Effect of acute hypoxia on muscle blood flow, VO2p, and [HHb] kinetics during leg extension exercise in older men

The adjustment of pulmonary oxygen uptake (VO_2p), heart rate (HR), limb blood flow (LBF), and muscle deoxygenation [HHb] was examined during the transition to moderate-intensity, knee-extension exercise in six older adults (70 ± 4 years) under two conditions: normoxia (FIO₂ = 20.9 %) and hypoxia (FIO₂ = 15 %). The subjects performed repeated step transitions from an active baseline (3 W) to an absolute work rate (21 W) in both conditions. Phase 2 VO_2p, HR, LBF, and [HHb] data were fit with an exponential model. Under hypoxic conditions, no change was observed in HR kinetics, on the other hand, LBF kinetics was faster (normoxia 34 ± 3 s; hypoxia 28 ± 2), whereas the overall [HHb] adjustment ( $ \tau^{\prime } = {\text{TD}} + \tau $ ) was slower (normoxia 28 ± 2; hypoxia 33 ± 4 s). Phase 2 VO_2p kinetics were unchanged (p < 0.05). The faster LBF kinetics and slower [HHb] kinetics reflect an improved matching between O₂ delivery and O₂ utilization at the microvascular level, preventing the phase 2 VO_2p kinetics from become slower in hypoxia. Moreover, the absolute blood flow values were higher in hypoxia (1.17 ± 0.2 L min^?1) compared to normoxia (0.96 ± 0.2 L min^?1) during the steady-state exercise at 21 W. These findings support the idea that, for older adults exercising at a low work rate, an increase of limb blood flow offsets the drop in arterial oxygen content (CaO₂) caused by breathing an hypoxic mixture.     

Local and systemic effects on blood lactate concentration during exercise with small and large muscle groups

To evaluate the relationship between lactate release and [lac]_art and to investigate the influence of the catecholamines on the lactate release, 14 healthy men [age 25±3 (SE) year] were studied by superimposing cycle on forearm exercise, both at 65% of their maximal power reached in respective incremental tests. Handgrip exercise was performed for 30 min at 65% of peak power. In addition, between the tenth and the 22nd minute, cycling with the same intensity was superimposed. The increase in venous lactate concentration ([lac]_ven) (rest: 1.3±0.4 mmol·l⁻¹; 3rd min: 3.9±0.8 mmol·l⁻¹) begins with the forearm exercise, whereas arterial lactate concentration ([lac]_art) remains almost unchanged. Once cycling has been added to forearm exercise (COMB), [lac]_art increases with a concomitant increase in [lac]_ven (12th min: [lac]_art, 3.2±1.3 mmol·l⁻¹; [lac]_ven, 5.7±2.2 mmol·l⁻¹). A correlation between oxygen tension (P_vO₂) and [lac]_ven cannot be detected. There is a significant correlation between [lac]_art and norepinephrine ([NE]) (y=0.25x+1.2; r=0.815; p<0.01) but no correlation between lactate release and epinephrine ([EPI]) at moderate intensity. Our main conclusion is that lactate release from exercising muscles at moderate intensities is neither dependent on P_vO₂ nor on [EPI] in the blood.     

Cardiorespiratory responses to exercise in acute hypoxia, hyperoxia and normoxia

There is a prevailing hypothesis that an acute change in the fraction of oxygen in inspired air (F _IO₂) has no effect on maximal cardiac output ( ), although maximal oxygen uptake ( ) and exercise performance do vary along with F _IO₂. We tested this hypothesis in six endurance athletes during progressive cycle ergometer exercise in conditions of hypoxia (F _IO₂=0.150), normoxia (F _IO₂=0.209) and hyperoxia (F _IO₂=0.320). As expected, decreased in hypoxia [mean (SD) 3.58 (0.45) l·min^–1, P<0.05] and increased in hyperoxia [5.17 (0.34) l·min^–1, P<0.05] in comparison with normoxia [4.55 (0.32) l·min^–1]. Similarly, maximal power ( ) decreased in hypoxia [334 (41) W, P<0.05] and tended to increase in hyperoxia [404 (58) W] in comparison with normoxia [383 (46) W]. Contrary to the hypothesis, was 25.99 (3.37) l·min^–1 in hypoxia (P<0.05 compared to normoxia and hyperoxia), 28.51 (2.36) l·min^–1 in normoxia and 30.13 (2.06) l·min^–1 in hyperoxia. Our results can be interpreted to indicate that (1) the reduction in in acute hypoxia is explained both by the narrowing of the arterio-venous oxygen difference and reduced , (2) reduced in acute hypoxia may be beneficial by preventing a further decrease in pulmonary and peripheral oxygen diffusion, and (3) reduced and in acute hypoxia may be the result rather than the cause of the reduced and skeletal muscle recruitment, thus supporting the existence of a central governor. Electronic Publication     

Severe hypoxia decreases oxygen uptake relative to intensity during submaximal graded exercise

Summary The effect of severe acute hypoxia (fractional concentration of inspired oxygen equalled 0.104) was studied in nine male subjects performing an incremental exercise test. For power outputs over 125 W, all the subjects in a state of hypoxia showed a decrease in oxygen consumption ( O₂) relative to exercise intensity compared with normoxia (P < 0.05). This would suggest an increased anaerobic metabolism as an energy source during hypoxic exercise. During submaximal exercise, for a given O₂, higher blood lactate concentrations were found in hypoxia than in normoxia (P < 0.05). In consequence, the onset of blood lactate accumulation (OBLA) was shifted to a lower O₂ ( O₂ 1.77 l·min^–1 in hypoxia vs 3.10 l·min^–1 in normoxia). Lactate concentration increases relative to minute ventilation ( _E) responses were significantly higher during hypoxia than in normoxia (P < 0.05). At OBLA, _E during hypoxia was 25% lower than in the normoxic test. This study would suggest that in hypoxia subjects are able to use an increased anaerobic metabolism to maintain exercise performance.     

Effect of low oxygen inhalation on changes in blood pH, lactate, and ammonia due to exercise

The present study examined the effect of hypoxia-induced respiratory alkalosis on exercise-induced metabolic acidosis and increases in plasma lactate and ammonia levels. Six male subjects underwent exercise of increasing intensity until exhaustion: (1) in normoxia (20.9% O₂) (=MAX), (2) in hypoxia (12% O₂) (=HP) in which hypoxic condition had been maintained from 60 min before to 30 min after exercise, and (3) the same intensity of exercise as HP in normoxia (=SUB). Arterialized blood was drawn from a superficial vein. Post-exercise blood pH was significantly higher in HP than in MAX (P<0.05), although plasma lactate was at the same level. For hypoxia as compared to normoxia, regression analysis confirmed a parallel shift of plasma lactate to higher pH levels indicating the effect of respiratory alkalosis (P<0.01). After exercise plasma levels of ammonia were lower in HP than in MAX (P<0.05). Regression analysis between ammonia and pH revealed nearly identical changes in hypoxia and normoxia at low pH. From these results, we conclude that: (1) hypoxia-induced respiratory alkalosis attenuated exhaustive exercise-induced metabolic acidosis, (2) plasma lactate concentration was determined by the relative exercise intensity, (3) the maximum plasma ammonia concentration under exhaustive exercise was reduced at hypoxia because of respiratory alkalosis.     

Effects of acute hypoxia and CO2 inhalation on systemic and peripheral oxygen uptake and circulatory responses during moderate exercise

Summary The effect of acute hypoxia and CO₂ inhalation on leg blood flow (LBF), on leg vascular resistance (LVR) and on oxygen supply to and oxygen consumption in the exercising leg was studied in nine healthy male subjects during moderate one-leg exercise. Each subject exercised for 20 min on a cycle ergometer in four different conditions: normoxia, normoxia +2% CO₂, hypoxia corresponding to an altitude of 4000 m above sea level, and hypoxia +1.2% CO₂. Gas exchange, heart rate (HR), arterial blood pressure, and LBF were measured, and arterial and venous blood samples were analysed for , , oxygen saturation, haematocrit and haemoglobin concentration. Systemic oxygen consumption was 1.83 l · min^–1 (1.48–2.59) and was not affected by hypoxia or CO₂ inhalation in hypoxia. HR was unaffected by CO₂, but increased from 136 beat · min^–1 (111–141) in normoxia to 155 (139–169) in hypoxia. LBF was 6.5 l · min^–1 (5.4–7.6) in normoxia and increased significantly in hypoxia to 8.4 (5.9–10.1). LVR decreased significantly from 2.23 kPa · l^–1 · min (1.89–2.99) in normoxia to 1.89 (1.53–2.52) in hypoxia. The increase in LBF from normoxia to hypoxia correlated significantly with the decrease in LVR. When CO₂ was added in hypoxia a significant correlation was also found between the decrease in LBF and the increase in LVR. In normoxia, the addition of CO₂ caused a significant increase in mean blood pressure. Oxygen consumption in the exercising leg (leg ) in normoxia was 0.97 l · min^–1 (0.72–1.10), and was unaffected by hypoxia and CO₂. It is concluded that the O₂ supply to the exercising leg and its are unaffected by hypoxia and CO₂. The increase in LBF in hypoxia is caused by a decrease in LVR. These changes can be counteracted by CO₂ inhalation. It is proposed that the regulatory mechanism behind these changes is that change in brain causes change in the central regulation of vascular tonus in the muscles.     

Impact of menstrual cycle phase on the exercise status of young,sedentary women

The purpose of the present study was to compare exercise status during the follicular (FP) and luteal (LP) phases of the menstrual cycle of a single group of young, sedentary women, where the marked differential in the blood concentrations of 17-oestradiol ([E₂]) and progesterone ([P₄]) has the potential to alter the metabolic response to exercise. Fourteen females [21.8 (4.0) years, peak oxygen uptake (V̇O_2peak) <45 ml·kg ^–1·min^–1] performed both incremental exercise to exhaustion and steady-state submaximal cycle ergometer exercise while measurements were made of several metabolic and hormonal variables. With the incremental exercise test, time to exhaustion, maximal power output and total work done were not different between the two phases, nor were the absolute values for V̇O_2peak or the corresponding values for ventilation (V̇E), respiratory frequency (f_R) and heart rate (HR). Resting, end-exercise and peak (post-exercise) plasma lactate concentrations and the lactate threshold were not different between the two phases either. However, as the workloads increased during the incremental protocol, plasma lactate concentration, carbon dioxide output (CO₂) and the respiratory exchange ratio (RER) all were lower during LP, while oxygen uptake (V̇O₂) was higher. With steady-state submaximal exercise, at workloads corresponding to 25% and 75% of menstrual cycle phase-specific O_2peak, V̇O₂ and the oxygen pulse (V̇O₂/HR) were higher and RER and plasma lactate concentration lower during LP. Regardless of phase, [E₂] increased with both incremental and steady-state submaximal exercise, while [P₄] was unchanged. It is concluded that while exercise capacity, as defined by O_2peak and the lactate threshold, is unaffected by cycle phase in young, sedentary women, the metabolic responses in the LP during both incremental and steady-state submaximal exercise suggest a greater dependence on fat as an energy source.     

Effect of acute mild hypoxia during exercise on plasma free and sulphoconjugated catecholamines

Catecholamine (CA) response to hypoxic exercise has been investigated during severe hypoxia. However, altitude training is commonly performed during mild hypoxia at submaximal exercise intensities. In the present study we tested whether submaximal exercise during mild hypoxia compared to normoxia leads to a greater increase of plasma concentrations of CA and whether plasma concentration of catecholamine sulphates change in parallel with the CA response. A group of 14 subjects [maximal oxygen uptake, 62.6 (SD 5.2) ml · min^–1 · kg^–1 body mass] performed two cycle ergometer tests of 1-h duration at the same absolute exercise intensities [191 (SD 6) W] during normoxia (NORM) and mild hypoxia (HYP) followed by 30 min of recovery during normoxia. Mean plasma concentrations of noradrenaline ([NA]), adrenaline ([A]), and noradrenaline sulphate ([NA-S]) were elevated (P < 0.01) after HYP and NORM compared with mean resting values and were higher after HYP [20.9 (SEM 3.1), 2.2 (SEM 0.24), 8.12 (SEM 1.5) nmol · 1^–1, respectively] than after NORM [(13.7 (SEM 0.9), 1.5 (SEM 0.14), 6.8 (SEM 0.7) nmol · 1^–1, respectively P < 0.01]. The higher plasma [NA-S] after HYP (P < 0.05) were still measurable after 30 min of recovery. From our study it was concluded that exercise at the same absolute submaximal exercise intensity during mild hypoxia increased plasma CA to a higher extent than during normoxia. Plasma [NA-S] response paralleled the plasma [NA] response at the end of exercise but, in contrast to plasma [NA], remained elevated until 30 min after exercise.     

Effect of acute normobaric hypoxia on quadriceps integrated electromyogram and blood metabolites during incremental exercise to exhaustion

This investigation analysed the effects of environmental hypoxia (EH) on changes in quadriceps integrated electromyogram (iEMG) and metabolite accumulation during incremental cycle ergometry. Trained male subjects (n = 14) were required to complete two maximal oxygen uptake tests, one test during EH (F _IO₂ = 0.135), the other during normoxia (F _IO₂ = 0.2093). The EMG were recorded at each exercise intensity from the vastus lateralis, rectus femoris and vastus medialis muscles over 60 cycle revolutions. Mean integral values were then calculated. Blood was collected from the radial vein of consenting subjects (n = 8) at the end of each exercise intensity. Oxygen saturation of arterial blood (S _aO₂) was estimated using pulse oximetry. Gas exchange variables were collected on-line every 15 s. The results indicated that, without exception, EH significantly reduced total exercise time. Mean time to exhaustion in EH was 26.34 (SD 2.58) min compared with 35.25 (SD 4.21) min during N. The S _aO₂ values indicated that severe arterial desaturation had been achieved by EH. Mean values for obtained in EH were 49 ml·kg·min^–1, compared with 59 ml · kg· min^–1 attained in N. Plasma lactate and ammonia concentrations were both significantly higher in EH. Increases in lactate and ammonia concentration were highly correlated in both N and EH. The onset of plasma lactate and ammonia accumulation occurred at the same exercise intensity in N. The iEMG responses of all three quadriceps muscles tended to be greater in the EH trials, although this difference was not significant. The basis for iEMG nonsignificance may have been related to large within sample variation in iEMG, sample size and the severity of the hypoxia induced.     

Effect of muscle mass on lactate formation during exercise in humans

To elucidate the mechanisms of lactate formation during submaximal exercise, eight men were studied during one- (1-LE) and two-leg (2-LE) exercise (approximately 11-min cycling) using the catheterization technique and muscle biopsies (quadriceps femoris muscle). The absolute exercise intensity and thus the energy demand for the exercising limb was the same [mean 114 (SEM 7) W] during both 1-LE and 2-LE. At the end of exercise partial pressure of O₂ and O₂ saturation in femoral venous blood were lower and arterial adrenaline and noradrenaline were higher during 2-LE than during 1-LE. Mean arterial blood lactate concentration increased to 10.8 (SEM 0.8) (2-LE) and 5.2 (SEM 0.4) mmol · 1^–1 (1-LE) after 10 min of exercise. The intramuscular metabolic response to exercise was attenuated during 1-LE [mean, lactate = 49 (SEM 9); glucose 6-P = 3.3 (SEM 0.3); nicotinamide adenine dinucleotide, reduced = 0.17 (SEM 0.02); adenosine 5-diphosphate 2.7 (SEM 0.1) mmol · kg dry mass^–1] compared to 2-LE [76 (SEM 6); 6.1 (SEM 0.7); 0.21 (SEM 0.02); 3.0 (SEM 0.1) mmol · kg dry mass^–1, respectively]. To elucidate whether the lower plasma adrenaline concentration could contribute to the attenuated metabolic response, additional experiments were performed on four of the eight subjects with infusion of adrenaline during 1-LE (1-LEE). Average plasma adrenaline concentration was increased during 1-LEE and reached 2–4 times higher levels than during 2-LE. Post-exercise muscle lactate and glucose 6-P contents were higher during 1-LEE than during 1-LE and were similar to those during 2-LE. Also, leg lactate release was elevated during 1-LEE versus 1-LE. It was concluded that during submaximal dynamic exercise the intramuscular metabolic response not only depended on the muscle power output, but also on the total muscle mass engaged. Plasma adrenaline concentrations and muscle oxygenation were found to be dependent upon the working muscle mass and both may have affected the metabolic response during exercise.     

Circulating leucocyte subpopulations in sedentary subjects following graded maximal exercise with hypoxia

Summary Ten healthy sedentary subjects [age, 27.5 (SD 3.5) years; height, 180 (SD 5) cm; mass, 69.3 (SD 6.3) kg] performed two periods of maximal incremental graded cycle ergometer exercise in a supine position. Randomly ordered and using an open spirometric system, one exercise was carried out during normoxia [maximal oxygen consumption ( O_2max)=38.6 (SD 3.5) ml·min^–1·kg^–1; maximal blood lactate concentration, 9.86 (SD 1.85) mmol·l^–1; test duration, 22.6 (SD 2.7) min], the other during hypoxia [ O_2max=33.2 (SD 3.2) ml·min^–1· kg^–1; maximal blood lactate concentration, 10.38 (SD 2.02) mmol·l^–1; test duration, 19.7 (SD 2.8) min]. At rest, immediately (0 p) and 60 min (60 p) after exercise, counts of leucocyte subpopulations (flow cytometry), cortisol and catecholamine concentrations were determined. At 0 p in contrast to normoxia, during hypoxia there was no significant increase of granulocytes. There were no significant differences between normoxia and hypoxia in the increases from rest to 0 p in counts of monocytes, total lymphocytes and lymphocyte subpopulations [clusters of differentiation (CD), CD3⁺, CD4⁺CD45RO^–, CD4⁺CD45RO⁺, CD8⁺CD45RO^–, CD8⁺CD45RO⁺, CD3⁺HLA-DR⁺, CD3^–CD16/CD56⁺, CD3⁺CD16/CD56⁺, CD 19⁺] as well as adrenaline, noradrenaline and cortisol concentrations. The counts of CD3 ^–CD16/CD56⁺-and CD8 ⁺CD45RO⁺-cells increased most. At 60 p, CD3^–CD16/CD56⁺ and CD3⁺CD16/CD56⁺-cell counts were below pre-exercise levels and under hypoxia slightly but significantly lower than under normoxia. We concluded that the exercise-induced mobilization and redistribution of most leucocyte and lymphocyte subpopulations were unimpaired under acute hypoxia at sea level. Reduced increases of granulocyte counts during the study and reduced cell numbers of natural killer cells and cytotoxic, not major histocompatibility complex-restricted T-cells, only indicated marginal effects on the immune system.     

The ventilation,lactate and electromyographic thresholds during incremental exercise tests in normoxia,hypoxia and hyperoxia

These experiments examined the effect of hypoxia and hyperoxia on ventilation, lactate concentration and electromyographic activity during an incremental exercise test in order to determine if coincident chances in ventilation and electromyographic activity occur during an incremental exercise test, despite an enhancement or reduction of peripheral chemoreceptor activity. In addition, these experiments were completed to determine if electromyographic activity and ventilation are enhanced or reduced in response to the inspiration of oxygen-depleted and oxygen-enriched air, respectively. Seven subjects performed three incremental exercise tests, until volitional exhaustion was achieved, while inspiring air with a fractional concentration of oxygen of either 66%, 21% or 17%. In addition, another single subject completed two tests while inspiring air with a fractional concentration of either 17% or 21%. During the tests, ventilation, mixed expired oxygen and carbon dioxide, arterialized venous blood and the electromyographic activity from the vastus lateralis were sampled. From these values ventilation, electromyographic and lactate thresholds were detected during normoxia, hypoxia and hyperoxia. The results showed that although ventilation and lactate concentration were significantly less during hyperoxia as compared to normoxia or hypoxia, the carbon dioxide production values were not significantly different between the normoxic, hypoxic and hyperoxic conditions. For a particular condition, the time, carbon dioxide production and oxygen consumption values that corresponded to the ventilation and electromyographic thresholds were not significantly different, but the values corresponding to the lactate threshold were significantly less than those for the electromyographic and ventilation thresholds. Comparisons between the three conditions showed that the time, carbon dioxide production and oxyen consumption values corresponding to each of these thresholds were not significantly different. These findings have led us to conclude that the changes in lactate concentration observed during exercise may not be directly related to the fractional concentration of inspired oxygen, and that the peripheral chemoreceptors may not be the sole mediators of the first ventilatory threshold. It is suggested that this threshold may be mediated by an increase in neural activity originating from higher motor centers or the exercising limbs, induced in response to the need to progressively recruit fast twitch muscle fibers as exercise power output is increased and as individual muscle fibers begin to fatigue.     

Lactate disposal in resting trained and untrained forearm skeletal muscle during high intensity leg exercise

Summary At a given oxygen uptake ( O₂) and exercise intensity blood lactate concentrations are lower following endurance training. While decreased production of lactate by trained skeletal muscle is the commonly accepted cause, the contribution from increased lactate removal, comprising both uptake and metabolic disposal, has been less frequently examined. In the present study the role of resting skeletal muscle in the removal of an arterial lactate load (approximately 11 mmol·-l^–1) generated during high intensity supine leg exercise (20 min at approximately 83% maximal oxygen uptake) was compared in the untrained (UT) and trained (T) forearms of five male squash players. Forearm blood flow and the venoarterial lactate concentration gradient were measured and a modified form of the Fick equation used to determine the relative contributions to lactate removal of passive uptake and metabolic disposal. Significant lactate uptake and disposal were observed in both forearms without any change in forearm O₂. Neither the quantity of lactate taken up [UT, 344.2 (SEM 118.8) mol·100 ml^–1; T, 330.3 (SEM 85.3) mol·100 ml^–1] nor the quantity disposed of [UT, 284.0 (SEM 123.3) mol·100 ml^–1, approximately 83% of lactate uptake; T, 300.8 (SEM 77.7) mol·100 ml^–1, approximately 91% of lactate uptake] differed between the two forearms. It is concluded that while significant lactate disposal occurs in resting skeletal muscle during high intensity exercise the lower blood lactate concentrations following endurance training are unlikely to result from an increase in lactate removal by resting trained skeletal muscle.     

Effect of lowered muscle temperature on the physiological response to exercise in men

Summary The effect of low muscle temperature on the response to dynamic exercise was studied in six healthy men who performed 42 min of exercise on a cycle ergometer at an intensity of 70% of their maximal O₂ uptake. Experiments were performed under control conditions, i.e. from rest at room temperature, and following 45 min standing with legs immersed in a water bath at 12°C. The water bath reduced quadriceps muscle temperature (at 3 cm depth) from 36.4 (SD 0.5)°C to 30.5 (SD 1.7)°C. Following cooling, exercise heart rate was initially lower, the mean difference ranged from 13 (SD 4) beats · min^–1 after 6 min of exercise, to 4 (SD 2) beats · min^–1 after 24 min of exercise. Steady-state oxygen uptake was consistently higher (0.21 · min^–1). However, no difference could be discerned in the kinetics of oxygen uptake at the onset of exercise. During exercise after cooling a significantly higher peak value was found for the blood lactate concentration compared to that under control conditions. The peak values were both reached after approximately 9 min of exercise. After 42 min of exercise the blood lactate concentrations did not differ significantly, indicating a faster rate of removal during exercise after cooling. We interpreted these observations as reflecting a relatively higher level of muscle hypoxia at the onset of exercise as a consequence of a cold-induced vasoconstriction. The elevated steady-state oxygen uptake may in part have been accounted for by the energetic costs of removal of the extra lactate released into the blood consequent upon initial tissue hypoxia.     

Effects of prolonged cycle ergometer exercise on maximal muscle power and oxygen uptake in humans

Summary The mechanical power (W_tot, W·kg^–1) developed during ten revolutions of all-out periods of cycle ergometer exercise (4–9 s) was measured every 5–6 min in six subjects from rest or from a baseline of constant aerobic exercise [50%–80% of maximal oxygen uptake (VO_2max)] of 20–40 min duration. The oxygen uptake [VO₂ (W·kg^–1, 1 ml O₂ = 20.9 J)] and venous blood lactate concentration ([la]_b, mM) were also measured every 15 s and 2 min, respectively. During the first all-out period, W_tot decreased linearly with the intensity of the priming exercise (W_tot = 11.9–0.25·VO₂). After the first all-out period (i greater than 5–6 min), and if the exercise intensity was less than 60% VO_2max, W_tot, VO₂ and [la]_b remained constant until the end of the exercise. For exercise intensities greater than 60% VO_2max, VO₂ and [la]_b showed continuous upward drifts and W_tot continued decreasing. Under these conditions, the rate of decrease of W_tot was linearly related to the rate of increase of V [(d W_tot/dt) (W·kg^–1·s^–1) = 5.0·10^–5 –0.20·(d VO₂/dt) (W·kg^–1·s^–1)] and this was linearly related to the rate of increase of [la]_b [(d VO₂/dt) (W·kg^–1·s^–1) = 2.310^–4 + 5.910^–5·(d [la]_b/dt) (mM·s^–1)]. These findings would suggest that the decrease of W_tot during the first all-out period was due to the decay of phosphocreatine concentration in the exercising muscles occurring at the onset of exercise and the slow drifts of VO₂ (upwards) and of W_tot (downwards) during intense exercise at constant W_tot could be attributed to the continuous accumulation of lactate in the blood (and in the working muscles).     

Influence of cerebral and muscle oxygenation on repeated-sprint ability

The study examined the influence of cerebral (prefrontal cortex) and muscle (vastus lateralis) oxygenation on the ability to perform repeated, cycling sprints. Thirteen team-sport athletes performed ten, 10-s sprints (with 30 s of rest) under normoxic (F_IO₂ 0.21) and acute hypoxic (F_IO₂ 0.13) conditions in a randomised, single-blind fashion and crossover design. Mechanical work was calculated and arterial O₂ saturation (S_pO₂) was estimated via pulse oximetry for every sprint. Cerebral and muscle oxy-(O₂Hb), deoxy-(HHb), and total haemoglobin (THb) were monitored continuously by near-infrared spectroscopy. Compared with normoxia, hypoxia induced larger decrements in S_pO₂ and work (11.6 and 7.6%, respectively; P < 0.05). In the muscle, we observed a fairly constant level of deoxygenation across sprints, with no effect of the condition. In normoxia, regional cerebral oxygenation increased during the first two sprints and slightly fluctuated thereafter. In contrast, this initial cerebral hyper-oxygenation was attenuated in hypoxia. Changes in [O₂Hb] and [HHb] occurred earlier and were larger in hypoxia compared with normoxia (P < 0.05), while regional blood volume (Δ[THb]) remained unaffected by the condition. Changes in cerebral [HHb] and mechanical work were strongly correlated in normoxia and hypoxia (R ² = 0.81 and R ² = 0.85, respectively; P < 0.05), although the slope of this relationship differed (normoxia, −351.3 ± 183.3 vs. hypoxia, −442.4 ± 227.2; P < 0.05). The results of this NIRS study show that O₂ availability influences prefrontal cortex, but not muscle, oxygenation during repeated, short sprints. By using a hypoxia paradigm, the study suggests that cerebral oxygenation contributes to the impairment of repeated-sprint ability.     

Atrial natriuretic peptide during and after maximal and submaximal exercise under normoxic and hypoxic conditions

Summary The present study was designed to investigate the influence of exercise intensity and duration as well as of inspiratory oxygen content on plasma atrial natriuretic peptide concentration ([ANP]) and furthermore to compare ANP with the effect on aldosterone concentration ([Aldo]). Ten untrained male subjects performed a maximal exercise test (ME) on a cycle ergometer and a submaximal test of 60-min duration at 60% of maximal performance (SE) under normoxia (N) and normobaric hypoxia (H) (partial pressure of oxygen: 12.3 kPa). Five subjects were exposed to hypoxia at rest for 90 min. The [ANP] was mostly affected by exercise intensity (5 min after ME-N, +298.1%, SEM 39.1%) and less by exercise duration (at the end of SE-N: +229.5%, SEM 33.2%). Hypoxia had no effect at rest and reduced the exercise response (ME-H, +184.3%, SEM 27.2%; SE-H, +172.4%, SEM 15.7%). In contrast to ANP, the Aldo response was affected more by duration at submaximal level (+290.1%, SEM 34.0%) than by short maximal exercise (+235.7%, SEM 22.2%). Exposure to hypoxia rapidly decreased [Aldo] (–28.5%, SEM 3.7% after 30 min, P<0.01), but did not influence the exercise effects (ME-H, +206.2%, SEM 26.4%; SE-H, +321.6%, SEM 51.6%). The [ANP] increase was faster than that of [Aldo] during the maximal tests and there was no difference during submaximal exercise. Changes in plasma volume (PV), sodium concentration, and osmolality (Osm) were most pronounced during maximal exercise (for ME-N: PV –13.1%, SD 3.6%, sodium +6.2 mmol·1^–1, SD 2.7, Osm +18.4 mosmol·kg H₂O^–1, SD 6.5). Regression analysis showed high correlations between changes in [ANP] and in Osm during and after maximal exercise and between changes in [ANP] and heart rate for submaximal exercise. It is concluded that besides other mechanisms increased Osm might be involved in the exercise-dependent increase of plasma [ANP].     

The effect of short and long duration exercise on serum erythropoietin concentrations

Summary The effects of short and long duration exercise on serum erythropoietin concentrations [EPO]_s were studied in seven male cross-country skiers of national team standard and eight male marathon runners, respectively. The short duration exercise was performed as 60 min of cycling at an intensity of 80%–95% of maximal heart rate. Arterial blood oxygen saturations monitored by pulse-oximetry remained unchanged throughout exercise. The partial pressure of O₂ at which haemoglobin was half-saturated with O₂ calculated from forearm venous blood gas tension and blood O₂ saturation, and the erythrocyte 2,3-diphosphoglycerate did not change significantly during the exercise. Blood lactate concentrations were increased at the end of exercise [from 1.3 (SEM 0.1) to 3.6 (SEM 0.3) mmol · 1^–1]. The [EPO]_s determined (by enzyme-linked immunosorbent assay) pre-exercise, 5 min, 6 h, 19 h, and 30 h after the exercise were unchanged [from 16.1 (SEM 2.6) to 19.1 (SEM 3.2), 17.9 (SEM 3.0), 17.0 (SEM 2.5), and 18.6 (SEM 2.9) U·l^–1, respectively]. The [EPO]_s were not correlated to the earlier parameters. The long duration exercise consisted of habitual training, a 3 week break from training followed by 2 and 4 weeks of re-training. The [EPO]_s, body fat (BF), and serum free-testosterone concentrations determined at the end of each period remained unchanged. The maximal oxygen uptakes were decreased after the break from training and increased during retraining (P=0.04). Body mass (m _b) increased after the break in training (P=0.02). The [EPO]_s were correlated to BF,r=0.42,P=0.02;m _b,r=0.45,P=0.01; and free-testosterone concentrations,r=0.44,P=0.01. Thus, short and long-duration exercise had no direct influence on [EPO]_s; but relationships among [EPO]_s, free-testosterone concentrations and body composition were noted.     

The effect of hypoxia on performance during 30 s or 45 s of supramaximal exercise

Summary The purpose of this study was to evaluate the effect of hypoxia (10.8±0.6% oxygen) on performance of 30 s and 45 s of supramaximal dynamic exercise. Twelve males were randomly allocated to perform either a 30 s or 45 s Wingate test (WT) on two occasions (hypoxia and room air) with a minimum of 1 week between tests. After a 5-min warm-up at 120 W subjects breathed the appropriate gas mixture from a wet spirometer during a 5-min rest period. Resting blood oxygen saturation was monitored with an ear oximeter and averaged 97.8 ± 1.5% and 83.2 ± 1.9% for the air (normoxic) and hypoxic conditions, respectively, immediately prior to the WT. Following all WT trials, subjects breathed room air for a 10-min passive recovery period. Muscle biopsies from the vastus lateralis were taken prior to and immediately following WT. Arterialized blood samples, for lactate and blood gases, were taken before and after both the warm-up and the performance of WT, and throughout the recovery period. Opencircuit spirometry was used to calculate the total oxygen consumption (Vo₂), carbon dioxide production and expired ventilation during WT. Hypoxia did not impair the performance of the 30-s or 45-s WT.Vo₃ was reduced during the 45-s hypoxic WT (1.71±0.21 I) compared with the normoxic trial (2.16±0.261), but there was no change during the 30-s test (1.22±0.11 vs 1.04±0.171 for the normoxic and hypoxic conditions, respectively). Muscle lactate (LA) increased more during hypoxia following both the 30-s and 45-s WT (67.1±25.0 mmol· kg^–1 dry weight) compared with normoxia (30.8 ± 18.0 mmol · kg^–1 dry weight). Hypoxia did not influence the change in intramuscular adenosine triphosphate, creatine phosphate and glucose-6-phosphate. The performance of WT during hypoxia was associated with a greater decrease in muscle glycogen (P<0.06). Throughout the recovery period, blood LA was lower following the hypoxia (8.43±2.88 mmol · l^–1) comparedwith normoxia (9.15±3.06 mmol · 1^–1). Breathing the hypoxic gas mixture prior to the performance of WT increased blood pH to 7.44±0.03, compared with 7.39±0.03 for normoxia. Blood pH remained higher during the 10-min recovery period following the hypoxic WT trials (7.24±0.08) compared with the normoxic WT (7.22±0.06). BloodP _{CO 2} was reduced prior to and immediately following WT during hypoxia, but there were no differences between the normoxic and hypoxic trials during the 10 min recovery period. These data indicate that more energy was transduced from the catabolism of glycogen to lactate during the hypoxic WT trials, which offset the reduced O₂ availability and maintained performance comparable with normoxic conditions. It is suggested that the induced respiratory alkalosis associated with breathing the hypoxic gas could account for the increased rate of muscle LA accumulation.     

Response of left ventricular diastolic filling to graded exercise relative to the lactate threshold

Summary During incremental exercise, the left ventricular ejection fraction increases up to the intensity of the anaerobic threshold and tends to level off at higher exercise intensities. Since there is a correlation between the response of peak filling rate and ejection fraction to exercise, this study was conducted to determine whether the response of left ventricular diastolic function is similar to the response of systolic function relative to lactate threshold. Twelve healthy men performed two exercise tests on a cycle ergometer. In the first test, lactate threshold and maximal power output were determined. In the second exercise test, gated radionuclide ventriculography was performed at rest, at the lactate threshold intensity, and at peak exercise to measure ejection fraction and peak filling rate. Ejection fraction increased significantly from rest [mean (SD): 62 (5)%] to lactate threshold [76 (7) %] and did not change significantly from lactate threshold to peak exercise [77 (7)%]. Likewise, peak filling rate (normalized for stroke counts) increased from resting [6.1 (0.9)V _s · s^–1] to lactate threshold [9.4 (1.8)V _s · s^–1] and did not change significantly from lactate threshold to peak exercise [9.6 (2.9)V _s · s^–1]. There was no correlation between the change in peak filling rate and the change in ejection fraction from rest to lactate threshold. Thus, during incremental exercise, left ventricular diastolic function responds qualitatively similar to systolic function.