The postural reduction in middle cerebral artery blood velocity is not explained by PaCO2

In the normocapnic range, middle cerebral artery mean velocity (MCA V _mean) changes ∼ 3.5% per mmHg carbon-dioxide tension in arterial blood (PaCO₂) and a decrease in PaCO₂ will reduce the cerebral blood flow by vasoconstriction (the CO₂ reactivity of the brain). When standing up MCA V _mean and the end-tidal carbon-dioxide tension (PETCO₂) decrease, suggesting that PaCO₂ contributes to the reduction in MCA V _mean. In a fixed body position, PETCO₂ tracks changes in the PaCO₂ but when assuming the upright position, cardiac output decreases and its distribution over the lung changes, while ventilation increases suggesting that PETCO₂ decreases more than PaCO₂. This study evaluated whether the postural reduction in PaCO₂ accounts for the postural decline in MCA V _mean. From the supine to the upright position, PETCO₂, PaCO₂, MCA V _mean, and the near-infrared spectrophotometry determined cerebral tissue oxygenation (CO₂Hb) were followed in seven subjects. When standing up, MCA V _mean (from 65.3±3.8 to 54.6±3.3 cm s⁻¹ ; mean ± SEM; P<0.05) and cO₂Hb (−7.2±2.2 μmol l⁻¹ ; P<0.05) decreased. At the same time, the ratio increased 49±14% (P<0.05) with the postural reduction in PETCO₂ overestimating the decline in PaCO₂ (−4.8±0.9 mmHg vs. −3.0±1.1 mmHg; P<0.05). When assuming the upright position, the postural decrease in MCA V _mean seems to be explained by the reduction in PETCO₂ but the small decrease in PaCO₂ makes it unlikely that the postural decrease in MCA V _mean can be accounted for by the cerebral CO₂ reactivity alone.     

Middle cerebral artery blood velocity and plasma catecholamines during exercise

During dynamic exercise, mean blood velocity (V_mean) in the middle cerebral artery (MCA) demonstrates a graded increase to work rate and reflects regional cerebral blood flow. At a high work rate, however, vasoactive levels of plasma catecholamines could mediate vasoconstriction of the MCA and thereby elevate V_mean at a given volume flow. To evaluate transcranial Doppler-determined V_mean at high plasma catecholamine levels, seven elite cyclists performed a maximal performance test on a bicycle ergometer. Results were compared with those elicited during five incremental exercise bouts and during rhythmic handgrip when plasma catecholamines are low. During rhythmic handgrip the V_mean was elevated by 21±3% (mean±SE), which was not statistically different from that established during moderate cycling. However, at the highest submaximal and maximal work intensities on the bicycle ergometer, V_mean increased by 31±3% and 48±4%, respectively, and this was significantly higher compared to handgrip (P<0.05). During maximal cycling, plasma adrenaline increased from 0.21±0.04 nmol L^-1 at rest to 4.18±1.46 nmol L^-1, and noradrenaline increased from 0.79±0.08 to 12.70±1.79 nmol L^-1. These levels were 12- to 16-fold higher than those during rhythmic handgrip (adrenaline: 0.34±0.03 nmol L^-1; noradrenaline: 0.78±0.05 nmol L^-1). The increase in V_mean during intense ergometer cycling conforms to some middle cerebral artery constriction elicited by plasma catecholamines. Such an influence is unlikely during rhythmic handgrip compared with low intensity cycling.     

Influence of upper body position on middle cerebral artery blood velocity during continuous positive airway pressure breathing

Continuous positive airway pressure (CPAP) is a treatment modality for pulmonary oxygenation difficulties. CPAP impairs venous return to the heart and, in turn, affects cerebral blood flow (CBF) and augments cerebral blood volume (CBV). We considered that during CPAP, elevation of the upper body would prevent a rise in CBV, while orthostasis would challenge CBF. To determine the body position least affecting indices of CBF and CBV, the middle cerebral artery mean blood velocity (MCA V _mean) and the near-infrared spectroscopy determined frontal cerebral hemoglobin content (cHbT) were evaluated in 11 healthy subjects during CPAP at different body positions (15° head-down tilt, supine, 15°, 30° and 45° upper body elevation). In the supine position, 10 cmH₂O of CPAP reduced MCA V _mean by 9 ± 3% and increased cHbT by 4 ± 2 μmol/L (mean ± SEM); (P < 0.05). In the head-down position, CPAP increased cHbT to 13 ± 2 μmol/L but left MCA V _mean unchanged. Upper body elevation by 15° attenuated the CPAP associated reduction in MCA V _mean (−7 ± 2%), while cHbT returned to baseline (1 ± 2 μmol/L). With larger elevation of the upper body MCA V _mean decreased progressively to −17 ± 3%, while cHbT remained unchanged from baseline. These results suggest that upper body elevation by ∼15° during 10 cmH₂O CPAP prevents an increase in cerebral blood volume with minimal effect on cerebral blood flow.     

Middle cerebral artery blood velocity,arterial diameter and muscle sympathetic nerve activity during post-exercise muscle ischaemia

During exercise the transcranial Doppler determined mean blood velocity (V_mean) increases in the middle cerebral artery (MCA) and reflects cerebral blood flow when the diameter at the site of investigation remains constant. Sympathetic activation could induce MCA vasoconstriction and in turn elevate V_mean at an unchanged cerebral blood flow. In 12 volunteers we evaluated whether V_mean relates to muscle sympathetic nerve activity (MSNA) in the peroneal nerve during rhythmic handgrip and post-exercise muscle ischaemia (PEMI). The luminal diameter of the dorsalis pedis artery (AD) was taken to reflect the MSNA influence on a peripheral artery. Rhythmic handgrip increased heart rate (HR) from 74 ± 20 to 92 ± 21 beats min^?1 and mean arterial pressure (MAP) from 87 ± 7 to 105 ± 9 mmHg (mean ± SD; P < 0.05). During PEMI, HR returned to pre-exercise levels while MAP remained elevated (101 ± 9 mmHg). During handgrip contralateral MCA V_mean increased from 65 ± 10 to 75 ± 13 cm s^?1 and this was more than on the ipsilateral side (from 63 ± 10 to 68 ± 10 cm s^?1; P < 0.05). On both sides of the brain V_mean returned to baseline during PEMI. MSNA did not increase significantly during handgrip (from 56 ± 24 to 116 ± 39 units) but the elevation became statistically significant during PEMI (135 ± 86 units, P < 0.05), while AD did not change. Taken together, during exercise and PEMI, V_mean changed independent of an elevation of MSNA by more than 140% and the dorsalis pedis artery diameter was stable. The results provide no evidence for a vasoconstrictive influence of sympathetic nerve activity on medium size arteries of the limbs and the brain during rhythmic handgrip and post-exercise muscle ischaemia.     

Middle cerebral artery blood velocity during exercise with β‐1 adrenergic and unilateral stellate ganglion blockade in humans

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V_mean) is attenuated during cycling with β‐1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocain; 8 mL; n=8) affects the attenuated exercise – MCA V_mean following cardio‐selective β‐1 adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V_mean were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V_mean increased to the same extent (11.4 ± 1.9 vs. 11.1 ± 1.9 cm s^?1). With the pharmacological intervention the exercise CO (10 ± 1 vs. 12 ± 1 L min^?1; n=5), HR (115 ± 4 vs. 134 ± 4 beats min^?1) and ΔMCA V_mean (8.7 ± 2.2 vs. 11.4 ± 1.9 cm s^?1) were reduced, and MAP was increased (100 ± 5 vs. 86 ± 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the β‐1 blockade induced attenuation in ΔMCA V_mean (10.2 ± 2.5 cm s^?1). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.     

Cerebral oxygenation is reduced during hyperthermic exercise in humans

Aim: Cerebral mitochondrial oxygen tension (P_mitoO₂) is elevated during moderate exercise, while it is reduced when exercise becomes strenuous, reflecting an elevated cerebral metabolic rate for oxygen (CMRO₂) combined with hyperventilation-induced attenuation of cerebral blood flow (CBF). Heat stress challenges exercise capacity as expressed by increased rating of perceived exertion (RPE). Methods: This study evaluated the effect of heat stress during exercise on P_mitoO₂ calculated based on a Kety-Schmidt-determined CBF and the arterial-to-jugular venous oxygen differences in eight males [27 ± 6 years (mean ± SD) and maximal oxygen uptake (VO_2max) 63 ± 6 mL kg⁻¹ min⁻¹]. Results: The CBF, CMRO₂ and P_mitoO₂ remained stable during 1 h of moderate cycling (170 ± 11 W, ∼50% of VO_2max, RPE 9–12) in normothermia (core temperature of 37.8 ± 0.4 °C). In contrast, when hyperthermia was provoked by dressing the subjects in watertight clothing during exercise (core temperature 39.5 ± 0.2 °C), P_mitoO₂ declined by 4.8 ± 3.8 mmHg (P < 0.05 compared to normothermia) because CMRO₂ increased by 8 ± 7% at the same time as CBF was reduced by 15 ± 13% (P < 0.05). During exercise with heat stress, RPE increased to 19 (19–20; P < 0.05); the RPE correlated inversely with P_mitoO₂ (r² = 0.42, P < 0.05). Conclusion: These data indicate that strenuous exercise in the heat lowers cerebral P_mitoO₂, and that exercise capacity in this condition may be dependent on maintained cerebral oxygenation.     

Effects of intermittent hypoxia on the cerebrovascular responses to submaximal exercise in humans

Intermittent hypoxia (IH) has been shown to alter the ventilatory and cardiovascular responses to submaximal exercise; however, the effect of IH on the cerebral blood flow (CBF) response to submaximal exercise has not been determined. This study tested the hypothesis that IH would blunt the CBF response during eucapnic and hypercapnic exercise. Nine healthy males underwent 10 consecutive days of isocapnic IH (oxyhaemoglobin saturation = 80%, 1 h day⁻¹). Ventilatory, cardiovascular, and cerebrovascular responses to cycle exercise (50, 100, and 150 W) were measured before and after IH. Carbon dioxide (5% CO₂), a mediator of CBF during exercise, was administered for 2 min of each exercise stage. Over the 10 days of IH, there was an increase in minute ventilation during the IH exposures (P < 0.05). Although exercise produced increases in middle cerebral artery mean velocity (MCA V _mean), and mean arterial pressure (P < 0.05), there was no effect of IH. Similarly, hypercapnic exercise increased and MCA V _mean (P < 0.05); however, the magnitude of the response was unchanged following IH. Our findings indicate that ten daily hypoxia exposures does not alter the CBF response to submaximal exercise.     

Influence of indomethacin on the ventilatory and cerebrovascular responsiveness to hypoxia

Indomethacin (INDO) has the potential to be a useful tool to explore the influence of cerebral blood flow and its responses to CO₂ on ventilatory control. However, the effect of INDO on the cerebrovascular and ventilatory response to hypoxia remains unclear; therefore, we examined the effect of INDO on ventilatory and cerebrovascular sensitivity to hypoxia and hypercapnia. We measured end-tidal gases, ventilation ([(V)\dot]_\textE ), (\dot{V}_{\text{E}} ), and middle cerebral artery velocity (MCAv) before and 90 min following INDO (100 mg) in 12 healthy participants at rest and during hyperoxic hypercapnia and isocapnic hypoxia. Following INDO, resting [(V)\dot]_\textE \dot{V}_{\text{E}} and end-tidal gases were unaltered (P > 0.05), whilst MCAv was lowered by 25 ± 19% (P < 0.001). INDO ingestion reduced MCAv-CO₂ reactivity by 46 ± 29% (2.9 ± 0.9 vs. 1.7 ± 0.9 cm s⁻¹ mmHg⁻¹; P < 0.001) and enhanced the [(V)\dot]_\textE \dot{V}_{\text{E}} -CO₂ sensitivity by 0.5 ± 0.5 L min⁻¹ mmHg⁻¹ (1.9 ± 1.5 vs. 2.3 ± 1.6 L min⁻¹ mmHg⁻¹; P < 0.05). No changes were observed in either the MCAv or [(V)\dot]_\textE \dot{V}_{\text{E}} responsiveness to isocapnic hypoxia following INDO ingestion (P > 0.05). These findings indicate that INDO does not alter cerebrovascular and ventilatory responsiveness to hypoxia, indicating a preserved peripheral chemoreflex in response to this pharmacological agent.     

Change in the peripheral CO2 chemoreflex from rest to exercise

A single-breath CO₂ test of peripheral chemosensitivity has recently been described, and elaborated based on model simulations. This study was designed to measure the peripheral CO₂ chemoreflex at rest and during heavy exercise to see if carotid chemosensitivity to CO₂ increased. Ten healthy, adult males performed an incremental exercise test to determine their ventilatory anaerobic threshold (VAT), and 20 minutes of steady-state exercise at a pre-determined power output above VAT. Arterialized venous blood was obtained during each minute of incremental exercise to verify development of metabolic acidosis. Carotid chemosensitivity was tested repeatedly at rest and in steady-state exercise by the ventilatory response to a single breath of 13% CO₂ in air. The peripheral chemoreflex for CO₂ for the group of subjects doubled from rest to exercise (mean 0.0961 · s^–1 · kPa^–1) with all subjects showing an increase. We conclude that the gain of the carotid CO₂ chemoreflex increases from rest to exercise at work above the VAT.     

Influence of sildenafil on lung diffusion during exposure to acute hypoxia at rest and during exercise in healthy humans

We sought to determine the influence of sildenafil on the diffusing capacity of the lungs for carbon monoxide (DL_CO) and the components of DL_CO (pulmonary capillary blood volume V _c, and alveolar–capillary membrane conductance D _M) at rest and following exercise with normoxia and hypoxia. This double-blind placebo-controlled, cross-over study included 14 healthy subjects (age = 33 ± 11 years, ht = 181 ± 8 cm, weight = 85 ± 14 kg, BMI = 26 ± 3 kg/m², peak normoxic VO₂ = 36 ± 6 ml/kg, mean ± SD). Subjects were randomized to placebo or 100 mg sildenafil 1 h prior to entering a hypoxic tent with an FiO₂ of 12.5% for 90 min. DLCO, V _c, and D _M were assessed at rest, every 3 min during exercise, at peak exercise, and 10 and 30 min post exercise. Sildenafil attenuated the elevation in PAP at rest and during recovery with exposure to hypoxia, but pulmonary arterial pressure immediately post exercise was not different between sildenafil and placebo. Systemic O₂ saturation and VO_2peak did not differ between the two conditions. DL_CO was not different between groups at any time point. V _C was higher with exercise in the placebo group, and the difference in D _M between sildenafil and placebo was significant only when corrected for changes in V _c (D _M/V _c = 0.57 ± 0.29 vs. 0.41 ± 0.16, P = 0.04). These results suggest no effect of sildenafil on DLCO, but an improvement in D _M when corrected for changes in V _c during short-term hypoxic exposure with exercise.     

<Emphasis Type="Italic">V</Emphasis>O<Subscript>2</Subscript>max during successive maximal efforts

The concept of VO₂max has been a defining paradigm in exercise physiology for >75 years. Within the last decade, this concept has been both challenged and defended. The purpose of this study was to test the concept of VO₂max by comparing VO₂ during a second exercise bout following a preliminary maximal effort exercise bout. The study had two parts. In Study #1, physically active non-athletes performed incremental cycle exercise. After 1-min recovery, a second bout was performed at a higher power output. In Study #2, competitive runners performed incremental treadmill exercise and, after 3-min recovery, a second bout at a higher speed. In Study #1 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (3.95 ± 0.75 vs. 4.06 ± 0.75 l min⁻¹). Maximal heart rate was not different (179 ± 14 vs. 180 ± 13 bpm) although maximal V _E was higher in the second bout (141 ± 36 vs. 151 ± 34 l min⁻¹). In Study #2 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (4.09 ± 0.97 vs. 4.03 ± 1.16 l min⁻¹), nor was maximal heart rate (184 + 6 vs. 181 ± 10 bpm) or maximal V _E (126 ± 29 vs. 126 ± 34 l min⁻¹). The results support the concept that the highest VO₂ during a maximal incremental exercise bout is unlikely to change during a subsequent exercise bout, despite higher muscular power output. As such, the results support the “classical” view of VO₂max.     

Exercise-induced breathing patterns of youth are related to age and intensity

The influences of sex, age, exercise intensity, and end-tidal CO₂ on the inspiratory drive ([V _T kg⁻¹]·T _i ⁻¹) and respiratory timing (T _i·T _tot ⁻¹) components of ventilation were examined in 295 youth (138 females, 157 males); similarly distributed 8–18 years of age. Ventilatory and metabolic measures were collected breath-by-breath at rest and during a slow walk (4.0 km h⁻¹), fast walk (5.6 km h⁻¹) and run (8.0 km h⁻¹). Regression modeling for drive (age, sex, and P_ETCO₂) found that sex was significant (R ² < 0.017; P < 0.05) for rest and running, but not walking. Compared to rest, drive increased by 120% for the slow walk, 217% for the fast walk and 258% for the run (P < 0.0001). Drive decreased with age (P < 0.0001): rest = 0.41 ml kg⁻¹ s⁻¹ year⁻¹; slow walk = 0.90 ml kg⁻¹ s⁻¹ year⁻¹; fast walk = 1.30 ml kg⁻¹ s⁻¹ year⁻¹; and run = 1.47 ml kg⁻¹ s⁻¹ year⁻¹. In the regression models for timing, sex provided ∼ 1% of the variance during the run, but was not significant during rest or walking. Timing increased with exercise intensity by approximately 0.02 units (P < 0.001), but decreased by ∼ 0.002 units year⁻¹ with age for all conditions (P < 0.003). Changes in drive and timing were marginally related to end-tidal CO₂ (exercise R ² < 0.063 for all models). These results suggest that in the control of inspiratory drive and timing during exercise in youth, sex is of minor importance but there are age-related changes which are marginally associated with CO₂.     

No effect of skin temperature on human ventilation response to hypercapnia during light exercise with a normothermic core temperature

Hyperthermia potentiates the influence of CO₂ on pulmonary ventilation ( [(V)\dot]_\textE \dot{V}_{\text{E}} ). It remains to be resolved how skin and core temperatures contribute to the elevated exercise ventilation response to CO₂. This study was conducted to assess the influences of mean skin temperature ( [`(T)]<sub>\textSK</sub> \overline{T}_{\text{SK}} ) and end-tidal PCO<sub>2</sub> (P<sub>ET</sub>CO<sub>2</sub>) on [(V)\dot]<sub>\textE</sub> \dot{V}_{\text{E}} during submaximal exercise with a normothermic esophageal temperature (T <sub>ES</sub>). Five males and three females who were 1.76 ± 0.11 m tall (mean ± SD), 75.8 ± 15.6 kg in weight and 22.0 ± 2.2 years of age performed three 1 h exercise trials in a climatic chamber with the relative humidity (RH) held at 31.5 ± 9.5% and the ambient temperature (T <sub>AMB</sub>) maintained at one of 25, 30, or 35°C. In each trial, the volunteer breathed eucapnic air for 5 min during a rest period and subsequently cycle ergometer exercised at 50 W until T <sub>ES</sub> stabilized at ~37.1 ± 0.4°C. Once T <sub>ES</sub> stabilized in each trial, the volunteer breathed hypercapnic air twice for ~5 min with P<sub>ET</sub>CO<sub>2</sub> elevated by approximately +4 or +7.5 mmHg. The significantly (P < 0.05) different increases of P<sub>ET</sub>CO<sub>2</sub> of +4.20 ± 0.49 and +7.40 ± 0.51 mmHg gave proportionately larger increases in [(V)\dot]<sub>\textE</sub> \dot{V}_{\text{E}} of 10.9 ± 3.6 and 15.2 ± 3.6 L min<sup>−1</sup> (P = 0.001). This hypercapnia-induced hyperventilation was uninfluenced by varying the [`(T)]_\textSK \overline{T}_{\text{SK}} to three significantly different levels (P < 0.001) of 33.2 ± 1.2°C, to 34.5 ± 0.8°C to 36.4 ± 0.5°C. In conclusion, the results support that skin temperature between ~33 and ~36°C has neither effect on pulmonary ventilation nor on hypercapnia-induced hyperventilation during a light exercise with a normothermic core temperature.     

Pulmonary oxygen uptake and muscle deoxygenation kinetics during recovery in trained and untrained male adolescents

Previous studies have demonstrated faster pulmonary oxygen uptake ( [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} ) kinetics in the trained state during the transition to and from moderate-intensity exercise in adults. Whilst a similar effect of training status has previously been observed during the on-transition in adolescents, whether this is also observed during recovery from exercise is presently unknown. The aim of the present study was therefore to examine [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics in trained and untrained male adolescents during recovery from moderate-intensity exercise. 15 trained (15 ± 0.8 years, [(V)\dot]\textO_2max \dot{V}{\text{O}}_{2\max} 54.9 ± 6.4 mL kg⁻¹ min⁻¹) and 8 untrained (15 ± 0.5 years, [(V)\dot]\textO_2max \dot{V}{\text{O}}_{2\max } 44.0 ± 4.6 mL kg⁻¹ min⁻¹) male adolescents performed two 6-min exercise off-transitions to 10 W from a preceding “baseline” of exercise at a workload equivalent to 80% lactate threshold; [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} (breath-by-breath) and muscle deoxyhaemoglobin (near-infrared spectroscopy) were measured continuously. The time constant of the fundamental phase of [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} off-kinetics was not different between trained and untrained (trained 27.8 ± 5.9 s vs. untrained 28.9 ± 7.6 s, P = 0.71). However, the time constant (trained 17.0 ± 7.5 s vs. untrained 32 ± 11 s, P < 0.01) and mean response time (trained 24.2 ± 9.2 s vs. untrained 34 ± 13 s, P = 0.05) of muscle deoxyhaemoglobin off-kinetics was faster in the trained subjects compared to the untrained subjects. [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics was unaffected by training status; the faster muscle deoxyhaemoglobin kinetics in the trained subjects thus indicates slower blood flow kinetics during recovery from exercise compared to the untrained subjects.     

Application of bioreactance for cardiac output assessment during exercise in healthy individuals

In patients with cardiac failure, bioreactance-based cardiac output (CO) monitoring provides a valid non-invasive method for assessing cardiac performance during exercise. The purpose of this study was to evaluate the efficacy of this technique during strenuous exercise in healthy, trained individuals. Fourteen recreational cyclists, mean (SD) age of 34 (8) years and relative peak oxygen uptake of (VO₂) 56 (6) ml kg⁻¹ min⁻¹, underwent incremental maximal exercise testing, whilst CO was recorded continuously using a novel bioreactance-based device (CO_bio). The CO_bio was evaluated against relationship with VO₂, theoretical calculation of arterial-venous oxygen difference (C(a − v) O₂) and level of agreement with an inert gas rebreathing method (CO_rb) using a Bland–Altman plot. Bioreactance-based CO measurement was practical and straightforward in application, although there was intermittent loss of electrocardiograph signal at high-intensity exercise. At rest and during exercise, CO_bio was strongly correlated with VO₂ (r = 0.84; P < 0.001), however, there was evidence of systematic bias with CO_bio providing lower values than CO_rb; mean bias (limits of agreement) −19% (14.6 to −53%). Likewise, calculated (C(a − v) O₂) was greater when determined using CO_bio than CO_rb (P < 0.001), although both devices provided values in excess of those reported in invasive studies. Bioreactance-based determination of CO provides a pragmatic approach to the continuous assessment of cardiac performance during strenuous exercise in trained individuals. Our findings, however, suggest that further work is needed to refine the key measurement determinants of CO using this device to improve measurement accuracy in this setting.     

A low carbohydrate diet affects autonomic modulation during heavy but not moderate exercise

The aim of this study was to examine the effects of low carbohydrate (CHO) availability on heart rate variability (HRV) responses during moderate and severe exercise intensities until exhaustion. Six healthy males (age, 26.5 ± 6.7 years; body mass, 78.4 ± 7.7 kg; body fat %, 11.3 ± 4.5%; [(V)\dot] \textO_{2 max} , \dot{V} {\text{O}}_{{2{ \max }}} , 39.5 ± 6.6 mL kg⁻¹ min⁻¹) volunteered for this study. All tests were performed in the morning, after 8–12 h overnight fasting, at a moderate intensity corresponding to 50% of the difference between the first (LT₁) and second (LT₂) lactate breakpoints and at a severe intensity corresponding to 25% of the difference between the maximal power output and LT₂. Forty-eight hours before each experimental session, the subjects performed a 90-min cycling exercise followed by 5-min rest periods and subsequent 1-min cycling bouts at 125% [(V)\dot] \textO_{2 max} \dot{V} {\text{O}}_{{2{ \max }}} (with 1-min rest periods) until exhaustion, in order to deplete muscle glycogen. A diet providing 10% (CHO_low) or 65% (CHO_control) of energy as carbohydrates was consumed for the following 2 days until the experimental test. The Poicaré plots (standard deviations 1 and 2: SD1 and SD2, respectively) and spectral autoregressive model (low frequency LF, and high frequency HF) were applied to obtain HRV parameters. The CHO availability had no effect on the HRV parameters or ventilation during moderate-intensity exercise. However, the SD1 and SD2 parameters were significantly higher in CHO_low than in CHO_control, as taken at exhaustion during the severe-intensity exercise (P < 0.05). The HF and LF frequencies (ms²) were also significantly higher in CHO_low than in CHO_control (P < 0.05). In addition, ventilation measured at the 5 and 10-min was higher in CHO_low (62.5 ± 4.4 and 74.8 ± 6.5 L min⁻¹, respectively, P < 0.05) than in CHO_control (70.0 ± 3.6 and 79.6 ± 5.1 L min⁻¹, respectively; P < 0.05) during the severe-intensity exercise. These results suggest that the CHO availability alters the HRV parameters during severe-, but not moderate-, intensity exercise, and this was associated with an increase in ventilation volume.     

Relationship of middle cerebral artery blood flow velocity to intensity during dynamic exercise in normal subjects

Summary Cerebral blood flow has been reported to increase during dynamic exercise, but whether this occurs in proportion to the intensity remains unsettled. We measured middle cerebral artery blood flow velocity (m) by transcranial Doppler ultrasound in 14 healthy young adults, at rest and during dynamic exercise performed on a cycle ergometer at a intensity progressively increasing, by 50 W every 4 min until exhaustion. Arterial blood pressure, heart rate, end-tidal, partial pressure of carbon dioxide (P _ETCO₂), oxygen uptake ( O₂) and carbon dioxide output were determined at exercise intensity. Mean vM increased from 53 (SEM 2) cm · s^–1 at rest to a maximum of 75 (SEM 4) cm · s^–1 at 57% of the maximal attained O₂( O_2max), and thereafter progressively decreased to 59 (SEM 4) cm · s^–1 at O_2max. The respiratory exchange ratio (R) was 0.97 (SEM 0.01) at 57% of O_2maxand 1.10 (SEM 0.01) at O_2max. The P _ETCO₂ increased from 5.9 (SEM 0.2) kPa at rest to 7.4 (SEM 0.2) kPa at 57% of O_2maxand thereafter decreased to 5.9 (SEM 0.2) kPa at O_2max. Mean arterial pressure increased from 98 (SEM 1) mmHg (13.1 kPa) at rest to 116 (SEM 1) mmHg (15.5 kPa) at 90% of O_2max, and decreased slightly to 108 (SEM 1) mmHg (14.4 kPa) at O_2max. In all the subjects, the maximal value of v _m was recorded at the highest attained exercise intensity below the anaerobic threshold (defined by R greater than 1). We concluded that cerebral blood flow as evaluated by middle cerebral artery flow velocity increased during dynamic exercise as a function of exercise intensity below the anaerobic threshold. At higher intensities, cerebral blood flow decreased, without however a complete return to baseline values, and it is suggested that this may have been at least in part explained by concomitant changes in arterial PCO₂.     

Role of adenosine in exercise‐induced human skeletal muscle vasodilatation

The role of adenosine in exercise‐induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline‐induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one‐legged, knee‐extensor exercise at ～48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (F_aBF) by ～20%, i.e. from 3.6 ± 0.5 to 2.9 ± 0.5 L min^?1, and leg vascular conductance (VC) from 33.4 ± 9.1 to 27.7 ± 8.5 mL min^?1 mmHg^?1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) F_aBF from 0.3 ± 0.03 L min^?1 to a 15‐fold peak elevation (P < 0.05) at 4.1 ± 0.5 L min^?1. Continuous infusion of adenosine at rest and during one‐legged exercise at ～62% of peak power output increased (P < 0.05) F_aBF dose‐dependently to level off (P = ns) at 8.3 ± 1.0 and 8.2 ± 1.4 L min^?1, respectively. One‐legged exercise alone increased (P < 0.05) F_aBF to 4.7 ± 1.7 L min^?1. Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least ～20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.     

Effectiveness of short-term heat acclimation for highly trained athletes

Effectiveness of short-term acclimation has generally been undertaken using untrained and moderately-trained participants. The purpose of this study was to determine the impact of short-term (5-day) heat acclimation on highly trained athletes. Eight males (mean ± SD age 21.8 ± 2.1 years, mass 75.2 ± 4.6 kg, [(V)\dot] \dot{V}O_2peak 4.9 ± 0.2 L min⁻¹ and power output 400 ± 27 W) were heat acclimated under controlled hyperthermia (rectal temperature 38.5°C), for 90-min on five consecutive days (T _a = 39.5°C, 60% relative humidity). Acclimation was undertaken with dehydration (no fluid-intake) during daily bouts. Participants completed a rowing-specific, heat stress test (HST) 1 day before and after acclimation (T _a = 35°C, 60% relative humidity). HST consisted 10-min rowing at 30% peak power output (PPO), 10 min at 60% PPO and 5-min rest before a 2-km performance test, without feedback cues. Participants received 250 mL fluid (4% carbohydrate; osmolality 240–270 mmol kg⁻¹) before the HST. Body mass loss during acclimation bouts was 1.6 ± 0.3 kg (2.1%) on day 1 and 2.3 ± 0.4 kg (3.0%) on day 5. In contrast, resting plasma volume increased by 4.5 ± 4.5% from day 1 to 5 (estimated from [Hb] & Hct). Plasma aldosterone increased at rest (52.6 pg mL⁻¹; p = 0.03) and end-exercise (162.4 pg mL⁻¹; p = 0.00) from day 1 to 5 acclimation. During the HST T _re and f _c were lowered 0.3°C (p = 0.00) and 14 b min⁻¹ (p = 0.00) after 20-min exercise. The 2-km performance time (6.52.7 min) improved by 4 s (p = 0.00). Meaningful physiological and performance improvements occurred for highly trained athletes using a short-term (5-day) heat acclimation under hyperthermia control, with dehydration.     

Myocardial function and aerobic fitness in adolescent females

A recent report indicated that variations in myocardial functional (systolic and diastolic) responses to exercise do not contribute to inter-individual differences in aerobic fitness (peak VO₂) among young males. This study was designed to investigate the same question among adolescent females. Thirteen highly fit adolescent football (soccer) players (peak VO₂ 43.5 ± 3.4 ml kg⁻¹ min⁻¹) and nine untrained girls (peak VO₂ 36.0 ± 5.1 ml kg⁻¹ min⁻¹) matched for age underwent a progressive cycle exercise test to exhaustion. Cardiac variables were measured by standard echocardiographic techniques. Maximal stroke index was greater in the high-fit group (50 ± 5 vs. 41 ± 4 ml m⁻²), but no significant group differences were observed in maximal heart rate or arterial venous oxygen difference. Increases in markers of both systolic (ejection rate, tissue Doppler S′) and diastolic (tissue Doppler E′, mitral E velocity) myocardial functions at rest and during the acute bout of exercise were similar in the two groups. This study suggests that among healthy adolescent females, like young males, myocardial systolic and diastolic functional capacities do not contribute to inter-individual variability in physiologic aerobic fitness.