Arterial hypoxemia in exercising thoroughbreds is not affected by pre-exercise nedocromil sodium inhalation

It has been reported that pulmonary injury (i.e. capillary stress failure) evoked histamine release from airway inflammatory/mast cells contributes to exercise-induced arterial hypoxemia (EIAH) and that pre-exercise inhalation of nedocromil sodium mitigated EIAH in human subjects 'Med. Sci. Sports Exercise 29, (1997) 10-16'. Because exercise-induced pulmonary hemorrhage due to capillary stress failure is routinely observed in racehorses, we examined whether nedocromil inhalation would similarly benefit EIAH and desaturation of hemoglobin in horses. Two sets of experiments, namely, placebo studies followed in 7 days by pre-exercise nedocromil sodium (30 puffs=60 mg) inhalation experiments were carried out on 7 healthy, sound, exercise-trained thoroughbred horses. In both treatments, arterial and mixed-venous blood-gas/pH measurements were made at rest pre- and post-placebo/drug inhalation, as well as during incremental exercise leading to galloping at 14 m/sec on a 3.5% uphill grade-a workload that elicited maximal heart rate and caused pulmonary hemorrhage in all horses in both treatments, thereby indicating capillary stress failure had occurred. In both treatments, significant (P<0.0001) EIAH of a similar magnitude had developed by 30 sec of maximal exertion, and further significant changes in arterial O(2) tension did not occur as exercise duration progressed to 120 sec. Thus, pre-exercise inhalation of nedocromil sodium was ineffective in modifying the development and/or severity of EIAH in the present study. These findings argue against the airway inflammatory mediator(s) release hypothesis for causing arterial hypoxemia in racehorses.     

Hyperhydration prior to a simulated second day of the 3-day moderate intensity equestrian competition does not cause arterial hypoxemia in Thoroughbred horses

Dehydration and the associated impairment of cardiovascular and thermoregulatory function comprise major veterinary problems in horses performing prolonged exercise, particularly under hot and humid conditions. For these reasons, there is considerable interest in using pre-exercise hyperhydration to help maintain blood volume in the face of the excessive fluid loss associated with sweat production during prolonged exertion. However, recently it was reported that pre-exercise hyperhydration causes arterial hypoxemia in horses performing moderate intensity exercise simulating the second day of an equestrian 3-day event competition (E3DEC) which may adversely affect performance (Sosa Leon et al. in Equine Vet J Suppl 34:425–429, 2002). These findings are contrary to data from horses performing short-term maximal exertion, wherein hyperhydration did not affect arterial O₂ tension/saturation. Thus, our objective in the present study was to examine the impact of pre-exercise hyperhydration on arterial oxygenation of Thoroughbred horses performing an exercise test simulating the second day of an E3DEC. Control and hyperhydration studies were carried out on seven healthy Thoroughbred horses in random order, 7 days apart. In the control study, horses received no medications. In the hyperhydration experiments, nasogastric administration of NaCl (0.425 g/kg) 5 h pre-exercise induced a plasma volume expansion of 10.9% at the initiation of exercise. This methodology for inducing hypervolemia was different from that of Sosa Leon et al. (2002). Blood-gas tensions/pH as well as plasma protein, hemoglobin and blood lactate concentrations were measured pre-exercise and during the exercise test. Our data revealed that pre-exercise hyperhydration neither adversely affected arterial O₂ tension nor hemoglobin-O₂ saturation at any time during the exercise test simulating the second day of an E3DEC. Further, it was observed that arterial blood CO₂ tension, pH, and blood lactate concentrations also were not affected by pre-exercise hyperhydration. However, hemodilution in hyperhydrated horses caused an attenuation of the expansion in the arterial to mixed-venous blood O₂ content gradient during phases B and D of the exercise protocol, which was likely offset by an increase in cardiac output. It is concluded that pre-exercise hyperhydration of horses induced in the manner described above is not detrimental to arterial oxygenation of horses performing an exercise test simulating the second day of an E3DEC.     

Repeated exercise-induced arterial hypoxemia in a healthy untrained woman

A healthy 36-year-old untrained (maximal oxygen consumption ( [Formula: see text] ): 39mL/kg/min) woman completed multiple graded exercise tests on a treadmill. Temperature-corrected arterial blood samples were obtained in addition to esophageal pressure. Significant hypoxemia (-13mmHg arterial oxygen tension decrease) and arterial oxyhemoglobin desaturation (-6% decrease) was observed relative to rest and occurred during submaximal exercise and worsened at maximal intensities. Expiratory flow limitation (28-40% intersection of tidal volume) was present at near-maximal intensities. Relieving mechanical ventilatory constraints with a helium inspirate (79% He:21% O(2)) partially reversed the hypoxemia. Conversely, increasing chemical ventilatory stimuli, with hypercapnia (3.5% CO(2)), failed to increase ventilation. Maintaining oxyhemoglobin saturation, via a mildly hyperoxic (26% O(2)) inspirate, increased exercise duration (+45s) and [Formula: see text] (+5mL/kg/min). We attribute the hypoxemia to an excessive [Formula: see text] resulting from ventilation-perfusion mismatch and secondarily to mechanical ventilatory constraints. We conclude that a healthy untrained woman can develop EIAH and this remains stable over a period of 6 months.     

Cerebral oxygenation decreases during exercise in humans with beta‐adrenergic blockade

Aim: Beta‐blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation. Methods: Acting as their own controls, eight healthy subjects performed a continuous incremental cycle test to exhaustion with or without administration of the non‐selective beta‐blocker propranolol. Changes in cerebral blood flow velocity were measured with transcranial Doppler ultrasound and those in cerebral oxygenation were evaluated using near‐infrared spectroscopy and the calculated cerebral mitochondrial oxygen tension derived from arterial to internal jugular venous concentration differences. Results: Arterial lactate and cardiac output increased to 15.3 ± 4.2 mm and 20.8 ± 1.5 L min^?1 respectively (mean ± SD). Frontal lobe oxygenation remained unaffected but the calculated cerebral mitochondrial oxygen tension decreased by 29 ± 7 mmHg (P < 0.05). Propranolol reduced resting heart rate (58 ± 6 vs. 69 ± 8 beats min^?1) and at exercise exhaustion, cardiac output (16.6 ± 3.6 L min^?1) and arterial lactate (9.4 ± 3.7 mm ) were attenuated with a reduction in exercise capacity from 239 ± 42 to 209 ± 31 W (all P < 0.05). Propranolol also attenuated the increase in cerebral blood flow velocity and frontal lobe oxygenation (P < 0.05) whereas the cerebral mitochondrial oxygen tension decreased to a similar degree as during control exercise (delta 28 ± 10 mmHg; P < 0.05). Conclusion: Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity.     

Effects of reduced frequency breathing on arterial hypoxemia during exercise

Summary It is uncertain that exercise with reduced frequency breathing (RFB) results in arterial hypoxemia. This study was designed to investigate whether RFB during exercise creates a true hypoxic condition in arterial blood by examining arterial oxygen saturation (SaO₂) directly. Six subjects performed ten 30 s periods of exercise on a Monark bicycle ergometer at a work rate of 210 W alternating with 30 s rest intervals. The breath was controlled to use 1 s each for inspiration and expiration, and two trials with different breathing patterns were used; a continuous breathing (CB) trial and an RFB trial consisting of four seconds of breath-holding at functional residual capacity (FRC). Alveolar oxygen pressure during exercise showed a slight but significant (p<0.05) reduction with RFB as compared to CB. However, a marked increase in alveolar-arterial pressure difference for oxygen (A-aDO₂) (p<0.05) with RFB over CB resulted in a marked (p<0.05) reduction in arterial oxygen pressure. Consequently, SaO₂ fell as low as 88.8% on average. Additional examination of RFB with breath-holding at total lung capacity showed no increases in A-aDO₂ in spite of the same amount of hypoventilation as compared with that at FRC. These results indicate that RFB during exercise can result in arterial hypoxemia if RFB is performed with breath-holding at FRC, this mechanism being closely related to the mechanical responses due to lung volume restriction.     

Acute hypoxic ventilatory response and exercise-induced arterial hypoxemia in men and women

Recent studies claim a higher prevalence of exercise-induced arterial hypoxemia (EIAH) in women relative to men and that diminished peripheral chemosensitivity is related to the degree of arterial desaturation during exercise in male endurance athletes. The purpose of this study was to determine the relationship between the acute ventilatory response to hypoxia (AHVR) and EIAH and the potential influence of gender in trained endurance cyclists and untrained individuals. Healthy untrained males (n = 9) and females (n = 9) and trained male (n = 11) and female (n = 10) cyclists performed an isocapnic AHVR test followed by an incremental cycle test to exhaustion. Oxyhemoglobin saturation (Sa(O(2)) was lower in trained men (91.4 +/- 0.9%) and women (91.3 +/- 0.9%) compared to their untrained counterparts (94.4 +/- 0.8% versus 94.3 +/- 0.7%) (P < 0.05). AHVR and maximal O(2) consumption were related for all subjects (r = -0.46), men (r = -0.45) and women (r = -0.53) (P < 0.05) but AHVR was unrelated to Sa(O(2)) for any groups (P > 0.05). We conclude that resting AHVR does not have a significant role in maintaining Sa(O(2)) during sea-level maximal cycle exercise in men or women.     

Acute hypervolaemia improves arterial oxygen pressure in athletes with exercise-induced hypoxaemia

The aim of this study was to determine the effect of acute plasma volume expansion on arterial blood-gas status during 6.5 min strenuous cycling exercise comparing six athletes with and six athletes without exercise-induced arterial hypoxaemia (EIAH). We hypothesized that plasma volume expansion could improve arterial oxygen pressure in a homogeneous sample of athletes - those with EIAH. In this paper we have extended the analysis and results of our recently published surprising findings that lengthening cardiopulmonary transit time did not improve arterial blood-gas status in a heterogeneous sample of endurance cyclists. One 500 ml bag of 10 % Pentastarch (infusion condition) or 60 ml 0.9 % saline (placebo) was infused prior to exercise in a randomized, double-blind fashion on two different days. Power output, cardiac output, oxygen consumption and arterial blood gases were measured during strenuous exercise. Cardiac output and oxygen consumption were not affected by acute hypervolaemia. There were group x condition interaction effects for arterial oxygen pressure and alveolar-arterial oxygen pressure difference, suggesting that those with hypoxaemia experienced improved arterial oxygen pressure (+4 mmHg) and lower alveolar-arterial oxygen pressure difference (-2 mmHg) with infusion. In conclusion, acute hypervolaemia improves blood-gas status in athletes with EIAH. The impairment of gas exchange occurs within the first minute of exercise, and is not impaired further throughout the remaining duration of exercise. This suggests that arterial oxygen pressure is only minimally mediated by cardiac output.     

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.     

Sympathetic influence on cerebral blood flow and metabolism during exercise in humans

This review focuses on the possibility that autonomic activity influences cerebral blood flow (CBF) and metabolism during exercise in humans. Apart from cerebral autoregulation, the arterial carbon dioxide tension, and neuronal activation, it may be that the autonomic nervous system influences CBF as evidenced by pharmacological manipulation of adrenergic and cholinergic receptors. Cholinergic blockade by glycopyrrolate blocks the exercise-induced increase in the transcranial Doppler determined mean flow velocity (MCA Vmean). Conversely, alpha-adrenergic activation increases that expression of cerebral perfusion and reduces the near-infrared determined cerebral oxygenation at rest, but not during exercise associated with an increased cerebral metabolic rate for oxygen (CMRO(2)), suggesting competition between CMRO(2) and sympathetic control of CBF. CMRO(2) does not change during even intense handgrip, but increases during cycling exercise. The increase in CMRO(2) is unaffected by beta-adrenergic blockade even though CBF is reduced suggesting that cerebral oxygenation becomes critical and a limited cerebral mitochondrial oxygen tension may induce fatigue. Also, sympathetic activity may drive cerebral non-oxidative carbohydrate uptake during exercise. Adrenaline appears to accelerate cerebral glycolysis through a beta2-adrenergic receptor mechanism since noradrenaline is without such an effect. In addition, the exercise-induced cerebral non-oxidative carbohydrate uptake is blocked by combined beta 1/2-adrenergic blockade, but not by beta1-adrenergic blockade. Furthermore, endurance training appears to lower the cerebral non-oxidative carbohydrate uptake and preserve cerebral oxygenation during submaximal exercise. This is possibly related to an attenuated catecholamine response. Finally, exercise promotes brain health as evidenced by increased release of brain-derived neurotrophic factor (BDNF) from the brain.     

Pulmonary vasodilatation and augmentation of right ventricular function following terbutaline infusion in severe chronic pulmonary disease

Twenty patients with a median age of 61 years and a median forced expired volume in 1 s (FEV1) after bronchodilating therapy of 0.55 l were studied in order to measure the effect of intravenous terbutaline on bronchial tone, cardiac function, pulmonary haemodynamics, gas exchange, and oxygen transport capacity during rest and in 10 patients during exercise. Terbutaline infusion during rest resulted in an increase in heart rate from 84 to 103 beats min-1 (P less than 0.01), a decrease in mean systemic arterial pressure from 95 to 80 mmHg (P less than 0.02), an unchanged mean pulmonary arterial pressure (18 mmHg), an increase in cardiac index from 2.89 to 3.86 l min-1 m-2 (P less than 0.01), an increase in right ventricular ejection fraction from 45 to 53% (P less than 0.01), an increase in left ventricular ejection fraction from 63 to 67% (NS), an unchanged arterial oxygen tension, and an increase in calculated oxygen delivery from 533 to 638 ml O2 min-1 m-2 (P less than 0.01). During exercise terbutaline infusion resulted in an increase in heart rate from 108 to 120 beats min-1 (P less than 0.05), a decrease in mean systemic arterial pressure from 117 to 106 mmHg (P less than 0.01), a decrease in mean pulmonary arterial pressure from 29 to 22 mmHg (P less than 0.01), an increase in cardiac index from 4.53 to 4.64 min-1 m-2 (NS), an unchanged arterial oxygen tension, and an increase in the calculated oxygen delivery from 834 to 856 ml O2 min-1 m-2 (NS). It was concluded that terbutaline augments right ventricular function: increases right ventricular ejection fraction and decreases right ventricular end-diastolic volume, and further decreases pulmonary vascular resistance without decreasing arterial oxygen tension, and increases oxygen delivery in patients with chronic pulmonary disease during rest and exercise.     

Effect of single-leg resistance exercise on regional arterial stiffness

To examine the effects of lower-limb unilateral resistance exercise on central and peripheral arterial stiffness, thirteen participants (7 male and 6 female, mean age = 21.5 ± 0.7 years) performed leg press exercise using their dominant leg. Pulse wave velocity (PWV) was used to measure central (carotid to femoral) and peripheral (femoral to dorsalis pedis of both legs) arterial stiffness before, 5 min post, and 25 min post exercise. No change was found in central PWV. A leg-by-time interaction was found as peripheral PWV in the non-exercised leg did not change (7.9 ± 0.3 m/s to 7.9 ± 0.3 m/s to 8.0 ± 0.3 m/s, P = 0.907) while peripheral PWV in the exercised leg significantly decreased from pre (8.7 ± 0.4 m/s) to 5 min post exercise (7.5 ± 0.3 m/s, P = 0.008) and 25 min post exercise (7.8 ± 0.3 m/s, P = 0.031). Systolic blood pressure (BP) increased significantly from pre (126.9 ± 3.4 mmHg) to 5 min post exercise (133.7 ± 4.3 mmHg, P = 0.023) and was not different than resting values 25 min post exercise (123.2 ± 3.1 mmHg). There was no change in diastolic BP. Compared to heart rate (HR) pre-exercise (55.4 ± 1.4 bpm), HR was significantly increased 5 min post exercise (70.7 ± 3.0 bpm, P = 0.001) and 25 min post exercise (69.1 ± 2.0, P = 0.001). Acute resistance exercise appears to decrease arterial stiffness in the exercised leg while having no effect on central arterial stiffness or arterial stiffness of the non-exercised leg. These findings suggest that regional changes rather than systemic alterations may influence arterial stiffness following acute resistance exercise.     

Effects of small changes of blood volume on oxygen delivery and tissue oxygenation

Circulatory effects of small (approximately 10%) changes in blood volume were examined in resting and exercising dogs: controls; group A (-200 ml blood); group B (+200 ml blood); group C (+200 ml 6% dextran). In exercise, cardiac output (Q) increased more in Group A than controls (510.4 ml . kg-1 . min-1 compared to 429.6 ml . kg-1 . min-1; P less than 0.05); oxygen delivery (cardiac output x arterial O2 content) and mixed venous oxygen tension (PVO2) were unchanged from exercising controls. Hypervolemia (group B) did not change Q or O2 delivery compared to controls, but caused a greater reduction in exercise PVO2 (29.3 mmHg compared to 33.1 mmHg in controls; P less than 0.01). Resting PVO2 as raised in group C (50.0 mmHg compared to 46.3 mmHg; P less than 0.05) and exercise PVO2 was reduced less (35.5 mmHg compared to 33.1 mmHg in controls; P less than 0.05). O2 delivery in exercise was higher than in controls (123.4 ml . kg-1 . min-1 compared to 94.3 ml . kg-1 . min-1; P less than 0.001). During exercise, O2 consumption was raised from base line to 34.9 ml . kg-1 . min-1 in controls and raised further to 41.4 ml . kg-1 . min-1 in group A, 44.4 ml . kg-1 . min-1 in group B, and 41.2 ml . kg-1 . min-1 in group C (P less than 0.01). Changes of blood volume that lie within physiological limits thus significantly modify the circulatory response to changed O2 requirements, and also change the metabolic cost of exercise.     

Augmented leg vasoconstriction in dynamically exercising older men during acute sympathetic stimulation

Vasoconstrictor responsiveness to acute sympathetic stimulation declines with advancing age in resting skeletal muscle. The purpose of the present study was to determine if age-related reductions in sympathetic vasoconstrictor responsiveness also occur in exercising skeletal muscle. Thirteen younger (20–30 years) and seven older (62–74 years) healthy non-endurance-trained men performed cycle ergometer exercise at ∼60 % of peak oxygen uptake while leg blood flow (femoral vein thermodilution), mean arterial blood pressure (radial artery catheter), and plasma adrenaline and noradrenaline concentrations were measured. After steady state was reached (i.e. ∼4 min), acute sympathetic stimulation was achieved by immersing a hand in ice water for 2–4 min (cold pressor test, CPT). CPT tended to cause a larger increase in mean arterial blood pressure in older men (older (O): 16 ± 3 mmHg; younger (Y): 10 ± 2 mmHg) during exercise, but increases in arterial noradrenaline were similar (O: 2.56 ± 0.96 nM; Y: 1.98 ± 0.40 nM). However, the older men demonstrated a larger percentage reduction in exercising leg vascular conductance (leg blood flow/mean arterial pressure) during CPT compared to younger men (O: -13.6 ± 3.1%; Y: -1.5 ± 4.3%; P = 0.04). Leg blood flow tended to increase in the younger men, but not in the older men ( P = 0.10). These results suggest, in contrast to what has been observed in resting skeletal muscle, that vasoconstrictor responsiveness to sympathetic stimulation is not reduced, but may be augmented in exercising muscle of healthy older humans. This could reflect a reduced ability of local substances (e.g. nitric oxide) to impair vasoconstriction in response to sympathetic stimulation during exercise in older humans.     

Acute dietary nitrate supplementation improves dry static apnea performance

Acute dietary nitrate (NO??) supplementation has been reported to lower resting blood pressure, reduce the oxygen (O?) cost of sub-maximal exercise, and improve exercise tolerance. Given the proposed effects of NO?? on tissue oxygenation and metabolic rate, it is possible that NO?? supplementation might enhance the duration of resting apnea. If so, this might have important applications both in medicine and sport. We investigated the effects of acute NO?? supplementation on pre-apnea blood pressure, apneic duration, and the heart rate (HR) and arterial O? saturation (SaO?) responses to sub-maximal and maximal apneas in twelve well-trained apnea divers. Subjects were assigned in a randomized, double blind, crossover design to receive 70 ml of beetroot juice (BR; containing ～5.0 mmol of nitrate) and placebo juice (PL; ～0.003 mmol of nitrate) treatments. At 2.5 h post-ingestion, the subjects completed a series of two 2-min (sub-maximal) static apneas separated by 3 min of rest, followed by a maximal effort apnea. Relative to PL, BR reduced resting mean arterial pressure by 2% (PL: 86±7 vs. BR: 84 ± 6 mmHg; P=0.04). The mean nadir for SaO? after the two sub-maximal apneas was 97.2±1.6% in PL and 98.5±0.9% in BR (P=0.03) while the reduction in HR from baseline was not significantly different between PL and BR. Importantly, BR increased maximal apneic duration by 11% (PL: 250 ± 58 vs. BR: 278±64s; P=0.04). In the longer maximal apneas in BR, the magnitude of the reductions in HR and SaO? were greater than in PL (P ≤ 0.05). The results suggest that acute dietary NO?? supplementation may increase apneic duration by reducing metabolic costs.     

Decrease in peak heart rate with acute hypoxia in relation to sea level VO(2max)

The aim of this study was to evaluate the influence of arterial oxygen saturation (SaO₂) on maximal heart rate during maximal exercise under conditions of acute hypoxia compared with normoxia. Forty-six males were divided into three groups depending on their sea level maximal oxygen consumption (O_2max): high [GH, O_2max=64.2 (3.3) ml.min^–1.kg^–1], medium [GM, 50.8 (3.9) ml.min^–1.kg^–1] and low [GL, 41.0 (1.9) ml.min^–1.kg^–1]. All subjects performed a maximal exercise test in two conditions of inspired oxygen tension (PIO₂, (149 mmHg and 70 mmHg). Among the GM group, seven subjects performed five supplementary incremental exercise tests at PIO₂ 136, 118, 104, 92, and 80 mmHg. Measurements of O_2max and SaO₂ using an ear-oxymeter were carried out at all levels of PIO₂. The decrease in SaO₂ and peak heart rate (HR_peak) with PIO₂ became significant from 104 and 92 mmHg. SaO₂ correlated with the decrease in HR_peak. For PIO₂=70 mmHg, the decrease in O_2max, SaO₂ and HR_peak was, respectively, 44%, 62%, and 17.0 bpm for GH, 38%, 68%, and 14.7 bpm for GM, and 34%, 68%, and 11.8 bpm for GL. During maximal exercise in hypoxia, SaO₂ was lower for GH than GM and GL (p<0.01). Among subjects in GH, five presented exercise-induced hypoxemia (EIH) when exercising in normoxia. The EIH group exhibited a greater decrement in HR_peak than the non-EIH group at maximal hypoxic exercise (21.2 bpm vs. 15.0 bpm; p<0.05). When subjects are exposed to acute hypoxia, the lower SaO₂, due either to lower PIO₂ or to training status, is associated with lower HR_peak.     

Reference values for gas exchange during exercise in healthy nonsmoking and smoking men

The gas exchange at rest and during exercise was measured in 50 healthy men, 25 lifelong nonsmokers and 25 smokers, between 20 and 65 years of age. Arterial blood samples were taken and expired air was collected at rest, supine and sitting, and during graded exercise. Prediction formulas for various gas exchange variables were obtained by multiple regression. Optimal conditions for gas transfer were present at light exercise. The arterial oxygen tension (PaO2) remained approximately constant during exercise, although in individual smokers and nonsmokers it decreased by up to 1.8 kPa (13.5 mmHg) between a workload of 50 W and the maximal workload. The lower limit for PaO2 at maximal exercise was about 10.7 kPa (80 mmHg). The alveolo-arterial difference in oxygen tension (PA-aO2) increased considerably with increased workload, from 1.09 +/- 1.05 kPa at 50 W to 3.1 +/- 0.9 kPa at maximal exercise. Ageing and tobacco smoking were associated with a decrease in PaO2 and an increase in PA-aO2 at rest in the supine position, but at maximal exercise neither PaO2 nor PA-aO2 was significantly influenced by age or tobacco smoking. In contrast, the dead space and total ventilation were increased during exercise by ageing and tobacco smoking.     

Cerebral oxygenation during intermittent supramaximal exercise

This study examined cerebral deoxygenation during intermittent supramaximal exercise in six healthy male subjects (age: 27.2 +/- 0.6 years (mean +/- S.E.). The subjects performed seven times exercise at an intensity corresponding to 150% of maximal oxygen uptake (VO2max) on cycle ergometer (30 s exercise/15 s rest). Cerebral oxygenation was measured by near-infrared spectroscopy (NIRS). The peak blood lactate concentration after exercise was 15.3 +/- 0.2 mmol/l. Cerebral oxygenation increased in first repetition compared with at rest (+ 5.7 +/- 0.6 microM; P < 0.05), but then decreased with time. Thus, in the last repetition cerebral oxygenation was - 8.5 +/- 0.4 microM (P < 0.05). There was no significant change in arterial oxygen saturation (99.6 +/- at rest, 98.4 +/- 0.2 at the final set of intermittent exercise), and there was no correlated change in end-tidal CO2 concentration with cerebral oxygenation (P > 0.05). These findings suggest that the fatigue resulting from dynamic severe exercise related to a decrease in the cerebral oxygenation level.     

Stress failure of pulmonary capillaries as a limiting factor for maximal exercise

The pulmonary blood-gas barrier has a basic physiological dilemma. On the one hand it needs to be extremely thin for efficient gas exchange. On the other hand it also needs to be immensely strong because the stresses on the pulmonary capillary wall become extremely high when the capillary pressure rises on exercise. Maximal hydrostatic pressures in human pulmonary capillaries during exercise are not accurately known but must exceed 30 mmHg. In some animals, for example thoroughbred horses, the capillary pressure rises to about 100 mmHg. These pressures cause stresses in the capillary wall of 5–10 × 10⁴ N·M^–2 (50–100 kPa) which approach the breaking strength of collagen. The strength of the capillary wall on the thin side of the blood-gas barrier can be attributed to the type IV collagen of the extracellular matrix. Raising the capillary pressure to similar levels in experimental preparations causes ultrastructural changes in the wall including disruption of the capillary endothelium, alveolar epithelium, and basement membrane in the interstitium. Essentially all thoroughbred racehorses bleed into their lungs during exercise because they break their capillaries, and some elite human athletes apparently do the same. Avoiding stress failure of pulmonary capillaries poses a challenging problem for some species. Stress failure is a hitherto overlooked factor limiting maximal exercise.     

Pulmonary gas exchange does not worsen during repeat exercise in women

The purposes were to determine (1) if repeat exercise worsens pulmonary gas exchange in women, and, (2) if the level of pulmonary edema obtained in these same women is related to the gas exchange impairment during exercise. Fourteen women (27 +/- 4 yrs; maximal oxygen uptake = 3.12 +/- 0.42 L/min) with minimal arterial PO2 (PaO2) ranging from 76 to 104 mmHg with a maximal alveolar-arterial PO2 difference (AaDO2) ranging from 7 to 35 mmHg performed three bouts of near-maximal exercise on a cycle ergometer (236 +/- 27 W) for 5 min each with 10 min of rest between sets. Cardiorespiratory parameters and oxygenation were measured at rest, throughout exercise and recovery. Chest radiographs were obtained before and 30 min after the interval training session (see Respir Physiol Neurobiol, 153 (2006) 181-190). Repeat exercise did not affect pulmonary gas exchange between sets 1 and 3 (change in PaO2 = 3 +/- 2 mmHg; change in AaDO2 = 1 +/- 2 mmHg P > 0.05). Arterial PCO2 decreased by 4 +/- 2 mmHg (P < 0.05) between sets 1 and 2, which did not reduce further in set 3. The level of PaO2 or AaDO2 was not related to the change in edema score or the post-exercise edema score (P > 0.05). In conclusion, pulmonary gas exchange is not worsened in women during interval training despite the mild edema triggered by exercise.     

Influence of cuff material on blood flow restriction stimulus in the upper body

The purpose of this study was to examine the acute skeletal muscle and perceptual responses to blood flow restriction (BFR) exercise to failure between narrow nylon and elastic inflatable cuffs at rest and during exercise. Torque and muscle thickness was measured pre, post, and 5, 20, 40, and 60 min post-exercise with muscle activation being measured throughout exercise. Resting arterial occlusion pressure was different between the nylon [139 (14) mmHg] and elastic [246 (71) mmHg, p < 0.001] cuffs. However, when exercising at 40 % of each cuff’s respective arterial occlusion pressure [nylon: 57 (7) vs. elastic: 106 (38) mmHg, p < 0.001], there were no differences in repetitions to failure, torque, muscle thickness, or muscle activation between the cuffs. Exercising with cuffs of different material but similar width resulted in the same acute muscular response when the cuffs were inflated to a pressure relative to each individual cuff.