Biomedical subjects

B Hanel

Publications and source records attributed to B Hanel.

At least 19 recordsLinked to original sources

PubMed2000

Pulmonary function after exercise with special emphasis on diffusion capacity.

The present work focuses on pulmonary gas exchange during repeated rowing to exhaustion and the recovery of pulmonary diffusion capacity for carbon monoxide (DL) after exercise in healthy young subjects. The components of DL are examined at rest using the single breath method at two different alveolar O2 tensions. Electrical impedance and 99mTechnetium labelled erythrocytes were used to evaluate the recovery of blood distribution. Special attention has been given to the role of the inspiratory muscles as a limiting factor for VO2max and performance. The documentation in this study of a reduced DL several hours after exercise conflicts with the prerequisites of optimal conditions for high metabolic rates in elite athletes. Even low intensity exercise induces a reduction in DL, and together with the fact that a diuretic does not attenuate this decrease, emphasises that the reduction in DM is not due to an interstitial pulmonary edema. The major part of the reduction is due to a decreased CBV reflected in a reduction of VC and a minor part is caused by an injury to the membrane component carried over from exercise. The ability in athletes to repeat exhaustive exercise within 2 h indicates that the slow recovery of DL is not combined with either impaired pulmonary gas exchange or performance. Thus, an acute diffusion limitation and a low pH cause the desaturation in some athletes during exhaustive exercise. Despite the inspiratory muscles having a slower response to endurance training compared with the cardiovascular system, selective training of the inspiratory muscles does not improve either VO2max or performance. This indicates that maximal inspiratory pressure is not a limiting factor for maximal exercise and that the stimuli to increase VA depends on an increased metabolic rate; stressing the role of the peripheral chemoreceptors. Together with the post-exercise decrease in ANP, the reduction in DL may be involved in the mechanism increasing the total blood volume in endurance trained athletes.

Adolescent↗

PubMed1999

Cardiovascular and neuroendocrine responses to exercise in hypoxia during impaired neural feedback from muscle.

Reflex mechanisms from contracting skeletal muscle have been shown to be important for cardiovascular, neuroendocrine, and extramuscular fuel-mobilization responses in exercise. Furthermore, because hypoxia results in exaggerated metabolic changes in contracting muscle, the present study evaluated whether enhancement of cardiovascular and neuroendocrine responses by hypoxia during exercise is influenced by neural feedback from contracting muscle. Seven healthy males cycled at 46% maximal O(2) uptake for 20 min both during normoxia and at 11.5% O(2), and both without and with epidural anesthesia (EA; 20 ml 0.25% bupivacain, resulting in cutaneous hypesthesia below T10-T12 and 25% reduction in maximal leg strength). Exercise to exhaustion was also performed at 7.8% O(2). The exercise-induced increases in heart rate; cardiac output; leg blood flow; plasma concentrations of growth hormone, adrenocorticotropin, cortisol, and catecholamines; renin activity; glucose production and disappearance; norepinephrine spillover [2, 190 +/- 341 ng/min (exercise at 11.5% O(2)) vs. 988 +/- 95 ng/min (exercise during normoxia)]; lactate release from and glucose uptake in the leg; and the decreases in plasma insulin and free fatty acids were exaggerated in hypoxia (P < 0.05). In muscle, concentrations of lactate, creatine, and inosine 5'-monophosphate were higher, and those of phosphocreatine were lower after exercise in hypoxia compared with normoxia. The exercise-induced increase in mean arterial blood pressure was not affected by hypoxia, but it was reduced by EA [108 +/- 4 mmHg (control) vs. 97 +/- 4 mmHg (EA); P < 0.05], and the reduction was more pronounced during severe hypoxia compared with normoxia. Apart from this, time to exhaustion at extreme hypoxia, circulatory responses, concentrations of neuroendocrine hormones, and extramuscular substrate mobilization were not diminished by EA. In conclusion, in essence the hypoxia-induced enhancement of systemic adaptation to exercise is not mediated by neural feedback from working muscle in humans.

Adult↗

PubMed1998

False-positive defects in technetium-99m sestamibi myocardial single-photon emission tomography in healthy athletes with left ventricular hypertrophy.

Exercise ECG and myocardial single-photon emission tomography (SPET) are fundamental in the non-invasive evaluation of patients suspected of having coronary artery disease (CAD). The purpose of the present study was to investigate the influence of physiological left ventricular hypertrophy (LVH) on myocardial sestamibi SPET in healthy young and old athletes. Eighteen young male elite athletes (ten rowers, five power/weight lifters and three triathletes) and 14 well-trained elderly rowers were studied. All underwent a bicycle test as part of a 2-day sestamibi SPET protocol. Attenuation correction was not performed. The studies were evaluated visually and quantitatively analysed by the CEqual program with its reference files and with a file from a local non-athletic age-matched population. Echocardiographic LVH was an inclusion criterion in the young athletes. Exercise ECG was normal in all subjects. In at least three of the young athletes a reversible defect was observed by visual analysis. On quantitative analysis one-third of the young athletes had "significant" (>10 pixels) defects compared with both the local reference base and the CEqual reference population. Nearly all defects were found in the anterior or inferior wall. The remaining subjects, including all old rowers, had normal SPET findings. Anterior and inferior wall defects are so common in healthy athletes with physiological LVH that the specificity of myocardial SPET, in contrast to exercise ECG, seems to be too low for evaluation of chest pain in this group. The mechanism of anterior and inferior defects may be related to hot spots (papillary muscles?) in the lateral wall. The specificity of SPET is maintained in athletes without LVH.

Adult↗

PubMed1997

Middle cerebral artery blood velocity during rowing.

Dynamic exercise increases the transcranial Doppler determined mean blood velocity in basal cerebral arteries corresponding to the cortical representation of the active limb(s) and independent of the concomitant rise in the mean arterial pressure. In 12 rowers we evaluated the middle cerebral artery blood velocity response to ergometer rowing when regulation of the cerebral perfusion is challenged by stroke synchronous fluctuation in arterial pressure. Rowing increased mean cerebral blood velocity (57 +/- 3 to 67 +/- 5 cm s-1; mean +/- SE) and mean arterial (86 +/- 6 to 97 +/- 6 mmHg) and central venous pressures (0 +/- 2 to 8 +/- 2 mmHg; P < 0.05). The force on the oar triggered an averaging procedure that demonstrated stroke synchronous sinusoidal oscillations in the cerebral velocity with a 12 +/- 2% amplitude upon the average exercise value. During the catch phase of the stroke, the mean velocity increased to a peak of 88 +/- 7 cm s-1 and it was in phase with the highest mean arterial pressure (125 +/- 14 mmHg), while the central venous pressure was highest after the stroke (20 +/- 3 mmHg). The results suggest that during rowing cerebral perfusion is influenced significantly by the rapid fluctuations in the perfusion pressure.

Adult↗

PubMed1997

Restricted postexercise pulmonary diffusion capacity and central blood volume depletion.

Pulmonary diffusion capacity for carbon monoxide (DLCO), regional electrical impedance (Z0), and the distribution of technetium-99m-labeled erythrocytes together with concentration of plasma atrial natriuretic peptide (ANP) were determined before and after a 6-min "all-out" row in nine oarsmen and in six control subjects. Two and one-half hours after exercise in the upright seated position, DLCO was reduced by 6 (-2 to 21; median and range) %, the thoracic-to-thigh electrical impedance ratio (Z0 thorax/Z0 thigh) rose by 14 (-1 to 29) %, paralleled by a 7 (-3 to 11) % decrease and a 3 (-5 to 12) % increase in the thoracic and thigh blood volume, respectively. These responses were associated with a decrease in the plasma ANP concentration from 15 (13-31) to 12 (9-27) pmol/l (P < 0.05). Similarly, in the supine position, Z0 thorax/Z0 thigh increased by 10 (-5 to 28) % when DLCO was reduced 12 (6-26) % (P < 0.05), whereas DLCO remained stable in the control group. The increase in Z0 thorax/Z0 thigh and the corresponding redistribution of the blood volume in both body positions show that approximately one-half of the postexercise reduction of DLCO is explained by a decrease in the pulmonary blood volume. The role of a reduced postexercise central blood volume is underscored by the lower plasma ANP, which aids in upregulating the blood volume after exercise in athletes.

Adult↗

PubMed1996

Lymphocyte, NK and LAK cell responses to maximal exercise.

To evaluate if exhaustion after maximal exercise suppresses the immune system; ten healthy male oarsmen (maximal oxygen uptake, 5.7 +/- 0.2 l.min-1; mean and SE) performed a six minute "all-out" bout on a rowing ergometer (394 +/- 12 watt). Rowing increased the blood leucocyte count as reflected in the concentrations of lymphocytes, monocytes, and neutrophils. Two hours after rowing the leucocyte and neutrophil numbers remained elevated, while the lymphocyte count decreased below the prevalue. The concentrations of cluster designation CD3+ (pan T), CD4+ (T subset), CD8+ (T subset), CD19+ (B cells), and CD16+ natural killer (NK) cells increased during rowing with the elevation in CD16+ cells being sevenfold. Only the concentration of CD3+ and CD8+ cells decreased below prevalues two hours after exercise. The lymphokine activated killer (LAK) cell activity of blood mononuclear cells (BMNC), and the NK cell activity of BMNC (%lysis per fixed number of BMNC), either unstimulated or stimulated with interleukin-2, interferon-alfa or indomethacin, also increased in response to rowing, and returned to the prevalues after two hours. In contrast, the BMNC proliferative responses did not change significantly. The evaluation of NK and LAK cell activities, and the proliferative responses of BMNC suggest that six minute maximal exercise does not suppress the immune response during recovery, even when a large muscle mass is involved.

Adult↗

PubMed1996

The heart of the senior oarsman: an echocardiographic evaluation.

We evaluated left ventricular mass and function in 15 oarsmen aged 78 (65-82) yr (median and range) and in 15 sedentary males aged 72 (65-81) yr by 2-D and M-mode echocardiography and cycle ergometry. The weekly time spent exercising among the oarsmen was 6 (2-18) h and two of the oarsmen were former national and international champions. The two groups of subjects had similar weight, height, and resting blood pressure. The oarsmen reached a maximal work rate of 142 (117-174) vs 113 (75-150) W for the sedentary group (P < 0.01). The internal diameters of the left ventricle were not significantly different, but the septum and posterior wall thicknesses were larger in the oarsmen (11 (8-20) vs 9 (7-11) mm, and 9 (8-13) vs 8 (7-19) mm, respectively, P < 0.023). Thus, the left ventricular mass index of the oarsmen was 19% larger (127 (101-284) vs 103 (74-134) g.m-2, P < 0.01). Also, the systolic function appeared to be superior in the oarsmen as the fractional shortening was 0.45 (0.28-0.55) vs 0.36 (0.18-0.49) in the controls (P < 0.05). In conclusion, we found that long-term rowing in the senior oarsman is associated with enlarged myocardial wall thickness, a normal systolic function, and a high work capacity.

Aged↗

PubMed1995

Restricted pulmonary diffusion capacity after exercise is not an ARDS-like injury.

Pulmonary diffusion capacity (DLCO) is reduced 2 h after various types of exercise, such as rowing, treadmill running, arm cranking and marathon running. The decrease in DLCO may involve alterations in the alveolar-capillary membrane as well as depletion of the central blood volume. We hypothesized that the reduction in DLCO might also be influenced by oxygen free radicals, acute phase proteins and endotoxin, which are also involved in the adult respiratory distress syndrome (ARDS). Ten competitive male oarsmen performed a 6 min 'all-out' ergometer row. Single breath DLCO was determined before and 2 h after rowing and venous blood samples were also obtained during the row. Absolute DLCO decreased by 11% (range 0-20%) 2 h after rowing, whereas the concentration of endotoxin did not change significantly and interleukin (IL)-1-alpha, IL-8 and tumour necrosis factor (TNF)-alpha were below the levels of detection before, during and 2 h after rowing. Oxygen free radicals were evaluated by oxidative modification of amino acids and DNA. Corrected for creatinine in urine voided 3 h post-exercise, the DNA repair product 8-oxo-7,8-dehydro-2-deoxyguanosine (8-oxodG) did not change significantly. The ratio of fluorescence due to dityrosine to that due to tryptophan in plasma proteins increased after exercise. This might reflect an effect of oxygen free radicals, but it might also indicate an altered relative composition of plasma proteins. These results suggest that the reduced pulmonary diffusion capacity following exercise is unrelated to factors typically associated with ARDS.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1995

Natural killer cell response to exercise in humans: effect of hypoxia and epidural anesthesia.

For the response of immunologically competent blood cells to exercise, the importance of afferent nerve impulses was evaluated. On separate days, seven males cycled in a recumbent position approximately 60% of maximal O2 uptake with and without sensory nerve blockade by lumbar epidural anesthesia. Blood samples were collected after 60 min of rest, 20 min of exercise, and 120 min postexercise. Subsequently, on each day, the subjects were exposed to 11.5% O2-88.5% N2 for 10 min. This was followed by 20 min of hypoxic exercise at the same work rate, and a final blood sample was obtained. The concentrations of lymphocytes expressing the cluster designation (CD) cell-surface antigens CD3, CD4, CD8, and CD14 became elevated during exercise, and these responses were enhanced by hypoxia (P < or = 0.01). The most pronounced changes were within the concentrations of CD16+ and CD56+ natural killer cells, which increased twofold during normoxic and fivefold during hypoxic exercise (P < or = 0.01). Sensory nerve blockade decreased the number of CD3+ and CD4+ cells and increased the percentage of CD16+ cells, independent of exercise and hypoxia (P < or = 0.05). Sensory nerve blockade caused minor enhancement in the increase of unstimulated natural killer cell activity during exercise (P = 0.07) and enhanced the interferon-alpha-stimulated activity at normoxia (P < or = 0.05), whereas no effect was detected at hypoxia. The results demonstrate that the responses of immunological competent cells to normoxic and hypoxic exercise are not abolished by blockade of nerve impulses from active muscle.

Adult↗

PubMed1994

Hypoxia and training-induced adaptation of hormonal responses to exercise in humans.

To establish whether or not hypoxia influences the training-induced adaptation of hormonal responses to exercise, 21 healthy, untrained subjects (2) years, mean (SE)] were studied in three groups before and after 5 weeks' training (cycle ergometer, 45 min.day-1, 5 days.week-1). Group 1 trained at sea level at 70% maximal oxygen uptake (VO2max), group 2 in a hypobaric chamber at a simulated altitude of 2500 m at 70% of altitude VO2max, and group 3 at a simulated altitude of 2500 m at the same absolute work rate as group 1. Arterial blood was sampled before, during and at the end of exhaustive cycling at sea level (85% of pretraining VO2max). VO2max increased by 12 (2)% with no significant difference between groups, whereas endurance improved most in group 1 (P < 0.05). Training-induced changes in response to exercise of noradrenaline, adrenaline, growth hormone, beta-endorphin, glucagon, and insulin were similar in the three groups. Concentrations of erythropoietin and 2,3-diphosphoglycerate at rest did not change over the training period. In conclusion, within 5 weeks of training, no further adaptation of hormonal exercise responses takes place if intensity is increased above 70% VO2max. Furthermore, hypoxia per se does not add to the training-induced hormonal responses to exercise.

Adaptation, Physiological↗

PubMed1994

Maximal inspiratory pressure following endurance training at altitude.

Effects of endurance training on maximal inspiratory pressure and fatigue were evaluated after 5 weeks. Twelve male and 9 female untrained subjects were matched in the three groups for sex and maximal oxygen uptake (VO2 max). Training was performed at 70% VO2max; 45 min day-1; 5 days week-1 (n = 7); and at the same relative (n = 7) and absolute (n = 7) work loads in a pressure chamber corresponding to 2500 m (560 mmHg). Work load was increased every week to maintain the training heart rate. Maximal respiratory pressure was measured at the mouth before and 30, 60 and 120 s after maximal exercise. With no significant difference between the three groups of subjects, VO2max increased from 2.96 (1.98-4.47) (median and range for 21 subjects) to 3.33 (2.50-4.72) 1 min-1 (p < 0.001) and ventilation (VE max) from 109 (57-147) to 123 (73-148) 1 min-1 (p < 0.001), while maximal heart rate decreased from 193 (180-211) to 192 (169-207) beats min-1 (p < 0.01). Maximal inspiratory pressure (87 (56-115) mmHg), inspiratory muscle fatigue (18 (-2-43)%, p < 0.001), and arterial oxygen tension during exercise (12.4 (9.9-15.6)kPa) were similar before and after training. The results demonstrate that training at simulated altitude at 2500 m does not increase VE max or VO2 max above the increases obtained from training at sea level. Furthermore, VEmax and VO2 max increased approximately 13% despite unchanged maximal inspiratory pressure and inspiratory muscle fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Restricted postexercise pulmonary diffusion capacity does not impair maximal transport for O2.

We evaluated whether the postexercise reduction of pulmonary diffusion capacity for carbon monoxide (DLco) is influenced by a second bout of rowing and whether it affects arterial O2 tension during maximal exercise. After exercise, DLco was reduced [from a median of 37 (range of 30-44) to 34 (27-40) ml.min-1.mmHg-1; n = 21; P < 0.001], and both the membrane diffusion capacity [from 80 (58-139) to 68 (54-104) ml.min-1.mmHg-1] and the pulmonary capillary blood volume [from 88 (74-119) to 79 (61-121) ml; P < 0.01] were affected. A second bout of exercise did not influence DLco or membrane diffusion capacity (n = 7), but during both bouts arterial O2 tension was reduced [from 105 (91-110) to 91 (77-102) Torr; P < 0.001] and arterial O2 saturation decreased [from 0.98 (0.97-0.99) to 0.95 (0.86-0.96); P < 0.001]. Furosemide (iv) did not affect DLco (n = 7), suggesting that it was influenced by the central blood volume rather than by pulmonary edema.

Adult↗

PubMed1994

Arterial blood pressure response to rowing.

Ten male oarsmen performed a 6-min bout of "all-out" exercise on a rowing ergometer in the laboratory. Intraarterial blood pressure was recorded from a catheter inserted percutaneously into the radial artery. Mean arterial pressure increased only modestly from 110 +/- 13 to 122 +/- 24 mm Hg (P < 0.05). Large fluctuations in pressure were superimposed on the normal blood pressure waveform during rowing. These rhythmic pressure fluctuations exhibited a one-to-one coupling with stroke rate and were 2-3 times the magnitude of the normal pulse pressure. Thus, the effective pulse pressure during the 1st minute of rowing (112 +/- 11 mm Hg) was markedly higher (P < 0.01) than the pulse pressure at rest (45 +/- 5 mm Hg) and remained so throughout the exercise bout. In five additional subjects in which central venous pressure (CVP) was measured, large stroke-related fluctuations in pressure were also seen in the CVP waveform. Similar fluctuations in blood pressure were observed during repetitive Valsalva maneuvers. These results suggest that the blood pressure response to rowing is principally influenced by a Valsalva-like maneuver performed at the catch of each stroke. The observed arterial pressure fluctuations may explain the degree of myocardial hypertrophy that occurs in the hearts of rowers.

Adult↗

PubMed1993

Influence of exercise intensity and duration on post-exercise pulmonary diffusion capacity.

Pulmonary diffusion capacity has been observed to be reduced by approximately 14% 2h after 4-6 min of maximal exercise. The purpose of this study was to determine if the decrease in pulmonary diffusion capacity also occurs when the duration of exercise intensity is shorter or when the exercise intensity is lower. We measured pulmonary diffusion capacity using the single breath method in 12 competitive rowers 22 (16-31) years old, 70 (56-100) kg body weight, and 180 (171-193) cm body height under two conditions: (1) 2h after 6 min of rowing at both 61% (58%-68%) and 76% (73%-78%) of maximal oxygen uptake; (2) 2h after 1, 2, or 3 min of all-out rowing. Values are presented as medians with ranges. Pulmonary diffusion capacity was reduced by 6% (2%-17%) after 6 min of rowing at 61% and by 10% (-7%-21%) after 6 min of rowing at 76% of maximal oxygen uptake (p < 0.03). Pulmonary diffusion capacity was reduced by 7% (3%-19%), 8% (2%-17%) and 7% (1%-16%) after 1, 2, and 3 min of all-out rowing (p < 0.01). We conclude that submaximal exercise at 61% of maximal oxygen uptake will affect pulmonary diffusion capacity following exercise as will shorter duration of maximal exercise. Although the mechanism for this fall in pulmonary diffusion capacity is unclear, the fact that it occurs after even mild exercise makes a significant change in pulmonary capillary membrane integrity or subclinical pulmonary edema unlikely.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1992

Recovery of pulmonary diffusing capacity after maximal exercise.

Pulmonary diffusing capacity (DICO), together with spirometric variables, arterial oxygen tension (paO2) and cardiac output were determined before and at intervals after maximal arm cranking, treadmill running and ergometer rowing. Independent of the type of exercise, D1CO increased immediately post-exercise from a median 13.6 (range 7.3-16.3) to 15.1 (9.3-19.6) mmol min-1 kPa-1 (P < 0.01). However, it decreased to 11.6 (6.9-15.5) mmol min-1 kPa-1 (P < 0.01) after 24 h with cardiac output and paO2 at resting values, and D1CO normalized after 20 h. Thoracic electrical impedance at 2.5 and 100 kHz increased slightly post-exercise, indicating a decrease in thoracic fluid balance, and there were no echocardiographic signs of left ventricular failure at the time of the decrease in D1CO. Also, active muscle (limb) circumference and volume, and an increase in haematocrit from 43.8 (38.0-47.0) to 47.1 (42.7-49.8) (P < 0.01), had normalized at the time of the decrease in D1CO. Vital capacity, forced vital capacity, forced expiratory volume in 1 s, peak and peak mid-expiratory flows did not change. However, total lung capacity increased from 6.8 (5.0-7.6) to 7.0 (5.1-7.8) litres (P < 0.05) immediately after exercise and remained elevated at 6.9 (5.1-8.7) litres (P < 0.05) when a decrease in D1CO was noted. The results demonstrate that independent of the type of maximal exercise, an approximate 15% reduction in D1CO takes place 2-3 h post-exercise, which normalizes during the following day of recovery.

Adult↗

PubMed1992

Middle cerebral artery flow velocity and blood flow during exercise and muscle ischemia in humans.

Changes in middle cerebral artery flow velocity (Vmean), measured by transcranial Doppler ultrasound, were used to determine whether increases in mean arterial pressure (MAP) or brain activation enhance cerebral perfusion during exercise. We also evaluated the role of "central command," mechanoreceptors, and/or muscle "metaboreceptors" on cerebral perfusion. Ten healthy subjects performed two levels of dynamic exercise corresponding to a heart rate of 110 (range 89-134) and 148 (129-170) beats/min, respectively, and exhaustive one-legged static knee extension. Measurements were continued during 2-2.5 min of muscle ischemia. MAP increased similarly during static [114 (102-133) mmHg] and heavy dynamic exercise [121 (104-136) mmHg] and increased during muscle ischemia after dynamic exercise. During heavy dynamic exercise, Vmean increased 24% (10-47%; P less than 0.01) over approximately 3 min despite constant arterial carbon dioxide tension. In contrast, static exercise with a higher rate of perceived exertion [18 (13-20) vs. 15 (12-18) units; P less than 0.01] was associated with no significant change in Vmean. Muscle ischemia after exercise was not associated with an elevation in Vmean, and it did not provoke an increase in Vmean after static exercise. Changes in Vmean during exercise were similar to those recorded with the initial slope index of the 133Xe clearance method. The data show that middle cerebral artery mean flow velocity reflects changes in cerebral perfusion during exercise. Furthermore, they support the hypothesis that cerebral perfusion during exercise reflects an increase in brain activation that is independent of MAP, central command, and muscle metaboreceptors but is likely to depend on influence of mechanoreceptors.

Adult↗

PubMed1992

Leg vasoconstriction during dynamic exercise with reduced cardiac output.

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 71 +/- 12 to 145 +/- 13 W (40-84% maximal oxygen uptake). Exercise was repeated after cardioselective (beta 1) adrenergic blockade (0.2 mg/kg metoprolol iv). Leg blood flow and cardiac output were determined with bolus injections of indocyanine green. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. beta 1-Blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively (P < 0.001). Mean arterial pressure was lower than control during light exercise with beta 1-blockade but did not differ from control with greater exercise intensities. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl.min-1.mmHg-1, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min (P < 0.01) and 4.6 +/- 0.4 cl.min-1.mmHg-1 (P < 0.05). During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

The effect of normoxic or hypobaric hypoxic endurance training on the hypoxic ventilatory response.

Cross-sectional studies in endurance athletes have demonstrated a diminished hypoxic ventilatory response (HVR) compared with mountaineers or sedentary controls. Conversely, short-term altitude acclimatization may increase the HVR. The longitudinal effect of training, either at sea level or altitude, on HVR has not been previously reported. We therefore studied 21 untrained men and women before and after 5 wk of cycle ergometer training at either sea level or 2,500 m. HVR was determined using the steady-state method (16). Minute ventilation (VE) was measured with a Tissot spirometer during the last minute of 5 min breathing room air, 8% and 12% O2, administered in random order. CO2 was added at the mouth in an effort to maintain end-tidal CO2 at baseline levels. Oxyhemoglobin saturation was measured directly from arterial blood with a hemoximeter (OSM 3). HVR was defined as the positive slope of the line relating VE to O2 saturation in l.min-1%-1. One group of subjects trained at sea level at 70% maximal oxygen uptake (VO2max; N = 7). A second group trained at 2,500 m in a hypobaric chamber, at the same relative exercise intensity (i.e., 70% altitude VO2max) or same absolute intensity (same power output) as group 1 (N = 14). Both groups trained on a bicycle ergometer for 45 min.d-1, 5 d.wk-1 for 5 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗