Maximum O2 uptake, O2 debt and deficit, and muscle metabolites in Thoroughbred horses

1988 ◽  
Vol 64 (2) ◽  
pp. 781-788 ◽  
Author(s):  
R. J. Rose ◽  
D. R. Hodgson ◽  
T. B. Kelso ◽  
L. J. McCutcheon ◽  
T. A. Reid ◽  
...  
Keyword(s):  
Peak Plasma ◽  
Co2 Production ◽  
Human Beings ◽  
O2 Uptake ◽  
Thoroughbred Horses ◽  
Muscle Ph ◽  
Exercise Muscle ◽  
Muscle Biopsies ◽  
O2 Deficit ◽  
O2 Debt

This study determined maximal O2 uptake (VO2max), maximal O2 deficit, and O2 debt in the Thoroughbred racehorse exercising on an inclined treadmill. In eight horses the O2 uptake (VO2) vs. speed relationship was linear until 10 m/s and VO2max values ranged from 131 to 153 ml.kg-1.min-1. Six of these horses then exercised at 120% of their VO2max until exhaustion. VO2, CO2 production (VCO2), and plasma lactate (La) were measured before and during exercise and through 60 min of recovery. Muscle biopsies were collected before and at 0.25, 0.5, 1, 1.5, 2, 5, 10, 15, 20, 40, and 60 min after exercise. Muscle concentrations of adenosine 5'-triphosphate (ATP), phosphocreatine (PC), La, glucose 6-phosphate (G-6-P), and creatine were determined, and pH was measured. The O2 deficit was 128 +/- 32 (SD) ml/kg (64 +/- 13 liters). The O2 debt was 324 +/- 62 ml/kg (159 +/- 37 liters), approximately two to three times comparative values for human beings. Muscle [ATP] was unchanged, but [PC] was lower (P less than 0.01) than preexercise values at less than or equal to 10 min of recovery. [PC] and VO2 were negatively correlated during both the fast and slow phases of VO2 during recovery. Muscle [La] and [G-6-P] were elevated for 10 min postexercise. Mean muscle pH decreased from 7.05 (preexercise) to 6.75 at 1.5 min recovery, and the mean peak plasma La value was 34.5 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of acetazolamide on metabolic and respiratory responses to exercise at maximal O2 uptake

1990 ◽  
Vol 68 (2) ◽  
pp. 617-626 ◽  
Author(s):  
R. J. Rose ◽  
D. R. Hodgson ◽  
T. B. Kelso ◽  
L. J. McCutcheon ◽  
W. M. Bayly ◽  
...  
Keyword(s):  
Muscle Metabolism ◽  
Blood Gases ◽  
Co2 Production ◽  
O2 Uptake ◽  
Blood Temperature ◽  
Arterial Ph ◽  
Muscle Ph ◽  
Venous Pco2 ◽  
Total Body ◽  
Exercise Muscle

Changes in blood gases, ions, lactate, pH, hemoglobin, blood temperature, total body metabolism, and muscle metabolites were measured before and during exercise (except muscle), at fatigue, and during recovery in normal and acetazolamide-treated horses to test the hypothesis that an acetazolamide-induced acidosis would compromise the metabolism of the horse exercising at maximal O2 uptake. Acetazolamide-treated horses had a 13-mmol/l base deficit at rest, higher arterial Po2 at rest and during exercise, higher arterial and mixed venous Pco2 during exercise, and a 48-s reduction in run time. Arterial pH was lower during exercise but not in recovery after acetazolamide. Blood temperature responses were unaffected by acetazolamide administration. O2 uptake was similar during exercise and recovery after acetazolamide treatment, whereas CO2 production was lower during exercise. Muscle [glycogen] and pH were lower at rest, whereas heart rate, muscle pH and [lactate], and plasma [lactate] and [K+] were lower and plasma [Cl-] higher following exercise after acetazolamide treatment. These data demonstrate that acetazolamide treatment aggravates the CO2 retention and acidosis occurring in the horse during heavy exercise. This could negatively affect muscle metabolism and exercise capacity.

Effect of induced metabolic acidosis on intracellular pH, buffer capacity and contraction force of human skeletal muscle

1985 ◽  
Vol 69 (5) ◽  
pp. 505-510 ◽  
Author(s):  
E. Hultman ◽  
S. Del Canale ◽  
H. Sjöholm
Keyword(s):  
Buffer Capacity ◽  
Recovery Period ◽  
Mean Values ◽  
Muscle Ph ◽  
Before And After ◽  
Ph Buffer ◽  
Total Capacity ◽  
Ph Decrease ◽  
Muscle Biopsies

1. Five volunteers were studied before and after oral administration of NH4Cl (0.3 g/kg body wt.) given in order to create a moderate acidosis. 2. The quadriceps femoris muscles were stimulated electrically for 75 s and muscle biopsies for determination of pH and metabolite content were taken before, at the end of contraction and after 10 min in the recovery period. 3. Muscle pH at rest (mean 7.04) was not significantly decreased after acidification despite an extracellular pH decrease of 0.15 unit. 4. After contraction muscle pH was significantly lower after NH4Cl. Mean values before and after acidification were 6.70 and 6.54 respectively. 5. The buffer capacity calculated as the total capacity of the muscle to buffer H+ produced during the isometric contraction before and after NH4Cl ingestion was reduced from 68.6 sl to 54.5 sl. 6. The force produced by contracting muscle was significantly lower at the end of the contraction period after NH4Cl ingestion, 44.6% of initial compared with 55.4% without NH4Cl.

Measurement of leucine metabolism in man from a primed, continuous infusion of L-[1-3C]leucine

1980 ◽  
Vol 238 (5) ◽  
pp. E473-E479 ◽  
Author(s):  
D. E. Matthews ◽  
K. J. Motil ◽  
D. K. Rohrbaugh ◽  
J. F. Burke ◽  
V. R. Young ◽  
...  
Keyword(s):  
Steady State ◽  
Continuous Infusion ◽  
Co2 Production ◽  
Human Beings ◽  
Priming Dose ◽  
Leucine Metabolism ◽  
Kinetics Of ◽  
13Co2 Enrichment

Leucine metabolism in vivo can be determined from a primed, continuous infusion of L-[1-13C]leucine by measuring, at isotopic steady state, plasm [-13C]leucine enrichment, expired 13CO2 enrichment, and CO2 production rate. With an appropriate priming dose of L-[1-13C]leucine and NaH13CO3, isotopic steady state is reached in less than 2 h, and the infusion is completed in 4 h. The method can determine rates of leucine turnover, oxidation, and incorporation into protein with typical relative uncertainties of 2, 10, and 4%, respectively. The method requires no more than 1 ml of blood and uses stable isotope rather than radioisotope techniques. Thus, the method is applicable to studies of human beings of all ages. L-[1-13C]leucine may be infused with a second amino acid labeled with 15N for simultaneous determination of the kinetics of two amino acids.

Comparison of indirect calorimetry and a new breath 13C/12C ratio method during strenuous exercise

1992 ◽  
Vol 263 (1) ◽  
pp. E64-E71 ◽  
Author(s):  
J. A. Romijn ◽  
E. F. Coyle ◽  
J. Hibbert ◽  
R. R. Wolfe
Keyword(s):  
Indirect Calorimetry ◽  
Fat Oxidation ◽  
Substrate Oxidation ◽  
Co2 Production ◽  
Strenuous Exercise ◽  
Ratio Method ◽  
O2 Uptake ◽  
Underlying Assumption ◽  
Oxidation Rates

A new stable isotope method for the determination of substrate oxidation rates in vivo is described and compared with indirect calorimetry at rest and during high-intensity exercise (30 min at 80-85% maximal O2 uptake capacity) in six well-trained cyclists. This method uses the absolute ratios of 13C/12C in expired air, endogenous glucose, fat, and protein in addition to O2 consumption and is independent of CO2 production (VCO2). Carbohydrate and fat oxidation rates at rest, calculated by both methods, were not significantly different. During exercise the breath 13C/12C ratio increased and reached a steady state after 15-20 min. Carbohydrate oxidation rates during exercise were 39.4 +/- 5.2 and 41.7 +/- 5.7 mg.kg-1.min-1 [not significant (NS)], and fat oxidation rates were 7.3 +/- 1.3 and 6.9 +/- 1.2 mg.kg-1.min-1 (NS), using indirect calorimetry, and the breath ratio method, respectively. We conclude that the breath 13C/12C ratio method can be used to calculate substrate oxidation under different conditions, such as the basal state and exercise. In addition, the results obtained by this new method support the validity of the underlying assumption that indirect calorimetry regards VCO2 as a reflection of tissue CO2 production, during exercise in trained subjects, even up to 80-85% maximal O2 uptake.

Measurement of metabolic rate in hyperoxia

1981 ◽  
Vol 51 (3) ◽  
pp. 725-731 ◽  
Author(s):  
H. G. Welch ◽  
P. K. Pedersen
Keyword(s):  
Metabolic Rate ◽  
Submaximal Exercise ◽  
Co2 Production ◽  
O2 Uptake ◽  
Vo2 Max ◽  
Conventional Calculation ◽  
Mixing Chamber ◽  
Douglas Bag ◽  
Douglas Bag Method ◽  
Fick Equation

The conventional Douglas bag calculation for estimating O2 uptake (VO2) during exercise in normoxia and hyperoxia, VO2 = VE . (FIO2 . FEN2/FIN2 - FEO2), was tested against two other valid calculations: the Fick equation, VO2 = VI . FIO2 - VE . FEO2, and the equation VO2 = VI - VE - VCO2 (VE and VI are expired and inspired ventilation, respectively; FEO2 and FIO2 are expired and inspired O2 contents, respectively; FEN2 and FIN2 are expired and inspired N2 contents, respectively; and VCO2 is CO2 production.). These calculations are based on different assumptions, in part, and are affected to a varying degree of errors in volume or gas fraction measurements. With the conventional Douglas bag technique, we found evidence of an overestimate of VO2 during hyperoxia. After the introduction of a mixing chamber for sampling expired air, the means of the three methods were not significantly different. The variability among the methods was least with the conventional calculation but increased with higher O2 fractions. The average VO2 for submaximal exercise in hyperoxia was not significantly different from that of normoxia. VO2 max was significantly higher in hyperoxia. The increased variability of the Douglas bag method in hyperoxia may lead to overestimates of VO2 max unless special precautions are taken.

Regulation of fat-carbohydrate interaction in skeletal muscle during intense aerobic cycling

1993 ◽  
Vol 265 (6) ◽  
pp. E852-E859 ◽  
Author(s):  
D. J. Dyck ◽  
C. T. Putman ◽  
G. J. Heigenhauser ◽  
E. Hultman ◽  
L. L. Spriet
Keyword(s):  
Skeletal Muscle ◽  
Pyruvate Dehydrogenase ◽  
Saline Control ◽  
Elevated Plasma ◽  
O2 Uptake ◽  
Muscle Lactate ◽  
Acid Cycle ◽  
Glucose Fatty Acid Cycle ◽  
Male Subjects ◽  
Muscle Biopsies

Six male subjects received either a saline (control) or Intralipid infusion during 30 min rest and 15 min cycling at 85% maximal O2 uptake (VO2max) to examine the regulation of fat-carbohydrate interaction (glucose-fatty acid cycle) in skeletal muscle. Muscle biopsies were sampled immediately before and at 3 and 15 min of exercise in both trials. A muscle biopsy was also taken at -30 min rest in the Intralipid trial. Intralipid infusion significantly elevated plasma free fatty acids above control during rest (0.21 +/- 0.04 to 0.94 +/- 0.09 mM) and exercise (5 min: 1.27 +/- 0.15 mM; 15 min: 1.42 +/- 0.13 mM). Muscle glycogen degradation was significantly lower in the Intralipid trial (109.7 +/- 29.3 vs. 194.7 +/- 32.1 mmol/kg dry muscle). Muscle lactate accumulation after 15 min was similar in both trials (control, 60.7 +/- 12.2 and Intralipid, 60.9 +/- 12.4 mmol/kg dry muscle). Muscle citrate increased at rest during Intralipid (0.32 +/- 0.06 to 0.58 +/- 0.06 mmol/kg dry muscle) but was not different between trials at 3 min (control, 0.73 +/- 0.07 and Intralipid, 0.68 +/- 0.06 mmol/kg dry muscle) and 15 min of cycling. Resting acetyl-CoA was unaffected by Intralipid and increased similarly in both trials at 3 min of cycling (control, 59.0 +/- 10.3 and Intralipid, 50.7 +/- 13.6 mumol/kg dry muscle) and remained unchanged at 15 min. Pyruvate dehydrogenase activity increased five- to sevenfold during exercise and was similar in both trials (15 min: control, 2.42 +/- 0.30 and Intralipid, 2.79 +/- 0.41 mmol.min-1 x kg wet wt-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose and oxygen metabolism in the fetal foal during late gestation

1995 ◽  
Vol 269 (6) ◽  
pp. R1455-R1461 ◽  
Author(s):  
A. L. Fowden ◽  
M. Silver
Keyword(s):  
Glucose Uptake ◽  
Glucose Utilization ◽  
Oxygen Metabolism ◽  
Endogenous Glucose Production ◽  
Late Gestation ◽  
Co2 Production ◽  
O2 Uptake ◽  
Fed State ◽  
Glucose Carbon ◽  
Lactate Uptake

With the use of [U-14C]glucose tracer methodology, the rates of umbilical uptake, utilization, oxidation, and production of glucose were determined in nine chronically catheterized fetal foals in the fed state between 268 and 325 days of gestation (term approximately 335 days). At the same time, the rates of umbilical O2 and lactate uptake were measured in all nine fetuses by Fick principle. The mean fetal rates of umbilical glucose uptake, glucose utilization, and CO2 production from glucose carbon were 36.9 +/- 2.5, 36.4 +/- 1.7, and 117.7 +/- 17.4 mumol.min-1.kg fetal body wt-1, respectively (n = 9). Endogenous glucose production was therefore negligible in the fetal foal in the fed state. Production of CO2 from glucose carbon accounted for 40.9 +/- 6.5% of the umbilical O2 uptake, which averaged 292 +/- 15 mumol.min-1.kg-1 (n = 9). No significant changes in fetal glucose or O2 metabolism were observed with increasing gestational age. The rates of umbilical glucose uptake, glucose utilization, and CO2 production from glucose carbon (P < 0.01), but not the rate of umbilical O2 uptake (P > 0.05), were positively correlated with the fetal blood glucose level. There was a significant umbilical lactate uptake in the fetuses older than 290 days (12.3 +/- 4.1 mumol.min-1.kg-1, n = 5, P < 0.05) but not in the younger animals (6.2 +/- 9.6 mumol.min-1.kg-1, n = 4, P > 0.05). Hence, glucose is used for both oxidative and nonoxidative metabolism in utero and is a major, although not the sole, oxidative substrate in the fetal foal during late gestation.

The effect of magnesium oxide supplementation on muscle glycogen metabolism before and after exercise and at slaughter in sheep

2001 ◽  
Vol 52 (7) ◽  
pp. 723 ◽  
Author(s):  
G. E. Gardner ◽  
R. H. Jacob ◽  
D. W. Pethick
Keyword(s):  
Magnesium Oxide ◽  
Muscle Glycogen ◽  
Glycogen Metabolism ◽  
Post Exercise ◽  
Exercise Regimen ◽  
Before And After ◽  
Series Of Experiments ◽  
Glycogen Repletion ◽  
Exercise Muscle ◽  
Muscle Biopsies

This study was a series of experiments designed to test the influence of supplemental magnesium oxide (MgO) on muscle glycogen concentration in sheep exposed to stress (exercise) and the commercial slaughter process, and to test the effectiveness of this supplement in the commercial scenario. In Expt 1, Merino wethers maintained on a mixed ration (metabolisable energy 11 MJ/kg and crude protein 16.3% in DM) were supplemented with MgO at the rate of 0%, 0.5%, or 1% of their ration for 10 days prior to a single bout of exercise and for 10 days prior to slaughter at a commercial abattoir. The exercise regimen consisted of 4 intervals of 15 min, with muscle biopsies taken by biopsy drill from the m. semimembranosis (SM) and m. semitendinosis (ST) pre-exercise and immediately post-exercise, and at 36 and 72 h post-exercise. Muscle biopsies were also taken 1 week prior to slaughter from the SM and ST, with further samples taken approximately 30 min post-slaughter. Ultimate pH (pHu) of the SM, ST, and m. longissimus dorsi (LD) was measured 48 h after slaughter. Sheep supplemented with MgO lost less muscle glycogen in the ST during exercise, and repleted more muscle glycogen in the SM during the post-exercise repletion phase, than unsupplemented sheep. The supplemented animals also had higher muscle glycogen concentrations in the ST at slaughter. In Expt 2, MgO was administered to Merino wether lambs for 4 days prior to slaughter in the form of a water-borne slurry at a rate equivalent to 1% of their ration. This treatment resulted in significantly reduced muscle glycogen concentrations in both the SM and ST at slaughter. In Expts 3–5, MgO was used as an ‘in-feed’ supplement in the commercial scenario. In each case, slaughter-weight Merino lambs were supplemented with MgO at the rate of 1% of their ration for 4 days prior to commercial slaughter. Positive responses were seen in 2 of the 3 experiments, with increased glycogen concentrations and a reduced pHu. The animals that demonstrated no response to MgO had the lowest pHu after slaughter, suggesting a minimal stress load, thus providing very little scope for an effect of the MgO supplement. We conclude that MgO can reduce the effects of exercise, leading to a subsequent reduction in glycogen loss, and an increase in the rate of glycogen repletion in skeletal muscle following exercise. The results support MgO supplementation as a viable option for reducing the stress associated with commercial slaughter.

O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate

1993 ◽  
Vol 75 (2) ◽  
pp. 755-762 ◽  
Author(s):  
T. J. Barstow ◽  
R. Casaburi ◽  
K. Wasserman
Keyword(s):  
Blood Lactate ◽  
Time Constant ◽  
Exercise Intensity ◽  
Power Output ◽  
Cycle Ergometer ◽  
O2 Uptake ◽  
Ergometer Exercise ◽  
Lactate Levels ◽  
Power Outputs ◽  
O2 Deficit

The dynamic responses of O2 uptake (VO2) to a range of constant power output levels were related to exercise intensity [as percent maximal VO2 and as below vs. above lactic acid threshold (LAT)] and to the associated end-exercise lactate in three groups of subjects: group I, untrained subjects performing leg cycle ergometer exercise; group II, the same subjects performing arm cycle exercise; and group III, trained cyclists performing leg cycle ergometer exercise. Responses were described by a double-exponential equation, with each component having an independent time delay, which reduced to a monoexponential description for moderate (below-LAT) exercise. When a second exponential component to the VO2 response was present, it did not become evident until approximately 80–100 s into exercise. An overall time constant (tau T, determined as O2 deficit for the total response divided by net end-exercise VO2) and a primary time constant (tau P, determined from the O2 deficit and the amplitude for the early primary VO2 response) were compared. The tau T rose with power output and end-exercise lactate levels, but tau P was virtually invariant, even at high end-exercise lactate levels. Moreover the gain of the primary exponential component (as delta VO2/delta W) was constant across power outputs and blood lactate levels, suggesting that the primary VO2 response reflects a linear system, even at higher power outputs. These results suggest that elevated end-exercise lactate is not associated with any discernible slowing of the primary rise in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

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