Single Bout Of Maximal Exercise Research Articles

596-P: Exercise Increases Plasma Neuronal Growth Regulator 1 (NEGR1) Concentrations in Human Subjects

Recent studies suggest that exercise-induced circulating factors are critical for the health benefits of exercise. In rodent models, we have identified NEGR1 as a cell adhesion molecule that is essential for remodeling white adipose tissue (WAT) innervation via sympathetic neurite outgrowth, and that NEGR1 is a secreted factor that may be involved inter-tissue communication. In humans, exercise training increases NEGR1 mRNA in subcutaneous WAT, but whether exercise regulates circulating NEGR1 in humans is not known. Here, we investigated the effects of a single bout of maximal exercise and exercise training on plasma NEGR1 in two different cohorts of obese subjects. Acute exercise (single bout until VO2MAX achieved) increased NEGR1 in plasma in all subjects (p<0.05; n=M3/F4). For the training study, obese subjects were randomized to one of three protocols: two different high intensity interval training (HIIT) protocols and one moderate continuous training (MCT) (Table), and blood samples were taken four days after the last training session. 1-HIIT and 4-HIIT similarly increased plasma NEGR1 concentrations, while there was no significant effect of MCT on NEGR1. In conclusion, we identify NEGR1 as a novel exercise-induced circulating factor in human subjects. We hypothesize that NEGR1 plays a role in tissue cross-talk mediating neuronal refinement in several tissues. Disclosure P.Nigro: None. N.P.Carbone: None. C.Bueno junior: None. M.Vamvini: None. L.Simpson: None. G.A.Hansbury: None. M.F.Hirshman: Stock/Shareholder; Abbott, AbbVie Inc., Amgen Inc., Colgate-Palmolive, Eli Lilly and Company, Medtronic. R.J.W.Middelbeek: Research Support; Novo Nordisk. L.Goodyear: None. Funding National Institutes of Health (R01DK099511, R01DK101043, K23DK114550, 5T32DK00726042, F32DK12643201); Joslin Diabetes Center (P30DK36836)

244-OR: Moderate Intensity Endurance Exercise Training Improves Late-Phase ß-Cell Function in Humans with Type 2 Diabetes

Type 2 diabetes (T2D) is associated with β-cell dysfunction. Although exercise is considered beneficial in T2D, the effects of moderate intensity endurance exercise training on β-cell function in humans with T2D are not known. GWAS uncovered Ras-Responsive Element Binding Protein 1 (RREB1) as a risk factor for T2D and in vitro studies suggest RREB1 impairs β-cell function; no studies have investigated exercise effects on RREB1. Here, we determined the effects of moderate intensity exercise training on β-cell function, RREB1, insulin, glucagon, and amylin in humans with T2D (7F/3M, 49±5y, BMI 30±3kg/m2) . Subjects completed 10-weeks of supervised exercise (Wks 1-3: 20-30min/day; 3X/wk; ∼50% VO2peak and Wks 4-10: 45-60min/day; 4X/wk; ∼70% VO2peak) . Fasting blood samples for OGTT, HbA1c, and hormones were obtained pre- and post-training (48hr) . Serum RREB1 was measured pre- and post-training and also in response to a single bout of maximal exercise. Training decreased HbA1c (7.7% to 7.2%, P=0.01) , pro-insulin (-18%, P=0.03) , pro-insulin/c-peptide ratio (-8%, P=0.03) , and glucose (OGTT: 90min, -18%, P=0.01; 120min, -15%, P<0.001) . Both β-cell function (late-phase disposition index, +38%, P=0.01) and insulin sensitivity (Stumvoll Index, +25%, P=0.01) improved. Body weight and composition, VO2peak, glucagon, amylin, c-peptide, and insulin were unchanged. Baseline RREB1 negatively correlated with the exercise-induced increase in late-phase disposition index (R= -0.71, P=0.03) , consistent with an inhibitory role of RREB1. Training did not alter serum RREB1, but interestingly, acute exercise decreased RREB1 both before (-51%, P<0.01) and after training (-11%, P=0.04) . Thus, RREB1 is an exercise-regulated serum factor whose decrease may function to improve β-cell function with exercise. In conclusion, moderate intensity exercise training, in the absence of increased VO2peak, improves late phase β-cell function and glucose control in humans with T2D. Disclosure H.Zhang: None. R.Middelbeek: Research Support; Novo Nordisk. L.Simpson: None. N.P.Carbone: None. L.J.Goodyear: None. Funding National Institutes of Health (K23-DK114550, R01-DK112283, 5P30DK36836, 5P30DK057521-20)

Thermosensory mapping of skin wetness sensitivity across the body of young males and females at rest and following maximal incremental running.

Humans lack skin receptors for wetness (i.e. hygroreceptors), yet we present a remarkable wetness sensitivity. Afferent inputs from skin cold-sensitive thermoreceptors are key for sensing wetness; yet, it is unknown whether males and females differ in their wetness sensitivity across their body and whether high intensity exercise modulates this sensitivity. We mapped sensitivity to cold, neutral and warm wetness across five body regions and show that females are more sensitive to skin wetness than males, and that this difference is greater for cold than warm wetness sensitivity. We also show that a single bout of maximal exercise reduced the sensitivity to skin wetness (i.e. hygro-hypoesthesia) of both sexes as a result of concurrent decreases in thermal sensitivity. These novel findings clarify the physiological mechanisms underpinning this fundamental human sensory experience. In addition, they indicate sex differences in thermoregulatory responses and will inform the design of more effective sport and protective clothing, as well as thermoregulatory models. Humans lack skin hygroreceptors and we rely on integrating cold and tactile inputs from A-type skin nerve fibres to sense wetness. Yet, it is unknown whether sex and exercise independently modulate skin wetness sensitivity across the body. We mapped local sensitivity to cold, neutral and warm wetness of the forehead, neck, underarm, lower back and dorsal foot in 10males (27.8±2.7years; 1.92±0.1m2 body surface area) and 10 females (25.4±3.9years; 1.68±0.1m2 body surface area), at rest and post maximal incremental running. Participants underwent our quantitative sensory test where they reported the magnitude of thermal and wetness perceptions (visual analogue scale) resulting from the application of a cold (5°C below skin temperature) wet (0.8mL of water), neutral wet and warm wet (5°C above skin temperature) thermal probe (1.32cm2 ) to five skin sites. We found that: (i) females were ∼14% to ∼17% more sensitive to cold-wetness than males, yet both sexes were as sensitive to neutral- and warm-wetness; (ii) regional differences were present for cold-wetness only, and these followed a craniocaudal increase that was more pronounced in males (i.e. the foot was ∼31% more sensitive than the forehead); and (iii) maximal exercise reduced cold-wetness sensitivity over specific regions in males (i.e. ∼40% decrease in foot sensitivity), and also induced a generalized reduction in warm-wetness sensitivity in both sexes (i.e. ∼4% to ∼6%). For the first time, we show that females are more sensitive to cold wetness than males and that maximal exercise induce hygro-hypoesthesia. These novel findings expand our knowledge on sex differences in thermoregulatory physiology.

The level of physical training modulates cytokine levels through P2X7 receptor in healthy subjects.

The P2X7 receptor-NLRP3 inflammasome complex (P2X7R-Infl) regulates inflammatory and immune responses. Physical exercise modulates heat-shock proteins (Hsps), influencing cytokine levels and oxidative stress; Hsp72 triggers P2X7R-Infl-dependent responses. We studied the effect of a single bout of maximal exercise on lymphomonocyte expression of P2X7R, NLRP3, caspase-1, NF-kB and Hsp72 and circulating levels of IL-1β, IL-18 and MCP-1, all modulated by P2X7R-Infl, in healthy sedentary (SED), trained (ATH), endurance (END) male individuals. Baseline P2X7R, NLRP3 and Caspase-1 expression progressively increased from SED to ATH and END; NF-kβ showed the same trend. Hsp72 did not differ among groups. Acute exercise strongly reduced P2X7R in all participants, irrespective of their degree of physical training. Inflammasome responses differed across groups: in SED, NLRP3 and Caspase-1 increased; in ATH, NLRP3 reduced and caspase-1 did not vary; in END, NLRP3 and Caspase-1 declined. Baseline IL-1β, higher in END, was unmodified after exercise; IL-18 decreased; MCP-1 doubled in SED, did not vary in ATH, declined in END. In the whole study population, significant direct relationships emerged between P2X7R expression and IL-1β, IL-18, MCP-1 levels, all P<.001; also Caspase-1 related with these markers. A multivariate analysis showed age, BMI and P2X7R as determinants of postexercise IL-1β levels. Endurance show higher P2X7R-Infl expression and function vs SED and ATH; however, maximal exercise determines prevailing pro-inflammatory vs anti-inflammatory responses in untrained and trained participants, respectively, highlighting a likely cause-effect relationship between degree of physical activity and P2X7R-Infl-mediated responses.

A single bout of maximal exercise improves lung function in patients with cystic fibrosis

BackgroundResponses to a single bout of exercise may provide critical information for maximizing improvements in pulmonary function following exercise training in cystic fibrosis (CF). We sought to determine if acute maximal exercise improves pulmonary function in patients with CF. MethodsThirty-three patients with CF completed a comprehensive assessment of pulmonary function to determine forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and lung clearance index (LCI) prior to and immediately following maximal aerobic exercise on a cycle ergometer. ResultsFollowing exercise, FVC (∆0.08±0.14L) and FEV1 (∆0.06±0.15L) increased, while LCI decreased (∆-0.71±0.93) (all p<0.05). Changes in FEV1 (%predicted) were associated with peak work (r=0.40, p=0.02) and peak pulmonary ventilation (r=0.45, p=0.01). ConclusionsA single bout of maximal exercise acutely improves pulmonary function in patients with CF and improvements may be related to peak work and peak pulmonary ventilation.

Effects of a single bout of maximal aerobic exercise on BDNF in bipolar disorder: A gender-based response

Acute exercise increases brain-derived neurotrophic factor (BDNF) serum levels in majorly depressed and anxious patients. However, to the best of our knowledge, no study has evaluated the acute effects of exercise on BDNF serum levels in Bipolar Disorder (BD). The objective of the present study was to evaluate the peripheral BDNF serum response to a single maximum session of exercise in BD participants and age- and gender-matched healthy participants. BD participants (n=18) and age- and gender-matched healthy participants (n=18) were recruited to perform a single bout of maximal exercise on a cycle ergometer. Blood samples were collected prior to and immediately after the exercise protocol. There was a significant group effect and a significant group x time x gender interaction. BD participants presented significantly higher BDNF serum levels when compared to their healthy control counterparts. Exercise increases the BDNF levels of BD women, but not men.

Antiatherosclerotic effect of exercise on the antioxidant properties of paraoxonase – A preliminary examination

The positive impact of properly performed exercise on the human body is well known. In this study, the effect of maximal exercise on the antioxidant activity of the blood enzyme, paraoxonase (PON), was determined. The aim of this study was to determine the influence of a single bout of maximal physical exercise on PON activity and to investigate the correlation of this activity with chosen biometric parameters and physical activity levels. In total, 15 subjects participated in this study. The average age of the subjects was 18 years (±2.74 years). Participants were subjected to maximum efforts on a treadmill until complete exhaustion resulted. They had their blood taken for analysis at three time points – before, at the end, and 2 h following the end of exercise. PON activity was determined by the ability to dispose of paraoxon. The subjects also filled in questionnaires in which they determined the amount and form of training carried out. Basic biometric data were collected from the subjects. This study demonstrates that the enzyme activity at the maximal effort is higher than at rest; however, it does not depend on the level of physical activity. PON activity 2 h following exercise, though higher than at rest, was not statistically significant. No relationship was found between PON activity and chosen parameters such as age, weight, BMI, lean, body mass. A single bout of maximal exercise increases PON activity. A positive trend was also observed with respect to the impact of the physical activity level on PON activity at rest.

Forearm Blood Flow Response to an Acute Maximal Exercise Bout in Obese and Normal Weight Males

One of the earliest sub-clinical stages associated with atherosclerosis is endothelial dysfunction (ED), which has been shown to predict future cardiovascular events. Chronic exercise is thought to improve endothelium-dependent vasodilation; however, few studies have evaluated the effects of acute exercise on vascular function (VF). In addition, no studies have compared VF responses in obese and non-obese individuals following acute exercise. PURPOSE:To evaluate VF, as determined by the assessment of forearm blood flow (FBF) and vascular reactivity (VR) before and up to 48 hours after a single bout of maximal exercise in obese and non-obese males. METHODS:Twelve obese (37.0 ± 1.1 kg/m2) and non-obese (21.9 ± 0.3 kg/m2) males volunteered to participate. FBF was assessed before (bFBF) and during reactive hyperemia (rhFBF). FBF measures were obtained prior to (PRE-E), immediately after (POST-E), and at 1 (POST-1), 2 (POST-2), 24 (POST-24), and 48 (POST-48) hours after exercise. Total excess flow, calculated as the difference between bFBF and rhFBF, was used as an indicator of VR. Blood samples were also obtained to evaluate the response of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), which are potential modifiers of VF. RESULTS:Although there was no main effect for group, there was a significant (P < 0.05) main effect for time in bFBF, rhFBF, and VR. A group × time interaction was not significant for bFBF, rhFBF, and VR. A Dunnett's post-hoc revealed that POST-E values were significantly (P < 0.05) increased compared to PRE-E values for bFBF, rhFBF, and VR (mean difference±S.E.: 330.21±40.31; 530.60±81.61; 200.39±54.13 ml/100 ml/min × sec, respectively), before returning to PRE-E values by POST-1 (mean differences±S.E. - bFBF, rhFBF, and VR: 49.12±40.31, 111.03±81.61, 61.91±54.14 ml/100 ml/min × sec). Concentrations of IL-6 and TNF-α were unchanged in response to exercise in both groups. CONCLUSIONS:An acute bout of maximal exercise significantly increased forearm endothelium-dependent vasodilation in non-obese and obese males. Although VR prior to exercise is significantly correlated to percent body fat (r=0.508, P=0.011), excess adiposity does not contribute to impairment in forearm blood flow in otherwise healthy obese males following an acute bout of maximal exercise.

Effect of single bout of maximal excercise on plasma antioxidant status and paraoxonase activity in young sportsmen

The purpose of this study was to elucidate the participation of plasma PON1 (paraoxonase activity [PON] and arylesterase activity [ARE]) in antioxidant defense in response to a single bout of maximal exercise. PON, ARE, lipid profile, lipid peroxidation (thiobarbituric acid reactive substances [TBARS]), total antioxidant status (ferric reducing ability of plasma [FRAP]), concentration of uric acid [UA], and total bilirubin (TBil) were determined in the plasma before, at the bout and 2 h after maximal exercise on a treadmill in young sportsmen. Chosen physiological parameters also were controlled during maximal exercise. Following maximal exercise, the unaltered level of TBARS and increased FRAP were registered. ARE increment was the highest (37.6%) of all measured variables but lasted for a short time. UA increment was lower than ARE but long-lasting and correlated with FRAP. PON activity increment was associated with the combined effect of body weight, lean, body mass index (BMI) and basal metabolic rate (BMR). We conclude that PON1 is a co-factor of the first line of antioxidant defense during maximal exercise. Its activity is associated with body composition and not the physical fitness of the subjects.

The Extended Time Course of Forearm Blood Flow Following a Maximal Bout of Exercise

Chronic exercise is thought to improve endothelium-dependent vasodilation; however, studies evaluating endothelial dysfunction (ED) following an exercise training program lack a standardized time frame in which to measure vascular function (VF). Although most studies require subjects to abstain from exercise for 24 hours prior to any VF measures, no study to date has assessed VF longer than 24 hours after the cessation of exercise. PURPOSE: To evaluate VF, as determined by the assessment of forearm blood flow (FBF) and vascular reactivity (VR) before and up to 48 hours after a single bout of maximal exercise in healthy male volunteers. METHODS: Twelve male subjects volunteered to participate. FBF was assessed before and during reactive hyperemia (RH). FBF measures were obtained prior to (PRE-E), immediately after (POST-E), and at 1 (POST-1), 2 (POST-2), 24 (POST-24), and 48 (POST-48) hours after exercise. Total excess flow, calculated as the difference between baseline FBF and FBF during RH, was used as an indicator of VR. Blood samples were also obtained at each time point to evaluate the response of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a), which are potential modifiers of VF. RESULTS: Baseline FBF and FBF during RH were significantly (P < 0.05) increased POST-E before returning to baseline values by POST-1. VR was significantly (P < 0.05) increased POST-E and was not significantly (P < 0.05) reduced until POST-48. Concentrations of IL-6 and TNF-a were unchanged in response to exercise. CONCLUSIONS: These results indicate that measurements used to verify improvements in VF following chronic exercise training should be employed more than 24 hours following a single bout of physical activity. Financial support was provided by the School of Education Research Initiation Awards Program at Virginia Commonwealth University

EVIDENCE FOR ALTERED ALPHA-ADRENORECEPTOR RESPONSIVENESS FOLLOWING A SINGLE BOUT OF MAXIMAL EXERCISE

PURPOSE: We studied hemodynamic responses to α- and β-receptor agonists in 8 healthy normotensive men on two different test days, each separated by at least one week, to test the hypothesis that adrenoreceptor responsiveness is altered within 24 h of performing a single bout of maximal exercise. METHODS: On one day, adrenoreceptor responsiveness was tested 24 h after each subject performed graded upright cycle exercise to volitional exhaustion. On another day, testing for adrenoreceptor responsiveness was repeated with no exercise (control). The order of exercise and control treatments was randomized and counterbalanced. Steady-state infusions of isoproterenol (ISO) were given at rates of 0.005, 0.01, and 0.02 μg/kg/min. Infusions of phenylephrine (PE) were given at rates of 0.25, 0.50, and 1.00 μg/kg/min. Slopes calculated from linear regressions between ISO and PE doses and changes in heart rate, blood pressure, and leg vascular resistance (occlusion plethysmography) for each subject were used to assess α- and β-adrenoreceptor responsiveness. RESULTS: Compared to control, exercise did not alter the slopes of heart rate (1987 ± 142 vs. 1773 ± 164 beats/μg/kg/min; t = 1.014, P = 0.331) and vasodilation (−429 ± 125 to −438 ± 140 pru/μg/kg/min; t = 0.015, P = 0.0908) to ISO infusion. In contrast, exercise was associated with greater (t = 6.323, P = 0.040) vascular resistance (15.1 ± 2.8 pru/μg/kg/min) and mean arterial pressure (18.6 ± 4.4 mmHg/μg/kg/min) responses to PE infusion compared to the control condition (9.0 ± 2.0 pru/μg/kg/min and 10.2 ± 2.3 mmHg/μg/kg/min, respectively). CONCLUSION: Our results provide evidence that a single bout of maximal exercise increases α1-adrenoreceptor responsiveness without affecting β1-cardiac and β2-vascular adrencoreceptor responses. Supported by the National Aeronautics and Space Administration.

Effects of maximal exercise on natural killer (NK) cell cytotoxicity and responsiveness to interferon-alpha in the young and old.

We investigated the effects of a graded maximal exercise treadmill test on natural killer (NK) cell number, activity, and responsiveness to interferon-alpha (IFN-alpha) in young (22+/-0.7 yrs) and elderly (65+/-0.8 yrs) sedentary subjects. NK cell cytotoxicity (NKCC) was determined using Ficoll purified peripheral blood mononuclear cells (PBMCs) by a 51Cr release assay against NK-sensitive (K562) and NK-insensitive (Daudi) target cells at various effector:target (E:T) ratios before and immediately after exercise. PBMCs were incubated with rhu IFN-alpha (125 and 250u/10(6) PBMCs) or without for 2 hrs before addition to the 51Cr release assay. There were no differences in unstimulated NKCC against K562 or Daudi targets between the old and the young despite significantly (p=.01) higher percentages of CD56+ NK cells (21.1+/-2.3% in old vs 12.5+/-2.5% in young, pre-exercise). IFN-alpha increased NKCC versus both targets, and NK cells from old subjects were hyporesponsive to IFN-alpha stimulation; this was especially evident at low E:T ratios versus Daudi cells. Maximal exercise significantly increased (50-200%) unstimulated NKCC versus K562 and Daudi targets similarly in both young and old and increased the percentage of CD56+ cells in the PBMC fraction to 33.3+/-3.7% and 23.3+/-3.6% in old and young, respectively. We found a significant correlation between %CD56+ and basal NKCC versus K562s and Daudi cells in the young (i.e., r=.55; p=.02 vs K562s), but not the old (i.e., r=.20; p=.29 vs K562s) subjects. This indicates that, in the young, part of the exercise-induced increase in NKCC is due to an increase in NK cell number. Maximal exercise did not affect unstimulated per cell killing of K562s, but tended to increase per cell killing of Daudis. These results indicate that CD56+ cells from old subjects have an intrinsic defect in their ability to perform cytolysis and respond to IFN-alpha. Furthermore, a single bout of maximal exercise increases NKCC and CD56+ cell number similarly in both young and old subjects regardless of the target cell used.

Restoration of peak vascular conductance after simulated microgravity by maximal exercise.

We sought to determine if (i) peak vascular conductance of the calf was reduced following prolonged exposure to simulated microgravity, and (ii) if maximal cycle ergometry performed at the end of microgravity exposure stimulated a restoration of peak calf vascular conductance. To do this, peak vascular conductance of the calf was recorded following ischaemic plantar flexion exercise to fatigue in seven men after 16 days of head-down tilt (HDT) under two conditions: (i) after one bout of maximal supine cycle ergometry completed 24 h prior to performance of ischaemic plantar flexion exercise, and (ii) in a control (no cycle ergometry) condition. Following HDT, peak vascular conductance was reduced in the control condition (0.38 +/- 0.02 to 0.24 +/- 0.02 ml 100 ml-1 min-1 mmHg-1; P = 0.04), but was restored when subjects performed cycle ergometry (0.33 +/- 0.05 to 0.28 +/- 0.04 ml 100 ml-1 min-1 mmHg-1; P = 0.46). After HDT, time to fatigue during ischaemic plantar flexion exercise was not different from pre-HDT 24 h after performance of exhaustive cycle ergometry (120 +/- 24 vs. 122 +/- 19 s), but was decreased in the control condition (116 +/- 11 vs. 95 +/- 8 s; P = 0.07). These data suggest that a single bout of maximal exercise can provide a stimulus to restore peak vascular conductance and maintain time to fatigue during performance of ischaemic plantar flexion exercise.

Restoration of plasma volume after 16 days of head-down tilt induced by a single bout of maximal exercise.

Seven healthy men performed maximal exercise 24 h before the end of 16 days exposure to 6 degrees head-down tilt (HDT) to test the hypothesis that such an exercise technique could restore plasma volume (PV) at the end of a simulated space mission. Exercise consisted of supine cycling with graded work rates increasing by 16 W/min to volitional fatigue and required an average of 16 min. The experimental protocol was a standard cross-over design in which the order of treatment (exercise or control) was counterbalanced across all seven subjects. PV, fluid intake (ad libitum), urine output, renal function, and hormones associated with fluid homeostasis were measured before HDT, 24 h before the end of HDT just prior to exercise, and at the end of HDT 24 h after exercise. HDT reduced PV by 16% in both control and exercise conditions. Maximal exercise completely restored plasma volume within 24 h to 3.9 +/- 3.2% of pre-HDT levels despite continued HDT. Compared with control, exercise induced a 660-ml larger positive fluid balance because of greater fluid intake and reduced urine volume during the 24 h after exercise. These results suggest that one bout of maximal leg exercise before return from 16 days of spaceflight may be completely effective in stimulating thirst and restoring plasma volume to preflight levels.

Quantification of anaerobic capacity

Anaerobic capacity may be defined as the maximal amount of ATP formed by the anaerobic processes during a single bout of maximal exercise. While several methods have been presented to measure a person's anaerobic capacity, none have become universally accepted. The muscle biopsy technique provides information on the anaerobic energy release from direct measures of ATP and CP breakdown and muscle lactate concentrations. As a practical measure of anaerobic capacity, the method may be limited, as it is an invasive, skilled technique. Furthermore, it has the limitation of measuring relative changes in concentrations, not amounts, such that the anaerobic contribution is estimated from estimates of the active muscle mass involvement. Measurement of lactate in blood after exhaustive exercise has frequently been used, but several factors suggest that, while it provides an indication of the extent of anaerobic glycolysis, it cannot be used as a quantitative measure of the anaerobic energy yield. The mean power during an all‐out effort on a bicycle ergometer has also been assumed to be a measure of anaerobic capacity, yet it provides only an indication of the ability to maintain high power outputs. Concerns over the duration of the test, the protocol and type of ergometer used and the contribution of the aerobic energy system to the energy supply also limit its validity as a measure of anaerobic capacity. The oxygen debt, defined as the recovery oxygen uptake above resting metabolic rates, has been discredited as a valid and reliable measure of the anaerobic capacity, as it is generally acknowledged that mechanisms other than the metabolism of lactate also contribute to the post‐exercise oxygen uptake. The recent work of Medbø et al. in re‐examining the issue of oxygen deficit has created considerable interest in its use as a measure of anaerobic capacity. The measurement of oxygen deficit directly depends on the accurate assessment of the energy cost of the work completed. This is not difficult during submaximal exercise, as the steady‐state oxygen uptake represents the energy costs. During exhaustive supramaximal exercise, the validity of the maximal accumulated oxygen deficit as a measure of the anaerobic capacity has been questioned, as the energy cost is estimated and not measured, either by assuming a given mechanical efficiency or by extrapolating the submaximal relationship between work intensity and oxygen uptake to supramaximal levels. Despite these theoretical objections, the maximal accumuiated oxygen deficit method remains a promising measure of the anaerobic capacity, as it provides a non‐invasive means of quantifying the anaerobic energy release during exhaustive exercise.