Oxygen cost of exercise hyperpnea: implications for performance.

We addressed two questions concerned with the metabolic cost and performance of respiratory muscles in healthy young subjects during exercise: 1) does exercise hyperpnea ever attain a "critical useful level"? and 2) is the work of breathing (WV) at maximum O2 uptake (VO2max) fatiguing to the respiratory muscles? During progressive exercise to maximum, we measured tidal expiratory flow-volume and transpulmonary pressure- (Ptp) volume loops. At rest, subjects mimicked their maximum and moderate exercise Ptp-volume loops, and we measured the O2 cost of the hyperpnea (VO2RM) and the length of time subjects could maintain reproduction of their maximum exercise loop. At maximum exercise, the O2 cost of ventilation (VE) averaged 10 +/- 0.7% of the VO2max. In subjects who used most of their maximum reserve for expiratory flow and for inspiratory muscle pressure development during maximum exercise, the VO2RM required 13-15% of VO2max. The O2 cost of increasing VE from one work rate to the next rose from 8% of the increase in total body VO2 (VO2T) during moderate exercise to 39 +/- 10% in the transition from heavy to maximum exercise; but in only one case of extreme hyperventilation, combined with a plateauing of the VO2T, did the increase in VO2RM equal the increase in VO2T. All subjects were able to voluntarily mimic maximum exercise WV for 3-10 times longer than the duration of the maximum exercise. We conclude that the O2 cost of exercise hyperpnea is a significant fraction of the total VO2max but is not sufficient to cause a critical level of "useful" hyperpnea to be achieved in healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanical constraints on exercise hyperpnea in endurance athletes.

We determined how close highly trained athletes [n = 8; maximal oxygen consumption (VO2max) = 73 +/- 1 ml.kg-1.min-1] came to their mechanical limits for generating expiratory airflow and inspiratory pleural pressure during maximal short-term exercise. Mechanical limits to expiratory flow were assessed at rest by measuring, over a range of lung volumes, the pleural pressures beyond which no further increases in flow rate are observed (Pmaxe). The capacity to generate inspiratory pressure (Pcapi) was also measured at rest over a range of lung volumes and flow rates. During progressive exercise, tidal pleural pressure-volume loops were measured and plotted relative to Pmaxe and Pcapi at the measured end-expiratory lung volume. During maximal exercise, expiratory flow limitation was reached over 27-76% of tidal volume, peak tidal inspiratory pressure reached an average of 89% of Pcapi, and end-inspiratory lung volume averaged 86% of total lung capacity. Mechanical limits to ventilation (VE) were generally reached coincident with the achievement of VO2max; the greater the ventilatory response, the greater was the degree of mechanical limitation. Mean arterial blood gases measured during maximal exercise showed a moderate hyperventilation (arterial PCO2 = 35.8 Torr, alveolar PO2 = 110 Torr), a widened alveolar-to-arterial gas pressure difference (32 Torr), and variable degrees of hypoxemia (arterial PO2 = 78 Torr, range 65-83 Torr). Increasing the stimulus to breathe during maximal exercise by inducing either hypercapnia (end-tidal PCO2 = 65 Torr) or hypoxemia (saturation = 75%) failed to increase VE, inspiratory pressure, or expiratory pressure. We conclude that during maximal exercise, highly trained individuals often reach the mechanical limits of the lung and respiratory muscle for producing alveolar ventilation. This level of ventilation is achieved at a considerable metabolic cost but with a mechanically optimal pattern of breathing and respiratory muscle recruitment and without sacrifice of a significant alveolar hyperventilation.     

Smaller lungs in women affect exercise hyperpnea

We subjected 29 healthy young women (age: 27 ± 1 yr) with a wide range of fitness levels [maximal oxygenuptake (O_{2 max}): 57 ± 6 ml · kg¹ · min¹;35-70ml · kg¹ · min¹]to a progressive treadmill running test. Our subjects had significantly smaller lung volumes and lower maximal expiratory flow rates, irrespective of fitness level, compared with predicted values for age-and height-matched men. The higher maximal workload in highly fit(O_{2 max} > 57 ml · kg¹ · min¹,n = 14) vs. less-fit(O_{2 max} < 56 ml · kg¹ · min¹,n = 15) women caused a higher maximalventilation (E) with increased tidal volume (VT)and breathing frequency (f_b) atcomparable maximal VT/vitalcapacity (VC). More expiratory flow limitation (EFL; 22 ± 4% ofVT) was also observed duringheavy exercise in highly fit vs. less-fit women, causing higherend-expiratory and end-inspiratory lung volumes and greater usage oftheir maximum available ventilatory reserves.HeO₂ (79% He-21%O₂) vs. room air exercise trialswere compared (with screens added to equalize external apparatusresistance). HeO₂ increasedmaximal expiratory flow rates (20-38%) throughout the range ofVC, which significantly reduced EFL during heavy exercise. When EFL wasreduced with HeO₂, VT,f_b, andE (+16 ± 2 l/min) weresignificantly increased during maximal exercise. However, in theabsence of EFL (during room air exercise),HeO₂ had no effect onE. We conclude that smaller lungvolumes and maximal flow rates for women in general, and especiallyhighly fit women, caused increased prevalence of EFL during heavyexercise, a relative hyperinflation, an increased reliance onf_b, and a greater encroachment onthe ventilatory "reserve." Consequently,VT andE are mechanically constrained duringmaximal exercise in many fit women because the demand for highexpiratory flow rates encroaches on the airways' maximum flow-volumeenvelope.

     

Independence of exercise hyperpnea and acidosis during high-intensity exercise in ponies

We investigated arterial PCO2 (PaCO2) and pH (pHa) responses in ponies during 6-min periods of high-intensity treadmill exercise. Seven normal, seven carotid body-denervated (2 wk-4 yr) (CBD), and five chronic (1-2 yr) lung (hilar nerve)-denervated (HND) ponies were studied during three levels of constant load exercise (7 mph-11%, 7 mph-16%, and 7 mph-22% grade). Mean pHa for each group of ponies became alkaline in the first 60 s (between 7.45 and 7.52) (P less than 0.05) at all work loads. At 6 min pHa was at or above rest at 7 mph-11%, moderately acidic at 7 mph-16% (7.32-7.35), and markedly acidic at 7 mph-22% (7.20-7.27) for all groups of ponies. Yet with no arterial acidosis at 7 mph 11%, normal ponies decreased PaCO2 below rest (delta PaCO2) by 5.9 Torr at 90 s and 7.8 Torr by 6 min of exercise (P less than 0.05). With a progressively more acid pHa at the two higher work loads in normal ponies, delta PaCO2 was 7.3 and 7.8 Torr by 90 s and 9.9 and 11.4 Torr by 6 min, respectively (P less than 0.05). CBD ponies became more hypocapnic than the normal group at 90 s (P less than 0.01) and tended to have greater delta PaCO2 at 6 min. The delta PaCO2 responses in normal and HND ponies were not significantly different (P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Control of exercise hyperpnea during hypercapnia in humans

Previous studies have yielded conflicting results on the ventilatory response to CO2 during muscular exercise. To obviate possible experimental errors contributing to such variability, we have examined the CO2-exercise interaction in terms of the ventilatory response to exercise under conditions of controlled hypercapnia. Eight healthy male volunteers underwent a sequence of 5-min incremental treadmill exercise runs from rest up to a maximum CO2 output (VCO2) of approximately 1.5 l . min-1 in four successive steps. The arterial PCO2 (PaCO2) at rest was stabilized at the control level or up to 14 Torr above control by adding 0-6% CO2 to the inspired air. Arterial isocapnia (SD = 1.2 Torr) throughout each exercise run was maintained by continual adjustment of the inspired PCO2. At all PaCO2 levels the response in total ventilation (VE) was linearly related to exercise VCO2. Hypercapnia resulted in corresponding increases in both the slope (S) and zero intercept (V0) of the VE-VCO2 curve; these being directly proportional to the rise in PaCO2 (means +/- SE: delta S/ delta PaCO2, 2.73 +/- 0.28 Torr-1; delta V0/ delta PaCO2, 1.67 +/- 0.18 l . min-1 . Torr-1). Thus the ventilatory response to concomitant hypercapnia and exercise was characterized by a synergistic (additive plus multiplicative) effect, suggesting a positive interaction between these stimuli. The increased exercise sensitivity in hypercapnia is qualitatively consistent with the hypothesis that VE is controlled to minimize the conflicting challenges due to chemical drive and the mechanical work of breathing (Poon, C. S. In: Modelling and Control of Breathing, New York: Elsevier, 1983, p. 189-196).     

Role of hilar nerve afferents in hyperpnea of exercise

The objective of this study was to determine the role of hilar nerve (lung vagal) afferents in the hyperpnea of exercise. Ten ponies were studied before and 2-4 wk and 3-12 mo after sectioning only the hilar branches of the vagus nerves (HND). After HND, lung volume feedback to the medullary centers was attenuated as indicated in the anesthetized state by 1) attenuation or absence of the Hering-Breuer inflation reflex (P less than 0.01) and 2) attenuation of the lengthened inspiratory time (TI) when the airway was occluded at end expiration (P less than 0.01). Moreover, after HND in the awake state, there was an increase in the ratio of TI to total cycle time (P less than 0.01). These changes verify a compromise in lung innervation comparable to cervical vagotomy. Resting arterial PCO2, PO2, and pH were not altered following HND (P greater than 0.10). Moreover, at three levels of mild and moderate treadmill exercise, no difference in either the temporal pattern or the absolute levels of arterial blood gases and arterial pH was found between pre- and post-HND studies (P greater than 0.10). In addition, minute ventilation (VE) at rest and during exercise was not altered by HND (P greater than 0.10). However, 2-4 wk after HND the increase in breathing frequency (f) during exercise was less, whereas the increase in tidal volume during exercise was greater than pre-HND (P less than 0.05). The reduced f was due to an increase in TI with no change in expiratory time. We conclude that lung afferents via the hilar nerves influence the pattern of breathing at rest and during exercise in ponies.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of hyperthermic hyperpnea elicited during rest and submaximal, moderate-intensity exercise.

We tested the hypothesis that, in humans, hyperthermic hyperpnea elicited in resting subjects differs from that elicited during submaximal, moderate-intensity exercise. In the rest trial, hot-water legs-only immersion and a water-perfused suit were used to increase esophageal temperature (T(es)) in 19 healthy male subjects; in the exercise trial, T(es) was increased by prolonged submaximal cycling [50% peak O(2) uptake (Vo(2))] in the heat (35 degrees C). Minute ventilation (Ve), ventilatory equivalent for Vo(2) (Ve/Vo(2)) and CO(2) output (Ve/Vco(2)), tidal volume (Vt), and respiratory frequency (f) were plotted as functions of T(es). In the exercise trial, Ve increased linearly with increases (from 37.0 to 38.7 degrees C) in T(es) in all subjects; in the rest trial, 14 of the 19 subjects showed a T(es) threshold for hyperpnea (37.8 +/- 0.5 degrees C). Above the threshold for hyperpnea, the slope of the regression line relating Ve and T(es) was significantly greater for the rest than the exercise trial. Moreover, the slopes of the regression lines relating Ve/Vo(2), Ve/Vco(2), and T(es) were significantly greater for the rest than the exercise trial. The increase in Ve reflected increases in Vt and f in the rest trial, but only f in the exercise trial, after an initial increase in ventilation due to Vt. Finally, the slope of the regression line relating T(es) and Vt or f was significantly greater for the rest than the exercise trial. These findings indicate that hyperthermic hyperpnea does indeed differ, depending on whether one is at rest or exercising at submaximal, moderate intensity.     

Oxygen cost of dynamic or isometric exercise relative to recruited muscle mass

Background

Oxygen cost of different muscle actions may be influenced by different recruitment and rate coding strategies. The purpose of this study was to account for these strategies by comparing the oxygen cost of dynamic and isometric muscle actions relative to the muscle mass recruited via surface electrical stimulation of the knee extensors.

Methods

Comparisons of whole body pulmonary Δ $\dot{V}$O₂ were made in seven young healthy adults (1 female) during 3 minutes of dynamic or isometric knee extensions, both induced by surface electrical stimulation. Recruited mass was quantified in T₂ weighted spin echo magnetic resonance images.

Results

The Δ $\dot{V}$O₂ for dynamic muscle actions, 242 ± 128 ml ? min^-1 (mean ± SD) was greater (p = 0.003) than that for isometric actions, 143 ± 99 ml ? min^-1. Recruited muscle mass was also greater (p = 0.004) for dynamic exercise, 0.716 ± 282 versus 0.483 ± 0.139 kg. The rate of oxygen consumption per unit of recruited muscle (${\dot{V}\text{O}}_{2^{\text{RM}}}$) was similar in dynamic and isometric exercise (346 ± 162 versus 307 ± 198 ml ? kg^-1 ? min^-1; p = 0.352), but the ${\dot{V}\text{O}}_{2^{\text{RM}}}$ calculated relative to initial knee extensor torque was significantly greater during dynamic exercise 5.1 ± 1.5 versus 3.6 ± 1.6 ml ? kg^-1 ? Nm^-1 ? min^-1 (p = 0.019).

Conclusion

These results are consistent with the view that oxygen cost of dynamic and isometric actions is determined by different circumstances of mechanical interaction between actin and myosin in the sarcomere, and that muscle recruitment has only a minor role.

     

Inspiratory muscle training lowers the oxygen cost of voluntary hyperpnea

The purpose of this study was to determine if inspiratory muscle training (IMT) alters the oxygen cost of breathing (Vo(2RM)) during voluntary hyperpnea. Sixteen male cyclists completed 6 wk of IMT using an inspiratory load of 50% (IMT) or 15% placebo (CON) of maximal inspiratory pressure (Pi(max)). Prior to training, a maximal incremental cycle ergometer test was performed to determine Vo(2) and ventilation (V(E)) at multiple workloads. Pre- and post-training, subjects performed three separate 4-min bouts of voluntary eucapnic hyperpnea (mimic), matching V(E) that occurred at 50, 75, and 100% of Vo(2 max). Pi(max) was significantly increased (P < 0.05) by 22.5 ± 8.7% from pre- to post-IMT and remained unchanged in the CON group. The Vo(2RM) required during the mimic trial corresponded to 5.1 ± 2.5, 5.7 ± 1.4, and 11.7% ± 2.5% of the total Vo(2) (Vo(2T)) at ventilatory workloads equivalent to 50, 75, and 100% of Vo(2 max), respectively. Following IMT, the Vo(2RM) requirement significantly decreased (P < 0.05) by 1.5% (4.2 ± 1.4% of Vo(2T)) at 75% Vo(2 max) and 3.4% (8.1 ± 3.5% of Vo(2T)) at 100% Vo(2 max). No significant changes were shown in the CON group. IMT significantly reduced the O(2) cost of voluntary hyperpnea, which suggests that a reduction in the O(2) requirement of the respiratory muscles following a period of IMT may facilitate increased O(2) availability to the active muscles during exercise. These data suggest that IMT may reduce the O(2) cost of ventilation during exercise, providing an insight into mechanism(s) underpinning the reported improvements in whole body endurance performance; however, this awaits further investigation.     

Role of neural afferents from working limbs in exercise hyperpnea

To determine the role of reflex discharge of afferent nerves from the working limbs in the exercise hyperpnea, 1.5- to 2.5-min periods of phasic hindlimb muscle contraction were induced in anesthetized cats by bilateral electrical stimulation of ventral roots L7, S1, and S2. Expired minute ventilation (VE) and end-tidal PCO2 (PETCO2) were computed breath by breath, and mean arterial PCO2 (PaCO2) was determined from discrete blood samples and, also in most animals, by continuous measurement with an indwelling PCO2 electrode. During exercise VE rose progressively with a half time averaging approximately 30 s, but a large abrupt increase in breathing at exercise onset typically did not occur. Mean PaCO2 and PETCO2 remained within approximately 1 Torr of control levels across the work-exercise transition, and PaCO2 was regulated at an isocapnic level after VE had achieved its peak value. Sectioning the spinal cord at L1-L2 did not alter these response characteristics. Thus, reflex discharge of afferent nerves from the exercising limbs was not requisite for the matching of ventilation to metabolic demand during exercise.     

Oxygen cost of inspiratory loading: resistive vs. elastic

We measured the O2 cost of breathing (VO2resp) against external inspiratory elastic (E) and resistive loads (R) when end-expiratory lung volume, tidal volume, breathing frequency, work rate, and pressure-time product were matched in each of six pairs of runs in six subjects. During E, peak inspiratory mouth pressure was 65.7 +/- 1.8% (SD) of the maximum at functional residual capacity. However, during resistive runs, peak inspiratory mouth pressure was 41.1 +/- 2.8% of the maximum at functional residual capacity. In 36 paired runs, where both work rate and pressure-time product were within 10%, VO2resp for E was less than for R (81 and 96 ml/min, respectively; P less than 0.01). During loaded and unloaded breathing with the same tidal volume, we measured the changes in anteroposterior diameter of the lower rib cage in five subjects. In four subjects we also recorded the electromyograms of several fixator and stabilizing muscles. During E and R, the change in anteroposterior diameter of the lower rib cage was -116 +/- 5 and -45 +/- 4% (SE), respectively, of the unloaded value (P less than 0.01), indicating greater deformation during E. Although the peak electromyographic activity was 72 +/- 16% greater during E (P less than 0.01), there was no difference between the loads for area under the electromyogram time curve (P greater than 0.05). However, the time to 50% peak activity was less during R (P less than 0.02). We conclude that, even when work rate and pressure-time product are matched, VO2resp during R is greater than that during E. This difference may be due to preferential recruitment of faster and less efficient muscle fibers.