Acta Physiologica

ELLINGSEN, I.; SYDNES, G.; HAUGE, A.; NICOLAYSEN, G.

doi: 10.1111/j.1748-1716.1988.tb08476.xpmid: 3147577

Conflicting opinions exist concerning the breathing pattern in man during resting and stimulated ventilation. Some but not all investigators have reported the existence of an abrupt change, a ‘breakpoint’, in the relation between mean tidal volume and mean inspiratory time. Different opinions exist as to whether the slope and the intercept for the relation between mean minute ventilation and mean tidal volume are identical regardless of the mode of stimulating the ventilation. We have studied 10 subjects, at rest and during graded stimulation of ventilation by CO2 inhalation and exercise. No breakpoint was observed in the relations between (I) mean tidal volume and mean inspiratory time and (2) mean tidal volume and mean expiratory time, even if a wide range of tidal volumes was achieved in our subjects. Carbon dioxide inhalation (normoxic or hyperoxic) and exercise gave different regression lines for the relation between mean minute ventilation and mean tidal volume in 8 out of 10 subjects with a larger slope during exercise. At exercise inspiratory time decreased with any increase in tidal volume, while during CO2 breathing no consistent change in inspiratory time was seen. Mean inspiratory flow was linearly related to exercise load and apparently also to arterial carbon dioxide pressure. We conclude that CO2 breathing gives a breathing pattern which is different from that obtained with exercise in the majority of normal subjects. Furthermore, we could not confirm the existence of breakpoints in relations describing the breathing pattern of normal man.

SAHLIN, K.; REN, J. M.; BROBERG, S.

doi: 10.1111/j.1748-1716.1988.tb08477.xpmid: 3227942

Six subjects cycled on two occasions for 10 min at power output of 188±11 W (x̄± SEM), which corresponded to 70 ± 2% of their maximal oxygen uptake (Vo2 max). The exercise intensity was either increased gradually in a stepwise manner over about 15 min (slow transition ‐ S), or increased directly (direct transition ‐ D) to the predetermined power output. Muscle samples from the quadriceps femoris muscle were taken at rest and immediately after exercise in both trials. During exercise with both D and S muscle lactate increased approximately 10 times (P < 0.0 1), phosphocreatine decreased about 50% (P < 0.01) and ADP increased about 20% (P < 0.05). There were no significant differences between S and D (P > 0.05). Furthermore, blood lactate, O2 deficit, O2 debt, and the calculated increase in muscle content of inorganic phosphate (Pi) were all similar between D and S (P < 0.05). It is concluded that the O2 deficit and the anaerobic energy utilization is not affected by the rate of transition from rest to exercise. Consequently, the O2 deficit at the onset of exercise is not due to a delay in O2 transport, but may be due to a limited peripheral O2 utilization as a result of metabolic adjustments at the cellular level. Increases in ADP and Pi are suggested to be primary metabolic regulators which activate both aerobic and anaerobic energy production resulting in the O2 deficit.

SJØGAARD, G.

doi: 10.1111/j.1748-1716.1988.tb08478.xpmid: 3227943

Seven men performed one‐legged isometric knee extension at 5% MVC for I h. Total body oxygen uptake amounted to 451 (42–471) ml min‐1 and oxygen uptake over the contracting leg to 200 (172–216) ml min‐1, with no changes occurring during the in contraction. Venous O2 tension decreased from 29.4 mmHg at rest to 23.1 mmHg with contraction and CO2 tension tended to increase from a resting value of 50.5 mmHg to 57.2 mmHg (ns.). No similar changes occurred in arterial O2 and CO2 tensions. There was a small but continuous glucose uptake at both rest and throughout the contraction, whereas a lactate release occurred only in the early phase (2 min) of contraction. Muscle glycogen content was 312 mmol kg‐1 dry wt at rest, no significant changes had occurred following 30 min or 1 h of contraction. Arterial and venous Hct and Hb values indicated that a flux of water occurred from the vascular bed to the contracting muscle, in which H2O increased from 3.06 I kg‐1 dry wt at rest to 3.30 1 kg‐1 dry wt after 1 h at 5 % MVC. Simultaneously potassium (K), was released from the muscle throughout contraction with a mean venous‐arterial difference of 0.25 mmol I‐1. With a plasma flow of 335 ml min‐1 kg‐1 wet wt the K loss amounted to 5 mmol kg‐1 wet wt or roughly 5% of the total muscle K content. Results from analysis of muscle K content were in line with this, since the mean K content of 460 mmol kg‐1 dry wt at the end of contraction tended to be lower than the mean resting value of 471 mmol kg‐1 dry wt (n.s.). These results indicate that during low‐level contractions, the muscle is able to maintain homeostasis with respect to energy turnover, but not with respect to intra‐/extracellular K concentration. This K imbalance may well play a role in muscle fatigue.

EVERTS, M. E.; RETTERSTØL, K.; CLAUSEN, T.

doi: 10.1111/j.1748-1716.1988.tb08479.xpmid: 2852445

Experiments were performed on isolated rat soleus and extensor digitorum longus (EDL) muscles of 4–week‐old rats. In the soleus, direct electrical stimulation for 10 min induced a frequency‐dependent increase in the ouabain‐suppressible 86Rb+ uptake, which was maximal (+110%) at a frequency of 2 Hz. In the EDL this frequency only induced a 31% increase. A supramaximal concentration of adrenaline (10μmol l‐1) stimulated ouabain‐suppressible 86Rb+ uptake by 80% and 27% in soleus and EDL, respectively. The combined effect of stimulation at 2 Hz and adrenaline was not significantly larger than each of the interventions alone in either of the muscles. The fractional loss of 22Na+ from soleus muscle was increased by around 50% by the exposure to adrenaline, electrical stimulation at 2 Hz or a combination of both. The effect of electrical stimulation on 22Na+ efflux was not prevented by addition of propranolol (I or 10μmol 1–1).

HANSSON, H.‐A.; ENGSTRÖM, A.M.C.; HOLM, S.; ROSENQVIST, A.‐I.

doi: 10.1111/j.1748-1716.1988.tb08480.xpmid: 3067520

Distribution of the trophic peptide somatomedin C (Sm‐C; insulin‐like growth factor I; IGF‐I) immunoreactivity was mapped in normal Achilles and tibialis anterior tendons. The spindle‐shaped tendon fibroblasts showed faint perinuclear staining. Fibroblasts in the paratenon mostly had a more intense IGF‐I immunoreactivity, i.e. faint to moderate. When analysing either tendon in detail, areas with more intense IGF‐I immunoreactivity could be recognized and seemed to correlate with areas of high mechanical stress. Increased mechanical load induced over 3 days elevated IGF‐I immunoreactivity throughout the cytoplasm of tendon fibroblasts. Peak intensity was reached in 7 days, and thereafter the IGF‐I immunoreactivity seemed to decrease irrespective of persistent high mechanical load. Training the animals on a treadmill for from 20 up to 60 min per day for 5 days induced after 3–5 days increased IGF‐I immunoreactivity throughout the cytoplasm of the tendon and paratenon fibroblasts. Sudden curtailment of loading the Achilles tendon resulted in a marked reduction of the IGF‐I immunoreactivity in most fibroblasts within 3 days. After a week only a small number of tendon fibroblasts showed any IGF‐I immunoreactivity. The IGF‐I immunoreactivity of tendon fibroblasts thus correlates to mechanical loading of the tendon. It is proposed that IGF‐I may have a trophic influence on tendon and paratenon cells by autocrine and/or paracrine mechanisms.

JUEL, C.

doi: 10.1111/j.1748-1716.1988.tb08481.xpmid: 2906515

The resting membrane potential (RMP), the intracellular free Na+ concentration ([Na+]1) and the intracellular free K+ concentration ([K+]1), were measured with double‐barrelled ion‐selective microelectrodes in mouse soleus muscles in vitro. In addition, the Na+ contents and K+ contents have been measured with the flame photometric technique. At rest the β2‐‐selective adrenoceptor agonist terbutaline (10‐5 m) increased the membrane potential and [K+]1, and decreased [Na+]1 when compared with control muscles. During a 5 min stimulation period the muscles, which were incubated with the β2‐adrenoceptor agonist, showed a smaller depolarization, a smaller decrease in [K+]1 and a smaller increase in [Na+]1 than stimulated control muscles. This difference was probably associated with an increased rate of Na‐K‐pumping in the β2‐adrenoceptor stimulated muscles. The P,‐agonist treated muscles were more resistant to fatigue than control muscles. This effect was significant with 10‐6 m terbutaline (25 °C). A depolarization obtained by increasing [K+]0 was shown to reduce the maximal tension. It is postulated, that the K+ shifts, which are responsible for the depolarization during muscle activity, are one of the mechanisms underlying muscle fatigue.

RØED, A.

doi: 10.1111/j.1748-1716.1988.tb08482.xpmid: 3227944

The site and mechanism of action of fatigue was investigated in the isolated rat phrenic nerve diaphrigm preparation, with indirect and direct stimulation at 20 Hz and recording of tension and EMG. An equal decay of the subtetanic tension during indirect and direct stimulation, and a parallel decay of tension and EMG, suggested a mechanism of fatigue localized to structures that were ‘seen’ by the EMG electrodes. A comparison of the responses to sub‐ and supra‐maximum direct stimulation did not show increased fatigue at sub‐maximum stimulation. Therefore, the fatigue was probably not caused by an increased threshold of the excitability of the sarcolemma. However, prolongation of the stimulus pulse during direct stimulation from 0.5 ms to 5 ms in the Citigued preparation caused a two‐phasic recovery of tension. The initial phase, but not the slow phase, was inhibited by tetrodotoxin (TTX). Thus a recovery of sarcolemma action potentials could explain the initial phase. The slow phase was probably caused by a mechanism localized at more distal potential‐dependent sites, probably in the T tubules.

STENBERG, A.; BOHMAN, S.‐O.; MORSING, P.; MÜLLER‐SUUR, C.; OLSEN, L.; PERSSON, A. E. G.

doi: 10.1111/j.1748-1716.1988.tb08483.xpmid: 3227945

The aim of the present investigation was to measure the back‐leak of pelvic urine to the blood circulation. In normopenic hydronephrotic, dehydrated hydronephrotic and dehydrated control kidneys the back‐leak was estimated from a servocontrolled machine which regulated infused saline to keep a preset pelvic pressure constant. The disappearance of fluid from the renal pelvis could be measured at different pressure levels, and a pressure‐dependent outflow of fluid was found. From these measurements a back‐leak conductance could be calculated which proved to be independent of pressure. In the lower pressure range (15–20 mmHg) there was a significantly lower conductance in the dehydrated controls compared with the dyhydrated hydronephrotic kidneys, while in the higher pressure range (25–30 mmHg) no difference was found. From electron microscopical studies the pyelorenal back‐leak of fluid in both hydronephrotic and control animals seemed to be most pronounced in the fornix region, as documented by a heavy presence of horseradish peroxidase in the intercellular spaces there. Other experiments with radioactively labelled inulin, which was injected into the pelvic cavity, indicated that most of the back‐leak occurred via the renal blood vessels and not through the lymphatic system. The importance of this back‐leak was evident from the measurements of the total kidney glomerular filtration rate (GFR) at a slightly increased pelvic pressure, where some of the urine with radioactive tracer flows back to circulation. The back‐leak of pelvic urine could also affect the concentration mechanism by removing diluted urine which had flowed over the renal papilla, and through water and urea diffusion increased papillary interstitial osmolarity.

BUGGE, J. F.; STOKKE, E. S.; KIIL, F.

doi: 10.1111/j.1748-1716.1988.tb08484.xpmid: 3067521

To examine the relationship between renal release of the prostaglandins E2 (PGE2) and I2 (PGI2) and renin during autoregulatory vasodilation, experiments were performed in anaesthetized dogs with denervated kidneys. Autoregulatory vasodilation was induced by reducing renal arterial pressure (RAP) or by raising ureteral pressure in steps. During progressive renal arterial constriction, PGE2 and PGI2 release reached maximal values (10.6±1.7 for PGE2 and 6.6±1.1 pmol min‐1 for PGI2 release) at RAP of 7–80 mmHg, associated with almost no increase in renin release. By further reduction of RAP, prostaglandin release was not significantly altered, whereas renin release reached maximal values (18.7 ± 2.4μg AI min‐1) when autoregulatory vasodilation was complete at RAP below 55–60 mmHg. During progressive elevation of ureteral pressure, the release of PGE2, PGI2 and renin increased in concert in a curvilinear fashion, reaching maximal values at a ureteral pressure of 85 mmHg. There was no further increase during ureteral occlusion and the plateau values averaged 23.6 ± 3.7 pmol min‐1 for PGE2, 8.0±1.6pmol min‐1 for PGI2 and 16.6 ± 3.4μg A1 min‐1 for renin. We conclude that vascular dilation enhances both prostaglandin and renin release. During reduction of RAP, preglomerular arteries are dilated at higher RAP than are afferent arterioles. Release of prostaglandins synthetized in arteries consequently occurs at higher RAP than release of renin, which is not enhanced until afferent arterioles ultimately dilate at RAP approaching 60 mmHg. In contrast, elevation of ureteral pressure provides nearly uniform enhancement of prostaglandin and renin release, indicating a more uniform dilation of the whole preglomerular vascular tree.

PETTERSSON, A.; RICKSTEN, S. E.; HEDNER, J.; HEDNER, T.

doi: 10.1111/j.1748-1716.1988.tb08485.xpmid: 2976237

Central haemodynamic parameters and cardiac performance were measured in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) control rats after a Io‐min infusion of rat ANP (103–125), I γg kg‐1 min‐1. Mean arterial blood pressure (MAP) decreased by approximately 10% in both groups of rats. Heart rate (HR) increased slightly in both strains during the infusion. In the normotensive group the fall in MAP was due to a reduction in cardiac output (CO) while in the SHR there was a decrease in CO as well as in total peripheral resistance (TPK). The ANP infusion also reduced central blood volume (CRV) and stroke volume (SV) in both groups of rats. The reduction in CRV and CO was significantly more pronounced in the WKY strain. Left ventricular end diastolic pressure (LVEDP) and cardiac contractility (dP/dt) did not change while central venous pressure (CVP) w‐as slightly decreased in the WKY group as a result of the ANP infusion. We conclude that ANP reduces MAP in normotensive animals by a reduction in CO. In the SHR a reduction in TPR also contributes to the fall in MAP. Atrial natriuretic peptide did not exert any negative inotropic effects, but the reduction of CO was due to an increased venous compliance.