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Biomedical subjects

F Lind

Publications and source records attributed to F Lind.

8 recordsLinked to original sources

Effects of sulphur hexafluoride on psychomotor performance.

The narcotic influence of sulphur hexafluoride on mental and psychomotor performance has been studied in 9 subjects at normal atmospheric pressure. Control experiments were performed with air and with nitrous oxide. Psychomotor, perceptual and cognitive abilities were assessed using a computerized test battery. Subjects were exposed to air and six different normoxic gas mixtures: 13, 26, and 39% N2O, and 39, 59, and 79% SF6. Significant performance impairments were found with 13% N2O and gradual further impairment with 26, and 39% N2O. During exposure to 39, 59, and 79% SF6 over-all performance was impaired by 5, 10, and 18%, respectively. Impairment was significant with 59 and 79% SF6. The results indicate that the relative narcotic potency of SF6: N2O is about 1:4 in humans. It is concluded that a normoxic SF6-O2 mixture can be inhaled for lung function studies without any harmful effects and that the short-lasting narcotic effect, although detectable with a test battery, would not impair the ability of the subject to perform simple breathing procedures.

Adult

Significance of airway resistance for the pattern of breathing and lung volumes in exercising humans.

The effects of increased airway resistance on lung volumes and pattern of breathing were studied in eight subjects performing leg exercise on a cycle ergometer. Airway resistance was changed 1) by increasing the density (D) of the respired gas by a factor of 4.2 and changing the inspired gas from O2 at 1.3 bar to air at 6 bar and 2) by increasing airway flow rates by exposing the subjects to incremental work loads of 0-200 W. Increased gas D caused a slower and deeper respiration at rest and during exercise and, at work loads greater than 120 W, depressed the responses of ventilation and mean inspiratory flow. Raised airway resistance induced by increases in D and/or airway flow rates altered respiratory timing by increasing the ratio of inspiratory time (TI) to total breath duration. Furthermore, analyses of the relationships between tidal volume and TI and between end-inspiratory volume and TI revealed elevation of Hering-Breuer inspiratory volume thresholds. We propose that this elevation, and hence exercise-induced increases of tidal volume, can largely be explained by previous observations that the threshold of the inspiratory off-switch mechanisms depends on central inspiratory activity (cf. C. von Euler, J. Appl. Physiol. 55: 1647-1659, 1983), which in turn increases with airway resistance (Acta Physiol. Scand. 120: 557-565, 1984).

Airway Resistance

Human skeletal muscle function and metabolism during intense exercise at high O2 and N2 pressures.

The maximal contractile force (peak torque) of the quadriceps femoris was studied during 60 repeated unilateral dynamic knee extensions in nine subjects under three different conditions, viz., during air breathing at normal (1 ATA) and raised (6 ATA) ambient pressures and during O2 breathing at 1.3 ATA. In six subjects the electromyographic (EMG) activity of the working muscle was recorded. Muscle biopsies were obtained from the vastus lateralis before, immediately after, and 1 min after exercise. Tissue specimens were subsequently assayed for various muscle metabolites. Peak torque, as an average of the 60 knee extensions, was higher (P less than 0.05) at 1.3 ATA than at 6 or 1 ATA. Peak torque of the exercising muscle declined more rapidly at 1 ATA than at 1.3 ATA, differing in the final 24 contractions by 14%. At 6 ATA peak torque of the initial 12 contractions was 6% lower (P less than 0.05) than at 1 ATA but equaled 1-ATA values in the latter third of the exercise bout. Although the EMG activity at 1 ATA increased relative to that at 6 ATA as exercise proceeded, the rate of force decline was greater at 1 ATA. Despite greater total work produced at 1.3 ATA than at 1 ATA, the metabolic response to exercise was not substantially altered at increased O2 pressure. However, the restitution rate of energy-rich phosphagens and the elimination of lactate during recovery were greater (P less than 0.05) at 1.3 ATA. These results suggest that hyperoxia may enhance the rate of energy release, whereas high N2 pressure and/or high hydrostatic pressure seem to interfere with neuromuscular activity.

Adenosine Triphosphate

Effects of blood volume distribution on ventilatory variables at rest and during exercise.

Ventilatory variables and heart rate (HR) were investigated in eight supine subjects during dynamic leg exercise at 0 and 100 W with and without the lower portion of the body exposed to a pressure of -50 mmHg (lower body negative pressure, LBNP). Resting values of inspired minute volume (V1), and respiratory drive in terms of mouth occlusion pressure (P0.1) were unchanged, whereas HR was higher during LBNP than in the control condition. Exercise values for HR in steady state were not affected by LBNP, whereas V1 was 15 and 11% lower and P0.1 was 20 and 11% lower in this condition at the 0 and 100 W workload levels, respectively. Time courses for V1 at the onset of 100 W exercise were similar with and without exposure to LBNP, indicating that the sudden increase in venous return occurring upon onset of pedalling during LBNP affords no significant stimulus in the initial development of exercise hyperpnoea. That exercise ventilation and P0.1 in steady state were reduced by LBNP suggests diminished humoral and/or locally induced chemical drive due to improved blood flow in exercising muscles resulting in reduced production of muscle metabolites or facilitation of their removal.

Adult

Breathing pattern and lung volumes during exercise.

The interrelationships of ventilation (V), tidal volume (VT), inspiratory (T1), expiratory (TE) and total breath (Ttot) durations, mean inspiratory (VT/TI) and expiratory (VT/TE) flows, and lung volumes were studied in normal subjects at rest and during exercise on a cycle ergometer. The ergometric load was increased by 10 W every minute, from zero W to 200 W. The TI/Ttot ratio increased with V in the range 15 to 60 1 X min-1, indicating that with increasing V the rate of increase of VT/TI decreased whereas that of VT/TE increased. Possible mechanisms responsible for the difference in behaviour of VT/TI and VT/TE are discussed. The VT-TI and VT-TE relationships both displayed three ranges with breakpoints at tidal volumes of about 1.4 and 2.4 1. The relations of TI and TE to end-inspiratory volume were approximately linear over the entire VT range studied, whereas the relations of TI and TE to end-expiratory volume showed three ranges with different characteristics. We conclude that the termination of inspiration during cycle exercise is dependent on volume-related afferent feedback from the lungs and/or chest walls, not only in the high but also in the low volume range.

Adult

Role of airway resistance in the control of ventilation during exercise.

To analyze the interdependence of respiratory drive, ventilation and airway resistance during exercise, mouth occlusion pressure (P0.1), minute ventilation (V) and mean inspiratory flow (VT/TI) were studied in eight normal subjects performing cycle-ergometer exercise at loads ranging from 0 W to 200 W under two different ambient conditions: 1) during oxygen breathing at 1.3 ATA, and 2) during air breathing at 6 ATA (PO2 = 1.3 ATA). Comparison of measurements at 6 ATA with those at 1.3 ATA indicated that a 4.2-fold increase in respired gas density (D) had little or no influence on the V and VT/TI responses whereas P0.1 at any given VT/TI was increased by a factor of 1.9. In both conditions, P0.1 increased at a faster rate than VT/TI as the work load increased. At loads higher than 40 W, the relationship between P0.1, D and VT/TI was found to approximate the equation P0.1 = K X D0.5(VT/TI)1.4, where K is a constant that varies among subjects. The results indicate that the ratio P0.1/(VT/TI), an estimate of respiratory impedance, increased with both D and VT/TI. Evidence is presented that the respiratory drive was reflexly enhanced in response to loading as airway resistance increased with D and/or VT/TI. We conclude that neural mechanisms compensating for internal flow-resistive loading play an important role in the control of ventilation during exercise, both at normal and at raised air pressures.

Adult

Breathing pattern and occlusion pressure during moderate and heavy exercise.

We studied changes in breathing pattern and mouth occlusion pressure (P0.1) in 11 healthy subjects performing graded steady-state exercise on a cycle ergometer up to the maximal load sustainable for 4 min. With increasing work intensity both the tidal volume (VT) and end-inspiratory volume relations to inspiratory (TI) and expiratory (TE) durations were linear in the moderate work load range; in the high load range VT and end-inspiratory volume tended to plateau with further decreases in TI and TE. The ratio of TI to total breath duration (TI/Ttot) increased with work intensity. Intraindividual coefficients of variation for VT, breathing frequency (f), mean inspiratory flow (VT/TI), and other respiratory variables decreased with increasing work intensity, indicating that breath-to-breath variations in breathing pattern became smaller as the level of ventilation increased. P0.1 rose with VT/TI as a power function with an exponent averaging 1.5 (range 1.3-1.9), indicating that the ratio P0.1/(VT/TI), an index of respiratory system impedance, increased with VT/TI and work intensity. We conclude that in moderate and heavy exercise the work of inspiration at a given ventilation is reduced because of the increase in TI/Ttot, the impedance of the respiratory system increases with work intensity because of both an increase in f and a flow-dependent rise in airway resistance, and the neuromuscular inspiratory activity is reflexly augmented because of internal flow-resistive loading.

Adult

Ventilatory and occlusion-pressure responses to incremental-load exercise.

Mouth occlusion pressure (P0.1), minute ventilation (V), and mean inspiratory and expiratory flows were studied in eight normal subjects at rest and during exercise on a cycle ergometer, the load of which was increased in steps of 10 W every minute. All four variables rose curvilinearly as the load was increased from 0 to 200 W. The ratio of P0.1 to mean inspiratory flow, like the ratio P0.1/V, increased with work load in the range 40-200 W, indicating that P0.1 increased considerably faster than mean inspiratory flow and V at rates higher than about 0.7 L X sec-1 and 15 L X min-1, respectively. Evidence is presented that the progressive divergence of the P0.1 and ventilatory responses was a result of raised respiratory impedance consequent to increasing respiratory frequency and resistance, and that, concurrently, the respiratory drive as assessed by P0.1 was enhanced because of an active load-compensating response. In this way, the respiratory drive increased with work load in a self-adjusting fashion, compensating for the impedance-dependent alterations in ventilatory responses. We also conclude that in moderate and heavy exercise P0.1 is a more representative index of the respiratory drive than are V and mean inspiratory flow.

Adult