Effects of priming exercise on VO2 kinetics and O2 deficit at the onset of stepping and cycling.

Breath-by-breath O2 uptake (VO2) kinetics and increase of blood lactate concentration (delta Lab) were determined at the onset of square-wave stepping (S) or cycling (C) exercise on six male subjects during 1) transition from rest (R) to constant work load, 2) transition from lower to heavier work loads, wherein the baseline VO2 (VO2 s) was randomly chosen between 20 and 65% of the subjects' maximal O2 uptake (VO2 max), and 3) inverse transition from higher to lower work loads and/or to rest. VO2 differences between starting and arriving levels were 20-60% VO2 max. In C, the VO2 on-response became monotonically slower with increasing VO2 s, the half time (t1/2) increasing from approximately 22 s for VO2 s = R to approximately 63 s when VO2 s approximately equal to 50% VO2 max. In S, the fastest VO2 kinetics (t1/2 = 16 s) was attained from VO2 s = 15-30% VO2 max, the t1/2 being approximately 25 s when starting from R or from 50% VO2 max. The slower VO2 kinetics in C were associated with a much larger delta Lab. The VO2 kinetics in recovery were essentially the same in all cases and could be approximated by a double exponential with t1/2 of 21.3 +/- 6 and 93 +/- 45 s for the fast and slow components, respectively. It is concluded that the O2 deficit incurred is the sum of three terms: 1) O2 stores depletion, 2) O2 equivalent of early lactate production, and 3) O2 equivalent of phosphocreatine breakdown.(ABSTRACT TRUNCATED AT 250 WORDS)

Slow upward drift of VO2 during constant-load cycling in untrained subjects.

The oxygen uptake kinetics during constant-load exercise when sitting on a bicycle ergometer were determined in 7 untrained subjects by measuring breath-by-breath VO2 during continuous exercise to volitional exhaustion (mean endurance time = 1160 +/- 172 s) at a pedal frequency of 70 revolutions.min-1. The power output, averaging 189.5 W, was set at 82.5% of that eliciting the individual VO2max during a 5 min incremental exercise test. Throughout the exercise period, the VO2 kinetics could be appropriately described by a two-component exponential equation of the form: VO2(t) = Ya[1 - exp(-kat)] + Yb[1 - exp(-kbt)] where VO2 is net oxygen consumption and t the time from work onset. VO2 measured at the end of exercise was close to VO2max (98% VO2max) and the mean values of Ya, ka, Yb and kb amounted to 1195 ml O2.min-1, 0.034 s-1, 1562 ml O2.min-1, and 0.005 s-1 respectively. The initial rate of increase in VO2 predicted from the above equation is slower than that calculated, for the same work intensity, on the basis of the data obtained by Morton (1985) in trained subjects. For t greater than 480 s, however, the two models yield substantially equal results.

[Principles of decisional analysis applied to the screening for occupational diseases: the example of occupational fluorosis]. / Principes d'analyse décisionnelle appliqués au dépistage de maladies professionnelles: exemple de la fluorose industrielle.

In this paper, two oral presentations are combined. The first described the broad aspects of decision analysis and the second mentioned those medical data which need to be gathered in order to apply the model to industrial fluorosis. For this purpose, biological and medical observations were collected, both from workers of the aluminium industry and from controls. The five successive steps for building up a decision tree are then demonstrated, the aim of which being to evaluate the fitness of a screening strategy. A computer programme has been developed which may be applied both to occupational or non occupational diseases. Referring to industrial fluorosis, the computerized decision tree showed that screening with preshift urinary fluor, clinical and radiological signs, plus bone fluor rate is required, as soon as the risk corresponds to a 7% prevalence of the disease.

After effects of chronic hypoxia on VO2 kinetics and on O2 deficit and debt.

Single breath O2 consumption (PB = 730, FI02 = 0.21) was measured at rest, during 10 min cycloergometric exercise at 125 W, and in the following recovery phase in seven subjects before, and 12 days after 6 weeks at 5,200 m or above. Peak blood lactate after exercise (Lâb) was measured. O2 deficits and debts and half times (t1/2) of the VO2 on- and off-kinetics were calculated. Before acclimatization, the VO2 on- and off-responses were close to a single exponential with t1/2 = 30 s. After return to sea level, the VO2 on-response curves were less steep in the initial phase, becoming closer to sigmoid. The t1/2, independent of the shape of the underlying function, was approximately 10 s longer. The VO2 off-responses during the initial 4 min of recovery were the same before and after acclimatization. Average O2 deficit was approximately 320 ml larger after acclimatization: the fast component of O2 debt was similar. Since steady state VO2 and Lâb were the same, the O2 deficit difference can be attributed to a greater utilization of O2 stores. Of these, about 1/3 is explained in terms of increased mixed venous blood O2 stores, due to increased [Hb] (16.6 vs 14.9 g X dl-1), while the remainder is ascribed essentially to increased Mb-bound O2. O2 stores utilization and replenishment is presumed to occur when muscle metabolism is low; as a consequence, while it is clearly detectable from the shape of the initial phase of the VO2 on-response, during recovery it is spread throughout, thus becoming more difficult to appreciate.

After effects of chronic hypoxia on cardiac output and muscle blood flow at rest and exercise.

Cardiac output (Q, by N2-CO2 rebreathing) and limb muscle blood flow (qm, from 133Xe clearance) were determined in eight male subjects at rest and during cycloergometric loads immediately before and 12 days after return from the 1981 Swiss Lhotse Shar (8,398 m) Expedition. Compared to control conditions, after exposure to hypoxia: 1) Q was unchanged at rest and at 75 watts (W) but was 18% less (P less than 0.01) at 150 W with constant heart rate (approximately 140 beats X min-1); 2) qm in the vastus lateralis was identical at rest but 26% and 39% less (P less than 0.05 and P less than 0.001, respectively) at two submaximal leg work loads (75 and 125 W); 3) qm in the biceps at 50 W was 34% less (P less than 0.01); 4) hemoglobin flow (QHb and qmHb), similarly to blood flow (Q and qm), was significantly reduced; 5) the qm adjustment rate, measured from the time required to attain a new steady state upon a square wave change of work load starting from rest, was slower, particularly at the lower work loads. From the above results as well as from corresponding morphometric findings showing in the same subjects: 1) a decrease of the ratio between fiber section and number of capillaries and 2) a rise of the mitochondrial to fiber volume ratio, it is concluded that during altitude acclimatization peripheral O2 delivery becomes more efficient.

Breath-by-breath alveolar gas exchange.

A method is described for breath-by-breath measurement of alveolar gas exchange corrected for changes of lung gas stores. In practice, the subject inspires from a spirometer, and each expired tidal volume is collected into a rubber bag placed inside a rigid box connected to the same spirometer. During the inspiration following any given expiration the bag is emptied by a vacuum pump. A computer monitors inspiratory and expiratory tidal volumes, drives four solenoid valves allowing appropriate operation of the system, and memorizes end-tidal gas fractions as well as mixed expired gas composition analyzed by mass spectrometer. Thus all variables for calculating alveolar gas exchange, based on the theory developed by Auchincloss et al. (J. Appl. Physiol. 21: 810-818, 1966), are obtained on a single-breath basis. Mean resting and steady-state exercise gas exchange data are equal to those obtained by conventional open-circuit measurements. Breathing rates up to 30 X min-1 can be followed. The breath-to-breath variability of O2 uptake at the alveolar level is less (25-35%) than that measured at the mouth as the difference between the inspired and expired volumes, both at rest and during exercise up to 0.7 of maximum O2 consumption.

A programmable electrically braked ergometer.

Research protocols require that the actual braking power (Wb) of electrically braked ergometers (EBE) is precisely set at the chosen power level, stable, and universally programmable. No commercially available EBEs appear to meet jointly the above conditions. In fact, EBE settings were found to deviate up to 25% from the reference level (WR), their Wb to drop as a result of increased temperature as much as 30% within 1 h of continuous operation, and the programming features to be limited and rigid. To overcome the above pitfalls a procedure for building or improving EBEs is presented whereby 1) the stator of the brake used as a dynamometer is mounted on ball bearings, the torque being transmitted to a strain gauge; 2) the number of revolutions of the rotor is measured on a cogwheel by a proximity detector and an impulse counter; and 3) the torque and impulse number signals are fed into a low-priced microcomputer controlling the brake's power supply. The device has proved to be satisfactory in following any preprogrammed exercise-forcing functions. In the range approximately 10-500 W, Wb = WR +/- 1%.

Human muscle adaptations to chronic hypoxia.

Maximal aerobic power (V02max) decreases with increasing altitude, the drop being about the same in acute and chronic hypoxia. To elucidate this well established but still rather inexplicable finding, experiments were carried out on a group of participants before and immediately after return from a mountaineering expedition to Mount Lhotse Shar (8398 m). The results of a typical subject exposed over a period of 5 weeks to an altitude of at least 5200 m indicate that: A) In the vastus lateralis muscle the number of capillaries to the number of fibers ratio was unchanged, the mean fiber diameter was reduced from 77.3 to 67.9 mu while the mitochondrial to fiber volume ratio increased from 6.7 to 7.9%; in addition, muscle protein concentration diminished by 37% and succinate dehydrogenase activity (SDH) was 48% less than in control conditions; B) Cardiac output and muscular (vastus lateralis) blood flow at submaximal work loads were reduced by 21% and 53%, respectively; C) The V02 on-response kinetics at the mouth upon rectangular submaximal work loads was delayed (t 1/2 = 37.5 vs. 27.0 s). From the above results it is concluded that the apparent lack of beneficial effects of acclimatization on maximal aerobic power is likely the consequence of the interaction of a number of positive (increased hematocrit, rightward shift of the 02 dissociation curve) and negative (reduced thoracic and peripheral blood flow, decreased muscle mass and oxidative enzymes activity) changes induced by hypoxia.