Relative Flow-Time Relationships in Single Breaths Recorded After Treadmill Exercise in Thoroughbred Horses

2007 ◽  
Vol 27 (8) ◽  
pp. 362-368 ◽  
Author(s):  
K. Kusano ◽  
R.A. Curtis ◽  
C.A. Goldman ◽  
D.L. Evans
1946 ◽  
Vol 19 (4) ◽  
pp. 1092-1098
Author(s):  
L. H. Cragg

Abstract The confusion existing in the use of symbols and names for Kraemer's “intrinsic viscosity” and other functions related to it is illustrated and deplored. The reasonable plea is made that one name be adopted for each function and that it be used with no other meaning. To stimulate discussion and ultimate action, the following names are proposed: “specific viscosity” for ηsp; “reduced viscosity” for ηsp/c, “inherent viscosity” for (ln ηr)/c; and “intrinsic viscosity” for [η], whether determined as “limiting reduced viscosity” limc→0 (ηsp/c), or as “limiting inherent viscosity” limc→0 (ηr/c), or as “limiting viscosity concentration coefficient” limc→0 (dηr/dc). Often, especially in routine practice, it is the relative kinematic viscosity νr, that is determined ; unless this is shown to be numerically equal to the relative viscosity ηr, the symbols and names of the derived functions should be modified accordingly: thus, (ln νr)/c inherent kinematic viscosity, [ν] intrinsic kinematic viscosity. Frequently, also, kinetic energy corrections are neglected; under these circumstances the suggested usage is tr, relative flow time, tsp/c reduced flow time, [t] intrinsic flow time, etc.


2005 ◽  
Vol 169 (2) ◽  
pp. 223-231 ◽  
Author(s):  
R.A. Curtis ◽  
K. Kusano ◽  
D.L. Evans ◽  
N.H. Lovell ◽  
D.R. Hodgson

1947 ◽  
Vol 25b (4) ◽  
pp. 333-350
Author(s):  
L. H. Cragg ◽  
T. M. Rogers ◽  
D. A. Henderson

From careful measurements of the relative flow times of solutions of GR-S in benzene, it has been established that the intrinsic flow time (and hence the intrinsic viscosity) of GR-S in benzene may be most precisely determined by the use of a function [Formula: see text], based on the Baker equation relating ηr, the relative viscosity, and c, the concentration; for the GR-S–benzene system the value of n may be taken as 8. For the greatest precision [t] is determined by linear (horizontal) extrapolation, to zero concentration, of the [Formula: see text] vs. c plot; in rapid routine work [t] may be evaluated as [Formula: see text] by measurements on only one solution of a concentration such that tr = 1.8 ± 0.4.


1987 ◽  
Vol 253 (6) ◽  
pp. R890-R895 ◽  
Author(s):  
J. M. Weber ◽  
G. P. Dobson ◽  
W. S. Parkhouse ◽  
D. Wheeldon ◽  
J. C. Harman ◽  
...  

This study characterizes the effects of exercise on the cardiac output (Q) and the metabolic rate (VO2) of trained Thoroughbred racehorses. Heart rate, Q, and arteriovenous (a-v)O2 difference were measured at rest and at three levels of submaximal treadmill exercise (1.6 m/s walk and 3-4 m/s trot at 6% incline, and 6.5 m/s horizontal canter). Heart rate and (a-v)O2 difference were also measured during maximal exercise (12.5 m/s gallop, 5% incline) to obtain an estimate of maximum O2 uptake (VO2max). The walk, trot, and canter represented 25, 45, and 55% VO2max. Mean heart rate went from 48.9 (rest) to 197 beats/min (gallop). Q ranged from 106 (rest) to 571 ml.min-1.kg-1 (canter), and stroke volume went from 1.34 (rest) to a maximum of 1.58 liters (walk). Thoroughbreds were able to bring hematocrit from 38 (rest) to 63% (gallop), and this adjustment allowed them to reach an impressive (a-v)O2 difference of 23 vol%, which represents a fivefold increase over resting values. These outstanding athletes probably support an aerobic scope of 40-fold.


1998 ◽  
Vol 84 (5) ◽  
pp. 1723-1730 ◽  
Author(s):  
S. R. Hopkins ◽  
W. M. Bayly ◽  
R. F. Slocombe ◽  
H. Wagner ◽  
P. D. Wagner

During short-term maximal exercise, horses have impaired pulmonary gas exchange, manifested by diffusion limitation and arterial hypoxemia, without marked ventilation-perfusion (V˙a/Q˙) inequality. Whether gas exchange deteriorates progressively during prolonged submaximal exercise has not been investigated. Six thoroughbred horses performed treadmill exercise at ∼60% of maximal oxygen uptake until exhaustion (28–39 min). Multiple inert gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained at rest and 5-min intervals during exercise. Oxygen uptake, cardiac output, and alveolar-arterial[Formula: see text] gradient were unchanged after the first 5 min of exercise. Alveolar ventilation increased progressively during exercise, from increased tidal volume and respiratory frequency, resulting in an increase in arterial[Formula: see text] and decrease in arterial[Formula: see text]. At rest there was minimalV˙a/Q˙inequality, log SD of the perfusion distribution (log SDQ˙) = 0.20. This doubled by 5 min of exercise (log SDQ˙ = 0.40) but did not increase further. There was no evidence of alveolar-end-capillary diffusion limitation during exercise. However, there was evidence for gas-phase diffusion limitation at all time points, and enflurane was preferentially overretained. Horses maintain excellent pulmonary gas exchange during exhaustive, submaximal exercise. AlthoughV˙a/Q˙inequality is greater than at rest, it is less than observed in most mammals and the effect on gas exchange is minimal.


1990 ◽  
Vol 69 (1) ◽  
pp. 42-45 ◽  
Author(s):  
J. I. Carlin ◽  
R. C. Harris ◽  
G. Cederblad ◽  
D. Constantin-Teodosiu ◽  
D. H. Snow ◽  
...  

Treadmill exercise of 2-min duration and increasing intensity resulted in increased formation of acetyl-CoA and acetylcarnitine in working muscle of Thoroughbred horses. At high work intensities a plateau was reached for both acetyl-CoA (approximately 50 mumols/kg dry muscle) and acetylcarnitine (approximately 20 mmol/kg dry muscle). Postexercise concentrations were significantly (P less than 0.001) correlated; [acetylcarnitine] = 349.[acetyl-CoA] + 2.4. The results indicate that approximately 350 mumols acetylcarnitine were accumulated for every 1 mumol acetyl-CoA. Under the conditions of exercise used it is probable that most of the acetyl-CoA formed is generated through the intramitochondrial decarboxylation of pyruvate. The acetyl groups of acetyl-CoA are apparently redistributed throughout the whole cell through formation of acetylcarnitine, which readily transverses the mitochondrial membrane. Despite the redistribution, however, the close correlation between acetylcarnitine and acetyl-CoA would indicate that equilibrium was maintained and that neither acetylcarnitine transferase nor carnitine/acetylcarnitine translocase were rate limiting. There is some question as to whether the changes observed relate directly to exercise itself or to the state in muscle 10 s or more after exercise.


2013 ◽  
Vol 24 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Hirokazu TSUBONE ◽  
Masakazu HANAFUSA ◽  
Maiko ENDO ◽  
Noboru MANABE ◽  
Atsushi HIRAGA ◽  
...  

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