d = 0.99) during exercise. Exercise-related area under curve (AUC) for CTX was increased by LCHF after Adaptation (p = 0.001, d = 1.52), with decreases in P1NP (p < 0.001, d = 1.27) and OC (p < 0.001, d = 2.0). CHO restoration recovered post-exercise CTX and CTX exercise-related AUC, while concentrations and exercise-related AUC for P1NP and OC remained suppressed for LCHF (p = 1.000 compared to Adaptation).Conclusion: Markers of bone modeling/remodeling were impaired after short-term LCHF diet, and only a marker of resorption recovered after acute CHO restoration. Long-term studies of the effects of LCHF on bone health are warranted.

Since the 1960s there has been an escalation in the purposeful utilization of altitude to enhance endurance athletic performance. This has been mirrored by a parallel intensification in research pursuits to elucidate hypoxia-induced adaptive mechanisms and substantiate optimal altitude protocols (e.g., hypoxic dose, duration, timing, and confounding factors such as training load periodization, health status, individual response, and nutritional considerations). The majority of the research and the field-based rationale for altitude has focused on hematological outcomes, where hypoxia causes an increased erythropoietic response resulting in augmented hemoglobin mass. Hypoxia-induced non-hematological adaptations, such as mitochondrial gene expression and enhanced muscle buffering capacity may also impact athletic performance, but research in elite endurance athletes is limited. However, despite significant scientific progress in our understanding of hypobaric hypoxia (natural altitude) and normobaric hypoxia (simulated altitude), elite endurance athletes and coaches still tend to be trailblazers at the coal face of cutting-edge altitude application to optimize individual performance, and they already implement novel altitude training interventions and progressive periodization and monitoring approaches. Published and field-based data strongly suggest that altitude training in elite endurance athletes should follow a long- and short-term periodized approach, integrating exercise training and recovery manipulation, performance peaking, adaptation monitoring, nutritional approaches, and the use of normobaric hypoxia in conjunction with terrestrial altitude. Future research should focus on the long-term effects of accumulated altitude training through repeated exposures, the interactions between altitude and other components of a periodized approach to elite athletic preparation, and the time course of non-hematological hypoxic adaptation and de-adaptation, and the potential differences in exercise-induced altitude adaptations between different modes of exercise.

Introduction We repeated our study of intensified training on a ketogenic low-carbohydrate (CHO), high-fat diet (LCHF) in world-class endurance athletes, with further investigation of a “carryover” effect on performance after restoring CHO availability in comparison to high or periodised CHO diets. Methods After Baseline testing (10,000 m IAAF-sanctioned race, aerobic capacity and submaximal walking economy) elite male and female race walkers undertook 25 d supervised training and repeat testing (Adapt) on energy-matched diets: High CHO availability (8.6 g∙kg-1∙d-1 CHO, 2.1 g∙kg-1∙d-1 protein; 1.2 g∙kg-1∙d-1 fat) including CHO before/during/after workouts (HCHO, n = 8): similar macronutrient intake periodised within/between days to manipulate low and high CHO availability at various workouts (PCHO, n = 8); and LCHF (

Purpose: The extent to which hepcidin regulation after acute bouts of exercise is influenced by baseline (resting) concentrations of key iron parameters remains uncertain. This investigation explored the influence of selected iron parameters and 25-km race walk time on 3-h post-exercise hepcidin-25 levels in international-level race walkers. Methods: Twenty-four male race walkers completed a graded exercise test and a 25-km race-walk trial. Throughout the 25-km race-walk, venous blood samples were collected pre-exercise, immediately post-exercise, and at 3-h post-exercise. Blood was analysed for serum ferritin, serum iron, Interleukin-6 (IL-6), and hepcidin-25 concentration. Results: IL-6 and hepcidin-25 increased (7.6- and 7.5-fold, respectively) in response to the 25-km race-walk trial (both p < 0.01). Significant individual relationships were evident between 3-h post-exercise hepcidin-25, baseline serum ferritin and serum iron (r > 0.62; p < 0.05). Multiple regression analysis showed that these two iron parameters, in addition to post-exercise IL-6 concentration and 25-km race-walk time, accounted for ~77% of the variance in 3-h post-exercise hepcidin-25 (p < 0.01). A median split by the cohort’s baseline serum ferritin concentration (LOW: 58.0 vs. HIGH: 101.8 µg/L; p < 0.01) showed a significant between group difference in the 3-h post-exercise hepcidin-25 (LOW: 6.0 ± 3.6 vs. 11.3 ± 5.4 nM; p = 0.01), despite no differences in baseline serum iron, post-exercise IL-6, or 25-km race-walk time (all p > 0.05). Conclusion: Despite exercise activating numerous hepcidin regulators, baseline iron status appears to play a dominant role in the regulation of hepcidin-25 in elite-level athletes subsequent to endurance exercise.

Purpose The short-term restriction of carbohydrate (CHO) can potentially influence iron regulation via modification of postexercise interleukin-6 (IL-6) and hepcidin levels. This study examined the effect of a chronic ketogenic low-CHO high-fat (LCHF) diet on iron status and iron-regulatory markers in elite athletes. Methods International-level race walkers (n = 50) were allocated to one of three dietary interventions: (i) a high-CHO diet (n = 16), (ii) a periodized CHO availability (n = 17), or (iii) an LCHF diet (n = 17) while completing a periodized training program for 3 wk. A 19- to 25-km race walking test protocol was completed at baseline and after adaptation, and changes in serum ferritin, IL-6, and hepcidin concentrations were measured. Results from high-CHO and periodized CHO were combined into one group (CHO; n = 33) for analysis. Results The decrease in serum ferritin across the intervention period was substantially greater in the CHO group (37%) compared with the LCHF (23%) group (P = 0.021). After dietary intervention, the postexercise increase in IL-6 was greater in LCHF (13.6-fold increase; 95% confidence interval [CI] = 7.1–21.4) than athletes adhering to a CHO-rich diet (7.6-fold increase; 95% CI = 5.5–10.2; P = 0.033). Although no significant differences occurred between diets, CI values indicate that 3 h postexercise hepcidin concentrations were lower after dietary intervention compared with baseline in CHO (β = −4.3; 95% CI = −6.6 to −2.0), with no differences evident in LCHF. Conclusion Athletes who adhered to a CHO-rich diet experienced favorable changes to the postexercise IL-6 and hepcidin response, relative to the LCHF group. Lower serum ferritin after 3 wk of additional dietary CHO might reflect a larger more adaptive hematological response to training.

Purpose: To determine whether combining training in heat with “Live High, Train Low” hypoxia (LHTL) further improves thermoregulatory and cardiovascular responses to a heat-tolerance test compared with independent heat training. Methods: A total of 25 trained runners (peak oxygen uptake = 64.1 [8.0] mL·min−1·kg−1) completed 3-wk training in 1 of 3 conditions: (1) heat training combined with “LHTL” hypoxia (H+H; FiO2 = 14.4% [3000 m], 13 h·d−1; train at Results: Submaximal heart rate (effect size [ES] = −0.60 [−0.89; −0.32]) and core temperature (ES = −0.55 [−0.99; −0.10]) were reduced in HOT until 1 wkP. Sweat rate (ES = 0.36 [0.12; 0.59]) and sweat sodium concentration (ES = −0.82 [−1.48; −0.16]) were, respectively, increased and decreased until 3 wkP in HOT. Submaximal heart rate (ES = −0.38 [−0.85; 0.08]) was likely reduced in H+H at 3 wkP, whereas CONT had unclear physiological changes. Perceived exertion and thermal sensation were reduced across all groups. Conclusions: Despite greater physiological stress from combined heat training and “LHTL” hypoxia, thermoregulatory adaptations are limited in comparison with independent heat training. The combined stimuli provide no additional physiological benefit during exercise in hot environments.

Objectives Adhering to a low carbohydrate (CHO) high fat (LCHF) diet can alter markers of iron metabolism in endurance athletes. This investigation examined the re-introduction of CHO prior to, and during exercise on the iron-regulatory response to exercise in a homogenous (in regard to serum ferritin concentration) group of athletes adapted to a LCHF diet. Design Parallel groups design. Methods Three weeks prior to the exercise trials, twenty-three elite race walkers adhered to either a CHO-rich (n = 14) or LCHF diet (n = 9). A standardised 19–25 km race walk was performed while athletes were still adhering to their allocated dietary intervention (Adapt). A second test was performed three days later, where all athletes were placed on a high CHO diet (CHO Restoration). Venous blood samples were collected pre-, post- and 3 h post-exercise and measured for interleukin-6 (IL-6) and hepcidin-25. Results The post-exercise IL-6 increase was greater in LCHF (p < 0.001) during both the Adapt (LCHF: 13.1-fold increase; 95% CI: 5.6–23.0, CHO: 8.0-fold increase; 5.1–11.1) and CHO Restoration trials (LCHF: 18.5-fold increase; 10.9–28.9, CHO: 6.3-fold increase; 3.9–9.5); outcomes were not different between trials (p = 0.84). Hepcidin-25 concentrations increased 3 h post-exercise (p < 0.001), however, they did not differ between trials (p = 0.46) or diets (p = 0.84). Conclusions The elevated IL-6 response in athletes adapted to a LCHF diet was not attenuated by an acute increase in exogenous CHO availability. Despite diet-induced differences in IL-6 response to exercise, post-exercise hepcidin levels were similar between diets and trials, indicating CHO availability has minimal influence on post-exercise iron metabolism.

Carbohydrate (CHO) availability could alter mucosal immune responses to exercise. This study compared the effect of three dietary approaches to CHO availability on resting and post-exercise s-IgA levels. Elite race walkers (n = 26) adhered to a high CHO diet (HCHO), periodised CHO availability (PCHO) or a low CHO/high fat diet (LCHF) for 3 weeks while completing an intensified training program. HCHO and PCHO groups consumed 8.0–8.5 g.kg−1 CHO daily, with timing of ingestion manipulated to alter CHO availability around key training sessions. The LCHF diet comprised 80% fat and restricted CHO to < 50 g.day−1. A race walk test protocol (19 km females, 25 km males) was completed at baseline, after adaptation, and following CHO restoration. On each occasion, saliva samples were obtained pre- and post-exercise to quantify s-IgA levels. Resting s-IgA secretion rate substantially increased ~ two-fold post-intervention in all groups (HCHO: 2.2 ± 2.2, PCHO: 2.8 ± 3.2, LCHF: 1.6 ± 1.6; fold-change± 95% confidence limits), however, no substantial differences between dietary treatments were evident. Post-exercise, substantial 20–130% increases in s-IgA concentration and 43–64% reductions in flow rate occurred in all dietary treatments, with trivial differences evident between groups. It appears that high volume training overrides any effect of manipulating CHO availability on mucosal immunity in elite athletes.

Purpose: To determine the effect of altitude training at 1600 and 1800 m on sea-level (SL) performance in national-level runners. Methods: After 3 wk of SL training, 24 runners completed a 3-wk sojourn at 1600 m (ALT1600, n = 8), 1800 m (ALT1800, n = 9), or SL (CON, n = 7), followed by up to 11 wk of SL racing. Race performance was measured at SL during the lead-in period and repeatedly postintervention. Training volume (in kilometers) and load (session rating of perceived exertion) were calculated for all sessions. Hemoglobin mass was measured via CO rebreathing. Between-groups differences were evaluated using effect sizes (Hedges g). Results: Performance improved in both ALT1600 (mean [SD] 1.5% [0.9%]) and ALT1800 (1.6% [1.3%]) compared with CON (0.4% [1.7%]); g = 0.83 (90% confidence limits −0.10, 1.66) and 0.81 (−0.09, 1.62), respectively. Season-best performances occurred 5 to 71 d postaltitude in ALT1600/1800. There were large increases in training load from lead-in to intervention in ALT1600 (48% [32%]) and ALT1800 (60% [31%]) compared with CON (18% [20%]); g = 1.24 (0.24, 2.08) and 1.69 (0.65, 2.55), respectively. Hemoglobin mass increased in ALT1600 and ALT1800 (∼4%) but not CON. Conclusions: Larger improvements in performance after altitude training may be due to the greater overall load of training in hypoxia compared with normoxia, combined with a hypoxia-mediated increase in hemoglobin mass. A wide time frame for peak performances suggests that the optimal window to race postaltitude is individual, and factors other than altitude exposure per se may be important.

Although short (up to 3 days) exposure to major shifts in macronutrient intake appears to alter acid–base status, the effects of sustained ( > 1 week) interventions in elite athletes has not been determined. Using a non‐randomized, parallel design, we examined the effect of adaptations to 21 days of a ketogenic low carbohydrate high fat (LCHF) or periodized carbohydrate (PCHO) diet on pre‐ and post‐exercise blood pH, and concentrations of bicarbonate (HCO3 −) and lactate (La−) in comparison to a high carbohydrate (HCHO) control. Twenty‐four (17 male and 7 female) elite‐level race walkers completed 21 days of either LCHF (n = 9), PCHO (n = 7), or HCHO (n = 8) under controlled diet and training conditions. At baseline and post‐intervention, blood pH, blood [HCO3 −], and blood [La−] were measured before and after a graded exercise test. Net endogenous acid production (NEAP) over the previous 48–72 h was also calculated from monitored dietary intake. LCHF was not associated with significant differences in blood pH, [HCO3 −], or [La−], compared with the HCHO diet pre‐ or post‐exercise, despite a significantly higher NEAP (mEq∙day−1) (95% CI = [10.44; 36.04]). Our results indicate that chronic dietary interventions are unlikely to influence acid–base status in elite athletes, which may be due to pre‐existing training adaptations, such as an enhanced buffering capacity, or the actions of respiratory and renal pathways, which have a greater influence on regulation of acid–base status than nutritional intake.

High altitude exposure can increase resting metabolic rate (RMR) and induce weight loss in obese populations, but there is a lack of research regarding RMR in athletes at moderate elevations common to endurance training camps. The present study aimed to determine whether 4 weeks of classical altitude training affects RMR in middle-distance runners. Ten highly trained athletes were recruited for 4 weeks of endurance training undertaking identical programs at either 2200m in Flagstaff, Arizona (ALT, n = 5) or 600m in Canberra, Australia (CON, n = 5). RMR, anthropometry, energy intake, and hemoglobin mass (Hbmass) were assessed pre- and posttraining. Weekly run distance during the training block was: ALT 96.8 ± 18.3km; CON 103.1 ± 5.6km. A significant interaction for Time*Group was observed for absolute (kJ.day-1) (F-statistic, p-value: F(1,8)=13.890, p = .01) and relative RMR (F(1,8)=653.453, p = .003) POST-training. No significant changes in anthropometry were observed in either group. Energy intake was unchanged (mean ± SD of difference, ALT: 195 ± 3921kJ, p = .25; CON: 836 ± 7535kJ, p = .75). A significant main effect for time was demonstrated for total Hbmass (g) (F(1,8)=13.380, p = .01), but no significant interactions were observed for either variable [Total Hbmass (g): F(1,8)=1.706, p = .23; Relative Hbmass (g.kg-1): F(1,8)=0.609, p = .46]. These novel findings have important practical application to endurance athletes routinely training at moderate altitude, and those seeking to optimize energy management without compromising training adaptation. Altitude exposure may increase RMR and enhance training adaptation,. During training camps at moderate altitude, an increased energy intake is likely required to support an increased RMR and provide sufficient energy for training and performance.