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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.

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 (V̇o2 peak60.7 ± 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% V̇o2 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.

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 ...

We investigated the hypothesis that the pulmonary oxygen uptake slow component is related to a progressive increase in muscle lactate concentration and that prior heavy exercise (PHE) with pronounced acidosis alters kinetics and reduces work efficiency. Subjects (n= 9) cycled at 75% of the peak for 10 min before (CON) and after (AC) PHE. 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 kinetics (phase II) was similar but the asymptote was 14% higher during AC. The slow increase in 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 and reduced gross exercise efficiency during AC. It is concluded that the 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 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 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.

This paper examines the time course of changes in plasma electrolyte and acid-base composition in response to NaHCO3and KHCO3ingestion. 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 NaHCO3or 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 [Formula: see text] 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[Formula: see text]. The decrease in [H+] in the KHCO3trial 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 NaHCO3and KHCO3produced 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.

MacDonald, Maureen, Preben K. Pedersen, and Richard L. Hughson. Acceleration ofV˙o 2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise. J. Appl. Physiol. 83(4): 1318–1325, 1997.—We examined the hypothesis that O2 uptake (V˙o 2) 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 ofV˙o 2 were determined from the mean response time (MRT; time to 63% of total change inV˙o 2) 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 V˙o 2 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 theV˙o 2 slow component from minute 3 to minute 6 of exercise, compared with normoxia. Prior exercise above VT accelerated the on-transient MRT and reduced theV˙o 2 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.

Udgivelsesdato: 2009-Nov The development of noncircular chain wheels for the enhancement of cycling performance has been in progress for a long time and continues apace. In this study we tested whether submaximal cycling using a non-circular (Biopace) versus a circular chain wheel resulted in lower peak crank torque at preset pedal rates as well as resulting in lower pedal rate and metabolic response at freely chosen pedal rate. Ten trained cyclists (mean+/-SD: 27+/-3 years of age, 182+/-4 cm tall, 77.5+/-7.0 kg of body mass, and peak oxygen uptake of 61.7+/-4.4 ml kg(-1) min(-1)) cycled with a Biopace and a circular chain wheel at 180 W at 65 and 90 rpm for recording of crank torque profiles, and at their freely chosen pedal rate for recording of pedal rate and metabolic response, including oxygen uptake and blood lactate concentration. Crank torque profiles were similar between the two chain wheels during cycling at preset pedal rates. During cycling at the freely chosen pedal rate (being 93+/-6 and 93+/-4 rpm for the Biopace and circular chain wheel, respectively), blood lactate concentration was significantly different between the two chain wheels, being on average 0.2 mmol l(-1) lower with the Biopace chain wheel. A musculoskeletal simulation model supported the idea that a contributing factor to the observed difference in blood lactate concentration may be slightly reduced muscle activity around the phase where peak crank torque occurs during cycling with the Biopace chain wheel. In that particular phase of the crank revolution, the observed slightly lower muscle activity may result from larger transfer of energy from the legs to the crank.

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.

It was tested whether cyclists perform better during all-out cycling following prolonged cycling at the pedal rate resulting in minimum oxygen uptake (VO(2)), i.e. the energetically optimal pedal rate (OPR) rather than at the freely chosen pedal rate (FCPR). Nine trained cyclists cycled at 180 W to determine individual OPR and FCPR. Baseline performance was determined by measuring mean power output (W(5min)) and peak VO(2) during 5-min all-out cycling at FCPR. Subsequently, on two separate days, the cyclists cycled 2.5 h at 180 W at OPR and FCPR, with each bout followed by a 5-min all-out trial. FCPR was higher (P < 0.05) than OPR at 180 W (95 +/- 7 and 73 +/- 11 rpm, respectively). During the prolonged cycling, VO(2), heart rate (HR), and rate of perceived exertion (RPE) were 7-9% higher (P < 0.05) at FCPR than at OPR and increased (P < 0.05) 2-21% over time. During all-out cycling following prolonged cycling at OPR and FCPR, W(5min) was 8 and 10% lower (P < 0.05) than at baseline, respectively. Peak VO(2) was lower (P < 0.05) than at baseline only after FCPR. The all-out trial power output was reduced following 2.5 h of cycling at 180 W at both OPR and FCPR. However, this aspect of performance was similar between the two pedal rates, despite a higher physiological load (i.e. VO(2), HR, and RPE) at FCPR during prolonged cycling. Still, a reduced peak VO(2) only occurred after cycling at FCPR. Therefore, during prolonged sub-maximal cycling, OPR is at least as advantageous as FCPR for performance optimization in subsequent all-out cycling.

The effects of training and/or ageing upon maximal oxygen uptake ( VO(2max)) and heart rate values at rest (HR(rest)) and maximal exercise (HR(max)), respectively, suggest a relationship between VO(2max) and the HR(max)-to-HR(rest) ratio which may be of use for indirect testing of VO(2max). Fick principle calculations supplemented by literature data on maximum-to-rest ratios for stroke volume and the arterio-venous O(2) difference suggest that the conversion factor between mass-specific VO(2max) (ml.min(-1).kg(-1)) and HR(max).HR(rest)(-1) is approximately 15. In the study we experimentally examined this relationship and evaluated its potential for prediction of VO(2max). VO(2max) was measured in 46 well-trained men (age 21-51 years) during a treadmill protocol. A subgroup ( n=10) demonstrated that the proportionality factor between HR(max).HR(rest)(-1) and mass-specific VO(2max) was 15.3 (0.7) ml.min(-1).kg(-1). Using this value, VO(2max) in the remaining 36 individuals could be estimated with an SEE of 0.21 l.min(-1) or 2.7 ml.min(-1).kg(-1) (approximately 4.5%). This compares favourably with other common indirect tests. When replacing measured HR(max) with an age-predicted one, SEE was 0.37 l.min(-1) and 4.7 ml.min(-1).kg(-1) (approximately 7.8%), which is still comparable with other indirect tests. We conclude that the HR(max)-to-HR(rest) ratio may provide a tool for estimation of VO(2max) in well-trained men. The applicability of the test principle in relation to other groups will have to await direct validation. VO(2max) can be estimated indirectly from the measured HR(max)-to-HR(rest) ratio with an accuracy that compares favourably with that of other common indirect tests. The results also suggest that the test may be of use for VO(2max) estimation based on resting measurements alone.

The metabolic active form of free fatty acids, long-chain acyl-coenzyme A (lc-acyl-CoA), binds to its 10-kDa binding protein with high affinity. In the present study, we investigated the content of lc-acyl-CoA binding protein (ACBP) in different skeletal muscle fibre types. Soleus had the highest expression of ACBP (0.33±0.02 μg mg protein-1) and the content was as high as in heart muscle. The content in mixed gastrocnemius (0.27±0.02 gg mg protein-1), extensor digitorum longus (0.21±0.01 gg mg protein-1) and white gastrocnemius (0.16±0.01 μg mg protein-1) were lower than in soleus and differed from each other (P

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 AgNO3-stimulated Ca2+release from 709 (range 560–877; before) to 774 (596–977) arbitrary units Ca2+⋅ 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 Ca2+uptake rate and Ca2+-ATPase capacity were observed following the training, despite that the relative density of Ca2+-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 Ca2+release, due to an enhanced total volume of SR, whereas SR Ca2+sequestration function is not altered.

This paper describes and quantifies acute responses of the kidneys in correcting plasma volume, acid-base, and ion disturbances resulting from NaHCO3 and KHCO3 ingestion. Renal excretion of ions and water was studied in five men after ingestion of 3.57 mmol/kg body mass of sodium bicarbonate (NaHCO3) and, in a separate trial, potassium bicarbonate (KHCO3). 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. NaHCO3 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 KHCO3 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 KHCO3 and NaHCO3 solutions.

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.

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.

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.

In order to test for possible sex differences in endurance capacity, groups of young, physically active women (n=6) and men (n=7) performed bicycle ergometer exercise at 80% and 90% of their maximal oxygen uptakes (\(\dot V_{{\text{O}}_{\text{2}} {\text{max}}}\)). The groups were matched for age and physical activity habits. At 80%\(\dot V_{{\text{O}}_{\text{2}} {\text{max}}}\) the women performed significantly longer (P

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.