Limits of Ultra: Towards an Interdisciplinary Understanding of Ultra-Endurance Running Performance.

Ultra-endurance running (UER) poses extreme mental and physical challenges that present many barriers to completion, let alone performance. Despite these challenges, participation in UER events continues to increase. With the relative paucity of research into UER training and racing compared with traditional endurance running distance (e.g., marathon), it follows that there are sizable improvements still to be made in UER if the limitations of the sport are sufficiently understood. The purpose of this review is to summarise our current understanding of the major limitations in UER. We begin with an evolutionary perspective that provides the critical background for understanding how our capacities, abilities and limitations have come to be. Although we show that humans display evolutionary adaptations that may bestow an advantage for covering large distances on a daily basis, these often far exceed the levels of our ancestors, which exposes relative limitations. From that framework, we explore the physiological and psychological systems required for running UER events. In each system, the factors that limit performance are highlighted and some guidance for practitioners and future research are shared. Examined systems include thermoregulation, oxygen delivery and utilisation, running economy and biomechanics, fatigue, the digestive system, nutritional and psychological strategies. We show that minimising the cost of running, damage to lower limb tissue and muscle fatigability may become crucial in UER events. Maintaining a sustainable core body temperature is critical to performance, and an even pacing strategy, strategic heat acclimation and individually calculated hydration all contribute to sustained performance. Gastrointestinal issues affect almost every UER participant and can be due to a variety of factors. We present nutritional strategies for different event lengths and types, such as personalised and evidence-based approaches for varying types of carbohydrate, protein and fat intake in fluid or solid form, and how to avoid flavour fatigue. Psychology plays a vital role in UER performance, and we highlight the need to be able to cope with complex situations, and that specific long and short-term goal setting improves performance. Fatigue in UER is multi-factorial, both physical and mental, and the perceived effort or level of fatigue have a major impact on the ability to continue at a given pace. Understanding the complex interplay of these limitations will help prepare UER competitors for the different scenarios they are likely to face. Therefore, this review takes an interdisciplinary approach to synthesising and illuminating limitations in UER performance to assist practitioners and scientists in making informed decisions in practice and applicable research.

Pulmonary O2 uptake on-kinetics in sprint- and endurance-trained athletes.

Pulmonary O2 uptake kinetics during "step" exercise have not been characterized in young, sprint-trained (SPT), athletes. Therefore, the objective of this study was to test the hypotheses that SPT athletes would have (i) slower phase II kinetics and (ii) a greater oxygen uptake "slow component" when compared with endurance-trained (ENT) athletes. Eight sub-elite SPT athletes (mean (+/-SD) age=25 (+/-7) y; mass=80.3 (+/-7.3) kg) and 8 sub-elite ENT athletes (age=28 (+/-4) y; mass=73.2 (+/-5.1) kg) completed a ramp incremental cycle ergometer test, a Wingate 30 s anaerobic sprint test, and repeat "step" transitions in work rate from 20 W to moderate- and severe-intensity cycle exercise, during which pulmonary oxygen uptake was measured breath by breath. The phase II oxygen uptake kinetics were significantly slower in the SPT athletes both for moderate (time constant, tau; SPT 32 (+/-4) s vs. ENT 17 (+/-3) s; p<0.01) and severe (SPT 32 (+/-12) s vs. ENT 20 (+/-6) s; p<0.05) exercise. The amplitude of the slow component (derived by exponential modelling) was not significantly different between the groups (SPT 0.55 (+/-0.12) L.min(-1) vs. ENT 0.50 (+/-0.22) L.min(-1)), but the increase in oxygen uptake between 3 and 6 min of severe exercise was greater in the SPT athletes (SPT 0.37 (+/-0.08) L.min(-1) vs. ENT 0.20 (+/-0.09) L.min(-1); p<0.01). The phase II tau was significantly correlated with indices of aerobic exercise performance (e.g., peak oxygen uptake (moderate-intensity r=-0.88, p<0.01; severe intensity r=-0.62; p<0.05), whereas the relative amplitude of the oxygen uptake slow component was significantly correlated with indices of anaerobic exercise performance (e.g., Wingate peak power output; r=0.77; p<0.01). Thus, it could be concluded that sub-elite SPT athletes have slower phase II oxygen uptake kinetics and a larger oxygen uptake slow component compared with sub-elite ENT athletes. It appears that indices of aerobic and anaerobic exercise performance differentially influence the fundamental and slow components of the oxygen uptake kinetics.

Sodium bicarbonate ingestion alters the slow but not the fast phase of VO2 kinetics.

PURPOSE: The influence of metabolic alkalosis (ALK) on pulmonary O2 uptake (pVO2) kinetics during high-intensity cycle exercise is controversial. The purpose of this study was to examine the influence of ALK induced by sodium bicarbonate (NaHCO3) ingestion on pVO2 kinetics, using a sufficient number of repeat-step transitions to provide high confidence in the results obtained. METHODS: Seven healthy males completed step tests to a work rate requiring 80% pVO2max on six separate occasions: three times after ingestion of 0.3 g x kg(-1) body mass NaHCO3 in 1 L of fluid, and three times after ingestion of a placebo (CON). Blood samples were taken to assess changes in acid-base balance, and pVO2 was measured breath-by-breath. RESULTS: NaHCO3 ingestion significantly increased blood pH and [bicarbonate] both before and during exercise relative to the control condition (P < 0.001). The time constant of the phase II pVO2 response was not different between conditions (CON: 29 +/- 6 vs ALK: 32 +/- 7 s; P = 0.21). However, the onset of the pVO2 slow component was delayed by NaHCO3 ingestion (CON: 120 +/- 19 vs ALK: 147 +/- 34 s; P < 0.01), resulting in a significantly reduced end-exercise pVO2 (CON: 2.88 +/- 0.19 vs ALK: 2.79 +/- 0.23 L x min(-1); P < 0.05). CONCLUSIONS: Metabolic alkalosis has no effect on phase II pVO2 kinetics but alters the pVO2 slow-component response, possibly as a result of the effects of NaHCO3 ingestion on muscle pH.

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.

Influence of acute plasma volume expansion on VO2 kinetics, VO2 peak, and performance during high-intensity cycle exercise.

The purpose of this study was to examine the influence of acute plasma volume expansion (APVE) on oxygen uptake (V(O2)) kinetics, V(O2peak), and time to exhaustion during severe-intensity exercise. Eight recreationally active men performed "step" cycle ergometer exercise tests at a work rate requiring 70% of the difference between the gas-exchange threshold and V(O2max) on three occasions: twice as a "control" (Con) and once after intravenous infusion of a plasma volume expander (Gelofusine; 7 ml/kg body mass). Pulmonary gas exchange was measured breath by breath. APVE resulted in a significant reduction in hemoglobin concentration (preinfusion: 16.0 +/- 1.0 vs. postinfusion: 14.7 +/- 0.8 g/dl; P < 0.001) and hematocrit (preinfusion: 44 +/- 2 vs. postinfusion: 41 +/- 3%; P < 0.01). Despite this reduction in arterial O(2) content, APVE had no effect on V(O2) kinetics (phase II time constant, Con: 33 +/- 15 vs. APVE: 34 +/- 12 s; P = 0.74), and actually resulted in an increased V(O2peak) (Con: 3.90 +/- 0.56 vs. APVE: 4.12 +/- 0.55 l/min; P = 0.006) and time to exhaustion (Con: 365 +/- 58 vs. APVE: 424 +/- 64 s; P = 0.04). The maximum O(2) pulse was also enhanced by the treatment (Con: 21.3 +/- 3.4 vs. APVE: 22.7 +/- 3.4 ml/beat; P = 0.04). In conclusion, APVE does not alter V(O2) kinetics but enhances V(O2peak) and exercise tolerance during high-intensity cycle exercise in young recreationally active subjects.

Influence of continuous and interval training on oxygen uptake on-kinetics.

PURPOSE: To examine the relative effectiveness of moderate-intensity continuous training and high-intensity interval training on pulmonary O2 uptake (VO2) kinetics at the onset of moderate- and severe-intensity cycle exercise in previously sedentary subjects. METHODS: Twenty-three healthy subjects (11 males; mean +/- SD age 24 +/- 5 yr; VO2peak 34.3 +/- 5.5 mL x kg(-1) x min(-1)) were assigned to one of three groups: a continuous training group that completed three to four sessions per week of 30-min duration at 60% VO2peak (LO); an interval training group that completed three to four sessions per week involving 20 x 1-min exercise bouts at 90% VO2peak separated by 1-min rest periods (HI); or a control group (CON). Before and after the 6-wk intervention period, all subjects completed a series of step exercise tests to moderate and severe work rates during which pulmonary VO2 was measured breath-by-breath. RESULTS: ANOVA revealed that continuous and interval training were similarly effective in reducing the phase II VO2 time constant during moderate (LO: from 31 +/- 8 to 23 +/- 5 s; HI: from 32 +/- 9 to 21 +/- 4 s; both P < 0.05; CON: from 30 +/- 6 to 29 +/- 7 s; NSD) and severe exercise (LO: from 35 +/- 6 to 24 +/- 7 s; HI: from 32 +/- 11 to 24 +/- 7 s; both P < 0.05; CON: from 27 +/- 7 to 25 +/- 5 s; NSD) and in reducing the amplitude of the VO2 slow component (LO: from 0.38 +/- 0.10 to 0.29 +/- 0.09 L x min(-1); HI: from 0.41 +/- 0.28 to 0.30 +/- 0.28 L x min(-1); both P < 0.05; CON: from 0.54 +/- 0.22 to 0.66 +/- 0.38 L.min; NSD). CONCLUSIONS: Six weeks of low-intensity continuous training and high-intensity interval training were similarly effective in enhancing VO2 on-kinetics following step transitions to moderate and severe exercise in previously untrained subjects.

Influence of hyperoxia on pulmonary O2 uptake kinetics following the onset of exercise in humans.

The purpose of this study was to examine the influence of hyperoxic gas (50% O2 in N2) inspiration on pulmonary oxygen uptake (V(O2)) kinetics during step transitions to moderate, severe and supra-maximal intensity cycle exercise. Seven healthy male subjects completed repeat transitions to moderate (90% of the gas exchange threshold, GET), severe (70% of the difference between the GET and V(O2) peak) and supra-maximal (105% V(O2) peak) intensity work rates while breathing either normoxic (N) or hyperoxic (H) gas before and during exercise. Hyperoxia had no significant effect on the Phase II V(O2) time constant during moderate (N: 28+/-3s versus H: 31+/-7s), severe (N: 32+/-9s versus H: 33+/-6s) or supra-maximal (N: 37+/-9s versus H: 37+/-9s) exercise. Hyperoxia resulted in a 45% reduction in the amplitude of the V(O2) slow component during severe exercise (N: 0.60+/-0.21 L min(-1) versus H: 0.33+/-0.17 L min(-1); P < 0.05) and a 15% extension of time to exhaustion during supra-maximal exercise (N: 173+/-28 s versus H: 198+/-41 s; P < 0.05). These results indicate that the Phase II V(O2) kinetics are not normally constrained by (diffusional) O2 transport limitations during moderate, severe or supra-maximal intensity exercise in young healthy subjects performing upright cycle exercise.

Influence of recombinant human erythropoietin treatment on pulmonary O2 uptake kinetics during exercise in humans.

We hypothesized that 4 weeks of recombinant human erythropoietin (RhEPO) treatment would result in a significant increase in haemoglobin concentration ([Hb]) and arterial blood O(2)-carrying capacity and that this would (1) increase peak pulmonary oxygen uptake during ramp incremental exercise, and (2) speed kinetics during 'severe'-, but not 'moderate'- or 'heavy'-intensity, step exercise. Fifteen subjects (mean +/- s.d. age 25 +/- 4 years) were randomly assigned to either an experimental group which received a weekly subcutaneous injection of RhEPO (150 IU kg(-1); n = 8), or a control group (CON) which received a weekly subcutaneous injection of sterile saline (10 ml; n = 7) as a placebo, for four weeks. The subjects and the principal researchers were both blind with respect to the group assignment. Before and after the intervention period, all subjects completed a ramp test for determination of the gas exchange threshold (GET) and , and a number of identical 'step' transitions from 'unloaded' cycling to work rates requiring 80% GET (moderate), 70% of the difference between the GET and (heavy), and 105% (severe) as determined from the initial ramp test. Pulmonary gas exchange was measured breath-by-breath. There were no significant differences between the RhEPO and CON groups for any of the measurements of interest ([Hb], kinetics) before the intervention. Four weeks of RhEPO treatment resulted in a 7% increase both in [Hb] (from 15.8 +/- 1.0 to 16.9 +/- 0.7 g dl(-1); P < 0.01) and (from 47.5 +/- 4.2 to 50.8 +/- 10.7 ml kg(-1).min(-1); P < 0.05), with no significant change in CON. RhEPO had no significant effect on kinetics for moderate (Phase II time constant, from 28 +/- 8 to 28 +/- 7 s), heavy (from 37 +/- 12 to 35 +/- 11 s), or severe (from 33 +/- 15 to 35 +/- 15 s) step exercise. Our results indicate that enhancing blood O(2)-carrying capacity and thus the potential for muscle O(2) delivery with RhEPO treatment enhanced the peak but did not influence kinetics, suggesting that the latter is principally regulated by intracellular (metabolic) factors, even during exercise where the requirement is greater than the , at least in young subjects performing upright cycle exercise.