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Biomedical subjects

M Jensen-Urstad

Publications and source records attributed to M Jensen-Urstad.

50 records · Page 3Linked to original sources

Effect of hypoxia on muscle oxygenation and metabolism during arm exercise in humans.

The influence of hypoxaemia on anaerobic energy production during arm exercise (AE) has been investigated. Six men were studied during maximal AE and during 10 min of sitting submaximal AE under both normoxic (AEN) and hypoxic (AEH, respiratory hypoxia, 12% O2) conditions. Peak pulmonary oxygen uptake (VO2) during maximal AE in normoxia and hypoxia was 2.25 +/- 0.15 and 2.18 +/- 0.14 l min-1, respectively (P < 0.05). The absolute workload was the same during submaximal AEN and AEH and corresponded to 54% of peak VO2 during normoxic maximal AE. To eliminate the potential influence of differences in catecholamine levels on the metabolic response, the submaximal experiments were performed during beta-adrenoceptor blockade. Oxygen deficit was 1.45 +/- 0.26 and 1.67 +/- 0.191 during AEN and AEH, respectively (n.s.). Oxygen extraction at steady state was lower during AEH than during AEN, and assuming a similar O2 demand this corresponds to a 14% higher muscle blood flow during AEH. At the onset of both AEN and AEH, O2 extraction (a-v O2) across the arm increased transiently above that at steady state, the increase being more pronounced during AEN than during AEH (P < 0.05). Muscle oxygenation, measured by near-infrared spectroscopy, demonstrated an initial decrease which was partially reversed as exercise proceeded. The reversal of muscle O2 desaturation was slower in all subjects during AEH (t1/2 = 2.4 +/- 0.2 min) than during AEN (t1/2 = 1.2 +/- 0.2 min; P < 0.01). After 10 min of exercise, arterial blood lactate was higher (P < 0.05) during AEH (5.5 +/- 0.2 mmol l-1) than during AEN (4.9 +/- 0.6 mmol l-1), whereas arterial plasma ammonia (NH3) was similar. The arteriovenous difference for both lactate and ammonia was similar during AEN and AEH. It is concluded that the high anaerobic energy production at the onset of AE is associated with a transient increase in O2 extraction and a transient decrease in muscle oxygenation. The effects of hypoxaemia on peak VO2, oxygen deficit and blood metabolites are less pronounced than previously described during submaximal leg exercise (LE).

Adult↗

Sudden death and physical activity in athletes and nonathletes.

Among young athletes, sudden deaths are predominantly associated with cardiomyopathies, coronary artery abnormalities and myocarditis, but coronary heart disease is a reality already in this group. The absolute risk of sudden death is, however, low and the benefits of routine medical screening are small. If an athlete has had any symptoms that arouse suspicion of cardiac disease, the athlete must be meticulously investigated, as an underlying life-threatening illness may be present. Among all nonathletes, as well as athletes > or = 30 years, the predominant cause of sudden death is coronary heart disease. A large number of studies have provided strong evidence suggesting the benefits of physical activity regarding prevention of cardiovascular death and disease. The immediate risk for sudden death is higher during physical activity than during other times, especially among usually sedentary individuals, but inactivity is much more dangerous in the long run. Regular exercise at moderate intensity gives large benefits with small risks. The benefits of irregular and intensive exercise are less clear and the risks higher. For the individual without known heart disease who exercises regularly, the risk for sudden death during physical activity is extremely small.

Adult↗

Effect of muscle mass on lactate formation during exercise in humans.

To elucidate the mechanisms of lactate formation during submaximal exercise, eight men were studied during one- (1-LE) and two-leg (2-LE) exercise (approximately 11-min cycling) using the catheterization technique and muscle biopsies (quadriceps femoris muscle). The absolute exercise intensity and thus the energy demand for the exercising limb was the same [mean 114 (SEM 7) W] during both 1-LE and 2-LE. At the end of exercise partial pressure of O2 and O2 saturation in femoral venous blood were lower and arterial adrenaline and noradrenaline were higher during 2-LE than during 1-LE. Mean arterial blood lactate concentration increased to 10.8 (SEM 0.8) (2-LE) and 5.2 (SEM 0.4) mmol.l-1 (1-LE) after 10 min of exercise. The intramuscular metabolic response to exercise was attenuated during 1-LE [mean, lactate = 49 (SEM 9); glucose 6-P = 3.3 (SEM 0.3); nicotinamide adenine dinucleotide, reduced = 0.17 (SEM 0.02); adenosine 5'-diphosphate 2.7 (SEM 0.1) mmol.kg dry mass-1] compared to 2-LE [76 (SEM 6); 6.1 (SEM 0.7); 0.21 (SEM 0.02); 3.0 (SEM 0.1) mmol.kg dry mass-1, respectively]. To elucidate whether the lower plasma adrenaline concentration could contribute to the attenuated metabolic response, additional experiments were performed on four of the eight subjects with infusion of adrenaline during 1-LE (1-LEE). Average plasma adrenaline concentration was increased during 1-LEE and reached 2-4 times higher levels than during 2-LE. Post-exercise muscle lactate and glucose 6-P contents were higher during 1-LEE than during 1-LE and were similar to those during 2-LE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗

Short-term effects of eating on vasoactive hormones and haemodynamics in patients with heart failure.

OBJECTIVES: To investigate if eating can influence the measurements of vasoactive hormones or their relationship to important haemodynamic variables. DESIGN: Haemodynamic variables and plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin and angiotensin enzyme (ACE) activity were measured. During the 24-h study period the patients ate ordinary hospital meals and thus were studied both in the absorptive and post-absorptive phases. SETTING: Two university hospitals in Sweden participated in the study. SUBJECTS: Ten patients with heart failure, due to ischaemic heart disease. INTERVENTION: Eating. MAIN OUTCOME MEASURES: Change in haemodynamic variables and plasma concentrations of vasoactive hormones related to eating. RESULTS: After a meal (absorptive phase) pulmonary capillary wedge pressure and plasma concentrations of ANP were significantly lower compared to the postabsorptive phase, 13 +/- 1.7 vs. 16 +/- 1.9 mmHg and 57 +/- 9.5 vs. 72 +/- 12.2 pmol l-1, respectively. The relationship between ANP and its main predictor, pulmonary capillary wedge pressure, was not altered during the study period. Plasma concentration of arginine vasopressin, ACE activity and mean right atrial pressure decreased with time and the cardiac index increased with time over the study period. CONCLUSIONS: A meal may significantly influence plasma concentrations of ANP. Studies on vasodilator treatment and its interactions with ANP should take account of these basal fluctuations. The present data confirm previous reports on haemodynamic improvement during the first 24 h of supine cardiac catheterization in patients with heart failure, and add new information about decreasing concentrations of arginine vasopressin and ACE.

Aged↗

Influence of angiotensin converting enzyme inhibition on relation of atrial natriuretic peptide concentration to atrial pressure in heart failure.

OBJECTIVE: To examine the relation between haemodynamics and atrial natriuretic peptide concentration during short term angiotensin converting enzyme inhibition. DESIGN: Patients were randomly allocated to receive placebo or one of three doses of the angiotensin converting enzyme inhibitor ramipril. SETTING: Cardiac units of two tertiary referral hospitals. SUBJECTS: 38 Patients with stable congestive heart failure caused by ischaemic heart disease. METHODS: Data were collected over a 24 hour period and assessed with the aim of distinguishing between the haemodynamic effects on plasma concentrations of atrial natriuretic peptide and the direct effects of the study drug, vasopressin concentrations, and angiotensin converting enzyme activity. RESULTS: Pulmonary capillary wedge pressure was the main predictor of the plasma concentration of atrial natriuretic peptide. A higher plasma concentration of this peptide with a given pulmonary capillary wedge pressure was found after 24 hours of treatment with 2.5 mg and 5 mg of ramipril. Plasma concentration of the active metabolite, change in arginine vasopressin concentration or degree of angiotensin converting enzyme inhibition did not significantly predict change in plasma concentration of atrial natriuretic peptide or in the ratio of atrial natriuretic peptide concentration to pulmonary capillary wedge pressure. CONCLUSIONS: A gradual increase in plasma concentration of atrial natriuretic peptide with a given pulmonary capillary wedge pressure, occurs during short term high degree inhibition of angiotensin converting enzyme. The causative mechanisms are yet to be identified. Such a change in the relation between central haemodynamics and atrial natriuretic peptide concentration may contribute to the beneficial effects of angiotensin converting enzyme inhibition in patients with congestive heart failure due to ischaemic heart disease.

Aged↗

Acute haemodynamic effects and pharmacokinetics of ramipril in patients with heart failure. A placebo controlled three-dose study.

The aim of the present study was primarily to evaluate the haemodynamic effects of the ACE-inhibitor ramipril which is active via its metabolite ramiprilat. Ramipril 1.25, 2.5 and 5 mg and placebo was administered orally to 4 groups of 12 patients with heart failure (NYHA III) in a double-blind randomised, parallel study. Haemodynamics were monitored for 24 h and blood was sampled and urine collected for up to 96 h. In the placebo-treated group the cardiac index (CI) was significantly increased (15.8%) and right atrial pressure decreased (26.6%). Ramipril 1.25 mg had insignificant haemodynamic effects compared to placebo and the 2.5 mg dose had significant effects on some haemodynamic variables. Ramipril 5 mg had pronounced and sustained effects on pulmonary artery pressure, which fell by 43.7%, and pulmonary capillary wedge pressure (PCWP; -59.1%); systemic vascular resistance was also decreased 21%. A significant effect on CI was only seen after 2.5 mg ramipril (+7.4%). The mean maximal degree of ACE inhibition was 73.2, 90.4 and 98.5%, respectively, after the three doses of ramipril. Complete inhibition of ACE-activity was seen at a mean plasma concentration of ramiprilat of 4.7 ng.ml-1. The degree of inhibition declined with a half life of about 75 h. There was a significant relation between the degree of ACE-inhibition and change in PCWP but not with the change in SVR. Ramipril was mainly eliminated in the form of ramiprilat and inactive metabolites.

Administration, Oral↗

High anaerobic energy release during submaximal arm exercise.

The anaerobic energy release during submaximal arm (AE) and leg exercise (LE) has been estimated from O2 deficit measured at the onset of exercise. Eight male subjects were studied during 8-10 min of arm or leg cycling at the same relative workload (53% of the peak exercise-induced increase in pulmonary oxygen uptake, VO2). The workloads were 78 +/- 4 W during AE and 173 +/- 11 W during LE and VO2 was 1.51 +/- 0.06 1 min-1 for AE and 2.33 +/- 0.15 1 min-1 for LE. The half-time of the VO2 on-response was considerably longer (P < 0.01) during AE (62 +/- 9 s) than during LE (33 +/- 4 s) and the peak blood lactate concentration was higher (P < 0.05) during AE (4.8 +/- 0.5 mmol.l-1) than during LE (3.5 +/- 0.4 mmol.l-1). Oxygen deficit was 1.64 +/- 0.16 and 1.78 +/- 0.16 1 for AE and LE respectively. Oxygen deficit was higher during AE than during LE when related to absolute workload (P < 0.01), or to VO2 at steady state (P < 0.001) or to limb volume (P < 0.001). The proportion of the total energy demand covered by anaerobic energy release at the onset of exercise (0-8 min) was about 54% higher (P < 0.01) during AE than during LE. It is concluded that the energy release to a greater extend is covered by anaerobic processes during AE than during LE.

Adult↗

Neuropeptide Y, noradrenaline and invasive haemodynamic data in mild to moderate chronic congestive heart failure.

Neuropeptide Y (NPY) is a peptide released together with noradrenaline (NA) from sympathetic nerve endings. Elevated plasma levels of NA and NPY-like immunoreactivity (LI) are found in patients with congestive heart failure. In order to assess any relationship found between plasma NPY-LI and haemodynamic data 12 patients with mild to moderate chronic congestive heart failure were studied during cardiac catheterization. All patients were treated with diuretics but not ACE inhibitors and were in New York Heart Association functional class II or III. Mean left ventricular ejection fraction determined by echocardiography was 34%. Plasma NPY-LI from mixed venous blood was elevated in five patients and NA in nine. Mean plasma NPY-LI was 29 +/- 3 pmoll-1 (mean +/- standard error of the mean) and NA 2.6 +/- 0.3 nmoll-1. Heart rate was 70 +/- 3 beats min-1, systolic blood pressure (SBP) 131 +/- 7 mmHg, stroke volume index (SVI) 29 +/- 1.9 ml m-2 and cardiac index (CI) 2.0 +/- 0.13 l min-1 m-2. Elevated levels of plasma NPY-LI (> 30 pmol l-1) were associated with lower SVI, CI, and SBP and a higher pulmonary vascular resistance. Elevated plasma NA (> 2 nmol l-1) did not correlate with haemodynamic data. Log NPY-LI correlated inversely with SVI (P < 0.01) and CI (P < 0.05) but not with plasma NA. It is concluded that log NPY-LI in mixed venous blood correlates inversely with SVI and CI in patients with mild to moderate chronic congestive heart failure.

Aged↗

High lactate and NH3 release during arm vs. leg exercise is not due to beta-adrenoceptor stimulation.

To investigate the differences in metabolic response between arm exercise (AE) and leg exercise (LE) and to elucidate the underlying mechanisms, seven men were studied during 20 min of AE or LE both with (beta) and without (control, C) nonselective beta-blockade (beta B) (propranolol). The work loads corresponded to 59 and 60% of peak pulmonary O2 uptake (VO2) during LE and AE, respectively. Pulmonary VO2 increased more slowly at the onset of exercise during AEC (half time = 61 +/- 9 s) than during LEC (half time = 35 +/- 3 s) and was not affected by beta B. At the onset of exercise the arteriovenous O2 difference across the exercising limb increased above that of steady state during AEC but not during LEC. This demonstrates that the adjustment of O2 delivery is slower than that of arm VO2 during AE. Despite the smaller exercising muscle mass, the release of lactate and NH3 was about twofold higher during AEC than during LEC. The difference in metabolic response between AE and LE was not altered by beta B. Lactate release was not reduced by beta B but, if anything, tended to increase during both AE and LE (beta vs. C). beta B increased NH3 release during LE (beta vs. C) but not during AE (beta vs. C). We conclude that AE compared with LE at the same relative work load is associated with a greater release of lactate and NH3, indicating a more severe metabolic stress during AE. Furthermore, the present data suggest that the increase in blood lactate at these submaximal exercise intensities is caused by factors other than beta-adrenoceptor stimulation.

Adult↗

Is the high lactate release during arm exercise due to a low training status?

To determine whether arm lactate release during arm exercise is related to the training status of the arms, seven arm-trained athletes were studied during 30 min of continuous arm exercise (AE) or leg exercise (LE) of increasing intensities corresponding to 30%, 50%, and 80% of peak VO2 during AE and LE respectively. Blood vessels were catheterized for determination of regional blood flows and substrate exchanges. The respiratory exchange ratio was higher during AE than LE (P less than 0.01). The arteriovenous oxygen difference, [(A-V)O2], for the leg during LE was 11-19% higher than the (A-V)O2 for the arm during AE (P less than 0.01). At the highest intensity the (A-V)O2 was 170 +/- 6 ml O2l-1 during LE, vs. 143 +/- 9 during AE (P less than 0.01). Arm blood flow in relation to limb volume was 56-95% higher during AE (P less than 0.05). Arterial lactate concentrations were 27-60% higher during AE (P less than 0.01) and lactate release from the exercising limb was 2-4 times higher (P less than 0.05) during AE compared to LE. Adrenaline and noradrenaline rose 6- and 21-fold, respectively, during AE and did not differ from corresponding LE values. During AE the (A-V)O2 difference across the arm, arterial lactate concentration, and arm lactate release were of the same magnitude in arm-trained and relatively less arm-trained subjects. Lactate release in relation to O2 uptake by the exercising limb was 7-37% lower during AE in arm-trained subjects compared to AE in arm-untrained subjects but was 3-6 times higher than the corresponding relation during LE (P less than 0.01). We conclude that AE is associated with a larger lactate release compared to LE. This difference is only to a minor extent influenced by intense training of the arms. The high arm vs. leg lactate release appears to be associated with differences in regional circulatory adaptation by the exercising limb.

Adult↗

Plasma levels of atrial natriuretic peptide at rest and during exercise in heart failure--influence of cardiac rhythm and haemodynamics.

The relationship between plasma levels of immunoreactive atrial natriuretic peptide (ir-ANP), arginine vasopressin (AVP), cardiac rhythm and different haemodynamic variables were studied at rest and during exercise in 16 patients with heart failure undergoing heart catheterization for clinically indicated reasons. Even though there was no significant relationship between pulmonary capillary wedge pressure (PCW) and ir-ANP at rest (r = 0.39; P = 0.14) changes in these variables with exercise correlated well (r = 0.71; P = 0.002). Change in right atrial mean pressure, heart rate, mean arterial blood pressure or cardiac index did not significantly influence change in plasma levels of ir-ANP. The correlation between PCW and AVP at rest (r = 0.92; P less than 0.001) disappeared during exercise. Calculated ir-ANP/PCW ratios decreased slightly during exercise, but were not influenced by initial atrial pressures or atrial fibrillation. These observations provide evidence for a similar responsiveness of ANP in patients with sinus rhythm and atrial fibrillation. The ability of rapid change in ANP plasma levels during exercise was preserved and proportional to changes in PCW over a wide pressure range in the studied patient group. This finding indicates that left atrium distension rather than right atrium distension is the major determinant for the release of ANP in patients with congestive heart failure. The observed rapid responsiveness of ANP to change in left atrial pressure may allow the hormone to modulate haemodynamic response during short periods of exercise.

Adult↗

Metabolism in exercising arm vs. leg muscle.

Arm and leg metabolism were compared by arterial and venous catheterization and blood flow measurements (by dye dilution techniques) in two groups of subjects performing 30-min continuous arm or leg exercise of increasing intensity corresponding to approximately 30, 50 and 80% of max oxygen uptake for arm or leg exercise. The absolute work-loads were 2.5-3 times higher during leg compared to arm exercise. Heart rates were the same in both types of exercise. r-Values were 0.97-1.07 during arm exercise. Arterial noradrenaline and adrenaline levels became higher during leg compared to arm exercise (P less than 0.05-0.01). Arterial lactate concentration was 50% higher for arm exercise at the two lower intensities (P less than 0.001) and the same at the highest intensity compared to leg exercise. Arm lactate release was three times higher (P less than 0.01) or the same as leg lactate output at corresponding exercise intensities. Arm and leg glucose uptake during exercise were of the same magnitude at the lower intensities. In contrast to the leg substrate exchange, arm lactate output was higher than the simultaneous glucose uptake (P less than 0.05-0.001), indicating a relatively higher rate of glycogen degradation. In conclusion, exercising arm compared to leg muscles working at the same relative intensities utilize more carbohydrate, mainly muscle glycogen resulting in higher lactate release by the exercising extremity. This cannot solely be explained on the basis of differences in the degree of training and occurs with lower catecholamine levels compared to leg exercise.

Adult↗

Arm blood flow at rest and during arm exercise.

To test the applicability of a dye-dilution method to quantitate total arm blood flow at rest and during arm exercise, indocyanine green was infused at a constant rate into the brachial artery. Eight subjects performed continuous 30-min arm exercises with an increase in intensity every 10 min (30, 60, and 90 W). The loads corresponded to 29 +/- 1, 48 +/- 2, and 78 +/- 4% (means +/- SE) of the maximal O2 uptake (VO2max 2.13 +/- 0.08 l/min) during arm exercise. VO2max during arm exercise was 61 +/- 1.7% of that during leg exercise. The dye concentration was analyzed in blood samples from three arm veins, two ipsi- and one contralateral, at shoulder level. Corresponding dye concentrations in both ipsilateral veins and a stable concentration difference between ipsi- and contralateral veins were achieved. Total arm blood flow was calculated to be 0.21 +/- 0.04 l/min at rest and 2.43 +/- 0.14 l/min at 90 W. Arm O2 uptake rose from 9 +/- 2 to 323 +/- 21 ml/min. Arm blood flow and O2 uptake each correlated linearly with both work load (r = 0.98) and pulmonary O2 uptake (r greater than or equal to 0.98). Mechanical efficiency for the arm and body was 34-44 and 16-19%, respectively. We conclude that arm blood flow can be determined by continuous infusion of indocyanine green.

Adult↗