Carbon monoxide exposure during exercise performance: muscle and cerebral oxygenation

Aim: To investigate the effect of carbon monoxide (CO) in the inspired air as anticipated during peak hours of traffic in polluted megalopolises on cerebral, respiratory and leg muscle oxygenation during a constant‐power test (CPT). In addition, since O₂ breathing is used to hasten elimination of CO from the blood, we examined the effect of breathing O₂ following exposure to CO on cerebral and muscle oxygenation during a subsequent exercise test under CO conditions. Methods: Nine men participated in three trials: (i) 3‐h air exposure followed by a control CPT, (ii) 1‐h air and 2‐h CO (18.9 ppm) exposure succeeded by a CPT under CO conditions (CPT_COA), and (iii) 2‐h CO and 1‐h 100% normobaric O₂ exposure followed by a CPT under CO conditions (CPT_COB). All exercise tests were performed at 85% of peak power output to exhaustion. Oxygenated (Δ[O₂Hb]), deoxygenated (Δ[HHb]) and total (Δ[tHb]) haemoglobin in cerebral, intercostal and vastus lateralis muscles were monitored with near‐infrared spectroscopy throughout the CPTs. Results: Performance time did not vary between trials. However, the vastus lateralis and intercostal Δ[O₂Hb] and Δ[tHb] were lower in CPT_COA than in CPT. During the CPT_COB, the intercostal Δ[O₂Hb] and Δ[tHb] were higher than in the CPT_COA. There were no differences in cerebral oxygenation between the trials. Conclusion: Inspiration of 18.9 ppm CO decreases oxygenation in the vastus lateralis and serratus anterior muscles, but does not affect performance. Breathing normobaric O₂ moderates the CO‐induced reductions in muscle oxygenation, mainly in the intercostals, but does not affect endurance.     

Muscle oxygenation kinetics at the onset of exercise do not depend on exercise intensity

The purpose of this study was to determine whether the onset kinetics of muscle oxygenation in localized working muscle (mOxy) was affected by differences in exercise intensity. Five healthy male subjects exercised for 6 min at 125 W, 150 W, and 175 W, and 1 min at 300 W on a cycle ergometer. mOxy was estimated by near-infrared spectroscopy (NIRS) with a continuous wave photometer. The NIRS probe was positioned on the vastus lateralis muscle of the right leg. The relative change in mOxy was calculated from the relative change of the oxygenated hemoglobin (OxyHb) and deoxygenated hemoglobin (DeoxyHb) concentration from their resting values ([mOxy]=[OxyHb]–[DeoxyHb]). Assuming an exponential time course with time delay, the time constants of the mOxy were 5.7 (SD 2.2) s at 125 W, 5.6 (SD 1.9) s at 150 W, 6.0 (SD 2.2) s at 175 W, and 5.6 (SD 2.1) s at 300 W. The time delays of the mOxy were 6.7 (SD 4.2) s at 125 W, 8.6 (SD 1.6) s at 150 W, 6.4 (SD 3.0) s at 175 W, and 5.4 (SD 2.9) s at 300 W. The mean response times of the mOxy were 12.5 (SD 2.7) s at 125 W, 14.2 (SD 2.4) s at 150 W, 12.4 (SD 4.4) s at 175 W, and 11.0 (SD 3.1) s at 300 W. These results indicate that the kinetics of mOxy were not affected by differences in exercise intensity.     

Reliability of erector spinae oxygenation and blood volume responses using near-infrared spectroscopy in healthy males

The purpose of this investigation was to (1) describe the trends in oxygenation (OXY) and blood volume (BV) of the right and left paraspinal muscles during the Biering-Sorensen muscle endurance (BSME) test using near infrared spectroscopy (NIRS), and (2) assess the test-retest reliability of OXY and BV changes during the BSME in healthy males. Seventeen healthy males [age=28.4 (9.8) years, height=1.75 (0.05) m, body mass=82.7 (9.1) kg; mean (SD)] completed two BSME trials within 1 week. NIRS probes were placed bilaterally at lumbar 3. The test was performed with the subject in the prone position using the following protocol: 2 min baseline, BSME, and 4 min recovery. The delta and range values of OXY and BV were used for analysis. Acceptable intra-class correlations were observed for endurance time and all the NIRS variables at the point of fatigue and at each 10% segment of the BSME during the two trials. Bland-Altman plots confirmed the reproducibility of the bilateral NIRS responses of the paravertebral muscles. The BV responses were more reliable than the OXY responses during the two trials. The OXY and BV responses of the paravertebral muscles during static contractions can be measured reliably using NIRS. Future studies should focus primarily on BV for analysis.     

Skeletal muscle StO<Subscript>2</Subscript> kinetics are slowed during low work rate calf exercise in peripheral arterial disease

The time course of muscle oxygen desaturation (StO₂ kinetics) following exercise onset reflects the dynamic interaction between muscle blood flow and muscle oxygen consumption. In patients with peripheral arterial disease (PAD), muscle StO₂ kinetics are slowed during walking exercise; potentially reflecting altered muscle oxygen consumption relative to blood flow. This study evaluated whether StO₂ kinetics measured using near infrared spectroscopy (NIRS) would be slowed in PAD during low work rate calf exercise compared with healthy subjects under conditions in which blood flow did not differ. Eight subjects with PAD and eight controls performed 3 min of calf exercise at 5, 10, 30, and 50% of maximal voluntary contraction (MVC). Calf blood flow responses were measured by plethysmography. Power outputs were similar between groups for all work rates. In PAD, the time constants of StO₂ kinetics were significantly slower than controls during 5% MVC (13.5 ± 1.7 vs. 6.9 ± 1.2 s, P < 0.05) and 10% MVC work rates (14.5 ± 2.7 vs. 6.8 ± 1.1 s, P < 0.05). Blood flow assessed when exercise was interrupted after 30 s did not differ between PAD and control subjects at these work rates. In contrast, the StO₂ time constants were not different between groups during 30 and 50% MVC work rates, where blood flow responses in PAD subjects were lower as compared with controls. Thus in PAD, the slowed StO₂ kinetic responses under conditions of unimpaired calf blood flow reflect slowed muscle oxygen consumption in PAD skeletal muscle during low work rate plantar flexion exercise as compared with healthy skeletal muscle.     

Effects of time pressure and precision demands during computer mouse work on muscle oxygenation and position sense

The present study investigated the effects of time pressure and precision demands during computer mouse work on muscle oxygenation and position sense in the upper extremity. Twenty-four healthy subjects (12 males and 12 females) performed a 45-min standardized mouse-operated computer task on two occasions. The task consisted of painting rectangles that were presented on the screen. On one occasion, time pressure and precision demands were imposed (more demanding task, MDT), whereas, on the other occasion, no such restraints were added (less demanding task, LDT). The order of the two task versions was randomized. Tissue oxygen saturation in the trapezius and extensor carpi radialis muscles was recorded throughout, and the position-matching ability of the wrist was measured before and after the tasks. In addition, measurements of autonomic nervous system reactivity and subjective ratings of tenseness and physical fatigue were obtained. Performance was measured in terms of the number of rectangles that were painted during the task. During MDT, oxygen saturation in extensor carpi radialis decreased (P<0.05) compared to LDT. These data were paralleled by increased electrodermal activity (P<0.05), skin blood flow (P<0.05), ratings of tenseness and fatigue (P<0.01), and increased performance (P<0.01) during MDT. Females exhibited lower oxygen saturation than males, during rest as well as during the computer tasks (P<0.01). Wrist repositioning error increased following LDT as compared to MDT (P<0.05). In conclusion, computer mouse work under time pressure and precision demands caused a decrease in forearm muscle oxygenation, but did not affect wrist position sense accuracy. We attribute our changes in oxygenation more to increased oxygen consumption as a result of enhanced performance, than to vasoconstriction.Presented in part at the 49th Nordiska Arbetsmiljömötet in Savonlinna Finland, August 25–27, 2003     

Cerebral blood flow and oxygenation at maximal exercise: the effect of clamping carbon dioxide

During exercise, as end-tidal carbon dioxide (P_ETCO2$P_{\text{E}{\text{T}}_{\text{C}{\text{O}}_2}}$) drops after the respiratory compensation point (RCP), so does cerebral blood flow velocity (CBFv) and cerebral oxygenation. This low-flow, low-oxygenation state may limit work capacity. We hypothesized that by preventing the fall in P_ETCO2$P_{\text{E}{\text{T}}_{\text{C}{\text{O}}_2}}$ at peak work capacity (W_max) with a newly designed high-flow, low-resistance rebreathing circuit, we would improve CBFv, cerebral oxygenation, and W_max. Ten cyclists performed two incremental exercise tests, one as control and one with P_ETCO2$P_{\text{E}{\text{T}}_{\text{C}{\text{O}}_2}}$ constant (clamped) after the RCP. We analyzed , middle cerebral artery CBFv, cerebral oxygenation, and cardiopulmonary measures. At W_max, when we clamped P_ETCO2$P_{\text{E}{\text{T}}_{\text{C}{\text{O}}_2}}$ (39.7 ± 5.2 mmHg vs. 29.6 ± 4.7 mmHg, P < 0.001), CBFv increased (92.6 ± 15.9 cm/s vs. 73.6 ± 12.5 cm/s, P < 0.001). However, cerebral oxygenation was unchanged (ΔTSI −21.3 ± 13.1% vs. −24.3 ± 8.1%, P = 0.33), and W_max decreased (380.9 ± 20.4 W vs. 405.7 ± 26.8 W, P < 0.001). At W_max, clamping P_ETCO2$P_{\text{E}{\text{T}}_{\text{C}{\text{O}}_2}}$ increases CBFv, but this does not appear to improve W_max.     

Intramuscular pressure and tissue oxygenation during low‐force static contraction do not underlie muscle fatigue

Aim: To test the hypothesis that time‐wise increase in intramuscular pressure (IMP) and subsequent decrease in muscle tissue oxygenation (TO₂) results in muscle fatigue development during a non‐exhaustive, low‐force contraction evidenced by changes in electromyogram (EMG) and particular mechanomyogram (MMG). Methods: Seven subjects performed static elbow flexion at 10% maximal voluntary contraction (MVC) for 10 min (10% MVC_{10 min}). Surface EMG, MMG, IMP and TO₂ measured by near‐infrared spectroscopy was recorded from m. biceps brachii during 10% MVC_{10 min} and during 5% MVC test contractions of 1 min duration performed before 10% MVC_{10 min}, 10 and 30 min post‐exercise. EMG and MMG were analysed for root mean square (rms) and mean power frequency (mpf). Results: During 10% MVC_{10 min} MMGrms increased from initial level of 0.04 ± 0.01 to 0.11 ± 0.07 m s⁻² in the last minute and MMGmpf and EMGmpf decreased from 34.9 ± 8.2 to 21.3 ± 3.8 Hz and from 71.7 ± 10.9 to 61.7 ± 10.0 Hz respectively. Similar changes were present in 5% MVC test contractions 30 min post‐exercise. Initially, TO₂ decreased by 6.9 ± 6.5% of resting level but returned to rest within 1 min. IMP remained constant during the contraction after an initial fourfold increase from resting level of 12.2 ± 10.4 mmHg. Conclusions: IMP was anticipated to increase with time of contraction due to e.g. increased muscle water content; but this was not confirmed. Consequently, muscle blood flow was unlikely to be impeded with contraction time, which may account for the maintenance of TO₂. Thus, decreased TO₂ did not underlie either acute or long‐term muscle fatigue development evidenced by changes in EMG and particular MMG variables.     

Near‐infrared spectroscopy determined brain and muscle oxygenation during exercise with normal and resistive breathing

To elevate effects of carbon dioxide (CO₂) retention by way of an increased respiratory load during submaximal exercise (150 W), the concentration changes of oxy‐ (ΔHbO₂) and deoxy‐haemoglobin (ΔHb) of active muscles and the brain were determined by near‐infrared spectroscopy (NIRS) in eight healthy males. During exercise, pulmonary ventilation increased to 33 (28–40) L min^–1 (median with range) with no effect of a moderate breathing resistance (reduction of the pneumotach diameter from 30 to 14 and 10 mm). The end‐tidal CO₂ pressure (P_ETCO ₂) increased from 45 (42–48) to 48 (46–58) mmHg with a reduction of only 1% in the arterial haemoglobin O₂ saturation (S_aO ₂). During control exercise (normal breathing resistance), muscle and brain ΔHbO₂ were not different from the resting levels, and only the leg muscle ΔHb increased (4 (–2–10) μM , P < 0.05). Moderate resistive breathing increased ΔHbO₂ of the intercostal and vastus lateralis muscles to 6 ± (–5–14) and 1 (–7–9) μM (P < 0.05), respectively, while muscle ΔHb was not affected. Cerebral ΔHbO₂ and ΔHb became elevated to 6 (1–15) and 1 (–1–6) μM by resistive breathing (P < 0.05). Resistive breathing caused an increased concentration of oxygenated haemoglobin in active muscles and in the brain. The results indicate that CO₂ influences blood flow to active skeletal muscle although its effect appears to be smaller than for the brain.     

Cerebral oxygenation decreases but does not impair performance during self-paced,strenuous exercise

Aim: The reduction in cerebral oxygenation (Cox) is associated with the cessation of exercise during constant work rate and incremental tests to exhaustion. Yet in exercises of this nature, ecological validity is limited due to work rate being either fully or partly dictated by the protocol, and it is unknown whether cerebral deoxygenation also occurs during self-paced exercise. Here, we investigated the cerebral haemodynamics during a 5-km running time trial in trained runners. Methods: Rating of perceived exertion (RPE) and surface electromyogram (EMG) of lower limb muscles were recorded every 0.5 km. Changes in Cox (prefrontal lobe) were monitored via near-infrared spectroscopy through concentration changes in oxy- and deoxyhaemoglobin (Δ[O₂Hb], Δ[HHb]). Changes in total Hb were calculated (Δ[THb] = Δ[O₂Hb] + Δ[HHb]) and used as an index of change in regional blood volume. Results: During the trial, RPE increased from 6.6 ± 0.6 to 19.1 ± 0.7 indicating maximal exertion. Cox rose from baseline to 2.5 km (↑Δ[O₂Hb], ↑Δ[HHb], ↑Δ[THb]), remained constant between 2.5 and 4.5 km, and fell from 4.5 to 5 km (↓Δ[O₂Hb], ↑Δ[HHb], ↔Δ[THb]). Interestingly, the drop in Cox at the end of the trial coincided with a final end spurt in treadmill speed and concomitant increase in skeletal muscle recruitment (as revealed by higher lower limb EMG). Conclusion: Results confirm the large tolerance for change in Cox during exercise at sea level, yet further indicate that, in conditions of self-selected work rate, cerebral deoxygenation remains within a range that does not hinder strenuous exercise performance.     

Cerebral and peripheral hemodynamics and oxygenation during maximal dry breath-holds

The effects of maximal apneas on cerebral and brachial blood flow and oxygenation are unknown in humans. Middle cerebral artery blood velocity (MCAV), cerebral and muscle oxygenation (Sc(O2) and Sm(O2)) and brachial blood flow (BBF) were measured during apneas in breath-hold divers (BHD) and non-divers (ND). Brain oxyhemoglobin (O(2)Hb) was maintained in both groups until the end of apnea, whereas deoxyhemoglobin increased more in BHD. Therefore, Sc(O2) decreased more in BHD due to longer apnea duration and smaller initial MCAV increase. MCAV increased significantly more in BHD versus ND at the end of apnea. Cerebral desaturation for approximately 13% occurred at the end of apnea in BHD despite increased cerebral oxygen delivery for approximately 50%. Larger reduction in muscle O(2)Hb was found in BHD, with similar peripheral vasoconstriction. These data indicate that BHD have decreased Sc(O2) at the end of breath-hold despite large increases in MCAV. This is partly due delayed initial cerebral vasodilation. This study provides further evidence for the oxygen-conserving effect in elite divers.     

Factors which alter the relationship between ventilation and carbon dioxide production during exercise in normal subjects

The slope of the linear relationship between ventilation and carbon dioxide production has been thought to indicate that is one of the major stimuli to . A group of 15 normal subjects undertook different incremental treadmill exercise protocols to explore the relationship between and . An incremental protocol using 1 instead of 3-min stages of exercise resulted in an increase in the to ratio [26.84 (SEM 1.23) vs 31.08 (SEM 1.36) (P < 0.008) for the first stage, 25.24 (SEM 0.86) vs 27.83 (SEM 0.91) (P < 0.005) for the second stage and 23.90 (SEM 0.86) vs 26.34 (SEM 0.81) (P = 0.001) for the third stage]. Voluntary hyperventilation to double the control level of during exercise resulted in an increase in the to slope [from 21.3 (SEM 0.71) for the control run to 35.1 (SEM 1.2) for the hyperventilation run (P < 0.001)]. Prolonged hyperventilation (5 min) during exercise at stage 2 of the Bruce protocol resulted in a continuted elevation of and the slope. A steady state of and metabolic gas exchange can only be said to have been present after at least 3 min of exercise. Voluntary hyperventilation increased the slope of the relationship between and . End-tidal carbon dioxide fell, but remained within the normal range. These results would suggest that a non-carbon dioxide factor may have been responsible for the increase we found in during exercise, and that factors other than increased dead space ventilation can cause an increased ventilation to slope, such as that seen in some pathophysiological conditions, such as chronic heart failure.     

Effects of intermittent hypoxia on SaO2, cerebral and muscle oxygenation during maximal exercise in athletes with exercise-induced hypoxemia

In a placebo-controlled study, the effects of intermittent hypoxic exposures (IHE) or a placebo control for 10 days, were examined on the extent of exercise-induced hypoxemia (EIH), cerebral and muscle oxygenation (near-infrared spectroscopy) and [Formula: see text] Eight athletes who had previously displayed EIH (fall in saturation of arterial oxygen (SaO(2)) of >4% from rest) during an incremental maximal exercise test, volunteered for the present research. Prior to (baseline), and 2 days following (post) the IHE or placebo, an incremental maximal exercise test was performed whilst SaO(2), heart rate, cerebral and muscle oxygenation and respiratory gas exchange were measured continuously. After IHE, but not placebo, EIH was less pronounced at [Formula: see text] (IHE group, SaO(2) at [Formula: see text] baseline 91.23 +/- 1.10%, post 94.10 +/- 2.19%; P < 0.01, mean +/- SD). This reduction was reflected in an increased ventilation (NS), a lower end-tidal CO(2) (P < 0.01), and lowered cerebral TOI during heavy exercise [Formula: see text] Conversely, muscle tHb at maximal exercise, was increased (2.4 +/- 1.8 DeltamuM, P = 0.01, mean +/- 95 CL) following IHE, whilst de-oxygenated Hb at 90% of [Formula: see text] was reduced (-0.9 +/- 0.8 DeltamuM, P = 0.02). These data indicate that exposure to IHE can attenuate the degree of EIH. Despite a potential compromise in cerebral oxygenation, exposure to IHE may induce some positive physiological adaptations at the muscle tissue level. We speculate that the unchanged [Formula: see text] following IHE might reflect a balance between these central (cerebral) and peripheral (muscle) adaptations.     

Oscillations in cerebral blood flow and cortical oxygenation in Alzheimer's disease

In Alzheimer's disease (AD) cerebrovascular function is at risk. Transcranial Doppler, near-infrared spectroscopy, and photoplethysmography are noninvasive methods to continuously measure changes in cerebral blood flow velocity (CBFV), cerebral cortical oxygenated hemoglobin (O₂Hb), and blood pressure (BP). In 21 patients with mild to moderate AD and 20 age-matched controls, we investigated how oscillations in cerebral blood flow velocity (CBFV) and O₂Hb are associated with spontaneous and induced oscillations in blood pressure (BP) at the very low (VLF = 0.05 Hz) and low frequencies (LF = 0.1 Hz). We applied spectral and transfer function analysis to quantify dynamic cerebral autoregulation and brain tissue oxygenation. In AD, cerebrovascular resistance was substantially higher (34%, AD vs. control: Δ = 0.69 (0.25) mm Hg/cm/second, p = 0.012) and the transmission of very low frequency (VLF) cerebral blood flow (CBF) oscillations into O₂Hb differed, with increased phase lag and gain (Δ phase 0.32 [0.15] rad; Δ gain 0.049 [0.014] μmol/cm/second, p both < 0.05). The altered transfer of CBF to cortical oxygenation in AD indicates that properties of the cerebral microvasculature are changed in this disease.     

Cerebral oxygenation and cerebral oxygen extraction in the preterm infant: the impact of respiratory distress syndrome

Haemodynamic factors play an important role in the etiology of cerebral lesions in preterm infants. Respiratory distress syndrome (RDS), a common problem in preterms, is strongly related with low and fluctuating arterial blood pressure. This study investigated the relation between mean arterial blood pressure (MABP), fractional cerebral oxygen saturation (ScO₂) and fractional (cerebral) tissue oxygen extraction (FTOE), a measure of oxygen utilisation of the brain, during the first 72 h of life. Thirty-eight infants (gestational age < 32 week) were included, 18 with and 20 without RDS. Arterial oxygen saturation (SaO₂), MABP and near infrared spectroscopy-determined ScO₂ were continuously measured. FTOE was calculated as a ratio: (SaO₂–ScO₂)/SaO₂. Gestational age and birth weight did not differ between groups, but assisted ventilation and use of inotropic drugs were more common in RDS infants (P<0.01). MABP was lower in RDS patients (P<0.05 from 12 up to 36 h after birth), but increased in both groups over time. ScO₂ and FTOE were not different between groups over time, but in RDS infants ScO₂ and FTOE had substantial larger variance (P<0.05 at all time points except at 36–48 h for ScO₂ and P<0.05 at 12–18, 18–24, 36–48 and 48–60 h for FTOE). During the first 72 h of life, RDS infants showed more periods of positive correlation between MABP and ScO₂ (P<0.05 at 18–24, 24–36 36–48 48–60 h) and negative correlation between MABP and FTOE (P<0.05 at 18–24, 36–48 h). Although we found that the patterns of cerebral oxygenation and extraction in RDS infants were not different as compared to infants without RDS, we suggest that the frequent periods with possible lack of cerebral autoregulation in RDS infants may make these infants more vulnerable to cerebral damage.     

Carbohydrate supplementation during prolonged cycling exercise spares muscle glycogen but does not affect intramyocellular lipid use

Using contemporary stable-isotope methodology and fluorescence microscopy, we assessed the impact of carbohydrate supplementation on whole-body and fiber-type-specific intramyocellular triacylglycerol (IMTG) and glycogen use during prolonged endurance exercise. Ten endurance-trained male subjects were studied twice during 3 h of cycling at 63 ± 4% of maximal O₂ uptake with either glucose ingestion (CHO trial; 0.7 g CHO kg⁻¹ h⁻¹) or without (CON placebo trial; water only). Continuous infusions with [U-¹³C] palmitate and [6,6-²H₂] glucose were applied to quantify plasma free fatty acids (FFA) and glucose oxidation rates and to estimate intramyocellular lipid and glycogen use. Before and after exercise, muscle biopsy samples were taken to quantify fiber-type-specific IMTG and glycogen content. Plasma glucose rate of appearance (R _a) and carbohydrate oxidation rates were substantially greater in the CHO vs CON trial. Carbohydrate supplementation resulted in a lower muscle glycogen use during the first hour of exercise in the CHO vs CON trial, resulting in a 38 ± 19 and 57 ± 22% decreased utilization in type I and II muscle-fiber glycogen content, respectively. In the CHO trial, both plasma FFA R _a and subsequent plasma FFA concentrations were lower, resulting in a 34 ± 12% reduction in plasma FFA oxidation rates during exercise (P < 0.05). Carbohydrate intake did not augment IMTG utilization, as fluorescence microscopy revealed a 76 ± 21 and 78 ± 22% reduction in type I muscle-fiber lipid content in the CHO and CON trial, respectively. We conclude that carbohydrate supplementation during prolonged cycling exercise does not modulate IMTG use but spares muscle glycogen use during the initial stages of exercise in endurance-trained men.     

Hypocapnia during hypoxic exercise and its impact on cerebral oxygenation,ventilation and maximal whole body O2 uptake

With hypoxic exposure ventilation is elevated through the hypoxic ventilatory response. We tested the hypothesis that the resulting hypocapnia reduces maximal exercise capacity by decreasing (i) cerebral blood flow and oxygenation and (ii) the ventilatory drive.     

The influence of circulatory difference on muscle oxygenation and fatigue during intermittent static dorsiflexion

This study aimed to examine the influences of circulatory difference on the utilization of O₂ and the progression of fatigue in the tibialis anterior (TA) muscle during dorsiflexion exercise, with reference to different body postures. The subjects performed intermittent static dorsiflexion at 50% of maximal voluntary contraction (MVC) up to exhaustion with the right leg either up or down relative to the heart. These exercises were performed with and without occluding muscle blood flow. Simultaneously with the surface electromyogram (EMG) measurement, total hemoglobin volume change and tissue oxygenation (S _tO₂) of TA were measured using near-infrared spectroscopy (NIRS). When the subjects performed an exhaustive intermittent dorsiflexion exercise at 50% MVC, the endurance time decreased in the leg up position. Also, the progression of fatigue in TA detected using EMG signals (i.e. integrated EMG and mean power frequency of EMG) was faster with the leg elevated. The NIRS data indicated a lower blood volume and S _tO₂ with the leg up than with the leg down during the exercise, which suggests that the deficit in the O₂ supply to exercising muscles demand was more apparent in the leg up position. However, these differences in EMG and NIRS data disappeared when the blood flow was restricted in both positions. From these results it is concluded that the difference in exercising muscle oxygenation between two different body postures influenced the progression of muscle fatigue and caused the difference in endurance performance.     

Changes in cerebral haemodynamics,regional oxygen saturation and amplitude-integrated continuous EEG during hypoxia-ischaemia and reperfusion in newborn piglets

Perinatal asphyxia models are necessary to obtain knowledge of the pathophysiology of hypoxia-ischaemia (HI) and to test potential neuroprotective strategies. The present study was performed in newborn piglets to obtain information about simultaneous changes in cerebral oxygenation and haemodynamics and electrocortical brain activity during a 60-min period of HI and up to 2 h of reperfusion using near infrared spectrophotometry (NIRS) and the amplitude-integrated EEG (aEEG). HI was induced by occluding both carotid arteries and decreasing the fraction of inspired oxygen (FiO(2)) to 0.08-0.12 for 60 min. The mean arterial blood pressure (MABP) and heart rate increased, the oxygenated haemoglobin (O(2)Hb) decreased, and the deoxygenated haemoglobin (HHb) increased, but total haemoglobin (tHb) remained stable during the 60-min HI period. The regional oxygen saturation (rSO(2)) was significantly decreased during the whole HI period, as was the electrocortical brain activity. Upon reperfusion and reoxygenation, the MABP normalised to baseline values but the heart rate remained increased. O(2)Hb and HHb recovered to baseline values and tHb remained unchanged. As indicated by the unchanged tHb values during the HI period, it was suggested that compensatory cerebral perfusion occurred during this period, probably via the vertebrobasilar arterial system. Furthermore, in this model a clear hyperperfusion period directly upon reperfusion and reoxygenation is not present. rSO(2) showed a quick recovery to baseline values, but the aEEG-measured electrocortical brain activity remained reduced following HI. In conclusion, the rSO(2) and aEEG showed a different time profile following perinatal asphyxia. The stable tHb during HI and reperfusion in this model differs from observations in human neonates.     

Rates of fluid ingestion alter pacing but not thermoregulatory responses during prolonged exercise in hot and humid conditions with appropriate convective cooling

The aim of the study was to examine the effects of fluid replacement on thermoregulation and cycling performance in hot, humid conditions. Six male cyclists (PPO = 426 ± 39 W) performed six 80 km time trials. Subjects replaced 0% (0); 33% (33); 66% (66); or 100% (100) of the weight lost during an “ad libitum” trial (Ad Lib). In another condition (WET), subjects rinsed their mouths at 10 km intervals. There was no trial effect on any thermoregulatory variables or on performance. When WET, 0, 33 (“LO”) were compared to Ad Lib; 66, 100 (“HI”), power output was higher in HI (209 ± 22 vs. 193 ± 22 W, p < 0.05). Restricting fluid below ad libitum rates impaired performance (LO group). Rates greater than ad libitum did not result in further improvements. Ad libitum fluid ingestion is optimal as it prevents athletes from ingesting too little or too much fluid.     

Age‐ and sex‐related differences in muscle phosphocreatine and oxygenation kinetics during high‐intensity exercise in adolescents and adults

The aim of this investigation was to examine the adaptation of the muscle phosphates (e.g. phosphocreatine (PCr) and ADP) implicated in regulating oxidative phosphorylation, and oxygenation at the onset of high intensity exercise in children and adults. The hypotheses were threefold: primary PCr kinetics would be faster in children than adults; the amplitude of the PCr slow component would be attenuated in children; and the amplitude of the deoxyhaemoglobin/myoglobin (HHb) slow component would be reduced in children. Eleven children (5 girls, 6 boys, 13 ± 1 years) and 11 adults (5 women, 6 men, 24 ± 4 years) completed two to four constant work rate exercise tests within a 1.5 T MR scanner. Quadriceps muscle energetics during high intensity exercise were monitored using ³¹P‐MRS. Muscle oxygenation was monitored using near‐infrared spectroscopy. The time constant for the PCr response was not significantly different in boys (31 ± 10 s), girls (31 ± 10 s), men (44 ± 20 s) or women (29 ± 14 s, main effects: age, p = 0.37, sex, p = 0.25). The amplitude of the PCr slow component relative to end‐exercise PCr was not significantly different between children (23 ± 23%) and adults (17 ± 13%, p = 0.47). End‐exercise [PCr] was significantly lower, and [ADP] higher, in females (18 ± 4 mM and 53 ± 16 µM) than males (23 ± 4 mM, p = 0.02 and 37 ± 11 µM, p = 0.02), but did not differ with age ([PCr]: p = 0.96, [ADP]: p = 0.72). The mean response time for muscle tissue deoxygenation was significantly faster in children (22 ± 4 s) than adults (27 ± 7 s, p = 0.01). The results of this study show that the control of oxidative metabolism at the onset of high intensity exercise is adult‐like in 13‐year‐old children, but that matching of oxygen delivery to extraction is more precise in adults. Copyright © 2010 John Wiley & Sons, Ltd.