C. M. Hesser
Karolinska Institutet
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Featured researches published by C. M. Hesser.
Respiration Physiology | 1977
C. M. Hesser; Dag Linnarsson; H. Bjurstedt
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.
Respiration Physiology | 1983
C. M. Hesser; F. Lind
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.
Archive | 1971
R. H. T. Edwards; A. Melcher; C. M. Hesser; O. Wigertz
We have recently been interested in the physiological adaptations accompanying the performance of a given total amount of work by a variety of patterns of intermittent and continuous exercise.
Respiration Physiology | 1968
C. M. Hesser; B. Katsaros; G. Matell
Abstract Gas exchange in lungs and tissues during 2-min periods of forced breath holding with oxygen was studied in 5 anesthetized, denitrogenated dogs. This was done by analysis of the changing relationships between gas levels in the pre- and postcapillary blood of the lungs and of lumped tissues in the cranial and caudal portions of the body. The CO2 a content dinerence across the pulmonary capillary bed (ΔCco2) decreased rapidly during the first 50 sec, and then became reversed. Since cardiac output remained essentially unchanged, the behavior of ΔCCO2 reflected the rate of CO2 exchange between blood and lungs. From the caudal body tissues CO2 was transferred to the blood throughout the apneic period, whereas the CO2 exchange in the cranial body tissues became reversed towards the end of breath holding. PCO2 rose faster in the inferior, and slower in the superior caval vein than it did in the pulmonary artery, the maximal increments after 2 min of apnea averaging 64, 44, and 57 per cent, respectively, of that obtaining in the arterial blood. In spite of slight reductions in O2 saturation, venous O2 tensions increased by 2 to 5 mm Hg (Bohr effect), implying slight increments of overall tissue O2 stores. Blood O2 store decreased at a rate corresponding to 2 per cent of metabolic O2 consumption. Alveolar-arterial PO2 difference increased only beyond 3 min of breath holding as the alveolar space was approaching the level of residual volume. Circulation (“appearance”) times from aortic arch to superior and inferior caval veins averaged 16.8 and 9.4 sec, respectively.
Acta Physiologica Scandinavica | 1960
Marianne Frankenhaeuser; V. Graff-Lonnevig; C. M. Hesser
Acta Physiologica Scandinavica | 1964
P.‐O. Barr; M. Beckman; H. Bjurstedt; J. Brismar; C. M. Hesser; G. Matell
Acta Physiologica Scandinavica | 1962
H. Bjurstedt; C. M. Hesser; G. Liljestrand; G. Matell
Acta Physiologica Scandinavica | 1984
F. Lind; C. M. Hesser
Acta Physiologica Scandinavica | 1965
C. M. Hesser; G. Matell
Acta Physiologica Scandinavica | 1974
Lennart Fagraeus; C. M. Hesser; Dag Linnarsson