Hyperbaric bradycardia and hypoventilation in exercising men: effects of ambient pressure and breathing gas.

We sought to determine whether hydrostatic pressure contributed to bradycardia and hypoventilation in hyperbaria. Eight men were studied during exercise at 50, 150, and 250 W while breathing 1) air at 1 bar, 2) helium-oxygen (He-O(2)) at 5.5 bar, 3) sulfur hexafluoride-oxygen (SF(6)-O(2)) at 1.3 bar, and 4) nitrogen-oxygen (N(2)-O(2)) at 5.5 bar. Gas densities were pairwise identical in 1) and 2), and 3) and 4), respectively. Increased hydrostatic pressure to 5.5 bar resulted in a modest but significant relative bradycardia on the order of 6 beats/min, in both the absence [1) vs. 2), P = 0. 0015] and presence [3) vs. 4), P = 0.029] of gases that are both denser than normal and mildly narcotic. In contrast, ventilatory responses appeared not to be influenced by hydrostatic pressure. Also, the combined exposure to increased gas density and mild-to-moderate inert gas narcosis at a given hydrostatic pressure [1) vs. 3), 2) vs. 4)] caused bradycardia (P = 0.032 and 0.061, respectively) of similar magnitude as 5.5-bar hydrostatic pressure. At the same time there was relative hypoventilation at the two higher workloads. We conclude that heart rate control, but not ventilatory control, is sensitive to relatively small increases in hydrostatic pressure.

Significance of airway resistance for the pattern of breathing and lung volumes in exercising humans.

The effects of increased airway resistance on lung volumes and pattern of breathing were studied in eight subjects performing leg exercise on a cycle ergometer. Airway resistance was changed 1) by increasing the density (D) of the respired gas by a factor of 4.2 and changing the inspired gas from O2 at 1.3 bar to air at 6 bar and 2) by increasing airway flow rates by exposing the subjects to incremental work loads of 0-200 W. Increased gas D caused a slower and deeper respiration at rest and during exercise and, at work loads greater than 120 W, depressed the responses of ventilation and mean inspiratory flow. Raised airway resistance induced by increases in D and/or airway flow rates altered respiratory timing by increasing the ratio of inspiratory time (TI) to total breath duration. Furthermore, analyses of the relationships between tidal volume and TI and between end-inspiratory volume and TI revealed elevation of Hering-Breuer inspiratory volume thresholds. We propose that this elevation, and hence exercise-induced increases of tidal volume, can largely be explained by previous observations that the threshold of the inspiratory off-switch mechanisms depends on central inspiratory activity (cf. C. von Euler, J. Appl. Physiol. 55: 1647-1659, 1983), which in turn increases with airway resistance (Acta Physiol. Scand. 120: 557-565, 1984).

Human skeletal muscle function and metabolism during intense exercise at high O2 and N2 pressures.

The maximal contractile force (peak torque) of the quadriceps femoris was studied during 60 repeated unilateral dynamic knee extensions in nine subjects under three different conditions, viz., during air breathing at normal (1 ATA) and raised (6 ATA) ambient pressures and during O2 breathing at 1.3 ATA. In six subjects the electromyographic (EMG) activity of the working muscle was recorded. Muscle biopsies were obtained from the vastus lateralis before, immediately after, and 1 min after exercise. Tissue specimens were subsequently assayed for various muscle metabolites. Peak torque, as an average of the 60 knee extensions, was higher (P less than 0.05) at 1.3 ATA than at 6 or 1 ATA. Peak torque of the exercising muscle declined more rapidly at 1 ATA than at 1.3 ATA, differing in the final 24 contractions by 14%. At 6 ATA peak torque of the initial 12 contractions was 6% lower (P less than 0.05) than at 1 ATA but equaled 1-ATA values in the latter third of the exercise bout. Although the EMG activity at 1 ATA increased relative to that at 6 ATA as exercise proceeded, the rate of force decline was greater at 1 ATA. Despite greater total work produced at 1.3 ATA than at 1 ATA, the metabolic response to exercise was not substantially altered at increased O2 pressure. However, the restitution rate of energy-rich phosphagens and the elimination of lactate during recovery were greater (P less than 0.05) at 1.3 ATA. These results suggest that hyperoxia may enhance the rate of energy release, whereas high N2 pressure and/or high hydrostatic pressure seem to interfere with neuromuscular activity.

Breathing pattern and occlusion pressure during moderate and heavy exercise.

We studied changes in breathing pattern and mouth occlusion pressure (P0.1) in 11 healthy subjects performing graded steady-state exercise on a cycle ergometer up to the maximal load sustainable for 4 min. With increasing work intensity both the tidal volume (VT) and end-inspiratory volume relations to inspiratory (TI) and expiratory (TE) durations were linear in the moderate work load range; in the high load range VT and end-inspiratory volume tended to plateau with further decreases in TI and TE. The ratio of TI to total breath duration (TI/Ttot) increased with work intensity. Intraindividual coefficients of variation for VT, breathing frequency (f), mean inspiratory flow (VT/TI), and other respiratory variables decreased with increasing work intensity, indicating that breath-to-breath variations in breathing pattern became smaller as the level of ventilation increased. P0.1 rose with VT/TI as a power function with an exponent averaging 1.5 (range 1.3-1.9), indicating that the ratio P0.1/(VT/TI), an index of respiratory system impedance, increased with VT/TI and work intensity. We conclude that in moderate and heavy exercise the work of inspiration at a given ventilation is reduced because of the increase in TI/Ttot, the impedance of the respiratory system increases with work intensity because of both an increase in f and a flow-dependent rise in airway resistance, and the neuromuscular inspiratory activity is reflexly augmented because of internal flow-resistive loading.

Role of airway resistance in the control of ventilation during exercise.

To analyze the interdependence of respiratory drive, ventilation and airway resistance during exercise, mouth occlusion pressure (P0.1), minute ventilation (V) and mean inspiratory flow (VT/TI) were studied in eight normal subjects performing cycle-ergometer exercise at loads ranging from 0 W to 200 W under two different ambient conditions: 1) during oxygen breathing at 1.3 ATA, and 2) during air breathing at 6 ATA (PO2 = 1.3 ATA). Comparison of measurements at 6 ATA with those at 1.3 ATA indicated that a 4.2-fold increase in respired gas density (D) had little or no influence on the V and VT/TI responses whereas P0.1 at any given VT/TI was increased by a factor of 1.9. In both conditions, P0.1 increased at a faster rate than VT/TI as the work load increased. At loads higher than 40 W, the relationship between P0.1, D and VT/TI was found to approximate the equation P0.1 = K X D0.5(VT/TI)1.4, where K is a constant that varies among subjects. The results indicate that the ratio P0.1/(VT/TI), an estimate of respiratory impedance, increased with both D and VT/TI. Evidence is presented that the respiratory drive was reflexly enhanced in response to loading as airway resistance increased with D and/or VT/TI. We conclude that neural mechanisms compensating for internal flow-resistive loading play an important role in the control of ventilation during exercise, both at normal and at raised air pressures.

Breathing pattern and lung volumes during exercise.

The interrelationships of ventilation (V), tidal volume (VT), inspiratory (T1), expiratory (TE) and total breath (Ttot) durations, mean inspiratory (VT/TI) and expiratory (VT/TE) flows, and lung volumes were studied in normal subjects at rest and during exercise on a cycle ergometer. The ergometric load was increased by 10 W every minute, from zero W to 200 W. The TI/Ttot ratio increased with V in the range 15 to 60 1 X min-1, indicating that with increasing V the rate of increase of VT/TI decreased whereas that of VT/TE increased. Possible mechanisms responsible for the difference in behaviour of VT/TI and VT/TE are discussed. The VT-TI and VT-TE relationships both displayed three ranges with breakpoints at tidal volumes of about 1.4 and 2.4 1. The relations of TI and TE to end-inspiratory volume were approximately linear over the entire VT range studied, whereas the relations of TI and TE to end-expiratory volume showed three ranges with different characteristics. We conclude that the termination of inspiration during cycle exercise is dependent on volume-related afferent feedback from the lungs and/or chest walls, not only in the high but also in the low volume range.

Ventilatory and occlusion-pressure responses to incremental-load exercise.

Mouth occlusion pressure (P0.1), minute ventilation (V), and mean inspiratory and expiratory flows were studied in eight normal subjects at rest and during exercise on a cycle ergometer, the load of which was increased in steps of 10 W every minute. All four variables rose curvilinearly as the load was increased from 0 to 200 W. The ratio of P0.1 to mean inspiratory flow, like the ratio P0.1/V, increased with work load in the range 40-200 W, indicating that P0.1 increased considerably faster than mean inspiratory flow and V at rates higher than about 0.7 L X sec-1 and 15 L X min-1, respectively. Evidence is presented that the progressive divergence of the P0.1 and ventilatory responses was a result of raised respiratory impedance consequent to increasing respiratory frequency and resistance, and that, concurrently, the respiratory drive as assessed by P0.1 was enhanced because of an active load-compensating response. In this way, the respiratory drive increased with work load in a self-adjusting fashion, compensating for the impedance-dependent alterations in ventilatory responses. We also conclude that in moderate and heavy exercise P0.1 is a more representative index of the respiratory drive than are V and mean inspiratory flow.

Pulmonary mechanisms and work of breathing at maximal ventilation and raised air pressure.

Pulmonary ventilation (V) and the interrelationships of airflow, transpulmonary pressure, and lung volume during inspiration and expiration were studied in eight healthy subjects who performed maximal exercise (MEx; 140% VO2 max), 15-s maximal voluntary ventilation (MVV), and forced inspiratory and expiratory vital capacity (FVC) maneuvers at 1, 3, and 6 ATA. Maximal exercise ventilation and MVV amounted to 149 +/- 7 (mean +/- SE) and 193 +/- 9 l . min-1, respectively, at 1 ATA and were both reduced by approximately 37% at 3 ATA and by 50% at 6 ATA. Expiratory peak flows during MEx and MVV were equal to the maximal flows obtained during FVC at comparable lung volumes, whereas inspiratory peak flows during MEx were 20% less than the FVC flows. Despite a sixfold increase in gas density, the rate of mechanical work of breathing decreased when the pressure was raised to 6 ATA, during MEx from 8 +/- 1 to 6 +/- 1 W, and during MVV from 28 +/- 5 to 18 +/- 3 W. With increasing gas density there was a shift of lung volumes in the inspiratory direction with consequent reductions of inspiratory-to-expiratory flow ratios. We conclude that depletion of energy stores in the inspiratory muscles contributed to limiting V during MEx at raised air pressure.

Responses to continuous negative-pressure breathing in man at rest and during exercise.

We studied the respiratory and circulatory effects in six healthy supine volunteers of continuous negative-pressure breathing (CNPB) at -15 and -30 cmH2O at rest and during dynamic leg exercies at 50% of individual working capacity. CNPB had no significant effects on respiratory minute volume, tidal volume, or arterial carbon dioxide tension. Mean arterial pressure remained essentially unchanged both at rest and during exercise, signifying that the reductions in intrathoracic pressure caused corresponding increases in left ventricular afterload. Nevertheless, cardiac output increased significantly in both conditions, causing reductions of mean central venous pressure that were considerably greater during exercise than at rest. These responses were reflected by increments in left ventricular work, amounting to 24 and 20% at rest and during exercise, respectively, at -30 cmH2O. We conclude that in CNPB at rest the increased activity of the left ventricle with associated juxtathoracic venous collapse protects the right heart and pulmonary circulation from congestion and that it does so even more effectively during exercise.

Combined effects of ethanol and hyperbaric air on body sway and heart rate in man.

Eight amateur divers took part in crossover experiments to study the combined effects of ethanol (0.72 g/kg b.wt.) and hyperbaric air (4 and 6 ATA) on heart rate and body-sway movements. Body sway with open and closed eyes was measured in lateral and sagittal directions by a statometer device. In the alcohol condition, there was an initial increase in body sway corresponding to the acute phase of ethanol intoxication. At a mean blood alcohol concentration of 0.77 mg/ml, this increase in body sway was statistically significant (P less than 0.01) compared with the alcohol-free condition. At 90 min from start of drinking, body sway scores at 1 ATA were not significantly different from alcohol-free measurements. On raising the pressure to 4 and 6 ATA, increased body sway occurred in both alcohol and alcohol-free conditions and, moreover, the rate of increase was more extreme in the alcohol condition. Significant pressure-alcohol interactions were established, suggesting a potentiating action of alcohol on the increase in body sway induced by acute exposure to high pressures of air. Heart-rate measurements with and without alcohol were not significantly different, although increases in ambient pressure caused a drop in heart rate in both conditions.

Respiratory and circulatory responses to sustained positive-pressure breathing and exercise in man.

To investigate the effects of sustained positive-pressure breathing (PPB) on the adaptation of respiratory and circulatory functions to exercise, 8 healthy volunteers were exposed to PPB of air at 15 and 30 cm H2O in the supine position at rest and while performing leg exercise at 50% of individual maximal working capacity. PPB was both subjectively and objectively better tolerated when combined with exercise than it was at rest. PPB at 30 cm H2O resulted in marked hyperventilation with alkalosis in the resting condition, but did not significantly affect respiratory minute volume, blood gases or acid-base balance during exercise. Cardiac output and left ventricular work were reduced by about one fifth and one third, respectively, both at rest and during exercise. In contrast to the case at normal airway pressure, exercise-induced increase in cardiac output was accompanied by an increment in stroke volume during PPB. Although mean arterial pressure (relative to atmospheric) was elevated by PPB at rest and during exercise, the driving pressure in systemic circuits (arterial minus central venous pressure) was reduced in both conditions. It is concluded that dynamic exercise counteracts deleterious effects of PPB by normalizing respiratory function and by improving cardiac filling by activation of the leg muscle and the abdominal pumps.

Roles of nitrogen, oxygen, and carbon dioxide in compressed-air narcosis.

In an attempt to determine the roles of nitrogen, oxygen, and carbon dioxide in compressed-air narcosis, the effects on performance (mental function and manual dexterity) of adding CO2 in various concentrations to the inspired gas under three different conditions were studied in eight healthy male volunteers. The three conditions were: (1) air breathing at 1.3 ATA; (2) oxygen breathing at 1.7 ATA; and (3) air breathing at 8.0 ATA (same inspired O2 pressure as in (2)). By relating performance to the changes induced in end-tidal (alveolar) gas pressures, and comparing the data from the three conditions, we arrived at the following results and conclusions. A rise in O2 pressure to 1.65 ATA, or in N2 pressure to 6.3 ATA at a constant high PO2 level, caused a significant decrement of 10% in mental function but no consistent effect on psychomotor function. A rise in end-tidal PCO2 of 10 mmHg caused an impairment of approximately 10% in both mental and psychomotor functions. The results suggest that, at raised partial pressures, all three gases have narcotic properties, and that the mechanism of CO2 narcosis differs fundamentally from that of N2 and O2 narcosis.

Dissociated ventilatory and central respiratory responses to CO2 at raised N2 pressure.

The effects of hyberbaric nitrogen on the responses of ventilation and central inspiratory activity (CIA) to progressive hypercapnia were studied in eight subjects rebreathing a) O2 at an ambient pressure of 1.3 bar (control), and b) air at 6.1 bar (PO2 = 1.3 bar, PN2 = 4.8 bar). Inspiratory occlusion pressure (P0.1), pulmonary ventilation, and end-tidal PCO2 were used for the computation of individual CIA and ventilatory CO2 response curves. Increasing the inspired PN2 to 4.8 bar caused, on the average, a 40% increase of P0.1 at PCO2 = 50 Torr, whereas the slope of the ventilatory CO2 response curve was reduced by 39%. It was concluded that, at raised air and nitrogen pressures, CIA is increased, although not sufficiently to prevent a reduction of ventilation brought about by the increased gas density and consequent increase in airway resistance. The increased airway resistance is thought to be responsible for the increase in CIA by causing a reflex stimulation of the respiratory centers.

Cardiorespiratory and metabolic responses to positive, negative and minimum-load dynamic leg exercise.

Cardiorespiratory and metabolic responses to steady-state dynamic leg exercise were studied in seven male subjects who performed positive and negative work on a modified Krogh cycle ergometer at loads of 0, 16, 33, 49, 98, and 147 W with a pedalling rate of 60 rpm. In positive work, O2 uptake increased with the ergometric load in a parabolic fashion. Net O2 uptake averaged averaged 220 ml-min-1 at 0 W (loadless pedalling), and was 75 ml-min-1 lower at the point of physiological minimum load which occurred in negative work at approximately 9 W. The O2 cost of loadless pedalling is for one-third attributed to the work of overcoming elastic and viscous resistance, the remaining part being due mainly to the work of antagonistic muscle contraction in the moving legs. Although at a given VO2, work rate was much higher in negative than in positive work, corresponding values for VE were similar, suggesting that the mechanical tension in working muscles is of little or no importance in the control of ventilation in steady-state exercise. Heart rate increased linearly with VO2 in both positive and negative work, with a steeper slope in negative work. Evidence is presented that none of the current definitions of muscular efficiency yields the true efficiency of muscular contraction in cycle ergometry, net efficiency calculation resulting in too low estimates, and work and delta efficiency calculations in overestimated values in the low-intensity work range, and in underestimated values in the high-intensity range.

Cardiorespiratory and metabolic costs of continuous and intermittent exercise in man.

1. Cardiorespiratory and metabolic responses to paired patterns of continuous and intermittent exercise with the same average power output were studied in eight men. Heart rate, ventilation and pulmonary gas exchange were measured during the different patterns of exercise performed on a cycle ergometer. The recovery oxygen volume was measured over 30 min of loadless pedalling. Needle biopsy samples of the vastus lateralis muscle were taken before, during and after completion of the exercise for measurement of muscle metabolites.2. Heart rate, ventilation, oxygen intake, respiratory exchange ratio, and blood lactate concentration were generally higher with intermittent compared with continuous exercise as were the accumulated totals for heart beats, ventilation and oxygen intake. Muscle biopsy samples tended to have higher lactate and lower phosphocreatine contents in intermittent exercise. The lactate concentration in muscle and blood water was the same during loadless pedalling before exercise but was significantly higher in muscle than blood during exercise. This concentration gradient was larger in intermittent than in continuous exercise.3. Work efficiency, calculated from the total oxygen cost of work in excess of a loadless pedalling control, was significantly lower in intermittent exercise. The explanation is thought to be connected with the observation that when the work was performed at a high rate in short bursts a large part of the oxidative recovery took place after the contraction during the rest periods, whereas in the low intensity continuous exercise the oxygen was mainly utilized while the work was being performed. This indicates that for part of the time in the intermittent exercise the muscle was working under anaerobic conditions. Although the possibility exists that the efficiency of resynthesis of phosphagen may be reduced in this form of activity, it is more likely that the result described is due to the greater amount of lactate formed in the intermittent exercise.