Reduced arterial O2 saturation during supine exercise in highly trained cyclists

Performance of intense dynamic exercise in highly trained athletes is associated with a reduced arterial haemoglobin saturation for O₂ (SaO ₂) and lower arterial PO ₂ (PaO ₂). We hypothesized that compared with upright exercise, supine exercise would be accompanied by a smaller reduction in SaO ₂ because of a lower maximal O₂ uptake (VPO _2max) and/or a more even ventilation–perfusion distribution. Eight elite bicyclists completed progressive cycle ergometry to exhaustion in both positions with concomitant determinations of ventilatory data, arterial blood gases and pH. During upright cycling VPO _2max averaged 75±1.6 mL O₂ min^-1 kg^-1 (±SEM) and it was 10.6±1.7% lower during supine cycling (P<0.001). Also the maximal pulmonary and alveolar ventilation were lower during supine cycling (by 15±2% and 21±3%, respectively; P< 0.001) which related to a 0.8±0.1 L lower tidal volume (P<0.001). In all subjects and independent of work posture PaO ₂ and SaO ₂ decreased from rest to exhaustion (from 99±3 to 82±2 Torr and 98.1±0.2 to 95.2±0.4%, respectively; P<0.001); alveolar–arterial PO ₂ difference increased from 6±2 to 37±3 Torr in both body positions. At exhaustion arterial PCO ₂ was lower in upright than in supine (33.4±0.6 vs. 35.9±0.9 Torr; P<0.01), suggesting a greater relative hyperventilation in upright. Arterial pH was similar in upright and supine at rest (both 7.41±0.01) and at exhaustion (7.31±0.01 vs. 7.32±0.01, respectively). We conclude that despite a lower VPO _2max and supposedly an improved ventilation–perfusion distribution, altering body position from upright to supine does not influence arterial O₂ desaturation during intense exercise.     

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

We examined the influence of hyperoxia on peak oxygen uptake (V˙O _2peak) and peripheral gas exchange during exercise with the quadriceps femoris muscle. Young, trained men (n=5) and women (n=3) performed single-leg knee-extension exercise at 70% and 100% of maximum while inspiring normal air (NOX) or 60% O₂ (HiOX). Blood was sampled from the femoral vein of the exercising limb and from the contralateral artery. In comparison with NOX, hyperoxic arterial O₂ tension (P_aO ₂) increased from 13.5 ± 0.3 (x ± SE) to 41.6 ± 0.3 kPa, O₂ saturation (S_aO ₂) from 98 ± 0.1 to 100 ± 0.1%, and O₂ concentration (C_aO ₂) from 177 ± 4 to 186 ± 4 mL L^–1 (all P < 0.01). Peak exercise femoral venous PO ₂ (P_vO ₂) was also higher in HiOX (3.68 ± 0.06 vs. 3.39 ± 0.7 kPa; P < 0.05), indicating a higher O₂ diffusion driving pressure. HiOX femoral venous O₂ saturation averaged 36.8 ± 2.0% as opposed to 33.4 ± 1.5% in NOX (P < 0.05) and O₂ concentration 63 ± 6 vs. 55 ± 4 mL L^–1 (P < 0.05). Peak exercise quadriceps blood flow (Q˙_leg), measured by the thermo-dilution technique, was lower in HiOX than in NOX, 6.4 ± 0.5 vs. 7.3 ± 0.9 L min^–1 (P < 0.05); mean arterial blood pressure at inguinal height was similar in NOX and HiOX at 144 and 142 mmHg, respectively. O₂ delivery to the limb (Q˙_leq times C_aO ₂) was not significantly different in HiOX and NOX. V˙O _2peak of the exercising limb averaged 890 mL min^–1 in NOX and 801 mL min^–1 in HiOX (n.s.) corresponding to 365 and 330 mL min^–1 per kg active muscle, respectively. The V˙O _2peak-to-P_vO ₂ ratio was lower (P < 0.05) in HiOX than in NOX suggesting a lower O₂ conductance. We conclude that the similar V˙O _2peak values despite higher O₂ driving pressure in HiOX indicates a peripheral limitation for V˙O _2peak. This may relate to saturation of the rate of O₂ turnover in the mitochondria during exercise with a small muscle group but can also be caused by tissue diffusion limitation related to lower O₂ conductance.     

Vasoconstriction in active calf persists after discontinuation of combined exercise with high-intensity elbow flexion

The present study aimed to determine whether vasoconstriction in active calf occurring during combined exercise diminished or persisted when added low- and high-intensity elbow flexion exercise ceased and single leg exercise continued. Six active women (mean age, 21.2 years) participated in this study. During 10-min plantar flexion exercise at 10% of maximum voluntary contraction (MVC), elbow flexion exercise at 10% MVC was added over the 3rd and 4th min. Calf blood flow did not change significantly upon superimposition and cessation of this elbow flexion exercise. However, when elbow flexion exercise at 50% MVC was added during the 7th and 8th min, calf blood flow above the resting value (2.23±0.23 mL 100 mL^-1 min^-1) decreased significantly (P<0.05) from 6.72±0.87 (6th min) to 5.14±1.36 mL 100 mL^-1 min^-1 after 2 min of combined exercise and was accompanied by a similar change in the non-exercising calf blood flow value. The vascular conductance of the exercising calf decreased significantly (P<0.01) from 6.48±1.08 (6th min) to 3.11±1.27 mL 100 mL^-1 min^-1 mmHg^-1 at the end of the 2nd min of combined plantar flexion exercise with elbow flexion exercise at 50% MVC. After elbow flexion exercise at 50% MVC was discontinued and plantar flexion exercise at 10% MVC alone was performed, the vascular conductance in the exercising calf remained significantly low for the next 2 min. These results indicate that the vasoconstriction induced by adding high-intensity arm exercise is persistent, suggesting a major contribution of metabo-receptor-mediated vasoconstriction rather than central command- and mechano-receptor-mediated vasoconstriction.     

Growth hormone and prolactin responses during partial and whole body warm‐water immersions

Aim: To elucidate the role of core and skin thermoreceptors in the release of growth hormone (GH) and prolactin (PRL), a sequence of two experiments using whole‐body (head‐out) and partial (one forearm) hot water immersions was performed. Methods: Experiment 1: Nine healthy men were exposed to head‐out and partial water immersions (25 min, 38–39 °C). Results: Head‐out immersion increased the core temperature (38.0 ± 0.1 vs. 36.7 ± 0.1 °C, P < 0.001) and plasma concentration of the hormones (GH, 16.1 ± 4.5 vs. 1.2 ± 0.4 ng mL^?1, P < 0.01; PRL, 9.1 ± 1.0 vs. 6.4 ± 0.4 ng mL^?1, P < 0.05). During the partial immersion the core temperature was slightly elevated (36.8 ± 0.1 vs. 36.6 ± 0.1, P < 0.001), the concentration of GH increased (4.8 ± 1.7 vs. 0.6 ± 0.3, P < 0.05), while plasma PRL decreased (7.6 ± 0.8, 6.0 ± 0.6, 5.2 ± 0.6, P < 0.01). Experiment 2: Seven volunteers immersed one forearm once in 39 °C and once in 38 °C water. The measurements were performed in 5‐min intervals. The GH concentration increased gradually from the beginning of the immersions (min 10; 39 °C: 1.9 ± 1.0 vs. 0.6 ± 0.3 ng mL^?1, P < 0.01; 38 °C: 0.19 ± 0.03 vs. 0.14 ± 0.03, P < 0.05) and peaked after their completion (39 °C: +10 min, 3.7 ± 2.0, P < 0.001; 38 °C: +15 min, 0.86 ± 0.61, P < 0.01). The core temperature was unchanged until min 15 of the 39 °C bath. Thereafter, it increased about 0.15 °C above the baseline (P < 0.01). Immersion in 38 °C water did not induce core temperature changes. Conclusions: Peripheral thermoreceptors are involved in GH release when the body is exposed to elevated environmental temperature while a substantial elevation of core temperature is a precondition of PRL release.     

Effect of drink pattern and solar radiation on thermoregulation and fluid balance during exercise in chronically heat acclimatized children

The purposes of this study were to examine the thermoregulatory and body fluid balance responses in chronically heat acclimatized children, i.e., indigenous to a tropical climate, during exercise in four outdoor conditions and the effects of dehydration on their thermoregulatory response. Nine children (age = 13.3 ± 1.9 yr, VO₂max = 45.5 ± 9.2 ml · kg^?1 · min^?1) cycled at 60% VO₂max each under four conditions: sun exposure voluntary drinking (SuVD), sun exposure forced drinking (SuFD), shaded voluntary drinking (ShVD), and shaded forced drinking (ShFD). Exercise sessions consisted of four 20-min exercise bouts alternating with 25-min rest periods. Globe temperature and the WBGT index were higher during SuVD and SuFD compared to ShVD and ShFD (P < 0.05). The change in rectal temperature, metabolic heat production, and heat storage did not differ among the conditions. Total water intake (% IBW) was higher during SuFD (4.1 ± 0.01) and ShFD (3.7 ± 0.1) compared to SuVD (2.1 ± 0.1) and ShVD (1.0 ± 0.1) and during SuVD compared to ShVD (P < 0.05). Sweating rate (L · hr^?1) was higher during SuFD (0.7 ± 0.1) and ShFD (0.6 ± 0.1) compared to SuVD (0.5 ± 0.1) and ShVD (0.4 ± 0.1) (P < 0.05). Total fluid loss did not differ among conditions (SuVD = 1.7 ± 0.4; SuFD = 1.5 ± 0.4; ShVD = 2.1 ± 0.2; ShFD = 1.3 ± 0.3). Results indicate that when exercising in a tropical climate, chronically heat acclimatized children demonstrate mild voluntary dehydration and adequate heat dissipation. © 1995 Wiley-Liss, Inc.     

Enhanced cerebral CO2 reactivity during strenuous exercise in man

Light and moderate exercise elevates the regional cerebral blood flow by ~20% as determined by ultrasound Doppler sonography (middle cerebral artery mean flow velocity; MCA V _mean). However, strenuous exercise, especially in the heat, appears to reduce MCA V _mean more than can be accounted for by the reduction in the arterial CO₂ tension (P _aCO₂). This study evaluated whether the apparently large reduction in MCA V _mean at the end of exhaustive exercise relates to an enhanced cerebrovascular CO₂ reactivity. The CO₂ reactivity was evaluated in six young healthy male subjects by the administration of CO₂ as well as by voluntary hypo- and hyperventilation at rest and during exercise with and without hyperthermia. At rest, P _aCO₂ was 5.1±0.2 kPa (mean ± SEM) and MCA V _mean 50.7±3.8 cm s⁻¹ and the relationship between MCA V _mean and P _aCO₂ was linear (double-log slope 1.1±0.1). However, the relationship became curvilinear during exercise (slope 1.8±0.1; P<0.01 vs. rest) and during exercise with hyperthermia (slope 2.3±0.3; P<0.05 vs. control exercise). Accordingly, the cerebral CO₂ reactivity increased from 30.5±2.7% kPa⁻¹ at rest to 61.4±10.1% kPa⁻¹ during exercise with hyperthermia (P<0.05). At exhaustion P _aCO₂ decreased 1.1±0.2 kPa during exercise with hyperthermia, which, with the determined cerebral CO₂ reactivity, accounted for the 28±10% decrease in MCA V _mean. The results suggest that during exercise changes in cerebral blood flow are dominated by the arterial carbon dioxide tension.     

Supplemental oxygen and muscle metabolism in mitochondrial myopathy patients

Patients with mitochondrial myopathy (MM) have a reduced capacity to perform exercise due to a reduced oxidative capacity. We undertook this study to determine whether skeletal muscle metabolism could be improved with oxygen therapy in patients with MM. Six patients with MM and six controls, matched for age, gender and physical activity, underwent ³¹P-magnetic resonance spectroscopy (³¹P-MRS) examination. ³¹P-MR spectra were collected at rest and in series during exercise and recovery whilst breathing normoxic (0.21 O₂) or hyperoxic (1.0 O₂) air. At rest, MM showed an elevated [ADP] (18 ± 3 μmol/l) and pH (7.03 ± 0.01) in comparison to the control group (12 ± 1 μmol/l, 7.01 ± 0.01) (P < 0.05) consistent with mitochondrial dysfunction. Oxygen supplementation did not change resting metabolites in either MM or the control group (P > 0.05). Inferred maximal ATP synthesis rate improved by 33% with oxygen in MM (21 ± 3 vs. 28 ± 5 mmol/(l min), P < 0.05) but only improved by 5% in controls (40 ± 3 vs. 42 ± 3 mmol/(l min), P > 0.05). We conclude that oxygen therapy is associated with significant improvements in muscle metabolism in patients with MM. These data suggest that patients with MM could benefit from therapies which improve the provision of oxygen.     

Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans

Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3-L4. This caused cutaneous sensory anaesthesia below T8-T9 and complete paralysis of the legs. Cycling was performed for 22.7 ± 2.7 min (mean, SE) (fatigue) and oxygen uptake (Vo₂) increased to 1.90 ± 0.13 1 min^-1. Compared with voluntary exercise at the same Vo₂, increases in heart rate (HR) (135 ± 7 vs. 130 ± 9 beats min^-1) and cardiac output (16.9 ± 1.1 vs. 17.3 ± 0.9 1 min^-1) were similar, and ventilation (54 ± 5 vs. 45 ± 4 1 min^-1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 ± 4 (rest) to 119 ± 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 ± 3 (rest) to 95 ± 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.     

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.     

Contribution of pH,diprotonated phosphate and potassium for the reflex increase in blood pressure during handgrip

The relative importance of pH, diprotonated phosphate (H₂PO₄^?) and potassium (K⁺) for the reflex increase in mean arterial pressure (MAP) during exercise was evaluated in seven subjects during rhythmic handgrip at 15 and 30% maximal voluntary contraction (MVC), followed by post-exercise muscle ischaemia (PEMI). During 15% MVC, MAP rose from 92 ± 1 to 103 ± 2 mmHg, [K⁺] from 4.1 ± 0.1 to 5.1 ± 0.1 mmol L^?1, while the intracellular (7.00 ± 0.01 to 6.80 ± 0.06) and venous pH fell (7.39 ± 0.01 to 7.30 ± 0.01) (P < 0.05). The intracellular [H₂PO₄^?] increased 8.4 ± 2 mmol kg^?1 and the venous [H₂PO₄^?] from 0.14 ± 0.01 to 0.16 ± 0.01 mmol L^?1 (P < 0.05). During PEMI, MAP remained elevated along with the intracellular [H₂PO₄^?] as well as a low intracellular and venous pH. However, venous [K⁺] and [H₂PO₄^?] returned to the level at rest. During 30% MVC handgrip, MAP rose to 130 ± 3 mmHg, [K⁺] to 5.8 ± 0.2 mmol L^?1, the intracellular and extracellular [H₂PO₄^?] by 20 ± 5 mmol kg^?1 and to 0.20 ± 0.02 mmol L^?1, respectively, while the intracellular (6.33 ± 0.06) and venous pH fell (7.23 ± 0.02) (P < 0.05). During post-exercise muscle ischaemia all variables remained close to the exercise levels. Analysis of each variable as a predictor of blood pressure indicated that only the intracellular pH and diprotonated phosphate were linked to the reflex elevation of blood pressure during handgrip.     

Oral creatine supplementation decreases plasma markers of adenine nucleotide degradation during a 1‐h cycle test

We investigated the effect of oral creatine supplementation (20 g d^?1 for 7 days) on metabolism during a 1‐h cycling performance trial. Twenty endurance‐trained cyclists participated in this double‐blind placebo controlled study. Five days after familiarization with the exercise test, the subjects underwent a baseline muscle biopsy. Thereafter, a cannula was inserted into a forearm vein before performing the baseline maximal 1‐h cycle (test 1 (T1)). Blood samples were drawn at regular intervals during exercise and recovery. After creatine (Cr) loading, the muscle biopsy, 1‐h cycling test (test 2 (T2)) and blood sampling were repeated. Resting muscle total creatine (TCr), measured by high performance liquid chromatography, was increased (P < 0.001) in the creatine group from 123.0 ± 3.8 ? 159.8 ± 7.9 mmol kg^?1 dry wt, but was unchanged in the placebo group (126.7 ± 4.7 ? 127.5 ± 3.6 mmol kg^?1 dry wt). The extent of Cr loading was unrelated to baseline Cr levels (r=0.33, not significant). Supplementation did not significantly improve exercise performance (Cr group: 39.1 ± 0.9 vs. 39.8 ± 0.8 km and placebo group: 39.3 ± 0.8 vs. 39.2 ± 1.1 km) or change plasma lactate concentrations. Plasma concentrations of ammonia (NH₃) (P < 0.05) and hypoxanthine (Hx) (P < 0.01) were lower in the Cr group from T1 to T2. Our results indicate that Cr supplementation alters the metabolic response during sustained high‐intensity submaximal exercise. Plasma data suggest that nett intramuscular adenine nucleotide degradation may be decreased in the presence of enhanced intramuscular TCr concentration even during submaximal exercise.     

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.     

Physiological and morphological effects of perfusing isolated rat kidneys with hyperosmolal mannitol solutions

Recently, we were able to modify the glomerular charge barrier using perfusates with low and normal ionic strengths keeping the osmolality unchanged. The concentration of fixed charges was reversibly reduced from 35 to 12 mEq L^–1 as the solution with low content of NaCl was introduced with no apparent effect on the size selectivity. It can be argued however, that the mannitol used for maintenance of osmolality may induce changes in glomerular permeability per se. To explore this possibility, isolated kidneys were perfused at 8° with hyperosmolal mannitol solutions (560 mOsm) and compared with those perfused with standard albumin solutions (295 mOsm). The vascular resistance (PRU₁₀₀) fell from 0.14 ± 0.01 to 0.11 ± 0.01 mmHg min 100 g mL^–1 as the mannitol solution was introduced (P < 0.001). As the blood pressure should remain unchanged, the flow was increased from 8 to 11 mL min^–1. The glomerular filtration rate (GFR) increased by 50% from 320 ± 40 to 490 ± 20 μL min^?1 g^–1 (P < 0.001). Despite these changes in haemodynamical parameters, there was no significant change in the fractional clearance for albumin. Kidneys perfused with the mannitol solution showed well-preserved histology, while there was a conspicuous collapse of the cortical tissue and signs of tubular epithelial swelling with the standard perfusate. Moreover, all glomeruli were perfused in the mannitol group, as revealed by fluorescence of FITC dextran, while the distribution was uneven in the control kidneys. We conclude that perfusion of isolated kidneys with a hyperosmolal mannitol solution increased GFR by increasing the number of functionally active nephrons with no apparent effect on the glomerular barrier, a pattern differing from alteration of ionic strength.     

Systemic nitric oxide clamping in normal humans guided by total peripheral resistance

Aim: We wanted to stabilize the availability of nitric oxide (NO) at levels compatible with normal systemic haemodynamics to provide a model for studies of complex regulations in the absence of changes in NO levels. Methods: Normal volunteers (23–28 years) were infused i.v. with the nitric oxide synthase (NOS) inhibitor N^G-nitro-l -arginine methyl ester (l -NAME) at 0.5 mg kg⁻¹ h⁻¹. One hour later, the NO donor sodium nitroprusside (SNP) was co-infused in doses eliminating the haemodynamic effects of l -NAME. Haemodynamic measurements included blood pressure (MABP) and cardiac output (CO) by impedance cardiography. Results: l -NAME increased MABP and total peripheral resistance (TPR, 1.02 ± 0.05 to 1.36 ± 0.07 mmHg s mL⁻¹, mean ± SEM, P < 0.001). With SNP, TPR fell to a stable value slightly below control (0.92 ± 0.05 mmHg s mL⁻¹, P < 0.05). CO decreased with l -NAME (5.8 ± 0.3 to 4.7 ± 0.3 L min⁻¹, P < 0.01) and returned to control when SNP was added (6.0 ± 0.3 L min⁻¹). A decrease in plasma noradrenaline (42%, P < 0.01) during l -NAME administration was completely reversed by SNP. Plasma renin activity decreased during l -NAME administration and returned towards normal after addition of SNP. In contrast, plasma aldosterone was increased by l -NAME and remained elevated. Conclusions: Concomitant NOS inhibition and NO donor administration can be adjusted to maintain TPR at control level for hours. This approach may be useful in protocols in which stabilization of the peripheral supply of NO is required. However, the dissociation between renin and aldosterone secretion needs further investigation.     

Immunomodulation by 8-week voluntary exercise in mice

This study was designed to evaluate the effects of voluntary exercise on macrophage and lymphocyte functions in mice. Male A/He inbred mice aged 19 weeks were divided into two groups: a group given voluntary exercise and a control group (n = 10 in each group). Exercise consisted of spontaneous running in wheels for 8 weeks (3 days week-1). Glucose consumption of peritoneal macrophages in the exercise group during incubation up to 72 h was significantly higher than that in the control group (70 and 13%, respectively). Also, activities of acid phosphatase (APH) (10.75 +/- 0.37 IU), beta-glucuronidase (GLU) (1.55 +/- 0.07 IU) and lactate dehydrogenase (LDH) (43.3 +/- 0.7 IU) in the peritoneal macrophages in the exercise group was significantly increased (P < 0.01). Compared with the control group, the exercise group had a significant increase of about twofold in macrophage production of nitric oxide (NO2-) stimulated by lipopolysaccharide (LPS) (11.1 +/- 0.1 vs. 5.9 +/- 0.1 microM mL-1 in exercise and control groups, respectively; P < 0.01). Stimulation indices both by concanavalin A (Con A) and phytohaemagglutinin were also significantly higher in the exercise group (P < 0.01). A significant increase in the splenocyte production of interleukin-2 (IL-2) stimulated by Con A was noticed in the exercise group (354.1 +/- 28.8 vs. 218.9 +/- 23.5 pg mL-1 in exercise and control groups, respectively; P < 0.01). These findings suggest that voluntary exercise enhances not only macrophage function but also lymphocyte responsiveness in mice. In the studies of voluntary exercise, evaluation of NO2- production, as an indicator of macrophage function, is recommended.     

Splanchnic and renal vasoconstrictor and metabolic responses to neuropeptide Y in resting and exercising man

The local clearance of neuropeptide Y (NPY) and whether NPY influences splanchnic and renal metabolism in man have not been investigated previously. The influence of NPY on splanchnic and renal blood flows at physiologically elevated levels has also not been investigated. The effects of a 40-min constant NPY infusion (3 pmol kg^-1 min^-1) at rest and during 130 min of exercise (50% of Vo_2max) were studied in six healthy subjects and compared with resting and exercising subjects receiving no NPY. Blood samples were drawn from arterial, hepatic and renal vein catheters for the determination of blood flows (indicators: cardiogreen and paraaminohippuric acid [PAH]), NPY, catecholamines, glucose, lactate and glycerol. NPY infusion was accompanied by: (1) significant fractional extraction of NPY-like immunoreactivity (NPY-Li) by splanchnic tissues at rest (58±5%) and during exercise (53±6%), while no arterial–venous differences could be detected across the kidney; (2) a reduction in splanchnic and renal blood flows of up to 18 and 13% respectively (P < 0.01–0.001) at rest without any additional changes during exercise; and (3) metabolic changes as reflected in: (a) a more marked fall in arterial glucose during exercise compared to the reference group (P < 0.05); (b) a 35% lower splanchnic glucose release (P < 0.01) during exercise due to diminished glycogenolysis (P < 0.01); and (c) a lower arterial lactate level (18%P < 0.05) together with unchanged splanchnic lactate uptake during exercise, suggesting reduced lactate production by extrahepatic tissues. The disappearance of plasma NPY-Li after the infusions was biphasic with two similar half-lives at rest (4 and 39 min) and during exercise (3 and 43 min).     

Low‐volume muscle endurance training prevents decrease in muscle oxidative and endurance function during 21‐day forearm immobilization

Aim: To examine the effects of low‐volume muscle endurance training on muscle oxidative capacity, endurance and strength of the forearm muscle during 21‐day forearm immobilization (IMM‐21d). Methods: The non‐dominant arm (n = 15) was immobilized for 21 days with a cast and assigned to an immobilization‐only group (Imm‐group; n = 7) or an immobilization with training group (Imm+Tr‐group; n = 8). Training comprised dynamic handgrip exercise at 30% of pre‐intervention maximal voluntary contraction (MVC) at 1 Hz until exhaustion, twice a week during the immobilization period. The duration of each exercise session was 51.7 ± 3.4 s (mean ± SE). Muscle oxidative capacity was evaluated by the time constant for phosphocreatine recovery (τ_offPCr) after a submaximal handgrip exercise using ³¹phosphorus‐magnetic resonance spectroscopy. An endurance test was performed at 30% of pre‐intervention MVC, at 1 Hz, until exhaustion. Results: τ _offPCr was significantly prolonged in the Imm‐group after 21 days (42.0 ± 2.8 and 64.2 ± 5.1 s, pre‐ and post‐intervention respectively; P < 0.01) but did not change for the Imm+Tr‐group (50.3 ± 3.0 and 48.8 ± 5.0 s, ns). Endurance decreased significantly for the Imm‐group (55.1 ± 5.1 and 44.7 ± 4.6 s, P < 0.05) but did not change for the Imm+Tr‐group (47.9 ± 3.0 and 51.7 ± 4.0 s, ns). MVC decreased similarly in both groups (P < 0.01). Conclusions: Twice‐weekly muscle endurance training sessions, each lasting approx. 50 s, effectively prevented a decrease in muscle oxidative capacity and endurance; however, there was no effect on MVC decline with IMM‐21d.     

Fibrinolytic markers and vasodilatory capacity following acute exercise among men of differing training status

We evaluated the effect of differing physical activity patterns on fibrinolysis and vasodilatory capacity using a cross-sectional design with 16 endurance-trained (ET) (mean ± SE) (28 ± 6 years), 14 resistance-trained (RT) (28 ± 7 years), and 10 untrained (UT) (26 ± 7 years) men. t-PA and PAI-1 activity and t-PA antigen were measured before and after a maximal treadmill test (VO_2peak). Vasodilatory capacity was assessed using strain-gauge plethysmography on the forearm following reactive hyperemia (RH) before and after the treadmill test. The ET group had a smaller body mass index (BMI) (22.8 ± 0.5 ET, 26.4 ± 0.4 RT, 25.1 ± 0.8 UT kg m⁻²) (P < 0.05) and a greater VO_2peak (57 ± 1 ET, 42 ± 2 RT, 45 ± 2 UT mL min⁻¹ kg⁻¹) (P < 0.05). Peak vasodilatory capacity (29.7 ± 2 ET, 32.0 ± 2 RT, 27.4 ± 2 UT mL min⁻¹ 100 mL of tissue) was similar between groups before and after exercise. Area under the curve for forearm blood flow was greater following acute exercise (212 vs. 122, P < 0.05), again with no differences between groups. t-PA activity and antigen increased following maximal exercise in all groups (P < 0.0001), with no group differences. PAI-1 activity decreased the least in RT after exercise (70% decrease vs. 86% ET and 82% UT; P < 0.05). The change in t-PA activity with exercise was not related to exercise-induced change in overall vasodilatory capacity. These findings demonstrate that in healthy young men different physical activity patterns do not appear to impact the exercise-induced changes in fibrinolysis or vasodilatory capacity.     

Live high:train low increases muscle buffer capacity and submaximal cycling efficiency

This study investigated whether hypoxic exposure increased muscle buffer capacity (βm) and mechanical efficiency during exercise in male athletes. A control (CON, n=7) and a live high:train low group (LHTL, n=6) trained at near sea level (600 m), with the LHTL group sleeping for 23 nights in simulated moderate altitude (3000 m). Whole body oxygen consumption (V˙O ₂) was measured under normoxia before, during and after 23 nights of sleeping in hypoxia, during cycle ergometry comprising 4×4‐min submaximal stages, 2‐min at 5.6 ± 0.4 W kg^–1, and 2‐min ‘all‐out’ to determine total work and V˙O _2peak. A vastus lateralis muscle biopsy was taken at rest and after a standardized 2‐min 5.6 ± 0.4 W kg^–1 bout, before and after LHTL, and analysed for βm and metabolites. After LHTL, βm was increased (18%, P < 0.05). Although work was maintained, V˙O _2peak fell after LHTL (7%, P < 0.05). Submaximal V˙O ₂ was reduced (4.4%, P < 0.05) and efficiency improved (0.8%, P < 0.05) after LHTL probably because of a shift in fuel utilization. This is the first study to show that hypoxic exposure, per se, increases muscle buffer capacity. Further, reduced V˙O ₂ during normoxic exercise after LHTL suggests that improved exercise efficiency is a fundamental adaptation to LHTL.     

Endotoxin‐induced shock in the pig – limited effects of low and high concentrations of inhaled nitric oxide

Aim: This study was carried out to study the prophylactic effects of inhalation of nitric oxide (NO) before and during the induction of endotoxic shock. Methods: Eighteen anaesthetized pigs received an infusion of 10–20 μg kg^?1 endotoxin during 2 h after pre‐treatment with the cortisol‐synthesis inhibitor metyrapone. Three groups were tested (n = 6 each) and received 0, 0.2 or 20 ppm inhaled NO from 30 min before start of endotoxin infusion until 4 h after start of endotoxin. Both 0.2 and 20 ppm NO were able to improve blood gas values. Results: Area above curve values of arterial P₂/FiO₂ from 0 to 4 h were 0.83 ± 0.09 kPa h (control), 0.78 ± 0.22 (0.2 ppm NO, non‐significant) and 0.31 ± 0.06 (20 ppm NO, P < 0.01, Mann–Whitney U‐test, compared to control). Area under curve values of PCO₂ from 0 to 4 h were 3.96 ± 0.66 kPa h (control), 1.20 ± 0.46 (0.2 ppm NO, P < 0.05, Mann–Whitney U‐test, compared to control) and 2.78 ± 1.06 (20 ppm NO group, non‐significant). The increase in pulmonary arterial pressure (PAP) was partly prevented by 20 ppm NO, but not by 0.2 ppm NO at 4 h. Inhaled NO did not affect the levels of BAL fluid total protein, tumour necrosis factor‐α, interleukin‐8 and neutrophil counts. Conclusions: The addition of a high (20 ppm), but not a low (0.2 ppm), concentration of NO to the inhaled air during endotoxin shock improves arterial oxygen tension and reduces pulmonary artery pressure. Neither dose affects lung mechanics or inflammatory indices, in spite of being given prophylactically.