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.

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)

Muscle metabolism during exercise in the heat in unacclimatized and acclimatized humans

1985 ◽  
Vol 59 (5) ◽  
pp. 1350-1354 ◽  
Author(s):  
D. S. King ◽  
D. L. Costill ◽  
W. J. Fink ◽  
M. Hargreaves ◽  
R. A. Fielding
Keyword(s):  
Muscle Glycogen ◽  
Respiratory Exchange Ratio ◽  
Muscle Metabolism ◽  
Submaximal Exercise ◽  
Intense Exercise ◽  
O2 Uptake ◽  
Heat Acclimatization ◽  
Fuel Selection ◽  
Muscle Ph ◽  
Male Subjects

The effect of heat acclimatization on aerobic exercise tolerance in the heat and on subsequent sprint exercise performance was investigated. Before (UN) and after (ACC) 8 days of heat acclimatization, 10 male subjects performed a heat-exercise test (HET) consisting of 6 h of intermittent submaximal [50% of the maximal O2 uptake] exercise in the heat (39.7 degrees C dB, 31.0% relative humidity). A 45-s maximal cycle ride was performed before (sprint 1) and after (sprint 2) each HET. Mean muscle glycogen use during the HET was lower following acclimatization [ACC = 28.6 +/- 6.4 (SE) and UN = 57.4 +/- 5.1 mmol/kg; P less than 0.05]. No differences were noted between the UN and ACC trials with respect to blood glucose, lactate (LA), or respiratory exchange ratio. During the UN trial only, total work output during sprint 2 was reduced compared with sprint 1 (24.01 +/- 0.80 vs. 21.56 +/- 1.18 kJ; P less than 0.05). This reduction in sprint performance was associated with an attenuated fall in muscle pH following sprint 2 (6.86 vs. 6.67, P less than 0.05) and a reduced accumulation of LA in the blood. These data indicate that heat acclimatization produced a shift in fuel selection during submaximal exercise in the heat. The observed sparing of muscle glycogen may be associated with the enhanced ability to perform highly intense exercise following prolonged exertion in the heat.

Exercise-induced hypercapnia in the horse

1989 ◽  
Vol 67 (5) ◽  
pp. 1958-1966 ◽  
Author(s):  
W. M. Bayly ◽  
D. R. Hodgson ◽  
D. A. Schulz ◽  
J. A. Dempsey ◽  
P. D. Gollnick
Keyword(s):  
Blood Gases ◽  
Co2 Production ◽  
Heavy Exercise ◽  
Severe Metabolic Acidosis ◽  
Short Term ◽  
Flow Rates ◽  
Thoroughbred Horses ◽  
Arterial Ph ◽  
Exercise Induced ◽  
Arterial Po2

The effects of exercise intensity and duration on blood gases in thoroughbred horses were studied to characterize the apparent exercise-induced failure in pulmonary gas exchange that occurs in these animals. In response to 2 min of exercise, arterial CO2 tension (PaCO2) decreased in mild and moderate exercise, returned to normocapnic levels in moderate to heavy exercise, and rose 5-10 Torr above resting values during very heavy exercise when CO2 production (VCO2) exceeded 20 times the resting value, and mixed venous CO2 tension approximated 140 Torr. Exercise-induced hypoxemia occurred at the onset of heavy exercise and was associated with the absence of a hyperventilatory response and an alveolar-arterial PO2 difference that increased four to six times above rest with very heavy exercise. PaCO2 was related to VCO2 but not fb, as changes in breathing frequency (fb) of 8-20 breaths/min at comparable VCO2 did not affect PaCO2. Prolonging very heavy exercise from 2 to 4 min caused a severe metabolic acidosis (arterial pH less than 7.15) and hypoxemia was maintained; however, CO2 was no longer retained, as PaCO2 gradually fell to below resting levels, due to an increased tidal volume at constant fb. We conclude that a truly compensatory hyperventilation to very heavy exercise in the horse is not achieved because of the excessive volumes and flow rates required by their extraordinarily high VCO2 and VO2. On the other hand, the frank CO2 retention during short-term high-intensity exercise occurs even though the horse is not apparently mechanically obligated to tolerate it.

Dietary effects on exercising muscle metabolism and performance by 31P-MRS

1994 ◽  
Vol 77 (3) ◽  
pp. 1108-1115 ◽  
Author(s):  
D. E. Larson ◽  
R. L. Hesslink ◽  
M. I. Hrovat ◽  
R. S. Fishman ◽  
D. M. Systrom
Keyword(s):  
Minute Ventilation ◽  
Muscle Metabolism ◽  
Exercise Duration ◽  
Quadriceps Muscle ◽  
Peak Exercise ◽  
Crossover Fashion ◽  
Resonance Spectroscopy ◽  
Phosphorylation Potential ◽  
Beneficial Effects ◽  
Muscle Ph

To determine how diet modulates short-term exercise capacity, skeletal muscle pH and bioenergetic state were examined by 31P-magnetic resonance spectroscopy in nine healthy volunteers. Subjects performed incremental quadriceps exercise to exhaustion after 5 days of high-carbohydrate (HCHO) or high-fat (HFAT) diet randomly assigned in crossover fashion and separated by a 2.5-day period of ad libitum mixed diet. Simultaneous measurements were made of pulmonary gas exchange, minute ventilation, and quadriceps muscle pH and phosphorylation potential. At rest and peak exercise, respiratory exchange ratio and minute ventilation were higher after HCHO than after HFAT (P < 0.05), reflecting greater CHO utilization. Peak O2 consumption (VO2) was not increased after HCHO (P > 0.05), but exercise duration was (339 +/- 34 s for HCHO vs. 308 +/- 25 s for HFAT; P < 0.05). HCHO was associated with a blunted early fall of phosphocreatine (PCr)/Pi vs. VO2 (-4.1 +/- 0.7 x 10(-2) min/ml for HCHO vs. -5.6 +/- 1.2 x 10(-2) min/ml for HFAT; P < 0.05). On both study days, the slope of PCr/Pi vs. VO2, before and after the PCr threshold, was correlated with exercise time. The results suggest that a diet rich in CHO improves exercise efficiency through beneficial effects on intracellular phosphorylation potential.

Respiratory, Ventilatory, Acid-Base and Ionoregulatory Physiology of the White Sucker Catostomus Commersoni: The Influence of Hyperoxia

1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Blood Gases ◽  
Catostomus Commersoni ◽  
Acid Base ◽  
Aortic Blood ◽  
Respiratory Parameters ◽  
Arterial Ph ◽  
O2 Extraction ◽  
Acid Base Status ◽  
Aortic Blood Pressure

Blood gases, acid-base status, plasma ions, respiration, ventilation and cardiovascular function were measured in white suckers, using standard cannulation methods. Basic respiratory parameters under normoxia were compared to those in the active, pelagic rainbow trout and in other benthic teleosts. Sustained environmental hyperoxia (350–550 torr) increased arterial O2 (102–392 torr) and venous O2 (17–80 torr) tensions so that blood O2 transport occurred entirely via physical solution. Dorsal aortic blood pressure and heart rate fell, the latter due to an increase in vagal tone. Ventilation volume declined markedly (by 50%) due to a decrease in ventilatory stroke volume, but absolute O2 extraction rose so that O2 consumption was unaffected. While the preceding effects were stable with time, arterial and venous CO2 tensions approximately doubled within 4 h, and continued to increase gradually thereafter. This CO2 retention caused an acidosis (7.993–7.814) which was gradually compensated by an accumulation of plasma [HCO3−]. However, even after 72 h, arterial pH remained significantly depressed by 0.10 units. The gradual rise in plasma [HCO3−] was accompanied by a progressive fall in both [Na+] and [Cl−]; [K+] and [Ca2+] remained unchanged. The responses of the sucker to hyperoxia are compared to those of the rainbow trout.

Ventilatory responses to the metabolic acidosis of treadmill and cycle ergometry

1976 ◽  
Vol 40 (6) ◽  
pp. 864-867 ◽  
Author(s):  
S. N. Koyal ◽  
B. J. Whipp ◽  
D. Huntsman ◽  
G. A. Bray ◽  
K. Wasserman
Keyword(s):  
Metabolic Acidosis ◽  
Treadmill Exercise ◽  
Cycle Ergometer ◽  
Cycle Ergometry ◽  
O2 Uptake ◽  
Ventilatory Responses ◽  
Arterial Ph ◽  
Ergometer Exercise ◽  
Type Of Exercise ◽  
Relationship Of

Ventilation and acid-base responses were studied at comparable levels of O2 uptake during cycle ergometer and treadmill exercise, to determine the extent to which the type of exercise affects these responses. Twenty male subjects performed 50-, 100-, and 150-W cycle ergometer exercise and three work rates of similar O2 uptake on a treadmill. At comparable oxygen uptakes, arterial lactate and VE were higher and arterial pH and bicarbonate were lower for cycle ergometer than treadmill exercise. These differences could be accounted for by the greater degree of metabolic acidosis during cycle ergometer work. The increment in VE over that predicted (from an extrapolation of the linear relationship of the VE-VO2 relationship for low work rates) was linearly related to the decrease in arterial bicarbonate; VE was increased by approximately 4 1/min for each meq/1 of bicarbonate decrease for both treadmill and cycle ergometry.

Pulmonary gas exchange in humans during exercise at sea level

1986 ◽  
Vol 60 (5) ◽  
pp. 1590-1598 ◽  
Author(s):  
M. D. Hammond ◽  
G. E. Gale ◽  
K. S. Kapitan ◽  
A. Ries ◽  
P. D. Wagner
Keyword(s):  
Gas Exchange ◽  
Sea Level ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
O2 Uptake ◽  
Heavy Exercise ◽  
Blood Temperature ◽  
O2 Diffusion

Previous studies have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during exercise at simulated altitude and suggested that similar changes could occur even at sea level. We used the multiple-inert gas-elimination technique to further study gas exchange during exercise in healthy subjects at sea level. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate, minute ventilation, respiratory rate, and blood temperature were recorded at rest and during steady-state exercise in the following order: rest, minimal exercise (75 W), heavy exercise (300 W), heavy exercise breathing 100% O2, repeat rest, moderate exercise (225 W), and light exercise (150 W). Alveolar-to-arterial O2 tension difference increased linearly with O2 uptake (VO2) (6.1 Torr X min-1 X 1(-1) VO2). This could be fully explained by measured VA/Q inequality at mean VO2 less than 2.5 l X min-1. At higher VO2, the increase in alveolar-to-arterial O2 tension difference could not be explained by VA/Q inequality alone, suggesting the development of diffusion limitation. VA/Q inequality increased significantly during exercise (mean log SD of perfusion increased from 0.28 +/- 0.13 at rest to 0.58 +/- 0.30 at VO2 = 4.0 l X min-1, P less than 0.01). This increase was not reversed by 100% O2 breathing and appeared to persist at least transiently following exercise. These results confirm and extend the earlier suggestions (8, 21) of increasing VA/Q inequality and O2 diffusion limitation during heavy exercise at sea level in normal subjects and demonstrate that these changes are independent of the order of performance of exercise.

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.

MUSCLE SURFACE pH: A NEW PARAMETER IN THE MONITORING OF THE CRITICALLY ILL CHILD

PEDIATRICS ◽  
1971 ◽  
Vol 47 (5) ◽  
pp. 880-885
Author(s):  
Robert M. Filler ◽  
John B. Das
Keyword(s):  
Critically Ill ◽  
Ph Monitoring ◽  
Vital Signs ◽  
Tissue Perfusion ◽  
Clinical Situation ◽  
Clinical Findings ◽  
Surface Ph ◽  
Arterial Ph ◽  
Muscle Ph ◽  
Critically Ill Child

In three severely ill infants, muscle surface pH was recorded continuously with a new miniaturized pH electrode for periods up to 100 hours. The clinical findings correlate with experimental results and indicate that muscle pH is a reflection of both arterial pH and the adequacy of tissue perfusion. Since muscle pH changes often precede changes in vital signs and arterial pH, muscle pH monitoring may provide the earliest warning of a deteriorating clinical situation. Although the present clinical experience is small, the findings appear to justify further trials with this method of monitoring sick infants.

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