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Biomedical subjects

L Kaijser

Publications and source records attributed to L Kaijser.

At least 37 records · Page 2Linked to original sources
PubMed1996

Comparable potent coronary constrictor effects of endothelin-1 and big endothelin-1 in humans.

BACKGROUND: Endothelin-1 (ET-1) is a potent vasoconstrictor produced from the precursor big ET-1 in endothelial cells. The coronary effects of these peptides in humans in vivo are unknown. Therefore, the effects of ET-1 and big ET-1 on coronary blood flow in relation to plasma ET-1 and big ET-1 levels were compared in healthy subjects. METHODS AND RESULTS: The peptides were infused intravenously at the rates of 0.2, 1, and 8 pmol/kg per minute. Each dose administered for 20 minutes except the highest dose of ET-1, which was administered for 10 minutes. ET-1 and big ET-1 evoked dose-related increases in mean arterial blood pressure from 93 +/- 4 to 107 +/- 4 mm Hg and from 89 +/- 2 to 122 +/- 5 mm Hg, respectively, at the highest dose. ET-1 and big ET-1 reduced coronary sinus blood flow, measured with thermodilution by a maximum of 25 +/- 4% and 28 +/- 8% and increased coronary vascular resistance by 50 +/- 9% and 107 +/- 26%, respectively. Coronary sinus, but not arterial, oxygen saturation was reduced in parallel with the coronary sinus blood flow. The effects of ET-1 and big ET-1 were similar at corresponding time points. During infusion of ET-1, a 19 +/- 5% extraction of ET-1 was observed over the coronary vascular bed (P < .05). Administration of big ET-1 elevated arterial plasma ET-1 levels by 2.4-fold, and after correction for the local extraction of ET-1, a myocardial production of ET-1 was observed. CONCLUSIONS: ET-1 and big ET-1 induce comparable increases in blood pressure and coronary constriction in humans in vivo. The results also suggest a net local removal of circulating ET-1 and big ET-1 and a local conversion of big ET-1 into ET-1 within the coronary vascular bed.

Adult↗
PubMed1996

Markedly improved skeletal muscle function with local muscle training in patients with chronic heart failure.

BACKGROUND: Reduced heart pump function and skeletal muscle abnormalities are considered important determinants for the low physical exercise capacity in chronic heart failure. Because of reduced ventricular function, traditional physical rehabilitation may cause underperfusion and low local work intensity, thereby producing suboptimal conditions for skeletal muscle training. HYPOTHESIS: The study was undertaken to determine the effects of local exercise training, designed as one- or two-legged knee extensor training, on exercise capacity in patients with moderate chronic heart failure. Because such exercise models use only about one quarter to half the muscle mass used in cycle ergometer training, the influence of a restricted circulatory capacity should therefore be limited. Further, we aimed to determine whether or not chronic heart failure skeletal musculature abnormalities are counteracted with such training. METHODS: Fourteen patients with chronic heart failure [age 58 +/- 3 years, ejection fraction (EF) 28 +/- 4%] were randomized to two different training protocols three times a week for 8 weeks and compared with a nontraining control group (n = 7, age 62 +/- 3, EF 27 +/- 3%). Group 2L (n = 7) underwent simultaneous two-legged knee extensor training (about 4 kg working muscle) for 15 min at 65-75% of VO2 max of the two-legged kick. Group 1L (n = 7) trained each leg at a time for 15 min of continuous one-legged dynamic knee extensor work with the same training load per muscle mass, that is, at 35% of VO2 max of the two-legged kick (about 2 kg working muscle). Peak VO2 of two-legged knee extensor exercise (l/min), two-legged endurance (W), and strength (Nm) were determined before and after the training period. The activity of citrate synthase (CS) was estimated in tissue samples from the quadriceps femoris muscle. RESULTS: Peak VO2 did not change with training. Two-legged knee extensor endurance exercise capacity increased by an average of 40-50% (p < 0.01) in all training patients in both the 2L and 1L groups, while no change was observed in the control group. Depressed skeletal muscle CS activity increased by 25-35% in both training groups (p < 0.01). Strength increased by 16% in the 2L group after training (p < 0.05), while no change was seen in the 1L and control groups. CONCLUSIONS: Skeletal muscle changes in stable moderate chronic heart failure are not entirely irreversible. A major factor contributing to these changes and to exercise limitation is deconditioning. Local muscle training is efficient and can at least partially improve skeletal muscle function in these patients. Different degrees of local activation, that is, one- or two-legged knee extensor exercise, do not seem to differ in terms of their effect on exercise capacity. Depressed skeletal muscle oxidative capacity adapts to such physical training with increased activity to an extent not different from that for healthy volunteers.

Adaptation, Physiological↗
PubMed1996

High intensity knee extensor training, in patients with chronic heart failure. Major skeletal muscle improvement.

Skeletal muscle adaptations to high intensity knee extensor strength and/or endurance training in patients with chronic heart failure were investigated. Eleven patients with chronic heart failure were randomized into two groups and exercised the m. quadriceps femoris 3 days/week for 8 weeks. After training, the maximal exercise intensity tolerated on the ergometer cycle was raised from 99 (32) to 114 (40) watts (W, P < 0.05) for all 11 patients. Peak dynamic knee extensor work rate showed the greatest increase after endurance training (40%, P < 0.01). Maximal dynamic and isometric strength were elevated by 40-45% (P < 0.05) after strength training. The cross-sectional area of m. quadriceps femoris was increased in the strength-trained legs (9%, P < 0.05), and the capillary per fibre ratio of m. vastus lateralis was raised by 47 and 58% in the endurance-trained legs (P < 0.05). The oxidative enzyme activity in m. vastus lateralis was significantly raised above 50% after endurance training, whereas glycolytic enzyme activity was unaltered. The peripheral skeletal musculature in patients with chronic heart failure adapts fairly quickly to high intensity knee extensor training. This results in a marked rise in local, and a small rise in total work capacity, indicating maintained plasticity of skeletal muscle in chronic heart failure patients.

Adaptation, Physiological↗
PubMed1996

Exercise capacity in heart failure patients: relative importance of heart and skeletal muscle.

The knee extensor and the whole-body exercise capacities were measured in 11 chronic heart failure (CHF) patients and 11 healthy age- and sex-matched controls, and were related to ejection fraction and to biochemical and histochemical markers of the musculature. The CHF patients had a 39% lower maximal oxygen uptake measured on an ergometer cycle than the healthy controls (1.54 +/- 0.57 vs. 2.51 +/- 0.70 1 min-1, P < 0.001). The low exercise capacity was markedly related to the ejection fraction (r = 0.77, P < 0.001). The maximal strength of m. quadriceps femoris was 15% lower in the CHF patients than in the controls (P < 0.05). The cross-sectional area (CSA) of m. quadriceps femoris explained 55% (r = 0.74, P < 0.001) of the difference in strength between both groups. The endurance capacity of m. quadriceps femoris was 30% lower in CHF patients than in controls, partly as a result of the 25% lower capillary density (P < 0.05) and the 27% lower aerobic enzyme capacity (P < 0.05), as estimated by the citrate synthase activity, in the CHF patients. The citrate synthase activity correlated with the maximal oxygen uptake (r = 0.61, P < 0.05). Moreover, the ejection fraction, together with the CSA of m. quadriceps femoris, explained 75% (r = 0.86%, P < 0.01) of the difference in maximal oxygen uptake between CHF patients and controls. These results demonstrate that CHF patients have both a lower local and a lower whole-body work capacity than healthy controls. This is a function of a smaller leg muscle mass and a lower capillary density and mitochondrial enzyme capacity in the CHF patients; however, a lowered pump capacity of the heart is the factor which limits the exercise capacity the most.

Aged↗
PubMed1995

Do highly physically active females have a lowered basal metabolic rate?

In several studies estimated energy intake has been found to be low compared with estimated energy expenditure in female athletes. It has therefore been suggested that female athletes may have a depressed basal energy expenditure (BMR). The main purpose of the present study was to explore this possibility by measuring BMR in physically extremely active females. Eight female dancers and 7 controls with low physical activity, all musicians, were studied; the variables measured included body weight, height, skinfold thickness and total body potassium. BMR was measured by indirect calorimetry. In conclusion, the present study lends no support to the idea of a lowered basal metabolic rate in female athletes as an explanation of the general finding of a lower estimated energy intake than energy expenditure in this type of subjects.

Adult↗
PubMed1995

Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance.

BACKGROUND: Cardiac creatine levels are depressed in chronic heart failure. Oral supplementation of creatine to healthy volunteers has been shown to increase physical performance. AIM: To evaluate the effects of creatine supplementation on ejection fraction, symptom-limited physical endurance and skeletal muscle strength in patients with chronic heart failure. METHODS: With a double-blind, placebo-controlled design 17 patients (age 43-70 years, ejection fraction < 40) were supplemented with creatine 20 g daily for 10 days. Before and on the last day of supplementation ejection fraction was determined by radionuclide angiography as was symptom-limited 1-legged knee extensor and 2-legged exercise performance on the cycle ergometer. Muscle strength as unilateral concentric knee extensor performance (peak torque, Nm at 180 degrees/s) was also evaluated. Skeletal muscle biopsies were taken for the determination of energy-rich phosphagens. RESULTS: Ejection fraction at rest and at work did not change. Performance before creatine supplementation did not differ between placebo and creatine groups. While no change was seen in the placebo group compared to baseline, creatine supplementation increased skeletal muscle total creatine and creatine phosphate by 17 +/- 4% (P < 0.05) and 12 +/- 4% (P < 0.05), respectively. Increments were seen only in patients with < 140 mmol total creatine/kg d.w. (P < 0.05). One-legged performance (21%, P < 0.05), 2-legged performance (10%, P < 0.05), and peak torque, Nm (5%, P < 0.05) increased. Both peak torque and 1-legged performance increased linearly with increased skeletal muscle phosphocreatine (P < 0.05). The increments in 1-legged, 2-legged and peak torque were significant compared to the placebo group, (P < 0.05). CONCLUSIONS: One week of creatine supplementation to patients with chronic heart failure did not increase ejection fraction but increased skeletal muscle energy-rich phosphagens and performance as regards both strength and endurance. This new therapeutic approach merits further attention.

Administration, Oral↗
PubMed1994

The effect of probucol on femoral atherosclerosis: the Probucol Quantitative Regression Swedish Trial (PQRST).

The Probucol Quantitative Regression Swedish Trial tested whether treatment of hypercholesterolemic persons with probucol for 3 years affected femoral atherosclerosis. The primary end point was the change in atheroma volume estimated as change in lumen volume of the femoral artery assessed by quantitative arteriography. Three hundred three patients with visible atherosclerosis were randomized to probucol 0.5 g, twice daily, or to placebo. All patients were given diet and cholestyramine, 8 to 16 g/day. Twenty-nine patients were excluded because of inadequate primary end point measurements. The mean age of the remaining 274 subjects (158 were men) was 55 years. Seventeen percent had intermittent claudication and 24% had angina pectoris. After 3 years, the probucol-treated patients had 17% lower serum cholesterol, 12% lower low-density lipoprotein cholesterol, 24% lower total high-density lipoprotein cholesterol, and 34% lower high-density lipoprotein2 cholesterol levels than control subjects. All lipoprotein differences between the treatment groups remained highly significant during the trial. There was no statistically significant change in lumen volume between the probucol and the control group. Furthermore, there was no difference between the treatment groups with regard to change in arterial edge roughness or amount of aorto-femoral atherosclerosis; neither were there any differences between the treatment groups with regard to change in ST-segment depressions on exercise tests or ankle/arm blood pressure (secondary end points). In the control group, lumen volume increased (p < 0.001) and roughness of the femoral artery decreased (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗
PubMed1994

Muscle strength from adolescence to adulthood--relationship to muscle fibre types.

The aim of the present study was to reinvestigate muscle strength and the relationship to muscle fibre and the level of physical activity in adult men and women previously studied during adolescence. A group of 55 men and 26 women were tested for maximal strength (handgrip, Sargent jump and two-hand lift) and completed a questionnaire concerning physical activity during their leisure time (activity index) at the ages of 16 and 27 years. Biopsy specimens were taken from the vastus lateralis and analysed for fibre type (percentage of I, IIA, IIB) and fibre area (area I, area IIA, area IIB). The sex differences in strength increased from age 16 to 17 years. Body dimension, sex, percentage of type II, mean fibre area and the activity index contributed to explaining 50-75% of the strength at both ages. Different changes in relationship between fibre type composition and strength in women and men was seen with increasing age. In the women, the relationship between strength and the percentage of type II fibres changed with age (from 16 to 27 years of age) from a positive correlation (only Sargent jump) to negative correlations for all the strength tests, i.e. the more type I fibres the stronger the subject. A positive correlation between strength and the level of physical activity during leisure time was revealed in the women at both ages. The positive correlation between strength and type II fibres in the 16-year-old men had disappeared at age 27. No systematic relationships between strength and the level of physical activity were seen in the men at either 16 or 27 years of age. It is suggested that women may be more dependent on physical activity than adult men to develop strength and the percentage of type I fibres reflects the degree of physical activity among adult women but not among adolescent women.

Adolescent↗
PubMed1994

The relation of coronary and peripheral arterial disease to the severity of femoral atherosclerosis in hypercholesterolaemia.

OBJECTIVES: The extent of atherosclerosis in the superficial femoral artery and the severity of arterial disease in the aorto-iliac and femoro-popliteal arterial districts were related to clinical diagnosis of coronary and peripheral atherosclerosis in hypercholesterolaemic patients. DESIGN: The study constitutes baseline cross-sectional data of a randomized double-blind clinical trial on Probucol, using both computer based and visual estimations of angiographies as endpoints. SUBJECTS: Two hundred and ninety men and women (mean age 54 years) with hypercholesterolaemia. MAIN OUTCOME MEASURES: Atherosclerosis was estimated with arteriographies. Lumen volume and edge roughness (vessel inner wall irregularity) of a 20 cm segment of the femoral artery were estimated by computer. A visual atherosclerosis score of the abdominal aorta to the popliteal arteries was made on both sides. RESULTS: Patients with peripheral arterial disease had significantly more advanced disease according to all three angiographic variables than those without symptoms of peripheral vascular disease. Both men and women with coronary artery disease had significantly lower femoral lumen volume and higher roughness values than patients without. Men with previous myocardial infarction had significantly higher mean visual scores of atherosclerosis than those without, while lumen volume and roughness did not differ in either sex. CONCLUSIONS: Femoral atherosclerosis is an expression of a generalized disease, associated with clinical symptoms of coronary artery disease. Femoral atherosclerosis is often accompanied by atherosclerosis also in the coronary arteries.

Adult↗
PubMed1994

Cardiovascular responses during one- and two-legged exercise in middle-aged men.

Eight healthy and regularly physically active men, 44-69 years old, performed one- and two-legged dynamic knee extension exercise at increasing work intensities, including one leading to exhaustion. Leg blood flow increased linearly in relation to work rate, reaching a peak value of 5.1 +/- 0.4 l min-1. With a mean weight of quadriceps femoris of 2.2 +/- 0.1 kg, a peak perfusion of 2.3 +/- 0.1 l kg-1 min-1 was attained. The maximal leg oxygen uptake was 0.72 +/- 0.07 l min-1 (0.33 +/- 0.03 l kg-1 min-1). At submaximal work the elevation in limb oxygen uptake accounted for between 70 and 100% of the rise in pulmonary oxygen uptake. Comparing two- with one-legged knee extension the cardiac output was 1.5 l min-1 higher at each work level, reaching 13.7 +/- 0.7 and 12.3 +/- 1.0, respectively at exhaustion, leaving 3.5 and 7.2 l min-1 of blood flow to the remaining body (cardiac output--leg blood flow). The mean arterial pressure was 119 +/- 5 mmHg at rest and increased to 155 mmHg for both test modes at the maximal work rate. The femoral arterial and venous plasma concentrations of lactate, ammonia and noradrenaline were significantly higher for two-legged as compared with one-legged exercise at the maximal load performed. However, the rate of release per leg, for both lactate and ammonia, did not differ between the two test conditions. It is concluded that physically active middle-aged men, with a well-retained muscle mass, can maintain a high skeletal muscle perfusion, similar to that of young males. However, the blood flow is achieved with a higher mean arterial pressure and an elevated sympathetic activity, as reflected by noradrenaline in plasma and spillover from the exercising limb.

Adult↗
PubMed1994

Exchange of purines in human liver and skeletal muscle with short-term exhaustive exercise.

The exchange of purines in liver and active skeletal muscle with short-term exhaustive exercise was investigated. Eight male subjects performed two similar 10-min bouts of exhaustive supine cycling, separated by 75 min of rest. Immediately after termination of the second bout, a tourniquet was applied to the upper part of the thigh for 10 min. After the first bout, the arterial concentration of hypoxanthine and uric acid increased from 4.1 +/- 0.3 (SE) to a peak value of 36.3 +/- 7.9 mumol/l (P < 0.05) and from 335 +/- 23 to a peak value of 421 +/- 28 mumol/l (P < 0.05), respectively. There was a net release of hypoxanthine from the muscle at 12 and 45 min postexercise and an uptake of hypoxanthine and inosine in the liver at 7 and 42 min postexercise. Uric acid was released from the liver at 7 and 42 min after exercise. Before the second exercise bout and at 2 and 10 min after the release of the tourniquet, there was a significant net uptake of uric acid by the muscle. The present study demonstrates that, after strenuous short-term exercise, the main source of plasma hypoxanthine is the muscle, with no net contribution of this purine from the liver. Hypoxanthine in the blood is taken up by the liver where most of it is converted to uric acid. After exercise and a short period of ischemia, uric acid is taken up by the muscle.

Adult↗
PubMed1994

Neuropeptide Y release from human heart is enhanced during prolonged exercise in hypoxia.

To evaluate the effect of hypoxemia on cardiac release of neuropeptide Y-like immunoreactivity (NPY-LI) and norepinephrine (NE), arterial and coronary sinus blood was sampled and coronary sinus blood flow was measured by thermodilution in nine healthy volunteers at rest and during supine cycle ergometer exercise while they breathed air and 12% O2, which reduced arterial O2 saturation to approximately 68%. Five subjects started to exercise for 30 min breathing air and continued for 30 min breathing 12% O2; four subjects breathed 12% O2 and air in the reverse order. The load was adjusted to give the same heart rate during O2 and air breathing. No significant cardiac net release of NPY-LI or NE was seen at rest. Exercise induced release of NPY-LI and NE. The net release of NPY-LI was 0.7 +/- 0.4 pmol/min during air breathing (average 12 and 30 min) and 2.8 +/- 0.6 pmol/min during 12% O2 breathing. The difference was not influenced by the order of the breathing periods. The NE coronary sinus-arterial difference was not significantly different between 12% O2 and air breathing, whereas the net release was significantly larger during 12% O2 breathing (0.6 +/- 0.1 vs. 0.4 +/- 0.1 nmol/min). Thus, NPY is released with NE from the heart during exercise. Arterial hypoxemia seems to be an additional stimulus of preferential NPY release.

Adult↗
PubMed1993

Increased expression of the lactate dehydrogenase M subunit in myocardial regions with decreased thallium uptake.

OBJECTIVE: In ischaemic heart disease, the heart muscle is subjected to repeated episodes of regional ischaemia or to a constant underperfusion. The purpose of the present investigation was to study the myocardial metabolic adaptation to this stress. METHODS: Eighteen male patients with ischaemic heart disease were studied by biopsies taken from the left ventricular septum during bypass surgery. Citrate synthase, total lactate dehydrogenase and its H and M subunits, coenzyme Q10, and myoglobin were determined in all biopsies. Concentrations of ATP, ADP, and AMP were determined and energy charge calculated in the biopsies from the patients with ischaemic heart disease. Biopsies from the septal region of hearts obtained from brain dead kidney and liver donors were used as reference and preoperative myocardial thallium scintigraphy was performed in the patients with ischaemic heart disease to relate the myocardial biochemical markers to thallium uptake at the biopsy site. RESULTS: Myocardial activities of citrate synthase as well as contents of coenzyme Q10 and myoglobin in patients with ischaemic heart disease were not different from those of the reference group, and no linear relation was found between these three markers on the one hand and thallium uptake on the other. The energy charge was directly related and the M subunit of lactate dehydrogenase inversely related to the thallium uptake. CONCLUSION: The results suggest an absence of adaptation to ischaemia in terms of increased myocardial oxidative capacity and O2 transport and storage capacity. Furthermore, it is indicated that a stressed energy metabolism with increasing severity of ischaemic heart disease enhances anaerobic metabolism and induces a shift in myocardial lactate dehydrogenase subunit fractions.

Adolescent↗
PubMed1993

Effects of ischaemic training on local aerobic muscle performance in man.

The aim of the study was to compare the effects of ischaemic and non-ischaemic training on aerobic performance. In 10 subjects, peak oxygen uptake (peak VO2) and time to fatigue (TTF) for one-legged exercise were measured before and after 4 weeks (4 times week-1) of one-legged training. Each training session started with one leg training for 45 min with 20% blood-flow reduction induced by local application of a supra-atmospheric external pressure of 50 mmHg (ischaemic leg; I-leg). We have previously shown that this decreases leg blood flow by about 20%. The contralateral leg (non-restricted-flow leg; N-leg), serving as a control, then trained with an identical power-output profile for 45 min but without flow restriction. In the I-leg the average training-induced increments in TTF and peak VO2 were 27 and 24%, respectively. In the N-trained leg TTF and peak-VO2 increased 10 and 14%, respectively. Both increments were significantly greater (P < 0.05) in the I-trained leg. Moreover, the performance increase in the I-trained leg was exaggerated (P < 0.05) in the ischaemic test condition, i.e. there was a specificity in the training response. In conclusion, ischaemia acts as an additive stimulus to training leading to an exaggerated increase in endurance and peak-VO2 compared to identical training without blood-flow restriction. The main explanation is probably an enhanced local adaptation in the I-trained leg.

Adult↗
PubMed1993

Muscle fibre types and enzyme activities after training with local leg ischaemia in man.

Eight healthy men performed supine one-legged training on a bicycle ergometer 45 min per leg four times per week for 4 week. The ergometer and lower body were inside a pressure chamber, the opening of which was sealed at the level of the crotch. One leg trained with impeded leg blood flow (I-leg), induced by an increased (50 mmHg) chamber pressure, at the highest tolerable intensity. The contralateral leg trained at the same power under normal pressure (N-leg). Before and after training biopsies were taken from the vastus lateralis of both legs and maximal one-legged exercise tests were executed with both legs. Biopsies were repeated when the subjects had been back to their habitual physical activity for 3 months. Training increased exercise time to exhaustion, but more in the I-leg than in the N-leg. After training, the I-leg had higher activity of citrate synthase (CS), a marker of oxidative capacity, and lower activity of the M-subunit of lactate dehydrogenase isoenzymes. It also had a higher percentage of type-I fibres and a lower percentage of IIB fibres, larger areas of all fibre types and a greater number of capillaries per fibre. It is concluded that ischaemic training changes the muscle metabolic profile in a direction facilitating aerobic metabolism. An altered fibre-type composition may contribute, but is not enough prerequisite for the change.

Adult↗
PubMed1993

Myocardial oxygen supply and lactate metabolism during marked arterial hypoxaemia.

Myocardial O2 delivery and changes in myocardial lactate metabolism during marked hypoxaemia (PaO2 5-5.4 kPa, Sa O2 70-75%) produced by 12% O2 breathing were studied in 12 healthy subjects at rest and during supine exercise up to maximal intensity. Blood for O2 and lactate analyses was sampled from catheters in an artery (a) and the coronary sinus (cs) and coronary sinus blood flow (CSBF) was measured by thermodilution. Lactate metabolism was evaluated in a subgroup of the subjects using i.v. infusion of [14C]lactate. At rest and during submaximal exercise up to heart rate 156 beats min-1 myocardial O2 uptake (MQO2) was maintained at the same level during hypoxaemia as during normoxaemia. This was achieved at rest mainly by a more complete O2 extraction, during exercise entirely by greater CSBF. During maximal exercise CSBF was 35% greater during hypoxaemia than normoxaemia, while there was no difference in cs O2 saturation. Maximal MQO2 was smaller during hypoxaemia than normoxaemia in spite of no difference in rate pressure product. The a-cs difference of lactate was reduced during hypoxaemia and there was a significant myocardial release of lactate, as calculated from [14C]lactate data, during hypoxaemic exercise, but not during hypoxaemic rest or normoxaemic rest and exercise. It is concluded that the heart has a coronary flow reserve of about 35%, which can be utilised under hypoxaemia. When this reserve is insufficient to supply the myocardium with oxygen lactate is produced to cover part of the myocardial ATP regeneration.

Adenosine Triphosphate↗
PubMed1993

Myocardial lactate release during prolonged exercise under hypoxaemia.

The possible appearance of myocardial lactate production during exercise under hypoxaemia, simulating an altitude of about 4500 metres above sea-level (masl) was investigated. Twelve healthy men were studied, after coronary sinus catheterization, during prolonged exercise breathing 12% O2 compared with men breathing air. Coronary sinus blood flow was measured by thermodilution. Exercise duration under each breathing condition was 30 min and the order normoxaemia/hypoxaemia was varied between subjects so as to compensate for any influence of a preceding exercise period on a subsequent one. Work load was adjusted so as to produce a heart rate (HR) of 130-140 beats min-1 during both hypoxaemia and normoxaemia. [14C]lactate was infused at a constant rate i.v. throughout the study to detect a possible myocardial lactate release simultaneously with a net uptake. Myocardial O2 uptake did not differ significantly between hypoxaemia and normoxaemia. The compensation for reduced blood oxygen content was achieved entirely by a greater coronary blood flow. Yet, the arterial-coronary sinus (a-cs) lactate difference was lower during hypoxaemia than normoxaemia and isotope data indicated that this was caused by a myocardial lactate release of approximately 90 mumol min-1 which was at hand during hypoxaemia but not normoxaemia, whether hypoxaemic exercise preceded or succeeded normoxaemic exercise. In conclusion, A 27% reduction in arterial oxygen saturation is almost compensated for by an increased coronary blood flow. However, during hypoxaemic exercise cardiac energy demand is to a smaller part, about 1%, covered by anaerobic metabolism.

Adult↗