The effect of progressive hypoxia on respiration in the dogfish (scyliorhinus canicula) at different seasonal temperatures

1975 ◽  
Vol 63 (1) ◽  
pp. 117-130 ◽  
Author(s):  
P. J. Butler ◽  
E. W. Taylor

1. Dogfish were acclimated to 7, 12 or 17 degrees C and exposed to progressive hypoxia at the temperature to which they had been acclimated. During normoxia, the Q10 values for oxygen uptake, heart rate, cardiac output and respiratory frequency over the full 10 degrees C range were: 2.1, 2.1, 2.1 and 2.5 respectively. Increased acclimation temperature had no effect on cardiac stroke volume or systemic vascular resistance, although there was a decrease in branchial vascular resistance, pHa and pHv. 2. Progressive hypoxia had no effect on heart rate or oxygen uptake at 7 degrees C, whereas at 12 degrees C and 17 degrees C there was bradycardia, and a reduction in O2 uptake, with the critical oxygen tension for both variables being higher at the higher temperature. Cardiac stroke volume increased during hypoxia at each temperature, such that cardiac output did not change significantly at 12 and 17 degrees C. Neither pHa nor pHv changed significantly during hypoxia at any of the three temperatures. 3. The influence of acclimation temperatures on experimental results from poikilotherms is pointed out. Previously-published results show quantitative differences. 4. The significance of the present results with respect to the functioning and location of oxygen receptors is discussed. It is argued that as the metabolic demand and critical oxygen tension of the whole animal are increased at high acclimation temperatures the same must be the case with the oxygen receptor. This would raise the stimulation threshold and could account for the bradycardia seen during hypoxia becoming manifest at higher values of PI,O2, Pa,O2 and Pv,O2 as the acclimation temperature is raised.

1977 ◽  
Vol 70 (1) ◽  
pp. 57-75 ◽  
Author(s):  
E. W. TAYLOR ◽  
S. SHORT ◽  
P. J. BUTLER

1. During normoxia, heart rate was governed by a vagal tone which increased at higher acclimation temperatures. This tonic influence was exerted predominantly via the branchial cardiac nerves. The increase in heart rate following atropinization or cardiac vagotomy was associated with a reduction in stroke flow in the ventral aorta in accordance with Starling's Law of the heart. 2. During slowly induced hypoxia there was a reflex bradycardia, the onset and extent of which varied with acclimation temperature, and which was mediated predominantly via the pair of branchial cardiac vagi. The branchial cardiac vagi were also wholely responsible for the transient marked bradycardia at the onset of rapidly induced hypoxia. 3. Direct measurement of blood flow to the anterior two pairs of branchial arteries demonstrated that they received approximately 37% of total cardiac output in normoxia and that this proportion was unchanged during hypoxia. 4. The bradycardia during hypoxia in control animals was partially offset by a rise in cardiac stroke volume so that cardiac output decreased slightly. Injection of the adrenergic -receptor blocker, Propranolol, abolished the increase in stroke flow during hypoxia, but did not effect the bradycardia, and the total blood flow was therefore reduced. 5. The values of PO2 during hypoxia from fish acclimated to 17 °C were significantly reduced from the control values following atropinization and either branchial cardiac vagotomy or total cardiac vagotomy. 6. The apparent power output of the heart was reduced during hypoxia at high acclimation temperatures due to the marked bradycardia.


1999 ◽  
Vol 19 (2) ◽  
pp. 235 ◽  
Author(s):  
Andrew T. Gannon ◽  
Vincent G. Demarco ◽  
Tom Morris ◽  
Michele G. Wheatly ◽  
Yu-Hsing Kao

2011 ◽  
Vol 26 (3) ◽  
pp. 102-106 ◽  
Author(s):  
B Sperlich ◽  
M Haegele ◽  
M Krüger ◽  
T Schiffer ◽  
H-C Holmberg ◽  
...  

Objective The effects of knee-high socks that applied different levels of compression (0, 10, 20, 30 and 40 mmHg) on various cardio-respiratory and metabolic parameters during submaximal running were analysed. Methods Fifteen well-trained, male endurance athletes (age: 22.2 ± 1.3 years; peak oxygen uptake: 57.2 ± 4.0 mL/minute/kg) performed a ramp test to determine peak oxygen uptake. Thereafter, all athletes carried out five periods of submaximal running (at approximately 70% of peak oxygen uptake) with and without compression socks that applied the different levels of pressure. Cardiac output and index, stroke volume, arterio-venous difference in oxygen saturation, oxygen uptake, arterial oxygen saturation, heart rate and blood lactate were monitored before and during all of these tests. Results Cardiac output ( P = 0.29) and index ( P = 0.27), stroke volume ( P = 0.50), arterio-venous difference in oxygen saturation ( P = 0.11), oxygen uptake ( P = 1.00), arterial oxygen saturation ( P = 1.00), heart rate ( P = 1.00) and arterial lactate concentration ( P = 1.00) were unaffected by compression (effect sizes = 0.00–0.65). Conclusion This first evaluation of the potential effects of increasing levels of compression on cardio-respiratory and metabolic parameters during submaximal exercise revealed no effects whatsoever.


2020 ◽  
Vol 30 (5) ◽  
pp. 674-680
Author(s):  
Eva R. Hedlund ◽  
Liselott Söderström ◽  
Bo Lundell

AbstractObjective:To evaluate heart rate against workload and oxygen consumption during exercise in Fontan patients.Method:Fontan patients (n = 27) and healthy controls (n = 25) underwent cardiopulmonary exercise testing with linear increase of load. Heart rate and oxygen uptake were measured during tests. Heart rate recovery was recorded for 10 minutes.Results:Heart rate at midpoint (140 ± 14 versus 153 ± 11, p < 0.001) and at maximal effort (171 ± 14 versus 191 ± 10 beats per minute, p < 0.001) of test was lower for patients than controls. Heart rate recovery was similar between groups. Heart rate in relation to workload was higher for patients than controls both at midpoint and maximal effort. Heart rate in relation to oxygen uptake was similar between groups throughout test. Oxygen pulse, an indirect surrogate measure of stroke volume, was reduced at maximal effort in patients compared to controls (6.6 ± 1.1 versus 7.5 ± 1.4 ml·beat−1·m−2, p < 0.05) and increased significantly less from midpoint to maximal effort for patients than controls (p < 0.05).Conclusions:Heart rate is increased in relation to workload in Fontan patients compared with controls. At higher loads, Fontan patients seem to have reduced heart rate and smaller increase in oxygen pulse, which may be explained by inability to further increase stroke volume and cardiac output. Reduced ability to increase or maintain stroke volume at higher heart rates may be an important limiting factor for maximal cardiac output, oxygen uptake, and physical performance.


1989 ◽  
Vol 147 (1) ◽  
pp. 263-277 ◽  
Author(s):  
N. CHIN LAI ◽  
JEFFREY B. GRAHAM ◽  
WILLIAM R. LOWELL ◽  
RALPH SHABETAI

Changes in pericardial pressure, pericardial fluid volume, cardiac stroke volume and heart rate induced by swimming were monitored for Triakis semifasciata (Girard). Maximum pericardial pressure (Pmax, 0.07±0.03 kPa) in resting sharks was typically above ambient, whereas minimum pressure (Pmin, −0.08±0.03 kPa) was slightly subambient. During swimming, both Pmax (0.23±0.03 kPa) and Pmin (−0.02±0.03 kPa) became elevated, as did heart rate (51±2 to 55±2 beats min−1) and fractional cardiac stroke volume (0.49±0.03 to 0.65±0.04ml). After swimming, all variables fell, except fractional cardiac stroke volume. Estimates of total cardiac output from fractional cardiac stroke volume data during rest, exercise and recovery were 33.1, 56.2 and 60.4 ml kg ‘1 min’ 1, respectively. The occurrence of both elevated pericardial pressure and cardiac output during swimming argues against a primary role for pericardial-induced vis a fronte filling as the principal mechanism responsible for increasing cardiac output with exercise. Pericardial fluid loss via the pericardioperitoneal canal (PPC) occurs during swimming as a result of steady-state elevation of pericardial pressure, a series of transient high pericardial pressures, or both. Good general agreement seen for net pericardial fluid loss (0.6 ml kg−) and the net increase in cardiac stroke volume (0.45 ml kg−) during swimming establishes fluid displacement as a mechanism for increasing cardiac stroke volume and suggests that this is the primary function of the PPC.


1982 ◽  
Vol 99 (1) ◽  
pp. 255-268
Author(s):  
J. D. Metcalfe ◽  
P. J. Butler

Cardiac output has been measured directly, and calculated by the Fick method, during normoxia and hypoxia in six artificially perfused dogfish (Scyliorhinus canicula) in an attempt to estimate the accuracy of this method in fish. The construction and operation of a simple extra-corporeal cardiac bypass pump is described. This pump closely mimics the flow pulse profiles of the fish's own heart and allows complete control of both cardiac stroke volume and systolic and diastolic periods. During normoxia (PO2 = 21 kPa) there was no significant difference between directly measured and calculated values for cardiac output. However, some shunting of blood past the respiratory surface of the gills may have been obscured by cutaneous oxygen uptake. In response to hypoxia (PO2 = 8.6 kPa) there is either a decrease in the amount of blood being shunted past the respiratory surface of the gills and/or an increase in cutaneous oxygen uptake such that the Fick calculated value for cardiac output is on average 38% greater than the measured value. It is proposed that the increase in the levels of circulating catecholamines that is reported to occur in response to hypoxia in this species may play an important role in the observed response to hypoxia. The results are discussed in terms of their implications for the calculation of cardiac output by the Fick principle in fish.


2011 ◽  
Vol 215 (1) ◽  
pp. 93-102 ◽  
Author(s):  
B. Speers-Roesch ◽  
J. G. Richards ◽  
C. J. Brauner ◽  
A. P. Farrell ◽  
A. J. R. Hickey ◽  
...  

1989 ◽  
Vol 66 (2) ◽  
pp. 949-954 ◽  
Author(s):  
A. M. Rivera ◽  
A. E. Pels ◽  
S. P. Sady ◽  
M. A. Sady ◽  
E. M. Cullinane ◽  
...  

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.


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