Relationship between cardiac output and oxygen uptake at the onset of exercise

The purpose of the present study was to assess the relationship between the rapidity of increased gas exchange (i.e. oxygen uptake ) and increased cardiac output ( ) during the transient phase following the onset of exercise. Five healthy male subjects performed multiple rest-exercise or light exercise (25 W)-exercise transitions on an electrically braked ergometer at exercise intensities of 50, 75, or 100 W for 6 min, respectively. Each transition was performed at least eight times for each load in random order. The was obtained by a breath-by-breath method, and was measured by an impedance method during normal breathing, using an ensemble average. On transitions from rest to exercise, rapidly increased during phase I with time constants of 6.8–7.3 s. The also showed a similar rapid increment with time constants of 6.0–6.8 s with an apparent increase in stroke volume (SV). In this phase I, increased to about 29.7%–34.1% of the steady-state value and increased to about 58.3%–87.0%. Thereafter, some 20 s after the onset of exercise a mono-exponential increase to steady-state occurred both in and with time constants of 26.7–32.3 and 23.7–34.4 s, respectively. The insignificant difference between and time constants in phase I and the abrupt increase in both and SV at the onset of exercise from rest provided further evidence for a cardiodynamic contribution to following the onset of exercise from rest.     

Cardiac output and oxygen uptake kinetics at the onset and offset of exercise

1. 1. The aim of the present study is to assess the relationship between rapidity of oxygen uptake (V_O2 and cardiac output (Q) kinetics at the transient phase of the onset and offset of exercise.

2. 2. Five healthy male subjects performed multiple rest-exercise-recovery transitions on an electrically braked ergometer, work rate was 50, 75, or 100 W for 6 min, respectively.

3. 3. V_O2 was obtained by a breath-by-breath method, and Q was measured by an impedance method during normal breath, using an ensemble averaged method.

4. 4. On transition from rest to exercise, V_O2 rapidly increased as phase I with a time constant of 7.0–7.8 s. Q also showed a similar rapid increment with a time constant of 6.3–6.8 s in phase I.

5. 5. In this phase I, V_O2 increased approx. 42–68% of steady state value and Q increased 71–84%. Thereafter, V_O2 and Q increased monoexponentially up to steady state with a time constant of 26.7–32.3 and 23.7–34.4 s, respectively.

6. 6. During recovery, V_O2 (with a time constant of 35.7–38.1 s and time delay (TD) of −1 to −2 s), while Q remained to sustain the value of steady state exercise with a couple of time delay (TD = 2–7 s), and thereafter decreased monoexponentially (with a time constant of 18.9–31.6 s).

7. 7. The stroke volume showed the similar behavior to the Q kinetics after exercise, while heart rate rapidly decreased (time constant = 10.6–21.2 s).

8. 8. It is suggested that the delayed Q kinetics after exercise might be attributable to the sustained level of venous return and that Q kinetics is not linked with V_O2 kinetics after exercise.

The redistribution of cardiac output in the dog during heat stress

In conscious Greyhound dogs, radioactive microsphere techniques have been used to measure cardiac output, its regional distribution, and proportion of the cardiac output passing through arteriovenous anastomoses (AVA's) in a thermoneutral environment and during severe heat stress. Heat stress resulted in a 74% increase in cardiac output and 4–6% of the cardiac output passed through AVA's. compared with about 1% under thermoneutral conditions: blood flow rate increased in skin of the lower legs and ears, tongue, maxillo turbinals, nasal mucosa, respiratory muscles and spleen, decreased in the thyroids, brain and spinal cord, and did not change significantly in the non-respiratory muscles, heart, pituitary, adrenals, kidneys, liver, stomach and intestines. Thus the circulatory requirements of the heat stressed dogs were met partly by an increase in cardiac output and partly by changes in its distribution. In contrast, the Merino sheep meets such a situation entirely by a redistribution of cardiac output. The present results may be taken as evidence that the Greyhound dog is less heat tolerant than the Merino sheep. The decreased brain blood flow during heat stress is similar to that which occurs in the sheep, but contrast with previous results obtained on anaestherized dogs. The less marked redistribution of cardiac output in the dog compared with the sheep, may explain the apparent difference in energy cost of panting in the two species.     

Decreased cardiac output at the onset of diabetes: renal mechanisms and peripheral vasoconstriction

Recently we reported that hindquarter blood flow, measured 24 h/day, decreased progressively over the first 6 days of type 1 diabetes in rats. That response, coupled with the tendency of mean arterial pressure to increase, suggested a vasoconstrictor response. The purpose of this study was to measure the changes in cardiac output together with the renal hemodynamic and excretory responses to allow integrative determination of whether vasoconstriction likely accompanies the onset of type 1 diabetes. Rats were instrumented with a Transonic flow probe on the ascending aorta and with artery and vein catheters, and cardiac output and mean arterial pressure were measured continuously, 24 h/day, throughout the study. The induction of diabetes, by withdrawing intravenous insulin-replacement therapy in streptozotocin-treated rats, caused a progressive decrease in cardiac output that was 85 +/- 5% of control levels by day 7. This was associated with significant increases in glomerular filtration rate, renal blood flow, and microalbuminuria as well as urinary fluid and sodium losses, with a negative cumulative sodium balance averaging 15.7 +/- 1.6 meq by day 7. Restoring insulin-replacement therapy reversed the renal excretory responses but did not correct the negative sodium balance, yet cardiac output returned rapidly to control values. Increasing sodium intake during the diabetic and recovery periods also did not significantly affect the cardiac output response during any period. These results indicate that cardiac output decreases significantly at the onset of type 1 diabetes without glycemic control, and although volume loss may contribute to this response, there also is a component that is not volume or sodium dependent. We suggest this may be due to vasoconstriction, but to what extent local blood flow autoregulation or active vasoconstriction may have mediated that response is not known.     

Exercise intensity influences cardiac baroreflex function at the onset of isometric exercise in humans.

We sought to examine the influence of exercise intensity on carotid baroreflex (CBR) control of heart rate (HR) and mean arterial pressure (MAP) at the onset of exercise in humans. To accomplish this, eight subjects performed multiple 1-min bouts of isometric handgrip (HG) exercise at 15, 30, 45 and 60% maximal voluntary contraction (MVC), while breathing to a metronome set at eupneic frequency. Neck suction (NS) of -60 Torr was applied for 5 s at end expiration to stimulate the CBR at rest, at the onset of HG (<1 s), and after approximately 40 s of HG. Beat-to-beat measurements of HR and MAP were recorded throughout. Cardiac responses to NS at onset of 15% (-12 +/- 2 beats/min) and 30% (-10 +/- 2 beats/min) MVC HG were similar to rest (-10 +/- 1 beats/min). However, HR responses to NS were reduced at the onset of 45% and 60% MVC HG (-6 +/- 2 and -4 +/- 1 beats/min, respectively; P < 0.001). In contrast to HR, MAP responses to NS were not different from rest at exercise onset. Furthermore, both HR and MAP responses to NS applied at approximately 40s of HG were similar to rest. In summary, CBR control of HR was transiently blunted at the immediate onset of high-intensity HG, whereas MAP responses were preserved demonstrating differential baroreflex control of HR and blood pressure at exercise onset. Collectively, these results suggest that carotid-cardiac baroreflex control is dynamically modulated throughout isometric exercise in humans, whereas carotid baroreflex regulation of blood pressure is well-maintained.     

Phase I dynamics of cardiac output, systemic O2 delivery, and lung O2 uptake at exercise onset in men in acute normobaric hypoxia

We tested the hypothesis that vagal withdrawal plays a role in the rapid (phase I) cardiopulmonary response to exercise. To this aim, in five men (24.6+/-3.4 yr, 82.1+/-13.7 kg, maximal aerobic power 330+/-67 W), we determined beat-by-beat cardiac output (Q), oxygen delivery (QaO2), and breath-by-breath lung oxygen uptake (VO2) at light exercise (50 and 100 W) in normoxia and acute hypoxia (fraction of inspired O2=0.11), because the latter reduces resting vagal activity. We computed Q from stroke volume (Qst, by model flow) and heart rate (fH, electrocardiography), and QaO2 from Q and arterial O2 concentration. Double exponentials were fitted to the data. In hypoxia compared with normoxia, steady-state fH and Q were higher, and Qst and VO2 were unchanged. QaO2 was unchanged at rest and lower at exercise. During transients, amplitude of phase I (A1) for VO2 was unchanged. For fH, Q and QaO2, A1 was lower. Phase I time constant (tau1) for QaO2 and VO2 was unchanged. The same was the case for Q at 100 W and for fH at 50 W. Qst kinetics were unaffected. In conclusion, the results do not fully support the hypothesis that vagal withdrawal determines phase I, because it was not completely suppressed. Although we can attribute the decrease in A1 of fH to a diminished degree of vagal withdrawal in hypoxia, this is not so for Qst. Thus the dual origin of the phase I of Q and QaO2, neural (vagal) and mechanical (venous return increase by muscle pump action), would rather be confirmed.     

Leukocytosis of exercise: role of cardiac output and catecholamines

The effect of propranolol (5 mg iv) on the leukocytosis of exercise was studied in seven normal young males. Leukocyte counts, plasma norepinephrine (NE), epinephrine (E), and cardiac output were measured at rest and in the steady state of several submaximal work loads when subjects exercised on a cycle ergometer. The results in control experiments were compared with those obtained on a different day with propranolol. Propranolol decreased heart rate at all work loads (P less than 0.001) but had no effect on the increase in cardiac output at increasing work loads. Plasma NE and E levels were similar at rest and in exercise in control and propranolol studies. There was no effect of propranolol on the increase in leukocyte counts with increasing work loads. Although propranolol did not affect the increase in total leukocyte count, the increase in lymphocyte count at higher work loads was less with propranolol. We conclude that the demargination of leukocytes from the pulmonary circulation in exercise is probably a mechanical effect of the increase in cardiac output. However, we have not excluded a contribution from a humoral event that would decrease the adherence of leukocytes to endothelium during exercise. The smaller increase in lymphocytes at higher work loads in the presence of propranolol suggests that catecholamines affect the lymphocyte count over and above their effect on cardiac output.