Net O2, CO2, lactate, and acid exchange by muscle during progressive working contractions

1984 ◽  
Vol 56 (1) ◽  
pp. 161-165 ◽  
Author(s):  
S. J. Chirtel ◽  
R. W. Barbee ◽  
W. N. Stainsby
Keyword(s):  
Acid Output ◽  
Motor Nerve ◽  
Venous Blood ◽  
Work Rate ◽  
O2 Uptake ◽  
Plantaris Muscle ◽  
Independent Variables ◽  
Co2 Output ◽  
Lactate Output ◽  
Acid Exchange

The net O2 uptake (VO2), CO2 output (VCO2), lactate output (L), and non-CO2 acid output (HA) by the gastrocnemius-plantaris muscle group of the dog were measured during progressively loaded isotonic tetanic contractions. Shortening during the 1/s contractions was maintained constant as load was increased by raising the stimulus voltage applied to the motor nerve. Contractions at each load continued for 5 min with two arterial and four venous blood samples obtained during the last minute at each load. Work rate (W) during the contractions was calculated from the load and the shortening. The VO2 increased linearly with time and W. The VCO2 generally followed VO2 with a modest lag during the first two work periods. L increased with time, W, and VO2. Maximal L was lower than that seen during repetitive maximal twitch contractions. HA also increased with time, W, and VO2 and was much larger than L at the higher work rates. It is concluded that L and HA are independent variables during progressive working contractions, as they were during repetitive twitch contractions. Both L and HA patterns may be explained as summations of the respective exchanges of L and HA with time by sequentially recruited groups of muscle fibers.

Plasma catecholamines and their effect on blood lactate and muscle lactate output

1984 ◽  
Vol 57 (2) ◽  
pp. 321-325 ◽  
Author(s):  
W. N. Stainsby ◽  
C. Sumners ◽  
G. M. Andrew
Keyword(s):  
Venous Blood ◽  
Plasma Catecholamines ◽  
Muscle Group ◽  
O2 Uptake ◽  
Plantaris Muscle ◽  
Muscle Lactate ◽  
Blood Samples ◽  
Lactate Output ◽  
Before And After

This study was designed to test the hypothesis that epinephrine (E) and norepinephrine (NE) increase net muscle lactate output (L) of in situ gastrocnemius-plantaris muscle group during contractions. Plasma [E] and [NE] were measured before and after the surgical isolation of the muscle and at 10-min intervals during the 60-min experiments. Plasma [E] and [NE] were increased threefold by intravenous infusions of E (n = 3) or NE (n = 3) at a rate of 1.5 micrograms X kg body wt-1 X min-1. Arterial and muscle venous blood samples for O2 and lactate concentrations were also obtained. The infusions began at min 11 and repetitive isometric contractions (4 tw/s) began at min 31. The presurgery plasma [E] and [NE] averaged 0.34 and 0.52 ng/ml, respectively, and rose to 1.12 and 1.19 ng/ml 10 min after surgery. Arterial and venous lactate concentrations (CaL and CvL) increased continuously during E infusion but remained constant during NE infusion. Maximal L during the first 10 min of contractions was significantly increased compared with an identical earlier study without infusions. O2 uptake was not changed by the infusions. It is concluded that E causes CaL to rise and that both E and NE increase maximal net lactate output during contractions.

Effects of ischemic and hypoxic hypoxia on VO2 and lactic acid output during tetanic contractions

1990 ◽  
Vol 68 (2) ◽  
pp. 574-579 ◽  
Author(s):  
W. N. Stainsby ◽  
W. F. Brechue ◽  
D. M. O'Drobinak ◽  
J. K. Barclay
Keyword(s):  
Lactic Acid ◽  
Mechanical Performance ◽  
Acid Output ◽  
Muscle Group ◽  
O2 Uptake ◽  
Major Goal ◽  
Plantaris Muscle ◽  
Rapid Reduction ◽  
Ischemic Hypoxia ◽  
Co2 Output

We measured O2 uptake (VO2), CO2 output (VCO2), and net lactic acid output (L) during a 30-min period of repetitive 1/s isotonic tetanic contractions of the dog gastrocnemius-plantaris muscle group. The conditions were modest ischemic hypoxia (ischemia), hypoxia hypoxia (hypoxia), and free-flow normoxia (control). The major goal was to assess the effects of these perturbations on L during contractions. Ischemia and hypoxia were initiated just before the start of the contractions and at minute 7 of contractions in separate groups of experiments. Whenever applied, both ischemia and hypoxia reduced VO2 compared with the control values. When ischemia was initiated at the start of contractions, L was reduced transiently compared with the controls. When ischemia began at minute 7, L was increased modestly but transiently compared with the controls. When hypoxia was initiated at the start of contractions, L was increased during the entire period of contractions. The L pattern was the same as in the controls, rising to a maximal value at 3 min and declining steadily to a lower value at 30 min. When hypoxia began at minute 7, L declined initially at a slower rate than it did in the controls and was thereby elevated above the controls from 9 to 30 min. Ischemia was associated with a more rapid reduction in mechanical performance than hypoxia. The data suggest that the mechanisms of the decreased mechanical performance and VO2 are different for ischemia and hypoxia.

Lactate accumulation during incremental exercise with varied inspired oxygen fractions

1983 ◽  
Vol 55 (4) ◽  
pp. 1134-1140 ◽  
Author(s):  
M. C. Hogan ◽  
R. H. Cox ◽  
H. G. Welch
Keyword(s):  
Cycle Ergometer ◽  
Work Rate ◽  
O2 Uptake ◽  
Lactate Accumulation ◽  
Oxygen Fraction ◽  
Co2 Output ◽  
Break Points ◽  
Expired Gas ◽  
Gas Fractions ◽  
Inspired Oxygen

Six subjects pedaled a stationary cycle ergometer to exhaustion on three separate occasions while breathing gas mixtures of 17, 21, or 60% O2 in N2. Each subject rode for 3 min at work rates of 60, 90, 105 W, followed by 15-W increases every 3 min until exhaustion. Inspired and expired gas fractions, ventilation (V), heart rate, and blood lactate were measured. O2 uptake (VO2) and CO2 output (VCO2) were calculated for the last minute of each work rate; blood samples were drawn during the last 5 s. “Break points” for lactate, V, VCO2, V/VO2, and expired oxygen fraction (FEO2) were mathematically determined. VO2 was not significantly different at any work rate among the three different conditions. Nor did maximal VO2 differ significantly among the three treatments (P greater than 0.05). Lactate concentrations were significantly lower during hyperoxia and significantly higher during hypoxia compared with normoxia. Lactate values at exhaustion were not significantly different among the three treatments. Four subjects were able to work for a longer period of time during hyperoxic breathing. The variations in lactate accumulation as reported in this study cannot be explained on the basis of differences in VO2. The results of this research lend support to the hypothesis that differences in the performance of subjects breathing altered fractions of inspired oxygen may be caused by differences in lactate (or H+) accumulation.

Effects of adrenergic agonists and antagonists on muscle O2 uptake and lactate metabolism

1987 ◽  
Vol 62 (5) ◽  
pp. 1845-1851 ◽  
Author(s):  
W. N. Stainsby ◽  
C. Sumners ◽  
P. D. Eitzman
Keyword(s):  
Adrenergic Receptor ◽  
Acid Output ◽  
Muscle Blood Flow ◽  
Lactate Concentration ◽  
Constant Load ◽  
Lactate Metabolism ◽  
O2 Uptake ◽  
Plantaris Muscle ◽  
Epinephrine Infusion ◽  
Arterial Lactate

To investigate adrenergic receptor-mediated responses in dog gastrocnemius-plantaris muscle, several catecholamine agonists, isoproterenol, epinephrine, norepinephrine, and phenylephrine, and two antagonists, propranolol and phenoxybenzamine, were given during repetitive, isotonic, tetanic contractions. The response variables that were measured were muscle blood flow, shortening during constant load contractions, and arterial and venous O2 and lactate concentrations. The calculated variables were O2 uptake (VO2), net lactic acid output (L), and power output. In the control experiments, the contractions increased VO2 to approximately 50 times rest by 2 min. Thereafter, shortening, work, and VO2 declined together by 17% at 30 min, indicating muscle fatigue. L increased rapidly to nearly 0.8 mumol X g-1 X min-1 by 2 min, declined to 0.3–0.4 mumol X g-1 X min-1 by 7 min, and was like rest at 15, 22.5, and 30 min. The arterial lactate concentration rose steadily from rest to 30 min of contractions. Epinephrine infusion stopped the decline of VO2 during the contractions, but this effect was not observed with the other agonists. Propranolol decreased VO2 compared with controls at 22.5 and 30 min of contractions. Phenoxybenzamine decreased VO2 compared with controls at all times during contraction, and the decline with time was present. Coinfusion of epinephrine with propranolol reduced the decline in VO2 observed with propranolol alone. Both epinephrine and isoproterenol increased L compared with controls. This epinephrine response was antagonized by propranolol but enhanced by phenoxybenzamine. Both isoproterenol and epinephrine infusions increased arterial lactate concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of reduced O2 delivery with anemia, hypoxia, or ischemia on peak VO2 and force in skeletal muscle

1993 ◽  
Vol 74 (1) ◽  
pp. 186-191 ◽  
Author(s):  
S. L. Dodd ◽  
S. K. Powers ◽  
E. Brooks ◽  
M. P. Crawford
Keyword(s):  
Venous Blood ◽  
Random Order ◽  
O2 Uptake ◽  
Plantaris Muscle ◽  
Experimental Conditions ◽  
Tension Development ◽  
O2 Concentration ◽  
O2 Delivery ◽  
Stimulation Pattern

This investigation was designed to describe alterations in O2 uptake (VO2) and tension development in a contracting in situ gastrocnemious-plantaris muscle preparation during three conditions of reduced O2 delivery [arterial O2 concentration X blood flow (Q)]. The three conditions, hypoxemia (H), ischemia (I), and anemia (A), were matched for O2 delivery. A normoxic normal flow condition was also utilized for comparison. H was produced by respiring the animals with 9% O2 in N2; I was produced by lowering Q, and A was produced by hemodilution with 6% dextran. The stimulation pattern for the isometric tetanic contractions used was 1 train/s, and each train was 200 ms, 70 Hz, and 6 V. The muscle was maximally contracted during each of the experimental conditions, and the conditions were administered in random order. In each bout the contractions continued for 5 min with 30 min of rest between bouts. Samples of arterial and muscle venous blood were obtained during the last 30 s of each bout. VO2 during I (125 ml.kg-1.min-1) was less than during N (145 ml.kg-1.min-1; P < 0.05) and greater than during H or A (104 and 101 ml.kg-1.min-1, respectively; P < 0.05). Venous PO2 (PVO2) was significantly lower during H (17.1 Torr) compared with the other conditions; no differences existed between N, I, and A (26.8, 26.0, and 28.1 Torr, respectively). Tension development was reduced by the reduction of O2 delivery during I, H, and A compared with N. Tension developed among the reduced O2 delivery groups was not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of beta-adrenergic blockade on respiratory and metabolic responses to exercise

1981 ◽  
Vol 51 (4) ◽  
pp. 788-793 ◽  
Author(s):  
O. P. Twentyman ◽  
A. Disley ◽  
H. R. Gribbin ◽  
K. G. Alberti ◽  
A. E. Tattersfield
Keyword(s):  
Venous Blood ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Adrenergic Blockade ◽  
Early Exercise ◽  
Co2 Output ◽  
Initial Reduction ◽  
Progressive Exercise ◽  
Constant Work Rate

The responses to oral propranolol (80 mg) and placebo were compared in normal subjects during three studies on a cycle ergometer (progressive exercise and two 5-min constant work rate studies at 50 and 70% maximum). Heart rate (HR), ventilation (VE), CO2 output (VCO2) and O2 uptake (VO2) were measured in each study and metabolites in venous blood in the 70% study. Propranolol reduced HR in all studies and endurance time during progressive exercise. During constant-work-rate exercise the changes with propranolol depended on time and work rate. At 50% max, VO2, VCO2, and VE were reduced in early exercise but were similar by min 5. At 70% max, VO2 and VCO2 were again lower initially with propranolol but then rose more rapidly. By min 5 VE was greater with propranolol, coinciding with a rapidly rising venous lactate. We interpret the initial reduction in VO2 and VCO2 to reduced cardiac output and muscle perfusion with propranolol. The resulting increase in anaerobic metabolism during heavy exercise would explain the increased VE at min 5. The metabolic data are compatible with glycogen being the predominant muscle fuel.

Derivation of CO2 output from oscillations in arterial pH

1987 ◽  
Vol 62 (3) ◽  
pp. 880-891 ◽  
Author(s):  
B. A. Cross ◽  
R. P. Stidwill ◽  
K. D. Leaver ◽  
S. J. Semple
Keyword(s):  
Maximum Rate ◽  
Venous Blood ◽  
Co2 Flux ◽  
Limited Range ◽  
Co2 Production ◽  
Mixed Venous Blood ◽  
Co2 Partial Pressure ◽  
Co2 Output ◽  
Arterial Ph ◽  
Small Rise

Theory predicts that the rate of rise of the oscillation in arterial CO2 partial pressure (PaCO2) is linearly dependent on CO2 flux from venous blood to alveolar gas. We have measured, in the anesthetized cat, CO2 output (VCO2) and oscillations in arterial pH. The pH signal was differentiated to give the maximum rate of fall of pH on the downstroke of the oscillation (dpH/dt decreases max). Since oscillations in pH are due to oscillations in arterial PCO2, dpH/dt decreases max was considered to be equivalent to the maximum rate of rise of the PCO2 oscillation. VCO2 was increased by ventilating the intestines with CO2 and by the intra-arterial infusion of 2,4-dinitrophenol. VCO2 was decreased by filling the intestines with isotonic tris(hydroxymethyl)methylamine buffer. The maximum range of VCO2 covered was 7.8–51 ml/min, and the mean range was from 13.6 +/- 1.3 to 29.7 +/- 1.6 (SE) ml/min. Although CO2 loading produced a small rise and CO2 unloading a small fall in mean PaCO2, the changes were not statistically significant, so that overall the response was close to isocapnia. Over the limited range of VCO2 studied there was a highly significant linear association between dpH/dt decreases max and VCO2 which supports the contention that the slope of the upstroke of the PaCO2 oscillation is determined by the CO2 flux from mixed venous blood to alveolar gas. As such this slope is a potential chemical signal linking ventilation to CO2 production.

Blood flow elevation increases VO2 maximum during repetitive tetanic contractions of dog muscle in situ

1993 ◽  
Vol 74 (4) ◽  
pp. 1499-1503 ◽  
Author(s):  
W. F. Brechue ◽  
B. T. Ameredes ◽  
G. M. Andrew ◽  
W. N. Stainsby
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Power Production ◽  
Arterial Supply ◽  
O2 Uptake ◽  
Plantaris Muscle ◽  
Control Series ◽  
Flow Through ◽  
Series Of Experiments

Blood flow through the gastrocnemius-plantaris muscle of the dog in situ was increased by a pump in the arterial supply during a 30-min period of 1/s isotonic tetanic contractions. Compared with a control series of experiments with normoxemia and spontaneous flow, the pump increased flow 84%, from 1.51 +/- 0.08 to 2.78 +/- 0.15 ml.g-1.min-1. The perfusion pressure was increased from 125 to 196 mmHg. The pump hyperemia increased maximal O2 uptake (VO2) at 5 min of contractions by 31%, from 8.97 +/- 0.44 to 12.89 +/- 0.30 mumol.g-1.min-1. The extraction was decreased, and venous PO2 (PVO2) was increased. Fatigue, measured as a drop in power production from the highest level at 10 s to 30 min, was 49% during pump hyperemia and 54% in the control conditions. VO2 decreased 30% from the 5-min value to the 30-min value with pump hyperemia and 28% over the same time in the control conditions. At maximal VO2, the ratio VO2/PVO2 was increased by pump hyperemia compared with control conditions, suggesting an increased O2 diffusing conductance of the muscles. We conclude that the elevated perfusion pressure of pump hyperemia increased flow to raise maximal VO2 mainly in areas of the muscle that had restricted flow under control conditions.

Maximal O2 uptake of in situ dog muscle during acute hypoxemia with constant perfusion

1990 ◽  
Vol 69 (2) ◽  
pp. 570-576 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
P. D. Wagner ◽  
J. B. West
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Peripheral Tissue ◽  
Diffusing Capacity ◽  
O2 Uptake ◽  
Lactate Output ◽  
O2 Diffusion ◽  
Arterial Po2 ◽  
Different Levels

We investigated the relationships among maximal O2 uptake (VO2max), effluent venous PO2 (PvO2), and calculated mean capillary PO2 (PCO2) in isolated dog gastrocnemius in situ as arterial PO2 (PaO2) was progressively reduced with muscle blood flow held constant. The hypothesis that VO2max is determined in part by peripheral tissue O2 diffusion predicts proportional declines in VO2max and PCO2 if the diffusing capacity of the muscle remains constant. The inspired O2 fraction was altered in each of six dogs to produce four different levels of PaO2 [22 +/- 2, 29 +/- 1, 38 +/- 1, and 79 +/- 4 (SE) Torr]. Muscle blood flow, with the circulation isolated, was held constant at 122 +/- 15 ml.100 g-1.min-1 while the muscle worked maximally (isometric twitches at 5-7 Hz) at each of the four different values of PaO2. Arterial and venous samples were taken to measure lactate, pH, PO2, PCO2, and muscle VO2. PCO2 was calculated using Fick's law of diffusion and a Bohr integration procedure. VO2max fell progressively (P less than 0.01) with decreasing PaO2. The decline in VO2max was proportional (R = 0.99) to the fall in both muscle PvO2 and calculated PCO2 while the calculated muscle diffusing capacity was not different among the four conditions. Fatigue developed more rapidly with lower PaO2, although lactate output from the muscle was not different among conditions. These results are consistent with the hypothesis that resistance to O2 diffusion in the peripheral tissue may be a principal determinant of VO2max.

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