Biomedical subjects

D Linnarsson

Publications and source records attributed to D Linnarsson.

67 records · Page 4Linked to original sources

PubMed1981

The effect of swimming on patients with ischemic heart disease.

Swimming is frequently recommended for cardiac rehabilitation, but little is known of its physiologic consequences in ischemic heart disease. Eight males who had had a myocardial infarction 8-17 months before the study were exercised to exhaustion or angina with 10 W/min-1 ramp on a cycle ergometer in sitting and supine positions. Oxygen uptake (VO2) was continuously measured to monitor the physiologic power requirement. All eight patients were taking beta blockers and four were taking digoxin. During sitting cycling, angina occurred in four and ST depression in five; during supine cycling, angina occurred in five and ST depression in six. VO2 was then measured while they swam at their own comfortable speed (mean 0.43 m/sec-1) in a swimming flume at water temperatures of 25.5 degrees C and 18 degrees C. In six, the water speed was gradually increased until they were limited by symptoms. Comfortable swimming at 25.5 degrees C was 87% (1.28 1/min-1) and at 18 degrees C 89% (1.30 1/min-1) of sitting peak VO2, while heart rates were 92% and 91% respectively. The mean peak VO2 and heart rate did not differ significantly between bicycle and swim tests (peak VO2 sitting 1.49 +/- 0.23, supine 1.42 +/- 0.24, 25.5 degrees C 1.60 +/- 0.17, 18 degrees C 1.52 +/- 0.19 1/min-1). Only two patients reported angina while swimming in warm water and one in cold water, although ST depression occurred in six in both swims. The subjective comfort and large muscle groups involved make swimming a good exercise, but the high relative energy cost and failure to identify ischemic symptoms indicate caution in cardiac patients, especially if their swimming skills are poor.

Aged↗

PubMed1978

Dissociated ventilatory and central respiratory responses to CO2 at raised N2 pressure.

The effects of hyberbaric nitrogen on the responses of ventilation and central inspiratory activity (CIA) to progressive hypercapnia were studied in eight subjects rebreathing a) O2 at an ambient pressure of 1.3 bar (control), and b) air at 6.1 bar (PO2 = 1.3 bar, PN2 = 4.8 bar). Inspiratory occlusion pressure (P0.1), pulmonary ventilation, and end-tidal PCO2 were used for the computation of individual CIA and ventilatory CO2 response curves. Increasing the inspired PN2 to 4.8 bar caused, on the average, a 40% increase of P0.1 at PCO2 = 50 Torr, whereas the slope of the ventilatory CO2 response curve was reduced by 39%. It was concluded that, at raised air and nitrogen pressures, CIA is increased, although not sufficiently to prevent a reduction of ventilation brought about by the increased gas density and consequent increase in airway resistance. The increased airway resistance is thought to be responsible for the increase in CIA by causing a reflex stimulation of the respiratory centers.

Adult↗

PubMed1977

Cardiopulmonary readjustments during graded immersion in water at 35 degrees C.

Six normal male volunteers, aged 25 to 34, suspended vertically in a harness that allowed them to completely relax their postural muscles, were studied in four randomly ordered conditions, namely in air at 28 degrees C, and immersed in water at 35 degrees C to the level of the hips, the xiphoid, or the chin. In each situation, several variables were measured by noninvasive techniques. Cardiac output rose from 5.11 min-1 (air) to 8.31-min-1 (chin), the increase in each of the three steps being significant at the 0.001 level. Heart rate dropped from 76 to 68 min-1 (P less than 0.001) from air to xiphoid immersion, but appeared to rise again (P less than 0.02) during chest immersion. Functional residual capacity decreased marginally during lower limb submergence, and considerably in each of the following stages. Pulmonary capillary blood volume rose significantly only during abdomen immersion. The arterial-endtidal PCO2 difference was minimally reduced as water reached hip level and then remained steady. Mixed venous PO2 increased during abdomen submergence, and PVCO2, was unaltered throughout. Analysis of the step-to-step changes demonstrates that some variables are set by a combination of processes which may counteract each other, and explains the difference between results obtained by previous investigators.

Adult↗

PubMed1977

Cardiorespiratory and metabolic responses to positive, negative and minimum-load dynamic leg exercise.

Cardiorespiratory and metabolic responses to steady-state dynamic leg exercise were studied in seven male subjects who performed positive and negative work on a modified Krogh cycle ergometer at loads of 0, 16, 33, 49, 98, and 147 W with a pedalling rate of 60 rpm. In positive work, O2 uptake increased with the ergometric load in a parabolic fashion. Net O2 uptake averaged averaged 220 ml-min-1 at 0 W (loadless pedalling), and was 75 ml-min-1 lower at the point of physiological minimum load which occurred in negative work at approximately 9 W. The O2 cost of loadless pedalling is for one-third attributed to the work of overcoming elastic and viscous resistance, the remaining part being due mainly to the work of antagonistic muscle contraction in the moving legs. Although at a given VO2, work rate was much higher in negative than in positive work, corresponding values for VE were similar, suggesting that the mechanical tension in working muscles is of little or no importance in the control of ventilation in steady-state exercise. Heart rate increased linearly with VO2 in both positive and negative work, with a steeper slope in negative work. Evidence is presented that none of the current definitions of muscular efficiency yields the true efficiency of muscular contraction in cycle ergometry, net efficiency calculation resulting in too low estimates, and work and delta efficiency calculations in overestimated values in the low-intensity work range, and in underestimated values in the high-intensity range.

Adolescent↗

PubMed1976

Autonomic origin of heart rate fluctuations at the onset of muscular exercise.

The time courses of the heart rate (HR) changes were studied in six healthy male subjects who performed step changes from rest to light dynamic leg exercise (50 W) in the sitting position during a) control, b) parasympathetic blockade (atropine, 2-2.5 mg iv), c) beta-adrenergic blockade (propranolol, 10 mg iv), and d) during combined blockade with both drugs. During the control and beta-blockade experiments all subjects showed an immediate, rapid increase in HR, reaching a peak value after about 10 s, whereafter an equally rapid transient drop by 10-20 beats/min took place reaching the lowest values about 17 s after the onset of work. HR then again increased to reach a steady-state level within 60-90 s. In the atropine experiments this response pattern was not evident at all, whereas in the experiments with combined blockade it could be distinguished to a small, but significant degree. It is concluded that the observed fluctuations of HR at the onset of light dynamic exercise can be explained by a rapid vagal withdrawal, followed by a transient increase in vagal tone.

Adult↗

PubMed1975

Time courses of pulmonary gas exchange and heart rate changes in supine exercise.

The time courses of ventilation (VE), O2 uptake (VO2), CO2 elimination (VCO2), respiratory exchange ratio (R), end-tidal PO2 and PCO2 and heart rate (HR) were studied in seven subjects performing light dynamic leg exercise in the supine position. Individual and group mean time courses in response to step changes in work load were computed and displayed graphically. A computer-based method was also used to fit mono- or bi-exponential mathematical functions to the recorded responses. The over-all rate of HR change in response to the transition from 0-load pedalling to exercise (on-response) was faster (mean response time, MRT = 31 s) than the corresponding VO2 response (MRT = 45 s) while VE responded considerably slower (MRT = 86 s). During the reverse transition (off-response), VO2 and VE changed with the same rate as in the on-response, while the HR-change was slower than during the on-response (MRT = 50 s). During the initial 15-sec period, VO2 changed only slightly, which contrasts to previous results in the sitting position, where 50% of the final change in VO2 has been reported to occur within the first 15-sec period, and where changes in blood distribution and stroke volume are known to be more pronounced than in the supine position. Our results emphasize the importance of central circulatory changes for the time course of VO2 at the start and end of exercise.

Adult↗

PubMed1974