ABSTRACT
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.
Subject(s)
Physical Endurance , Running , Humans , Physical Endurance/physiology , Running/physiology , Nutritional Status , Body Temperature Regulation , FatigueABSTRACT
Following the start of low-intensity exercise in healthy humans, it has been established that the kinetics of skeletal muscle O(2) delivery is faster than, and does not limit, the kinetics of muscle O(2) uptake (V(O(2)(m))). Direct data are lacking, however, on the question of whether O(2) delivery might limit (V(O(2)(m))) kinetics during high-intensity exercise. Using multiple exercise transitions to enhance confidence in parameter estimation, we therefore investigated the kinetics of, and inter-relationships between, muscle blood flow (Q(m)), a-(V(O(2))) difference and (V(O(2)(m))) following the onset of low-intensity (LI) and high-intensity (HI) exercise. Seven healthy males completed four 6 min bouts of LI and four 6 min bouts of HI single-legged knee-extension exercise. Blood was frequently drawn from the femoral artery and vein during exercise and Q(m), a-(V(O(2))) difference and (V(O(2)(m))) were calculated and subsequently modelled using non-linear regression techniques. For LI, the fundamental component mean response time (MRT(p)) for Q(m) kinetics was significantly shorter than (V(O(2)(m))) kinetics (mean ± SEM, 18 ± 4 vs. 30 ± 4 s; P < 0.05), whereas for HI, the MRT(p) for Q(m) and (V(O(2)(m))) was not significantly different (27 ± 5 vs. 29 ± 4 s, respectively). There was no difference in the MRT(p) for either Q(m) or (V(O(2)(m))) between the two exercise intensities; however, the MRT(p)for a-(V(O(2)) difference was significantly shorter for HI compared with LI (17 ± 3 vs. 28 ± 4 s; P < 0.05). Excess O(2), i.e. oxygen not taken up (Q(m) x (V(O(2))), was significantly elevated within the first 5 s of exercise and remained unaltered thereafter, with no differences between LI and HI. These results indicate that bulk O(2) delivery does not limit (V(O(2)(m))) kinetics following the onset of LI or HI knee-extension exercise.
Subject(s)
Exercise/physiology , Muscle, Skeletal/blood supply , Muscle, Skeletal/metabolism , Adult , Exercise Test , Humans , Kinetics , Male , Oxygen/blood , Oxygen Consumption , Young AdultABSTRACT
Rowers regularly undertake rowing training within 24 h of performing bouts of strength training; however, the effect of this practice has not been investigated. This study evaluated the impact of a bout of high-intensity strength training on 2,000 m rowing ergometer performance and rowing-specific maximal power. Eight highly trained male club rowers performed baseline measures of five separate, static squat jumps (SSJ) and countermovement jumps (CMJ), maximal rowing ergometer power strokes (PS) and a single 2,000 m rowing ergometer test (2,000 m). Subsequently, participants performed a high-intensity strength training session consisting of various multi-joint barbell exercises. The 2,000 m test was repeated at 24 and 48 h post-ST, in addition SSJ, CMJ and PS tests were performed at these time points and also at 2 h post-ST. Muscle soreness, serum creatine kinase (CK) and lactate dehydrogenase (LDH) were assessed pre-ST and 2, 24 and 48 h post-ST. Following the ST, there were significant elevations in muscle soreness (2 and 24 h, P < 0.01), CK (2, 24 and 48 h, P < 0.01), and LDH (2 h, P < 0.05) in comparison to baseline values. There were significant decrements across all time points for SSJ, CMJ and PS, which ranged between 3 and 10% (P < 0.05). However, 2,000 m performance and related measurements of heart rate and blood lactate were not significantly affected by ST. In summary, a bout of high-intensity strength training resulted in symptoms of muscle damage and decrements in rowing-specific maximal power, but this did not affect 2,000 m rowing ergometer performance in highly trained rowers.
Subject(s)
Athletic Performance/physiology , Muscle Strength/physiology , Resistance Training/methods , Sports , Adolescent , Adult , Biomarkers/blood , Blood Chemical Analysis , Ergometry , Exercise Test , Humans , Male , Muscular Diseases/blood , Muscular Diseases/diagnosis , Muscular Diseases/pathology , Muscular Diseases/physiopathology , Physical Endurance/physiology , Sports/physiology , Time Factors , Young AdultABSTRACT
There is limited published research on the practices of strength and conditioning (S &C) coaches in Great Britain. Information about training program design would be useful in developing models of good practice and ecologically valid intervention studies. The aim of this research was to quantify the training practices of coaches responsible for the S&C of rowing athletes. A questionnaire was developed that consisted of 6 sections: (a) personal details, (b) physical testing, (c) strength and power development, (d) flexibility development, (e) unique aspects of the program, and (f) any further relevant comments regarding the athletes prescribed training program. Twenty-two rowing and 10 S&C coaches with an average of 10.5 ± 7.2 years' experience agreed to complete the questionnaire. Approximately, 34% coached rowers of Olympic standard, 34% coached national standard, 3% coached regional standard, 19% coached club standard, and 10% coached university standard rowers. All coaches agreed that strength training enhanced rowing performance and the majority (74%) indicated that athletes' strength trained 2-3 times a week. Almost all coaches (94%) reported their rowers performed strength training, with 81% using Olympic lifting, and 91% employing a periodized training model. The clean (63%) and squat (27%) were rated the most important prescribed exercises. Approximately 50% of coaches used plyometrics such as depth jumps, box drills, and standing jumps. Ninety-four percent indicated they conducted physical testing on their rowers, typically assessing cardiovascular endurance (80%), muscular power (70%), muscular strength (70%), and anaerobic capacity (57%). This research represents the only published survey to date on the S&C practices in rowing within Great Britain.
Subject(s)
Athletic Performance/physiology , Muscle Strength/physiology , Muscle, Skeletal/physiology , Physical Fitness , Adult , Athletes , Female , Humans , Male , Physical Endurance/physiology , Resistance Training , Surveys and Questionnaires , United Kingdom , Weight Lifting/physiologyABSTRACT
We hypothesised that dichloroacetate (DCA) would reduce blood lactate accumulation, pulmonary carbon dioxide output (.V(CO2)) and ventilation (.V(E)) at sub-maximal work rates, and improve exercise tolerance during incremental exercise in healthy humans. Nine males (mean+/-SD, age 27+/-4 years) completed, in random order, two ramp incremental cycle ergometer tests to the limit of tolerance following the intravenous infusion of DCA (75 mg/kg body mass in 80 ml saline) or an equivalent volume of saline (as placebo). Relative to control, blood [lactate] was significantly reduced by DCA immediately before exercise (CON: 0.7+/-0.2 vs. DCA: 0.5+/-0.2mM; P<0.05) and throughout exercise until 630s (P<0.05). Blood [HCO(3)(-)] was significantly higher in the DCA condition from 360s until 720s of exercise (P<0.05). .V(CO2) and .V(E) were both lower throughout exercise in the DCA condition, with the differences reaching significance at 90 and 180s for .V(CO2) (P<0.05) and at 90, 180, 450, 540, 630, and 810s for .V(E) (P<0.05). Exercise tolerance was not significantly altered (CON: 1029+/-109 vs. DCA: 1045+/-101s). Infusion of DCA resulted in reductions in blood [lactate], .V(CO2) and .V(E) during sub-maximal incremental exercise, consistent with the existence of a link between the bicarbonate buffering of metabolic acidosis and increased CO(2) output. However, the reduced blood lactate accumulation during sub-maximal exercise with DCA did not enhance exercise tolerance.
Subject(s)
Dichloroacetic Acid/pharmacology , Exercise/physiology , Pulmonary Gas Exchange/drug effects , Pulmonary Ventilation/drug effects , Adult , Bicarbonates/blood , Energy Metabolism , Exercise Tolerance , Heart Rate/drug effects , Humans , Lactic Acid/blood , Male , Oxygen Consumption/drug effects , Physical Exertion/drug effects , Young AdultABSTRACT
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.
Subject(s)
Lung/physiology , Oxygen Consumption , Physical Endurance/physiology , Sports/physiology , Adult , Bicycling/physiology , Humans , Kinetics , Male , Running/physiology , Track and Field/physiologyABSTRACT
We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 +/- 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 +/- 2.3 min vs. postintervention group (POST): 19.4 +/- 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 +/- 1.6 min vs. POST: 22.0 +/- 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 +/- 13 s vs. POST: 43 +/- 10 s) or the trained leg (PRE: 38 +/- 8 s vs. POST: 40 +/- 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 +/- 7 vs. POST: 7 +/- 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 +/- 8 vs. POST: 12 +/- 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.
Subject(s)
Exercise/physiology , Muscle, Skeletal/metabolism , Phosphocreatine/metabolism , Physical Endurance/physiology , Physical Fitness/physiology , Adult , Algorithms , Bicycling , Ergometry , Humans , Hydrogen-Ion Concentration , Kinetics , Magnetic Resonance Spectroscopy , Male , Models, Statistical , Muscle, Skeletal/chemistryABSTRACT
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.
Subject(s)
Acid-Base Imbalance/blood , Oxygen Consumption/drug effects , Sodium Bicarbonate/pharmacology , Adult , Exercise Test , Humans , Hydrogen-Ion Concentration/drug effects , Kinetics , Lactic Acid/blood , Male , Oxygen Consumption/physiologyABSTRACT
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.
Subject(s)
Adaptation, Physiological/physiology , Energy Metabolism/physiology , Exercise/physiology , Oxygen Consumption/physiology , Posture/physiology , Pulmonary Gas Exchange/physiology , Adult , Exercise Test , Humans , Hyperemia/metabolism , Lactic Acid/blood , Lung/metabolism , Male , Muscle, Skeletal/metabolism , Oxygen/analysis , Oxygen/metabolism , Spectroscopy, Near-InfraredABSTRACT
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.
Subject(s)
Exercise Tolerance/physiology , Oxygen Consumption/physiology , Oxygen/metabolism , Physical Exertion/physiology , Plasma Substitutes/administration & dosage , Plasma Volume/physiology , Task Performance and Analysis , Adult , Exercise Test , Exercise Tolerance/drug effects , Humans , Male , Metabolic Clearance Rate/drug effects , Oxygen Consumption/drug effects , Physical Exertion/drug effects , Plasma Volume/drug effects , Polygeline/administration & dosageABSTRACT
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.
Subject(s)
Exercise , Oxygen Consumption/physiology , Adult , Exercise Test/methods , Humans , Kinetics , Male , Physical Endurance , United KingdomABSTRACT
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.
Subject(s)
Exercise/physiology , Hyperoxia/rehabilitation , Inhalation/physiology , Oxygen Consumption/physiology , Adult , Exercise Test/methods , Humans , Hyperoxia/physiopathology , Male , Pulmonary Gas Exchange/physiology , Time FactorsABSTRACT
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.