Biomedical subjects

P Robach

Publications and source records attributed to P Robach.

11 recordsLinked to original sources

PubMed2006

Effects of ATP-induced leg vasodilation on VO2 peak and leg O2 extraction during maximal exercise in humans.

During maximal whole body exercise VO2 peak is limited by O2 delivery. In turn, it is though that blood flow at near-maximal exercise must be restrained by the sympathetic nervous system to maintain mean arterial pressure. To determine whether enhancing vasodilation across the leg results in higher O2 delivery and leg VO2 during near-maximal and maximal exercise in humans, seven men performed two maximal incremental exercise tests on the cycle ergometer. In random order, one test was performed with and one without (control exercise) infusion of ATP (8 mg in 1 ml of isotonic saline solution) into the right femoral artery at a rate of 80 microg.kg body mass-1.min-1. During near-maximal exercise (92% of VO2 peak), the infusion of ATP increased leg vascular conductance (+43%, P<0.05), leg blood flow (+20%, 1.7 l/min, P<0.05), and leg O2 delivery (+20%, 0.3 l/min, P<0.05). No effects were observed on leg or systemic VO2. Leg O2 fractional extraction was decreased from 85+/-3 (control) to 78+/-4% (ATP) in the infused leg (P<0.05), while it remained unchanged in the left leg (84+/-2 and 83+/-2%; control and ATP; n=3). ATP infusion at maximal exercise increased leg vascular conductance by 17% (P<0.05), while leg blood flow tended to be elevated by 0.8 l/min (P=0.08). However, neither systemic nor leg peak VO2 values where enhanced due to a reduction of O2 extraction from 84+/-4 to 76+/-4%, in the control and ATP conditions, respectively (P<0.05). In summary, the VO2 of the skeletal muscles of the lower extremities is not enhanced by limb vasodilation at near-maximal or maximal exercise in humans. The fact that ATP infusion resulted in a reduction of O2 extraction across the exercising leg suggests a vasodilating effect of ATP on less-active muscle fibers and other noncontracting tissues and that under normal conditions these regions are under high vasoconstrictor influence to ensure the most efficient flow distribution of the available cardiac output to the most active muscle fibers of the exercising limb.

Adenosine Triphosphate↗

PubMed2006

Is it more effective for highly trained swimmers to live and train at 1200 m than at 1850 m in terms of performance and haematological benefits?

OBJECTIVES: The effects of living and training have not been compared at different altitudes in well trained subjects. METHODS: Nine international swimmers lived and trained for 13 days similarly at 1200 m (T1200) and 1850 m (T1850). The two altitude training periods were separated by six weeks of sea level training. Before and after each training trip, subjects performed, at an altitude of 1200 m, an incremental exercise test to exhaustion of 5 x 200 m swims and a maximal test over 2000 m. RESULTS: There was no difference in Vo(2)max after each training trip: the before values were 58.5 (5.6) and 60.4 (6.7) ml/kg/min and the after values were 56.2 (5.2) and 57.1 (4.7) ml/kg/min for T1200 and T1850 respectively. The 2000 m performance had improved during T1200 (1476 (34) to 1448 (45) seconds) but not during T1850 (1458 (35) v 1450 (33) seconds). Mean cell volume increased during T1850 (86.6 (2.8) to 88.7 (2.9) microm(3)) but did not change during T1200 (85.6 (2.9) v 85.7 (2.9) microm(3)). The proportion of reticulocytes decreased during T1200 (15.2 (3.8)% to 10.3 (3.4)%) and increased during T1850 (9.3 (1.6)% to 11.9 (3.5)%). CONCLUSIONS: The short term effects of 13 days of training at 1200 m on swimming performance appear to be greater than the same type of training for the same length of time at 1850 m. As mean cell volume and proportion of reticulocytes only increased during training at 1850 m, the benefits of training at this altitude may be delayed and appear later on.

Adaptation, Physiological↗

PubMed2005

Living high-training low altitude training: effects on mucosal immunity.

Secretory immunoglobulin A (sIgA) is the major immunoglobulin of the mucosal immune system. Whereas the suppressive effect of heavy training on mucosal immunity is well documented, little is known regarding the influence of hypoxia exposure on sIgA during altitude training. This investigation examined the impact of an 18-day Living high-training low (LHTL) training camp on sIgA levels in 11 (six females and five males) elite cross-country skiers. Subjects from the control group (n=5) trained and lived at 1,200 m of altitude, whereas, subjects from the LHTL group (n=6) trained at 1,200 m, but lived at a simulated altitude of 2,500, 3,000 and 3,500 m (3x6-day, 11 h day(-1)) in hypoxic rooms. Saliva samples were collected before, after each 6-day phases and 2 weeks thereafter (POST). Salivary sIgA, protein and cortisol were measured. There was a downward trend in sIgA concentrations over the study, which reached significance in LHTL (P<0.01), but not in control (P=0.08). Salivary IgA concentrations were still lower baseline at POST (P<0.05). Protein concentration increased in LHTL (P<0.05) and was negatively correlated with sIgA concentration after the 3,000 and 3,500 m-phase and at POST (P<0.05 all). Cortisol concentrations were unchanged over the study and no relationship was found between cortisol and sIgA. In summary, data were strongly suggestive of a cumulative negative effect of physical exercise and hypoxia on sIgA levels during LHTL training. Two weeks of active recovery did not allow for proper sIgA recovery. The mechanism underlying this depression of sIgA could be mediated by neural factors.

Adult↗

PubMed2001

Operation Everest III (Comex'97): the effect of simulated sever hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise.

Eight subjects were placed in a decompression chamber for 31 days at pressures from sea level (SL) to 8848 m altitude equivalent. Whole blood lipid peroxidation (LP) was increased at 6000 m by a mean of 23% (P<0.05), at 8000 m by 79% (P<0.01) and at 8848 m by 94% (P<0.01). (All figures are means.) Two days after return to sea level (RSL), it remained high, by 81% (P<0.01), while corresponding erythrocyte GSH/GSSG ratios decreased by 31, 46, 49, 48%, respectively (each P<0.01). Erythrocyte SOD and plasma ascorbate did not change significantly. At sea level, maximal exercise induced a 49% increase in LP (P<0.01), and a 27% decrease in erythrocyte GSH/GSSG ratio relative to resting values (P<0.05). At 6000 m, the LP was enhanced further from 23 (P<0.05) to 66% (P<0.01), and after RSL from 81 (P<0.01) to 232% (P<0.01), while pre-exercise GSH/GSSG ratios did not change significantly. Exercise did not change plasma ascorbate relative to sea level or to 6000 m, but decreased after RSL by 32% (P<0.01). These findings suggest that oxidative stress is induced by prolonged hypobaric hypoxia, and is maintained by rapid return to sea level, similar to the post-hypoxic re-oxygenation process. It is increased by physical exercise.

Acclimatization↗

PubMed2000

Operation Everest III: energy and water balance.

We hypothesized that hypoxia decreases energy intake and increases total energy requirement and, additionally, that decreased barometric pressure increases total water requirement. Energy and water balance was studied over 31 days in a hypobaric chamber at 452-253 Torr (corresponding to 4,500-8,848 m altitude), after 7 days acclimatization at 4,350 m. Subjects were eight men, age 27+/-4 years (mean+/-SD), body mass index 22.9+/-1.5 kg/m2. Food and water intake was measured with weighed dietary records, energy expenditure and water loss with labelled water. Insensible water loss was calculated as total water loss minus urinary and faecal water loss. Energy intake at normoxia was 13.6+/-1.8 MJ/d. Energy intake decreased from 10.4+/-2.1 to 8.3+/-1.9 MJ/d (P<0.001) and energy expenditure from 13.3+/-1.6 to 12.1+/-1.8 MJ/d (P<0.001) over the first and second 15-day intervals of progressive hypoxia. Absolute insensible water loss did not change (1.67+/-0.26 and 1.66+/-0.37 l/d), however, adjusted for energy expenditure it increased with ambient pressure reduction (P<0.05). In conclusion, hypoxia induced a negative energy balance, mainly by a reduction of energy intake. Overall insensible water loss was unchanged because the increase in respiratory evaporative water loss was counterbalanced by a decrease in metabolic rate that probably limited the hypoxia-induced increase in ventilation.

Acclimatization↗

PubMed2000

Operation Everest III: role of plasma volume expansion on VO(2)(max) during prolonged high-altitude exposure.

We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O(2) uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively. VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery of VO(2)(max).

Adult↗

PubMed2000

Peripheral chemoreflex function in hyperoxia following ventilatory acclimatization to altitude.

After a period of ventilatory acclimatization to high altitude (VAH), a degree of hyperventilation persists after relief of the hypoxic stimulus. This is likely, in part, to reflect the altered acid-base status, but it may also arise, in part, from the development during VAH of a component of carotid body (CB) activity that cannot be entirely suppressed by hyperoxia. To test this hypothesis, eight volunteers undergoing a simulated ascent of Mount Everest in a hypobaric chamber were acutely exposed to 30 min of hyperoxia at various stages of acclimatization. For the second 10 min of this exposure, the subjects were given an infusion of the CB inhibitor, dopamine (3 microg. kg(-1). min(-1)). Although there was both a significant rise in ventilation (P < 0.001) and a fall in end-tidal PCO(2) (P < 0.001) with VAH, there was no progressive effect of dopamine infusion on these variables with VAH. These results do not support a role for CB in generating the persistent hyperventilation that remains in hyperoxia after VAH.

Acclimatization↗

PubMed1999

Operation Everest III (COMEX '97). Effects of prolonged and progressive hypoxia on humans during a simulated ascent to 8,848 M in a hypobaric chamber.

Exposure to high altitude induces physiological or pathological modifications that are not always clearly attributable to a specific environmental factor: hypoxia, cold, stress, inadequate food. The principal goal of hypobaric chamber studies is to determine the specific effect of hypoxia. Eight male volunteers ("altinauts"), aged 23 to 37 were selected. They were first preacclimatized in the Observatoire Vallot (4,350 m) before entering the chamber. The chamber was progressively decompressed down to 253 mmHg barometric pressure, with a recovery period of 3 days at 5,000 m in the middle of the decompression period. They spent a total of 31 days in the chamber. Eighteen protocols were organized by 14 European teams, exploring the limiting factors of physical and psychological performance, and the pathophysiology of acute mountain sickness (AMS). All subjects reached 8,000 m and 7 of them reached the simulated altitude of 8,848 m. Three altinauts complained of transient neurological symptoms which resolved rapidly with reoxygenation. Body weight decreased by 5.4 kg through a negative caloric balance. Only four days after the return to sea-level, subjects had recovered 3.4 kg, i.e. 63% of the total loss. At 8,848 m (n = 5), PaO2 was 30.6 +/- 1.4 mmHg, PCO2 11.9 +/- 1.4 mmHg, pH 7.58 +/- 0.02 (arterialized capillary blood). Hemoglobin concentration increased from 14.8 +/- 1.4 to 18.4 +/- 1.5 g/dl at 8,000 m and recovered within 4 days at sea-level. AMS score increased rapidly at 6,000 m and was maximal at 7,000 m, especially for sleep. AMS was related to alteration in color vision and elevation of body temperature. VO2MAX decreased by 59% at 7,000 m. The purpose of this paper is to give a general description of the study and the time course of the main clinical and physiological parameters. The altinauts reached the "summit" (for some of them three consecutive times) in better physiological conditions than it would have been possible in the mountains, probably because acclimatization and other environmental factors such as cold and nutrition were controlled.

Acclimatization↗

PubMed1997

Recovery processes after repeated supramaximal exercise at the altitude of 4,350 m.

We tested the hypothesis that prolonged exposure to high altitude would impair the restoration of muscle power during repeated sprints. Seven subjects performed two 20-s Wingate tests (WT1 and WT2) separated by 5 min of recovery, at sea level (N) and after 5-6 days at 4,350 m (H). Mean power output (MPO) and O2 deficit were measured during WT. O2 uptake (VO2) and ventilation (VE) were measured continuously. Blood velocity in the femoral artery (FBV) was recorded by Doppler ultrasound during recovery. Arterialized blood pH and concentrations of bicarbonate ([HCO3-]), venous plasma lactate ([La-]), norepinephrine ([NE]), and epinephrine ([Epi]) were measured before and after WT1 and WT2. MPO decreased between WT1 and WT2 by 6.9% in N (P < 0.05) and by 10.7% in H (P < 0.01). H did not further decrease MPO. O2 deficit decreased between WT1 and WT2 in H only (P < 0.01). Peak VO2 after WT was reduced by 30-40% in H (P < 0.01), but excess postexercise O2 consumption was not significantly lowered in H. During recovery in H compared with N, VE, exercise-induced acidosis, and [NE] were higher, [Epi] tented to be higher, [La-] was not altered, and [HCO3-] and FBV were lower. The similar [La-] accumulation was associated with a higher exercise-induced acidosis and a larger increase in [NE] in H. We concluded from this study that prolonged exposure to high altitude did not significantly impair the restoration of muscle power during repeated sprints, despite a limitation of aerobic processes during early recovery.

Adult↗

PubMed1996

Water balance and acute mountain sickness before and after arrival at high altitude of 4,350 m.

The present study is a first attempt to measure water balance and its components at altitude by using labeled water and bromide dilution and relating the results with acute mountain sickness (AMS). Water intake, total water output, and water output in urine and feces were measured over a 4-day interval before and a subsequent 4-day interval after transport to 4,350 m. Total body water and extracellular water were measured at the start and at the end of the two intervals. There was a close relationship between energy intake and water intake, and the relationship was unchanged by the altitude intervention. Subjects developing AMS reduced energy intake and water intake cor respondingly. The increase in total body water (TBW) in subjects developing AMS was accompanied by a reduction in total water loss. They did not show the increased urine output, compensating for the reduced evaporative water loss at altitude. Subjects showed a significant increase in TBW after 4 days at altitude. Subjects with AMS showed the biggest shifts in extracellular water relative to TBW. In conclusion, fluid retention in relation to AMS is independent of a change in water requirements due to altitude exposure. Subjects developing AMS were those showing a fluid shift of at least 1 liter from the intracellular to the extracellular compartment or from the extracellular to the intracellular compartment.

Adult↗

PubMed1995

[Cardiovascular effects of a calcium channel blocker in hypoxia caused by altitude].

OBJECTIVE: High altitude pulmonary oedema can be successfully treated and prevented by calcium channel blockers. Moreover, calcium entering in the cells could explain the congestive phenomena of acute mountain sickness (AMS). These findings led us to study the action of a calcium channel blocker, isradipine, in the prevention of non-complicated AMS. METHODS: In a double blind randomized study, 20 healthy volunteers received 5 mg of isradipine (n = 6) or placebo (n = 6) for 8 days. After 5 days of treatment in normoxia, the subjects were rapidly transported to an altitude of 4350 m. The efficiency of the treatment was then estimated by the AMS symptom score, haemodynamic parameters and renal function. RESULTS: The administration of isradipine did not significantly modify AMS symptom score nor most of other parameters measured in high altitude hypoxia. Heart rate was an average of 15 b/min lower in the isradipine group, probably because of a direct action of isradipine on the sinus node. Otherwise, the effects of hypoxia were similar in both groups and were in accordance with the literature. There was no clear explanation for the increase in cardiac output and stroke volume when the subjects moved from supine to standing position. Renal blood flow, measured by Doppler or para-aminohippuric acid clearance was not modified by hypoxia. Cerebral blood flow was elevated, due to the direct vasodilator effect of hypoxia. However this increase did not seem to be the main mechanism responsible for the congestive phenomena. On the other hand, the increase in capillary permeability (demonstrated by the increased transcapillary escape rate of albumin, and albuminuria) appeared to play a major role in the pathogenesis of AMS and high altitude cerebral oedema. Isradipine had no protective effect on these phenomena and its use should be restricted to the treatment of high altitude pulmonary oedema.

Adult↗