Increased steady-state VO2 and larger O2 deficit with CO2 inhalation during exercise.

AIM: To examine whether inhalation of CO(2) -enriched gas would increase steady-state VO(2) during exercise and enlarge O(2) deficit. METHODS: Ten physically active men (VO(2) 53.7 ± 3.6 mL min(-1) kg(-1) ; x ± SD) performed transitions from low-load cycling (baseline; 40 W) to work rates representing light (≈ 45% VO(2); 122 ± 15 W) and heavy (≈ 80% VO(2); 253 ± 29 W) exercise while inhaling normal air (air) or a CO(2) mixture (4.2% CO(2) , 21% O(2) , balance N(2) ). Gas exchange was measured with Douglas bag technique at baseline and at min 0-2, 2-3 and 5-6. RESULTS: Inhalation of CO(2) -enriched air consistently induced respiratory acidosis with increases in PCO(2) and decreases in capillary blood pH (P < 0.01). Hypercapnic steady-state VO(2) was on average about 6% greater (P < 0.01) than with air in both light and heavy exercise, presumably because of increased cost of breathing (ΔVE 40-50 L min(-1) ; P < 0.01), and a substrate shift towards increased lipid oxidation (decline in R 0.12; P < 0.01). VO(2) during the first 2 min of exercise were not significantly different whereas the increase in VO(2) from min 2-3 to min 5-6 in heavy exercise was larger with CO(2) than with air suggesting a greater VO(2) slow component. As a result, O(2) deficit was greater with hypercapnia in heavy exercise (2.24 ± 0.51 L vs. 1.91 ± 0.45 L; P < 0.05) but not in light (0.64 ± 0.21 L vs. 0.54 ± 0.20 L; ns). CONCLUSION: Inhalation of CO(2)-enriched air and the ensuing respiratory acidosis increase steady-state VO(2) in both light and heavy exercise and enlarges O(2) deficit in heavy exercise.

Non-linear relationship between oxygen uptake and power output in the Astrand nomogram-old data revisited.

For the last decade there have been considerable discussion concerning the linearity / non-linearity of the oxygen uptake (V(O2)) - power output (W) relationship with strong experimental evidence of non-linearity provided mainly by breath-by-breath measurements. In this study, we attempted to answer the question whether the V(O2) - W relationship in the Astrand nomogram, as presented in the Textbook of Work Physiology, P.-O. Astrand et al. (2003), page 281, based on the Douglas bag method, is indeed linear, as stated by the authors before, or if a change point in V(O2), described by Zoladz et al. (1998) Eur J Appl Physiol 78: 369-377, can possibly be detected in those data. The V(O2) - W data were taken from the Astrand nomogram referenced above and from the Table 9.5 on page 282 in the same reference and tested for the presence of the change point in V(O2), using our two-phase model (see the reference above). In the first phase, a linear V(O2) - W relationship was assumed, whereas in the second one (above the so-called change point) an additional increase in V(O2) above the values expected from the linear model was allowed. It was found that in the data taken from the Astrand nomogram (data for men), as well as in the data taken from the Table 9.5, statistically significant change points in V(O2) were present at the power output of 150 W. The documentation of the presence of a change point in the V(O2) - W relationship in the Astrand data provides further evidence for the existence of a non-linearity in the V(O2) - W relationship in incremental exercise tests of humans, also in V(O2) data based upon the Douglas bag method.

The potential for mitochondrial fat oxidation in human skeletal muscle influences whole body fat oxidation during low-intensity exercise.

The purpose of this study was to investigate fatty acid (FA) oxidation in isolated mitochondrial vesicles (mit) and its relation to training status, fiber type composition, and whole body FA oxidation. Trained (Vo(2 peak) 60.7 +/- 1.6, n = 8) and untrained subjects (39.5 +/- 2.0 ml.min(-1).kg(-1), n = 5) cycled at 40, 80, and 120 W, and whole body relative FA oxidation was assessed from respiratory exchange ratio (RER). Mit were isolated from muscle biopsies, and maximal ADP stimulated respiration was measured with carbohydrate-derived substrate [pyruvate + malate (Pyr)] and FA-derived substrate [palmitoyl-l-carnitine + malate (PC)]. Fiber type composition was determined from analysis of myosin heavy-chain (MHC) composition. The rate of mit oxidation was lower with PC than with Pyr, and the ratio between PC and Pyr oxidation (MFO) varied greatly between subjects (49-93%). MFO was significantly correlated to muscle fiber type distribution, i.e., %MHC I (r = 0.62, P = 0.03), but was not different between trained (62 +/- 5%) and untrained subjects (72 +/- 2%). MFO was correlated to RER during submaximal exercise at 80 (r = -0.62, P = 0.02) and 120 W (r = -0.71, P = 0.007) and interpolated 35% Vo(2 peak) (r = -0.74, P = 0.004). ADP sensitivity of mit respiration was significantly higher with PC than with Pyr. It is concluded that MFO is influenced by fiber type composition but not by training status. The inverse correlation between RER and MFO implies that intrinsic mit characteristics are of importance for whole body FA oxidation during low-intensity exercise. The higher ADP sensitivity with PC than that with Pyr may influence fuel utilization at low rate of respiration.

Cycling efficiency in humans is related to low UCP3 content and to type I fibres but not to mitochondrial efficiency.

The purpose of this study was to investigate the hypothesis that cycling efficiency in vivo is related to mitochondrial efficiency measured in vitro and to investigate the effect of training status on these parameters. Nine endurance trained and nine untrained male subjects (V(O2peak) = 60.4 +/- 1.4 and 37.0 +/- 2.0 ml kg(-1) min(-1), respectively) completed an incremental submaximal efficiency test for determination of cycling efficiency (gross efficiency, work efficiency (WE) and delta efficiency). Muscle biopsies were taken from m. vastus lateralis and analysed for mitochondrial respiration, mitochondrial efficiency (MEff; i.e. P/O ratio), UCP3 protein content and fibre type composition (% MHC I). MEff was determined in isolated mitochondria during maximal (state 3) and submaximal (constant rate of ADP infusion) rates of respiration with pyruvate. The rates of mitochondrial respiration and oxidative phosphorylation per muscle mass were about 40% higher in trained subjects but were not different when expressed per unit citrate synthase (CS) activity (a marker of mitochondrial density). Training status had no influence on WE (trained 28.0 +/- 0.5, untrained 27.7 +/- 0.8%, N.S.). Muscle UCP3 was 52% higher in untrained subjects, when expressed per muscle mass (P < 0.05 versus trained). WE was inversely correlated to UCP3 (r = -0.57, P < 0.05) and positively correlated to percentage MHC I (r = 0.58, P < 0.05). MEff was lower (P < 0.05) at submaximal respiration rates (2.39 +/- 0.01 at 50% V(O2max)) than at state 3 (2.48 +/- 0.01) but was neither influenced by training status nor correlated to cycling efficiency. In conclusion cycling efficiency was not influenced by training status and not correlated to MEff, but was related to type I fibres and inversely related to UCP3. The inverse correlation between WE and UCP3 indicates that extrinsic factors may influence UCP3 activity and thus MEff in vivo.

Prior heavy exercise eliminates VO2 slow component and reduces efficiency during submaximal exercise in humans.

We investigated the hypothesis that the pulmonary oxygen uptake (VO2) slow component is related to a progressive increase in muscle lactate concentration and that prior heavy exercise (PHE) with pronounced acidosis alters VO2 kinetics and reduces work efficiency. Subjects (n= 9) cycled at 75% of the peak VO2 (VO2peak) for 10 min before (CON) and after (AC) PHE. VO2 was measured continuously (breath-by-breath) and muscle biopsies were obtained prior to and after 3 and 10 min of exercise. Muscle lactate concentration was stable between 3 and 10 min of exercise but was 2- to 3-fold higher during AC (P < 0.05 versus CON). Acetylcarnitine (ACn) concentration was 6-fold higher prior to AC and remained higher during exercise. Phosphocreatine (PCr) concentration was similar prior to exercise but the decrease was 2-fold greater during AC than during CON. The time constant for the initial VO2 kinetics (phase II) was similar but the asymptote was 14% higher during AC. The slow increase in VO2 between 3 and 10 min of exercise during CON (+7.9 +/- 0.2%) was not correlated with muscle or blood lactate levels. PHE eliminated the slow increase in VO2 and reduced gross exercise efficiency during AC. It is concluded that the VO2 slow component cannot be explained by a progressive acidosis because both muscle and blood lactate levels remained stable during CON. We suggest that both the VO2 slow component during CON and the reduced gross efficiency during AC are related to impaired contractility of the working fibres and the necessity to recruit additional motor units. Despite a pronounced stockpiling of ACn during AC, initial VO2 kinetics were not affected by PHE and PCr concentration decreased to a lower plateau. The discrepancy with previous studies, where initial oxidative ATP generation appears to be limited by acetyl group availability, might relate to remaining fatiguing effects of PHE.

Biological variation in variables associated with exercise training.

To be able to identify a training induced change in a certain variable, it is necessary to know the background variation. In this study the coefficient of variation (total, between-subjects, within-subjects), the relative sources of variance (between-subjects and within-subjects), and the critical difference (within-subjects) were estimated in four categories of variables (performance and physiological variables, metabolic and hormonal variables, immunological variables, and mood state variables) in 15 moderately trained male runners measured on three different occasions over a period of 7 weeks. In the performance and physiological variables, 78.9 % of the variance was due to variation between subjects and they had the lowest critical difference (11.9 %). In contrast, the metabolic and hormonal variables had the highest critical difference (59.9 %) and 53.4 % of the variance was due to variations within subjects. The immunological and psychological variables had about two thirds of the variance arising from variation between subjects. However, the critical difference for the immunological variables was high (47.4 %), while it was relatively low for the psychological variables (26.8 %). The low critical difference and variation within subjects of the psychological and in particular the performance and physiological variables indicate that they may be beneficial as primary markers of training induced changes.

Enhanced sarcoplasmic reticulum Ca(2+) release following intermittent sprint training.

To evaluate the effect of intermittent sprint training on sarcoplasmic reticulum (SR) function, nine young men performed a 5 wk high-intensity intermittent bicycle training, and six served as controls. SR function was evaluated from resting vastus lateralis muscle biopsies, before and after the training period. Intermittent sprint performance (ten 8-s all-out periods alternating with 32-s recovery) was enhanced 12% (P < 0.01) after training. The 5-wk sprint training induced a significantly higher (P < 0.05) peak rate of AgNO(3)-stimulated Ca(2+) release from 709 (range 560-877; before) to 774 (596-977) arbitrary units Ca(2+). g protein(-1). min(-1) (after). The relative SR density of functional ryanodine receptors (RyR) remained unchanged after training; there was, however, a 48% (P < 0.05) increase in total number of RyR. No significant differences in Ca(2+) uptake rate and Ca(2+)-ATPase capacity were observed following the training, despite that the relative density of Ca(2+)-ATPase isoforms SERCA1 and SERCA2 had increased 41% and 55%, respectively (P < 0.05). These data suggest that high-intensity training induces an enhanced peak SR Ca(2+) release, due to an enhanced total volume of SR, whereas SR Ca(2+) sequestration function is not altered.

NaHCO(3) and KHCO(3) ingestion rapidly increases renal electrolyte excretion in humans.

This paper describes and quantifies acute responses of the kidneys in correcting plasma volume, acid-base, and ion disturbances resulting from NaHCO(3) and KHCO(3) ingestion. Renal excretion of ions and water was studied in five men after ingestion of 3.57 mmol/kg body mass of sodium bicarbonate (NaHCO(3)) and, in a separate trial, potassium bicarbonate (KHCO(3)). Subjects had a Foley catheter inserted into the bladder and indwelling catheters placed into an antecubital vein and a brachial artery. Blood and urine were sampled in the 30-min period before, the 60-min period during, and the 210-min period after ingestion of the solutions. NaHCO(3) ingestion resulted in a rapid, transient diuresis and natriuresis. Cumulative urine output was 44 +/- 11% of ingested volume, resulting in a 555 +/- 119 ml increase in total body water at the end of the experiment. The cumulative increase (above basal levels) in renal Na(+) excretion accounted for 24 +/- 2% of ingested Na(+). In the KHCO(3) trial, arterial plasma K(+) concentration rapidly increased from 4.25 +/- 0.10 to a peak of 7.17 +/- 0.13 meq/l 140 min after the beginning of ingestion. This increase resulted in a pronounced, transient diuresis, with cumulative urine output at 270 min similar to the volume ingested, natriuresis, and a pronounced kaliuresis that was maintained until the end of the experiment. Cumulative (above basal) renal K(+) excretion at 270 min accounted for 26 +/- 5% of ingested K(+). The kidneys were important in mediating rapid corrections of substantial portions of the fluid and electrolyte disturbances resulting from ingestion of KHCO(3) and NaHCO(3) solutions.

Hyperoxia does not increase peak muscle oxygen uptake in small muscle group exercise.

We examined the influence of hyperoxia on peak oxygen uptake (VO2peak) and peripheral gas exchange during exercise with the quadriceps femoris muscle. Young, trained men (n=5) and women (n=3) performed single-leg knee-extension exercise at 70% and 100% of maximum while inspiring normal air (NOX) or 60% O2 (HiOX). Blood was sampled from the femoral vein of the exercising limb and from the contralateral artery. In comparison with NOX, hyperoxic arterial O2 tension (PaO2) increased from 13.5 +/- 0.3 (x +/- SE) to 41.6 +/- 0. 3 kPa, O2 saturation (SaO2) from 98 +/- 0.1 to 100 +/- 0.1%, and O2 concentration (CaO2) from 177 +/- 4 to 186 +/- 4 mL L-1 (all P < 0. 01). Peak exercise femoral venous PO2 (PvO2) was also higher in HiOX (3.68 +/- 0.06 vs. 3.39 +/- 0.7 kPa; P < 0.05), indicating a higher O2 diffusion driving pressure. HiOX femoral venous O2 saturation averaged 36.8 +/- 2.0% as opposed to 33.4 +/- 1.5% in NOX (P < 0.05) and O2 concentration 63 +/- 6 vs. 55 +/- 4 mL L-1 (P < 0.05). Peak exercise quadriceps blood flow (Qleg), measured by the thermo-dilution technique, was lower in HiOX than in NOX, 6.4 +/- 0. 5 vs. 7.3 +/- 0.9 L min-1 (P < 0.05); mean arterial blood pressure at inguinal height was similar in NOX and HiOX at 144 and 142 mmHg, respectively. O2 delivery to the limb (Qleq times CaO2) was not significantly different in HiOX and NOX. VO2peak of the exercising limb averaged 890 mL min-1 in NOX and 801 mL min-1 in HiOX (n.s.) corresponding to 365 and 330 mL min-1 per kg active muscle, respectively. The VO2peak-to-PvO2 ratio was lower (P < 0.05) in HiOX than in NOX suggesting a lower O2 conductance. We conclude that the similar VO2peak values despite higher O2 driving pressure in HiOX indicates a peripheral limitation for VO2peak. This may relate to saturation of the rate of O2 turnover in the mitochondria during exercise with a small muscle group but can also be caused by tissue diffusion limitation related to lower O2 conductance.

Role of skeletal muscle in plasma ion and acid-base regulation after NaHCO3 and KHCO3 loading in humans.

This paper examines the time course of changes in plasma electrolyte and acid-base composition in response to NaHCO3 and KHCO3 ingestion. It was hypothesized that skeletal muscle is involved in the correction of the ensuing plasma disturbance by exchanging ions, gasses, and fluids between cells and extracellular fluids. Five male subjects, with catheters in a brachial artery and antecubital vein, ingested 3.57 mmol/kg body mass NaHCO3 or KHCO3. While seated, blood samples were taken 30 min before ingestion of the solution, at 10-min intervals during the 60-min ingestion period, and periodically for 210 min after ingestion was complete. Blood was analyzed for gases, hematocrit, plasma ions, and total protein. With NaHCO3, arterial plasma Na+ concentration ([Na+]) increased from 143 +/- 1 to 147 +/- 1 (SE) meq/l, H+ concentration ([H+]) decreased by 6 +/- 1 neq/l, and PCO2 increased by 5 +/- 1 mmHg. There was no detectable net Na+ uptake by tissues. An increased plasma strong ion difference ([SID]) accounted fully for the decrease in plasma [H+]. With KHCO3, K+ concentration increased from 4.25 +/- 0.10 to 7.17 +/- 0.13 meq/l, plasma volume decreased by 15.5 +/- 2.3%, [H+] decreased by 4 +/- 1 neq/l, and there was no change in PCO2. The decrease in [H+] in the KHCO3 trial primarily arose in response to the increased [SID]. Net K+ uptake by tissues accounted for 37 +/- 5% of the ingested K+. In conclusion, ingestion of NaHCO3 and KHCO3 produced markedly different fluid and ionic disturbances and associated regulatory responses by skeletal muscle. Accordingly, the physicochemical origins of the acid-base disturbances also differed between treatments. The tissues did not play a role in regulating plasma [Na+] after ingestion of NaHCO3. In contrast, the net influx of K+ to tissues played an important role in removing K+ from the extracellular compartment after ingestion of KHCO3.

Improved running economy following intensified training correlates with reduced ventilatory demands.

PURPOSE: To compare the effects of three types of intensive run training on running economy (RE) during exhaustive running and to establish possible relationships with changes in ventilatory function and/or muscle fiber type distribution. METHODS: Thirty-six male recreational runners were divided into three groups and assigned to either exhaustive distance training (DT), long-interval training (LIT), or short-interval training (SIT) three times 20-30 minxwk(-1) for 6 wk. VO(2 max) and RE were measured during treadmill running before and after training. Muscle fiber type distribution of the vastus lateralis muscle was established from biopsy material. RESULTS: VO(2max) (Lxmin(-1) increased by 5.9% (P < 0.0001), 6.0% (P < 0.0001), and 3.6% (P < 0.01) in DT, LIT, and SIT, respectively, and running speed at VO(2max) by 9% (P < 0.0001), 10% (P < 0.0001), and 4% (P < 0.05), respectively. Time-to-exhaustion at 87% of pretraining VO(2max) (mean 3.83) mxs(-1) increased by 94% in DT (P < 0.0001), 67% in LIT (P < 0.0001). Running economy improved by 3.1% in DT (P < 0.05), 3.0% in LIT (P < 0.01), and 0.9% SIT (NS): pulmonary ventilation (VE) was on average 11 Lxmin(-1) lower following training (P < 0.0001). The individual decrements in VE correlated with improvements in RE (r = 0.77; P < 0.0001) and may account for 25-70% of the decrease in aerobic demand. Muscle fiber composition, and respiratory exchange ratio, stride length, and stride frequency during running were unaltered with training. CONCLUSIONS: Recreational runners can improve RE and aerobic run performance by exchanging parts of their conventional aerobic distance training with intensive distance or long-interval running, whereas short-interval running is less efficient. The improvement in RE may relate to reduced ventilatory demands. Muscle fiber type distribution was unaltered with training and showed no associations with RE.

Acceleration of VO2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise.

We examined the hypothesis that O2 uptake (VO2) would change more rapidly at the onset of step work rate transitions in exercise with hyperoxic gas breathing and after prior high-intensity exercise. The kinetics of VO2 were determined from the mean response time (MRT; time to 63% of total change in VO2) and calculations of O2 deficit and slow component during normoxic and hyperoxic gas breathing in one group of seven subjects during exercise below and above ventilatory threshold (VT) and in another group of seven subjects during exercise above VT with and without prior high-intensity exercise. In exercise transitions below VT, hyperoxic gas breathing did not affect the kinetic response of VO2 at the onset or end of exercise. At work rates above VT, hyperoxic gas breathing accelerated both the on- and off-transient MRT, reduced the O2 deficit, and decreased the VO2 slow component from minute 3 to minute 6 of exercise, compared with normoxia. Prior exercise above VT accelerated the on-transient MRT and reduced the VO2 slow component from minute 3 to minute 6 of exercise in a second bout of exercise with both normoxic and hyperoxic gas breathing. However, the summated O2 deficit in the second normoxic and hyperoxic steps was not different from that of the first steps in the same gas condition. Faster on-transient responses in exercise above, but not below, VT with hyperoxia and, to a lesser degree, after prior high-intensity exercise above VT support the theory of an O2 transport limitation at the onset of exercise for workloads >VT.

Calcium content and respiratory control index of skeletal muscle mitochondria during exercise and recovery.

The purpose of this study was to evaluate the relationship between mitochondrial Ca2+ concentration and the respiratory control index (RCI; state III/state IV) in isolated mitochondria before and after exhaustive exercise at 75% of maximal O2 consumption. Muscle biopsies of 100-150 mg from 12 moderately trained men were sampled at rest, immediately after exercise, and 30 or 60 min after exercise. The mitochondrial Ca2+ content after exhaustive exercise was significantly higher than the preexercise level [15.1 (range 39.4) vs. 11.6 (range 6.5) nmol/mg protein, respectively; P < 0.05], and RCI increased from 11.6 (range 14.4) at rest to 13.7 (range 15.0) at exhaustion (P < 0.05). After 60 min of recovery, the mitochondrial Ca2+ content was still high [18.8 (range 29.9) nmol/mg protein], but the RCI value was significantly depressed because of the increased state IV value and, in fact, was lower than the preexercise value [8.6 (range 5.1); P < 0.05]. Our results show that the mitochondrial Ca2+ content is increased in human skeletal muscle after prolonged exhaustive exercise and that this is followed by an elevated RCI value, with slightly increased state III and decreased state IV respiration. The restoration of the elevated mitochondrial Ca2+ level is slow and could be related to an increased state IV respiration, which together indicate uncoupled Ca2+ respiration during recovery.

Reduced arterial O2 saturation during supine exercise in highly trained cyclists.

Performance of intense dynamic exercise in highly trained athletes is associated with a reduced arterial haemoglobin saturation for O2 (SaO2) and lower arterial PO2 (PaO2). We hypothesized that compared with upright exercise, supine exercise would be accompanied by a smaller reduction in SaO2 because of a lower maximal O2 uptake (VO2max) and/or a more even ventilation-perfusion distribution. Eight elite bicyclists completed progressive cycle ergometry to exhaustion in both positions with concomitant determinations of ventilatory data, arterial blood gases and pH. During upright cycling VO2max averaged 75 +/- 1.6 mL O2 min-1 kg-1 (+/-SEM) and it was 10.6 +/- 1.7% lower during supine cycling (P < 0.001). Also the maximal pulmonary and alveolar ventilation were lower during supine cycling (by 15 +/- 2% and 21 +/- 3%, respectively; P < 0.001) which related to a 0.8 +/- 0.1 L lower tidal volume (P < 0.001). In all subjects and independent of work posture PaO2 and SaO2 decreased from rest to exhaustion (from 99 +/- 3 to 82 +/- 2 Torr and 98.1 +/- 0.2 to 95.2 +/- 0.4%, respectively; P < 0.001); alveolar-arterial PO2 difference increased from 6 +/- 2 to 37 +/- 3 Torr in both body positions. At exhaustion arterial PCO2 was lower in upright than in supine (33.4 +/- 0.6 vs. 35.9 +/- 0.9 Torr; P < 0.01), suggesting a greater relative hyperventilation in upright. Arterial pH was similar in upright and supine at rest (both 7.41 +/- 0.01) and at exhaustion (7.31 +/- 0.01 vs. 7.32 +/- 0.01, respectively). We conclude that despite a lower Vo2max and supposedly an improved ventilation-perfusion distribution, altering body position from upright to supine does not influence arterial O2 desaturation during intense exercise.

Calcium content and respiratory control index of isolated skeletal muscle mitochondria: effects of different isolation media.

Calcium (Ca) content measured with graphite furnace atomic absorption spectrometry and polarographical measurement of respiratory control index (RCI) were performed on isolated skeletal muscle mitochondria. Four different isolation media were used in order to develop a method for isolating physiologically intact mitochondria in small samples with an endogenous Ca content as close as possible to in vivo conditions. With ruthenium red in the isolation medium, the mean Ca content decreased fourfold to 19.3 +/- 6.8 nmol/mg protein and RCI increased about 25% to 6.9 +/- 1.1 compared with a standard medium. With EGTA or EGTA plus ruthenium red, the mean Ca content decreased further to 5.8 +/- 1.0 and 5.1 +/- 0.9 nmol/mg protein and the mean RCI values increased to 8. 4 +/- 1.2 and 8.8 +/- 1.3, respectively. Isolated mitochondria from human muscle samples using EGTA and ruthenium red in the isolation medium had mean Ca values of 11.0 +/- 0.9 nmol/mg protein and mean RCI values of 12.2 +/- 1.6. The data indicate that the Ca concentration in the skeletal muscle mitochondria is inversely proportional to RCI, and the mitochondrial functional property is significantly improved upon lowering the intramitochondrial Ca accumulation by the incorporation of a chelating agent (EGTA) and a potent Ca antagonist, ruthenium red, in the isolation media.

Effects of detraining on endurance capacity and metabolic changes during prolonged exhaustive exercise.

The effects of 4 wk of detraining on maximal O2 uptake (VO2max) and on endurance capacity defined as the maximal time to exhaustion at 75% of VO2max were studied in nine well-trained endurance athletes. Detraining consisted of one short 35-min high-intensity bout per week as opposed to the normal 6-10 h/wk. Detraining had no effect on VO2max (4.57 +/- 0.10 vs. 4.54 +/- 0.08 l/min), but endurance capacity decreased by 21% from 79 +/- 4 to 62 +/- 4 min (P < 0.001). Endurance exercise respiratory exchange ratio was higher in the detrained than in the trained state (0.91 +/- 0.01 vs. 0.89 +/- 0.01; P < 0.01). Muscle [K+] values were unchanged during exercise and were similar in the trained and detrained states. Muscle [Mg2+] values were similar at rest and at minute 40 (30.3 +/- 0.9 vs. 30.8 +/- 0.6 mmol/kg dry wt) but increased significantly at exhaustion to 33.8 +/- 1.0 mmol/kg dry wt in the trained state and to 33.9 +/- 0.9 mmol/kg dry wt in the detrained state. The elevated muscle [Mg2+] at exhaustion could contribute to fatigue in prolonged exercise through an inhibition of Ca2+ release from sarcoplasmic reticulum. It is concluded that the endurance capacity can vary considerably during detraining without changes in VO2max. Altered substrate utilization or changes in electrolyte regulation may account for the reduced endurance capacity.

Increased working capacity with hyperoxia in humans.

The purpose of the study was to examine the influence of oxygen-breathing on maximal oxygen uptake (VO2max) and submaximal endurance performance. Six young women and five men rode a cycle-ergometer while breathing compressed air (normoxia, NOX) or a 55% O2 in N2 mixture (hyperoxia, HOX). The VO2max increased significantly by 12% (P less than 0.01) with HOX in the women but not in the men (+4%; nonsignificant). Maximal heart rate was also increased with HOX in the women but not in the men. Endurance time during work to exhaustion at 80% of normoxic VO2max was 41% longer in HOX than in NOX (P less than 0.025) with no significant difference between the men and the women. The variation among individuals was large. The oxygen uptake and respiratory quotient were not different in the two endurance tests, but pulmonary ventilation (VE) and blood lactate concentration were lower in HOX than in NOX, especially during the latter part of the task. Plasma base deficit (BDpl) increased initially by 3.5 mmol.l-1 during HOX and then stabilized. In NOX, a continuous increase was seen and the change was more than twice as large. Relative to BDpl, VE was higher in HOX than in NOX indicating a more efficient ventilatory compensation of the metabolic acidosis. The reduced ventilatory demand and lower metabolic acidosis in HOX in combination with lower relative exercise intensity may have contributed to the longer time to exhaustion. However, the pattern of individual variation suggested that other mechanisms were also involved.

Carbohydrate supercompensation and muscle glycogen utilization during exhaustive running in highly trained athletes.

Three female and three male highly trained endurance runners with mean maximal oxygen uptake (VO2max) values of 60.5 and 71.5 ml.kg-1.min-1, respectively, ran to exhaustion at 75%-80% of VO2max on two occasions after an overnight fast. One experiment was performed after a normal diet and training regimen (Norm), the other after a diet and training programme intended to increase muscle glycogen levels (Carb). Muscle glycogen concentration in the gastrocnemius muscle increased by 25% (P less than 0.05) from 581 mmol.kg-1 dry weight, SEM 50 to 722 mmol.kg-1 dry weight, SEM 34 after Carb. Running time to exhaustion, however, was not significantly different in Carb and Norm, 77 min, SEM 13 vs 70 min, SEM 8, respectively. The average glycogen concentration following exhaustive running was 553 mmol.kg-1 dry weight, SEM 70 in Carb and 434 mmol.kg-1 dry weight, SEM 57 in Norm, indicating that in both tests muscle glycogen stores were decreased by about 25%. Periodic acid-Schiff staining for semi-quantitative glycogen determination in individual fibres confirmed that none of the fibres appeared to be glycogen-empty after exhaustive running. The steady-state respiratory exchange ratio was higher in Carb than in Norm (0.92, SEM 0.01 vs 0.89, SEM 0.01; P less than 0.05). Since muscle glycogen utilization was identical in the two tests, the indication of higher utilization of total carbohydrate appears to be related to a higher utilization of liver glycogen. We have concluded that glycogen depletion of the gastrocnemius muscle is unlikely to be the cause of fatigue during exhaustive running at 75%-80% of VO2max in highly trained endurance runners. Furthermore, diet- and training-induced carbohydrate super-compensation does not appear to improve endurance capacity in such individuals.

Plasma noradrenaline response to a multistage exercise test in young men at increased risk of developing essential hypertension.

Venous plasma noradrenaline (PNA) was recorded during a multistage exercise test in order to assess the possible role of excess sympathetic nervous system activity in young men at increased risk of developing essential hypertension, and to analyse whether any such involvement was associated with heredity and/or borderline hypertension. Four groups were evaluated: 28 normotensive (NTO) and 20 borderline hypertensive (BHO) offspring of hypertensives, 12 borderline hypertensives with normotensive parents (BH) and 28 normotensives with normotensive parents (NT). Analysis of variance showed that heredity per se was associated with an increased PNA response to light exercise. In NT, PNA correlated with age at rest and light exercise (r = 0.39-0.58, P less than 0.05-0.005). When the influence of age was controlled for by dividing the subjects into two age groups a more pronounced increase in PNA response to light exercise was found in the youngest age group of offspring hypertensives (17-26 years), whereas no differences between the groups were observed in the upper age group (27-40 years). Our results indicate the presence of a hyperreactivity of the sympathetic nervous system during light exercise in young offspring of hypertensives.