Is the O2 deficit an accurate quantitative measure of the anaerobic energy production during intense exercise?
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Anaerobiosis↗
Biomedical subjects
J Bangsbo
Publications and source records attributed to J Bangsbo.
Substrates for muscle glycogen synthesis in recovery from intense exercise in man.
1. Intramuscular glyconeogenesis from lactate after intense exercise was examined by using the one-legged knee extension model which enables evaluation of metabolism in a well-defined muscle group. 2. In seven subjects measurements of leg blood flow and arterial-venous differences of various substrates were performed in individuals after intense, exhaustive knee extensor exercise lasting 3.0 min. Muscle glycogen and lactate concentrations were determined in the quadriceps muscle immediately after exercise and three times during 1 h of recovery. 3. Muscle glycogen increased from 93.7 +/- 6.7 (+/- S.E.M.) to 108.8 +/- 8.1 mmol (kg wet wt)-1 during the recovery period. Muscle lactate was 27.1 +/- 2.1 mmol (kg wet wt)-1 at the end of exercise and decreased to 14.5 +/- 2.1, 6.7 +/- 1.1, and 3.0 +/- 0.5 mmol (kg wet wt)-1 after 3, 10 and 60 min of recovery, respectively. 4. More than two-thirds of the lactate that accumulated in the muscle during the intense exercise was released into the blood. It was estimated that between 13 and 27% of the lactate could have been converted to glycogen. This corresponded to a glycogen resynthesis rate from lactate of 0.17-0.34 and 0.002 mmol glucosyl units min-1 (kg wet wt)-1 for the first 10 and last 50 min of recovery, respectively. 5. The O2 debt of the leg was 1.5 l of which the resynthesis of ATP, creatine phosphate (CP) and glycogen and reloading of haemoglobin (Hb) and myoglobin (Mb) only could account for one-third. It is proposed that the elevated oxygen uptake during recovery is linked to the metabolic use of intramuscular triacylglycerol.
Adult↗
Activity profile of competition soccer.
In order to study the movement pattern of soccer players, 14 top-level players were filmed during several competitive matches. In addition, the relationship between the observed activity during match play and blood lactate values was examined. The mean distance covered during competitive matches was 10.80 km, and the average individual difference between matches was 0.92 km, with no difference in regard to high intensity activities. Midfielders covered a 10% longer (p less than 0.05) distance (11.4 km) than defenders and forwards, with no difference concerning high intensity running. There was a significant correlation (r = 0.61, p less than 0.05) between the amount of high intensity running during the match and lactate concentration in the blood. The results suggest that high intensity running can be used for making comparisons in soccer and that the interpretation of blood lactate in soccer is limited to giving an indication of the type of activity that has been carried out a few minutes before sampling.
Adult↗
Lactate and potassium fluxes from human skeletal muscle during and after intense, dynamic, knee extensor exercise.
This study examines lactate and K+ fluxes from muscle to blood during and after intense exercise. Ten men performed exhaustive dynamic exercise (mean load 65 W, mean duration 3.18 min) with the knee extensors of one leg. The mean lactate efflux was 15.5 (range 8.9-24.0) mmol min-1 at exhaustion, and it was linearly related to the lactate gradient. A linear relationship was also obtained if the H+ gradient was taken into account. Muscle pH decreased from 7.14 at rest to 6.71 (range 6.50-6.87) at exhaustion. At rest and during late recovery blood lactate was distributed across the erythrocyte membrane according to the membrane potential (intra-/extracellular ratio of 0.5), but during rapid lactate release this ratio decreased to 0.2. In-vitro experiments demonstrated a time constant of 1.2 min for lactate efflux from the erythrocytes. Approximately 70% of the K+ ions released from the muscle to the blood accumulated in the plasma; the rest were taken up by other tissues. However, erythrocytes were not involved as a dilution space. The small change in erythrocyte K+ concentration was due to cellular volume changes. During recovery the kinetics of K+ reuptake by the muscle were described by a very fast (less than 1 min) and a slow component (greater than 1 min): the magnitude of the former was equivalent to what had accumulated in the plasma. Individuals displayed a wide range of intramuscular lactate concentrations and pH values at exhaustion. Further, the pH changes were not as extreme as previously reported, suggesting that pH may not be the only factor involved in the fatigue process. A possible role for the potassium shifts as a limiting factor for muscle function is discussed.
Adult↗
Anaerobic energy production and O2 deficit-debt relationship during exhaustive exercise in humans.
1. Eight subjects performed one-legged, dynamic, knee-extensor exercise, first at 10 W followed by 10 min rest, then at an intense, exhaustive exercise load (65 W) lasting 3.2 min. After 60 min recovery, exercise was performed for 8-10 min each at 20, 30, 40 and 50 W. Measurements of pulmonary oxygen uptake, heart rate, blood pressure, leg blood flow, and femoral arterial-venous differences of oxygen content and lactate were performed as well as determination of ATP, creatine phosphate (CP) inosine monophosphate (IMP) and lactate concentrations on biopsy material from the quadriceps muscle before and immediately after the intense exercise, and at 3, 10 and 60 min into recovery. 2. Individual linear relations (r = 0.95-1.00) between the power outputs for submaximal exercise and oxygen uptakes (leg and pulmonary) were used to estimate the energy demand during intense exercise. Pulmonary and leg oxygen deficits determined as the difference between energy demand and oxygen uptake were 0.46 and 0.48 l (kg active muscle)-1, respectively. Limb and pulmonary oxygen debts (oxygen uptake during 60 min of recovery - pre-exercise oxygen uptake) were 0.55 and 1.65 l (kg active muscle)-1, respectively. 3. During the intense exercise, muscle [ATP] decreased by 30% and [CP] by 60% from resting concentrations of 6.2 and 22.4 mmol (kg wet wt)-1, respectively, and [IMP] increased to 1.1 mmol (kg wet wt)-1. Muscle [lactate] increased from 2 to 28.1 mmol (kg wet wt)-1, and the concomitant net lactate release was 14.8 mmol (kg wet wt)-1 or about 1/3 of the total net lactate production. During recovery 70% of the accumulated lactate was released to the blood, and the nucleotides and CP returned to about 40 and 85% of pre-exercise values at 3 and 10 min of recovery, respectively. 4. Total reduction in ATP and CP (and elevation of IMP) during the intense exercise amounted to 16.4 mmol ATP (kg wet wt)-1, which together with the lactate production accounted for 83.1 mmol ATP (kg wet wt)-1. In addition 6-8 mmol ATP (kg wet wt)-1 are made available related to accumulation of glycolytic intermediates including pyruvate (and alanine). Estimated leg oxygen deficit corresponded to an ATP production of 94.7 mmol ATP kg-1; this value included 3.1 mmol kg-1 related to unloading of HbO2 and MbO2.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
Ammonia metabolism during intense dynamic exercise and recovery in humans.
This study examined the dynamics for ammonia (NH3) metabolism in human skeletal muscle during and after intense one-legged exercise. Subjects (n = 8) performed dynamic leg extensor exercise to exhaustion (3.2 min). Muscle NH3 release increased rapidly to a maximum of 314 +/- 42 mumol/min and declined immediately on cessation of exercise. Recovery was complete in approximately 20 min. Arterial [NH3] increased less rapidly and reached its maximum 2-3 min into recovery. These data demonstrate that NH3 clearance is more sensitive to the cessation of exercise than is NH3 release from skeletal muscle. Muscle [NH3] increased three to fourfold during exercise and represented 74 +/- 8% of the total net NH3 formation. Thus the change in muscle [NH3] alone underestimates the NH3 production. There was no evidence that the muscle-to-venous blood NH3 ratio shifts in accordance with the H+ data. Thus other factors must contribute to the NH3 release from active muscle. The total net NH3 formed corresponded with the intramuscular inosine 5'-monophosphate accumulation, suggesting that the NH3 was derived from AMP deamination. Changes in the known modulators of AMP deaminase (ATP, ADP, H+) were moderate, so the mechanisms initiating the deamination remain obscure.
Adenine Nucleotides↗
Hormonal response to exercise in humans: influence of hypoxia and physical training.
Hypoxia and physical training alter the responses of glucoregulatory hormones to absolute work loads in opposite directions. These effects have tentatively been ascribed to changes in maximal O2 consumption (VO2 max) and ensuing changes in relative work loads. However, hypoxia as well as training may more specifically influence the hormonal response. We therefore differentiated the influence of hypoxia, training, and VO2 max, respectively, on the hormonal response to bicycle exercise. Responses to hypoxia in a low-pressure chamber (PB = 465 vs. 730 Torr) were studied at given absolute and relative (85% VO2 max) work loads in seven endurance-trained athletes (T) and 7 age and weight-matched sedentary subjects (C). Concentrations in plasma of norepinephrine, growth hormone, adrenocorticotropic hormone, and cortisol were always closely related to the relative work load. However, the epinephrine response in T, but not in C, was at the same relative work load higher during hypoxia (5.84 +/- 0.83 nmol/l) than during normoxia (4.26 +/- 0.44, P less than 0.05). These results indicate that the hormonal response is influenced by hypoxia and physical training, mainly via changes in the relative work load. However, in trained subjects both at rest and during exercise, an enhancing effect of hypoxia per se on the epinephrine response is seen, probably due to an increased adrenal medullary secretory responsiveness in long-term endurance-trained subjects.
Adrenocorticotropic Hormone↗
Inhibition of nitric oxide synthesis by systemic N(G)-monomethyl-L-arginine administration in humans: effects on interstitial adenosine, prostacyclin and potassium concentrations in resting and contracting skeletal muscle.
We examined whether the formation or the release of the vasodilators adenosine, prostacyclin (PGI(2)) and potassium (K(+)) increase in skeletal muscle interstitium in response to nitric oxide synthase (NOS) inhibition. Five subjects performed one-legged knee extensor exercise at 30 W without (controls) and with prior N(G)-nitro-L-arginine methyl ester (L-NAME) infusion (4 mg/kg, intravenously). Samples from the interstitial fluid were obtained at rest, during exercise and after exercise with the microdialysis technique. Interstitial adenosine in controls increased (p<0.05) from 0.11+/-0.03 micromol/l at rest to 0.48 +/-0.06 micromol/l during exercise. Interstitial adenosine during exercise in L-NAME was similar (p>0.05) to controls. The 6-keto-prostaglandin F1alpha concentration in controls was 1.17+/-0.20 ng/ml at rest and increased (p<0.05) to 1.97+/-0.30 ng/ml during exercise and was further elevated (p<0.05) to 2.76+/-0.38 ng/ml after exercise and these concentrations were not different (p>0.05) in L-NAME. The interstitial K(+) concentration in controls increased (p< 0.05) from 4.1+/-0.1 mmol/l at rest to 9.5+/-0.5 mmol/l during exercise. The interstitial K(+) concentration during exercise (6.7+/- 0.4 mmol/l) was lower (p<0.05) in L-NAME than in controls. The present findings demonstrate that the muscle interstitial concentrations of adenosine, PGI(2) and K(+) during exercise are not increased with systemic NOS inhibition. Thus, the lack of effect of NOS inhibition on the rate of blood flow to contracting human skeletal muscle does not appear to be due to compensatory formation or release of adenosine, PGI(2) and K(+) in the muscle interstitium. The present study also supports a role for PGI(2) in the regulation of blood flow during exercise.
6-Ketoprostaglandin F1 alpha↗