Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep.

We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the gender difference in the sleep apnea/hypopnea syndrome. We studied eight men (age 25-35 yr) and eight women in the midluteal phase of the menstrual cycle (age 21-43 yr); we repeated studies in six women during the midfollicular phase. Hypocapnia was induced via nasal mechanical ventilation for 3 min, with respiratory frequency matched to eupneic frequency. Tidal volume (VT) was increased between 110 and 200% of eupneic control. Cessation of mechanical ventilation resulted in hypocapnic central apnea or hypopnea, depending on the magnitude of hypocapnia. Nadir minute ventilation in the recovery period was plotted against the change in end-tidal PCO(2) (PET(CO(2))) per trial; minute ventilation was given a value of 0 during central apnea. The apneic threshold was defined as the x-intercept of the linear regression line. In women, induction of a central apnea required an increase in VT to 155 +/- 29% (mean +/- SD) and a reduction of PET(CO(2)) by -4.72 +/- 0.57 Torr. In men, induction of a central apnea required an increase in VT to 142 +/- 13% and a reduction of PET(CO(2)) by -3.54 +/- 0.31 Torr (P = 0.002). There was no difference in the apneic threshold between the follicular and the luteal phase in women. Premenopausal women are less susceptible to hypocapnic disfacilitation during NREM sleep than men. This effect was not explained by progesterone. Preservation of ventilatory motor output during hypocapnia may explain the gender difference in sleep apnea.

Airway obstruction during exercise and isocapnic hyperventilation in asthmatic subjects.

We compared pulmonary mechanics measured during long-term exercise (LTX = 20 min) with long-term isocapnic hyperventilation (LTIH = 20 min) in the same asthmatic individuals (n = 6). Peak expiratory flow (PEF) and forced expiratory volume in 1 s (FEV(1)) decreased during LTX (-19.7 and -22.0%, respectively) and during LTIH (-6.66 and 10. 9%, respectively). In contrast, inspiratory pulmonary resistance (RL(I)) was elevated during LTX (57.6%) but not during LTIH (9.62%). As expected, airway function deteriorated post-LTX and post-LTIH (FEV(1) = -30.2 and -21.2%; RL(I) = 111.8 and 86.5%, respectively). We conclude that the degree of airway obstruction observed during LTX is of a greater magnitude than that observed during LTIH. Both modes of hyperpnea induced similar levels of airway obstruction in the posthyperpnea period. However, the greater airway obstruction during LTX suggests that a different process may be responsible for the changes in airway function during and after the two modes of hyperpnea. This finding raises questions about the equivalency of LTIH and LTX in the study of airway function during exercise-induced asthma.

The effect of rapid eye movement (REM) sleep on upper airway mechanics in normal human subjects.

1. It has been proposed that the upper airway is more compliant during rapid eye movement (REM) sleep than during non-rapid eye movement (NREM) sleep. The purpose of this study was to test this hypothesis in a group of subjects without sleep-disordered breathing. 2. On the first night, the effect of sleep stage on the relationship of retropalatal cross-sectional area (CSA; visualized with a fibre-optic scope) to pharyngeal pressure (PPH) measured at the soft palate during eupnoeic breathing was studied. Breaths during REM sleep were divided into phasic (associated with eye movements) and tonic (not associated with eye movements). There was a significant decrease in pharyngeal CSA during NREM sleep compared with wakefulness. There was no further decrease observed during either tonic or phasic REM sleep. Pharyngeal compliance, defined as the slope of the regression CSA versus PPH, was significantly increased during NREM sleep compared with wakefulness and REM sleep, with the compliance during both tonic and phasic REM sleep being similar to that observed in wakefulness. 3. On the second night, the effect of sleep stage on pressure-flow relationships of the upper airway was investigated. There was a trend towards the upper airway resistance being highest in NREM sleep compared with wakefulness and REM sleep. 4. We conclude that the upper airway is stiffer and less compliant during REM sleep than during NREM sleep. We postulate that this difference is secondary to differences in upper airway vascular perfusion between REM and NREM sleep.

High frequency diaphragmatic fatigue detected with paired stimuli in humans.

PURPOSE: The purpose of this study was to determine whether high frequency fatigue was present in the diaphragm after intense whole body endurance exercise. METHODS: We used bilateral phrenic nerve stimulation (BPNS) before and during recovery from whole body exercise to detect fatigue in the diaphragm. To detect high frequency fatigue we used paired stimuli at 10, 20, 50, 70, and 100 Hz frequency and determined the transdiaphragmatic pressure (Pdi) response to the second stimulation (T2). RESULTS: The subjects (N = 10) exercised at 93.3 +/- 2.3% of their VO2max for 9.9 +/- 0.5 min. The Pdi response to "twitch" and 10 Hz "tetanic" stimulation was decreased immediately after exercise versus pre-exercise values (-23.4 +/- 3.3%). The T2 amplitude was substantially reduced at all frequencies immediately after exercise (-28.0%), but by 30 min into recovery the T2 amplitude at 70 and 100 Hz was not different from pre-exercise values. In contrast, at 10 and 20 Hz the T2 response was still significantly reduced. CONCLUSIONS: We interpret these data to mean that high frequency fatigue as well as low frequency fatigue were present in the diaphragm after intense whole body endurance exercise.

Long-term facilitation of ventilation in humans during NREM sleep.

The purpose of this study was to determine whether episodic hypoxic exposure would elicit long term facilitation (LTF) of ventilation (V(I)) in sleeping humans. Twenty subjects gave written informed consent. Of these, six subjects were unable to maintain stable stage 2 sleep or deeper for a majority of the experiment and their data were excluded from the analysis. On night 1 after subjects had reached stable sleep (stage 2 or deeper), the subjects breathed room air for 5 minutes, followed by 3 minutes of hypoxia (F(I)O2 = 8%). This sequence was repeated 10 times, and the breathing pattern was observed for a further 60 minutes. Subjects returned to the laboratory for a second visit, which served as a sham night. Instrumentation and study time were the same as on night 1, but subjects breathed room air only. Airflow, tidal volume (V(T)), end tidal O2 and CO2, and estimation of arterial O2 saturation (%) were measured. Seven of the subjects had long-term facilitation (LTF), which was manifested as a significant increase in V(I) that persisted for up to 40 minutes following the last hypoxic exposure. In the other seven subjects, no substantial increase in V(I) was found. We could not explain this difference based on body size (BMI), gender, level of hypoxemia, or magnitude of the hyperpnea during hypoxia. The difference between the two groups was that the LTF group consisted of habitual snorers, and that the NLTF were not inspiratory-flow-limited during the experiment.

Effect of induced hypocapnic hypopnea on upper airway patency in humans during NREM sleep.

We wished to determine the effect of reduced ventilatory drive (hypopnea) on upper airway patency in humans during non-rapid-eye-movement (NREM) sleep. We studied nine subjects (58 trials) spanning the spectrum of susceptibility to upper airway collapse including normals, snorers and patients with mild sleep apnea. Hypocapnic hypopnea was induced by abrupt cessation of brief (1 min) nasal mechanical hyperventilation. Surface inspiratory EMG (EMGinsp) was used as an index of drive. Upper airway resistance and supraglottic pressure-flow plots were used as indexes of upper airway patency. Termination of nasal mechanical ventilation resulted in reduced VE to 4904 of pre-mechanical ventilation eupneic control. Upper airway resistance at a fixed flow did not change significantly in inspiration or expiration. Likewise, pressure-flow plots showed no increase in upper airway resistance except in one subject. However, maximum flow (Vmax) decreased during hypopnea in four subjects who demonstrated inspiratory flow-limitation (IFL) during eupneic control. In contrast, no IFL was noted in subjects who showed no evidence of IFL during eupnea. We concluded: (1) Reduced ventilatory drive does not compromise upper airway patency in normal subjects during NREM sleep; (2) the reduction in Vmax during hypopnea in subjects with IFL during eupneic control, suggests that reduced drive is associated with increased upper airway compliance in these subjects; and (3) upper airway susceptibility to narrowing/closure is an important determinant of the response to induced hypopnea during NREM sleep.

Respiratory muscle work compromises leg blood flow during maximal exercise.

We hypothesized that during exercise at maximal O2 consumption (VO2max), high demand for respiratory muscle blood flow (Q) would elicit locomotor muscle vasoconstriction and compromise limb Q. Seven male cyclists (VO2max 64 +/- 6 ml.kg-1.min-1) each completed 14 exercise bouts of 2.5-min duration at VO2max on a cycle ergometer during two testing sessions. Inspiratory muscle work was either 1) reduced via a proportional-assist ventilator, 2) increased via graded resistive loads, or 3) was not manipulated (control). Arterial (brachial) and venous (femoral) blood samples, arterial blood pressure, leg Q (Qlegs; thermodilution), esophageal pressure, and O2 consumption (VO2) were measured. Within each subject and across all subjects, at constant maximal work rate, significant correlations existed (r = 0.74-0.90; P < 0.05) between work of breathing (Wb) and Qlegs (inverse), leg vascular resistance (LVR), and leg VO2 (VO2legs; inverse), and between LVR and norepinephrine spillover. Mean arterial pressure did not change with changes in Wb nor did tidal volume or minute ventilation. For a +/-50% change from control in Wb, Qlegs changed 2 l/min or 11% of control, LVR changed 13% of control, and O2 extraction did not change; thus VO2legs changed 0.4 l/min or 10% of control. Total VO2max was unchanged with loading but fell 9.3% with unloading; thus VO2legs as a percentage of total VO2max was 81% in control, increased to 89% with respiratory muscle unloading, and decreased to 71% with respiratory muscle loading. We conclude that Wb normally incurred during maximal exercise causes vasoconstriction in locomotor muscles and compromises locomotor muscle perfusion and VO2.

Aerobic fitness effects on exercise-induced low-frequency diaphragm fatigue.

We used bilateral phrenic nerve stimulation (BPNS; at 1, 10, and 20 Hz at functional residual capacity) to compare the amount of exercise-induced diaphragm fatigue between two groups of healthy subjects, a high-fit group [maximal O2 consumption (VO2max) = 69.0 +/- 1.8 ml.kg-1.min-1, n = 11] and a fit group (VO2max = 50.4 +/- 1.7 ml.kg-1.min-1, n = 13). Both groups exercised at 88-92% VO2max for about the same duration (15.2 +/- 1.7 and 17.9 +/- 2.6 min for high-fit and fit subjects, respectively, P > 0.05). The supramaximal BPNS test showed a significant reduction (P < 0.01) in the BPNS transdiaphragmatic pressure (Pdi) immediately after exercise of -23.1 +/- 3.1% for the high-fit group and -23.1 +/- 3.8% (P > 0.05) for the fit group. Recovery of the BPNS Pdi took 60 min in both groups. The high-fit group exercised at a higher absolute workload, which resulted in a higher CO2 production (+26%), a greater ventilatory demand (+16%) throughout the exercise, and an increased diaphragm force output (+28%) over the initial 60% of the exercise period. Thereafter, diaphragm force output declined, despite a rising minute ventilation, and it was not different between most of the high-fit and fit subjects. In summary, the high-fit subjects showed diaphragm fatigue as a result of heavy endurance exercise but were also partially protected from excessive fatigue, despite high ventilatory requirements, because their hyperventilatory response to endurance exercise was reduced, their diaphragm was utilized less in providing the total ventilatory response, and possibly their diaphragm aerobic capacity was greater.

Respiratory muscle fatigue during exercise: implications for performance.

Heavy whole-body exercise, requiring a 10- to 15-fold increase in minute ventilation, encroaches on the capacities of the respiratory muscle system to respond. Recently, using the technique of bilateral phrenic nerve stimulation, it has been shown that heavy endurance exercise (> 85% of VO2max) lasting > 8-10 min causes diaphragmatic fatigue (15-30% reduction in transdiaphragmatic pressures when electrically stimulated at low frequencies [1-20 Hz] supramaximally). The fatigue appears to be due to an interaction of diaphragmatic work (i.e., pressure production) combined with effects related to exercise intensity (i.e., increased blood flow competition with the locomotor muscles and increased production of metabolic by-products) and requires > 60 min for recovery. Fitness (i.e., as implied from VO2max) appears to allow greater diaphragmatic work for a similar degree of fatigue. Unloading the respiratory muscles (with helium/oxygen gas or using a pressure-assist device) during heavy exercise < 90-95% of VO2max does not appear to alter exercise time, VO2max, or minute ventilation, implying that respiratory muscle fatigue plays little role in altering human performance at these work intensities. However, unloading the respiratory system with helium at work intensities > 90-95% of VO2max has been shown to improve exercise time. This would imply that respiratory muscle fatigue may play a role in limiting human performance at the extremes of human performance or that other factors related to the respiratory system (i.e., alterations in the sensation of dyspnea or mechanical load) may play an important role.

Airway obstruction during exercise in asthma.

Airway obstruction (AO) in exercise-induced asthma (EIA) is considered a postexercise phenomenon. However, many with EIA complain of respiratory distress during exercise. We evaluated AO in six asthmatic subjects during a short (SX = 6 min) and a long (LX = 20 min) exercise session. We measured peak expiratory flow (PEF) rate, forced expiratory volume in one second (FEV1), and forced expiratory flow at 50% of vital capacity (Vmax50) and calculated expiratory and inspiratory pulmonary resistance (RLe and RLi). Rated perceived exertion (RPE) was evaluated as a measure of dyspnea. All three indices of airflow significantly decreased following SX and LX, but RLi and RLe increased. During SX, PEF, FEV1, and Vmax50 did not decrease, but RLi decreased. During LX, PEF, FEV1, and Vmax50 decreased (20.0, 26.0, and 17.7%, respectively), whereas RLi and RLe significantly increased (74.0 and 53.0%). Rated perceived exertion correlated highly with RLi during exercise (r = 0.95). In summary, there was little or no AO during SX but a frank AO during LX in asthmatic subjects. We conclude that AO occurs during LX and that the manifestation of dyspnea is associated with AO during exercise, as well as in recovery.

Contribution of diaphragmatic power output to exercise-induced diaphragm fatigue.

In nine normal humans we compared the effects on diaphragm fatigue of whole body exercise to exhaustion (86-93% of maximal O2 uptake for 13.2 +/- 2.0 min) to voluntary increases in the tidal integral of transdiaphragmatic pressure (integral of Pdi) while at rest at the same magnitude and frequency and for the same duration as those during exercise. After the endurance exercise, we found a consistent and significant fall (-26 +/- 2.9%, range -19.2 to -41.0%) in the Pdi response to supramaximal bilateral phrenic nerve stimulation at all stimulation frequencies (1, 10, and 20 Hz). Integral of Pdi.fB (where fB is breathing frequency) achieved during exercise averaged 509 +/- 81.0 cmH2O/min (range 304.0-957.0 cmH2O/min). At rest, voluntary production of integral of Pdi.fB, which was < 550-600 cmH2O/min (approximately 4 times the resting eupenic integral of Pdi.fB or 60-70% of Pdi capacity), did not result in significant diaphragmatic fatigue, whereas sustained voluntary production of integral of Pdi.fB in excess of these threshold values usually did result in significant fatigue. Thus, with few exceptions (5 of 23 tests) the ventilatory requirements of whole body endurance exercise demanded a level of integral of Pdi.fB that, by itself, was not fatiguing. The rested first dorsal interosseous muscle showed no fatigue in response to supramaximal ulnar nerve stimulation after whole body exercise. We postulate that the effects of locomotor muscle activity, such as competition for blood flow distribution and/or extracellular fluid acidosis, in conjunction with a contracting diaphragm account for most of the exercise-induced diaphragm fatigue.

Longitudinal effects of aging on lung function at rest and exercise in healthy active fit elderly adults.

We retested 18 healthy, active, and highly fit [maximal O2 consumption (VO2max) 201 +/- 12% of predicted] older adults over a 6-yr period (mean age 67-->73 yr) to determine the longitudinal effects of aging on lung function at rest and during exercise. In the 6-yr period, total lung capacity (TLC), functional residual capacity, and diffusion capacity did not change; vital capacity, forced expiratory volume in 1 s, and maximal volitional flow rates decreased; and residual volume and closing capacity/TLC increased 11-13%, all of which were greater than predicted from cross-sectional data. At maximum exercise over the 6-yr period, VO2max fell 11.2 +/- 3.4% (45.0-->40.3 ml.kg-1.min-1), six (of 18) subjects showed significant arterial hypoxemia (arterial O2 saturation < or = 92%), and maximum heart rate and minute ventilation-to-O2 consumption ratio (VF/VO2) were unchanged. At any given submaximal work rate, VE and breathing frequency were higher, the degree of expiratory flow limitation increased, and end-expiratory and end-inspiratory lung volumes were unchanged but remained significantly higher relative to young adults. We conclude that in contrast to implications from cross-sectional data, our longitudinal findings demonstrate that habitual physical activity and high aerobic capacity modify neither the normal deterioration in resting lung function nor the increased levels of ventilatory work during exercise that occur with healthy aging over the sixth and seventh decades of life.

Hypoxic effects on exercise-induced diaphragmatic fatigue in normal healthy humans.

We examined the effects of hypoxia on exercise-induced diaphragmatic fatigue. Eleven subjects with a mean maximal O2 uptake of 52.4 +/- 0.7 ml.kg-1.min-1 completed one normoxic (arterial O2 saturation 96-94%) and one hypoxic (inspiratory O2 fraction = 0.15; arterial O2 saturation 83-77%) exercise test at 85% maximal O2 uptake to exhaustion on separate days. Supramaximal bilateral phrenic nerve stimulation (BPNS) was used to determine the pressure generation of the diaphragm pre- and postexercise at 1, 10, and 20 Hz. There was increased flow limitation during hypoxic vs. normoxic exercise. There was a decrease in hypoxic exercise time (normoxic 24.9 +/- 0.7 min vs. hypoxic 15.8 +/- 0.8 min; P < 0.05). After exercise the BPNS transdiaphragmatic pressure (Pdi) was significantly reduced at 1 and 10 Hz after both exercise tests. The BPNS Pdi was recovered to control values by 60 min postnormoxic exercise but was still reduced 90 min posthypoxic exercise. The mean percent fall in the stimulated BPNS Pdi was similar (normoxic -24.8 +/- 4.7%; hypoxic -18.8 +/- 3.0%) after both exercise conditions. Experiencing the same amount of diaphragm fatigue in a shorter time period in hypoxic exercise may have been due to 1) the increased expiratory flow limitation and diaphragmatic muscle work, 2) decreased O2 transport to the diaphragm, and/or 3) increased levels of circulating metabolites.

An integrative view of limitations to muscular performance.

First we describe the changing site of limitation to maximal O2 transport with increasing fitness in mammals. The capacity for diffusion and airway/parenchymal flow rate and volume are markedly overbuilt in the sedentary subject's lung, but undergo little change with increased training/fitness; accordingly, as demand for O2 transport increases in the highly fit, the limits for maximal diffusion and ventilation are surpassed or met at maximal exercise. Secondly, low-frequency diaphragmatic fatigue occurred with by heavy endurance exercise. This fatigue resulted from increased diaphragmatic work together with the major contribution from the secondary effects of increased locomotor muscle activity; namely, metabolic acidosis and increased requirement for blood flow.

Oxygen uptake kinetics in cardiac transplant recipients.

Our purpose was to examine the gas exchange response to exercise in heart transplant (HT) patients and to characterize the O2 uptake kinetics (tau VO2) during successive square-wave on-transients from loadless cycling to moderate exercise. We hypothesized that with a slow heart rate response (and O2 transport limitation) O2 kinetics would be slowed but that with a repeated exercise initiated while the heart rate remained elevated the tau VO2 would be faster. Six male HT patients performed two ramp-function tests to determine peak O2 uptake (1.32 +/- 0.23 l/min) and ventilation threshold (1.02 +/- 0.16 l/min). Patients subsequently completed two repeats of a square-wave forcing function and repeated this on 2 days. Alveolar gas exchange was measured breath by breath. A monoexponential fit of signal-averaged data of the first exercise on-transient (between days) yielded a significantly slower tau VO2 in HT subjects than in healthy men (mean age 47 yr; n = 8) (77 +/- 26 vs. 45 +/- 4 s). With successive exercise (2nd transition) initiated while HR remained elevated the tau VO2 of HT patients was 46 +/- 17 s. The faster O2 kinetics of the second transition suggests that O2 delivery was enhanced and therefore that the tau VO2 may reflect bioenergetic processes controlling the rate of oxidative metabolism.

Exercise on-transient gas exchange kinetics are slowed as a function of age.

The purpose was to characterize gas exchange kinetics following the on-transient of exercise in men aged 30-80 yr. Forty-six men completed square wave exercise tests from loadless cycling to subventilatory threshold (V(E)T) work rates with gas exchange measured breath-by-breath. Signal averaged data were fit with a monoexponential equation to derive time constants (tau) for gas exchange and ventilation (tau VO2, tau VCO2, tau VE) and heart rate (tau HR). There was a significant slowing of ventilation and gas exchange kinetics across age with linear regression yielding an increase of 0.67 s.yr-1 for tau VO2 (39 s in young to 61 s in old), 0.57 s.yr-1 for tau VCO2, and 0.65 s.yr-1 for tau VE, whereas tau HR (44 to 41 s) was not changed significantly. The slowed VO2 kinetics with age may reflect limitations in muscle blood flow or in control of the rate of oxidative metabolism. The less marked slowing of tau VCO2 compared with tau VO2 across age may reflect reduced CO2 storage capacity with loss of muscle tissue. The tau VE change across age was similar to that for tau VCO2 (tau VE/tau VCO2 unchanged). The present study demonstrated marked age-related slowing of gas exchange dynamics at exercise onset.

Effects of aerobic endurance training on gas exchange kinetics of older men.

The kinetics of gas exchange at the on-transient of exercise are appreciably slowed in older individuals. Eight older men (72 yr) completed 6 months of aerobic cycle training. Ventilation and gas exchange kinetics were determined at the onset of a below threshold (ventilatory threshold, V(E)T) square wave exercise function and compared with control values (N = 4, age 70 yr). Gas exchange data were measured breath-by-breath and signal averaged data were fit with a monoexponential function to determine the time constants (tau). The training group showed significant increases in VO2max (20%) and VO2 at V(E)T (21%). The tau for oxygen uptake kinetics decreased significantly (62.2 +/- 15.5 to 31.9 +/- 7.0 s). The tau VCO2 (70.9 +/- 10.9 to 43.8 +/- 11.4 s) and tau VE (89.2 +/- 18.0 to 50.4 +/- 11.3) also were significantly faster posttraining; however, tau HR (38.1 +/- 20.5 to 28.6 +/- 7.2) was not significantly altered. Thus, with a vigorous training program, the kinetics of gas exchange of older individuals were faster, and approached values reported in fit young subjects.

Exercise-induced diaphragmatic fatigue in healthy humans.

1. Twelve healthy subjects (33 +/- 3 years) with a variety of fitness levels (maximal oxygen uptake (VO2, max) = 61 +/- 4 ml kg-1 min-1, range 40-80), exercised at 95 and 85% VO2, max to exhaustion (mean time = 14 +/- 3 and 31 +/- 8 min, expired ventilation (VE) over final minute of exercise = 149 +/- 9 and 126 +/- 10 l min-1). 2. Bilateral transcutaneous supramaximal phrenic nerve stimulation (BPNS) was performed before and immediately after exercise at four lung volumes, and 400 ms tetanic stimulations were performed at 10 and 20 Hz. The coefficients of variation of repeated measurements for the twitch transdiaphragm pressures (Pdi) were +/- 7-10% and for compound muscle action potentials (M wave) +/- 10-15%. 3. Following exercise at 95% of VO2, max, group mean Pdi twitch values were reduced at all lung volumes (range -8 +/- 3 to -32 +/- 5%) and tetanically stimulated Pdi values were reduced at both 10 and 20 Hz (-21 +/- 3 and -13 +/- 2%, respectively) (P = 0.001-0.047). Following exercise at 85% VO2, max, stimulated Pdi values were reduced at all lung volumes and stimulating frequencies, but only significantly so with the twitch at functional residual capacity (-15 +/- 5%). Stimulated Pdi values recovered partially by 30 min post-exercise and almost completely by an average time of 70 min. 4. The fall in stimulated Pdi values post-exercise was significantly correlated with the percentage increase in diaphragmatic work (integral of Pdi min-1) from rest to end-exercise and the relative intensity of the exercise. 5. The integral of Pdi min-1 and the integral of Po min-1 (Po, esophageal pressure) rose together from rest through the fifth to tenth minute of exercise, after which integral of Pdi min-1 plateaued even though integral of Po min-1, VE and inspiratory flow rate all continued to rise substantially until exercise terminated. Thus, the relative contribution of the diaphragm to total respiratory motor output was progressively reduced with exercise duration. 6. We conclude that significant diaphragmatic fatigue is caused by the ventilatory requirements imposed by heavy endurance exercise in healthy persons with a variety of fitness levels. The magnitude of the fatigue and the likelihood of its occurrence increases as the relative intensity of the exercise exceeds 85% of VO2, max.

Influence of ageing on aerobic parameters determined from a ramp test.

The purpose of this study was to examine the four parameters of aerobic function, the maximum oxygen uptake (VO2max), ventilation threshold (ThVE), efficiency, and the effective time constant for oxygen consumption (tau'VO2), across age. In particular, the study was designed to observe whether there may be accelerated declines in aerobic function beyond 60 years of age. Seventy-nine sedentary men aged 30-84 years were studied. Each subject performed two maximal cycle ramp function tests, and data were collected on a breath-by-breath basis. The VO2max, from a plateau in VO2, was achieved in 87% of the subjects using the ramp test. The VO2max showed a significant decrease with increasing age (from linear regression, r = -0.81) at a rate averaging 0.037 l.min-1.year-1. The ThVE also declined with increasing age, but at a slower rate (0.013 l.min-1.year-1). The tau'VO2 was significantly increased across the age groups from 69 s for those aged 30-40 years to 98 s for those aged 60 years or more. There was no evidence of accelerated decline in these aerobic parameters beyond age 60 years, and there were no differences in efficiency (27.5-29.9%) across age. Although other forcing functions should be used to confirm this characterization of the oxygen kinetics, this slowed response with age would result in greater oxygen deficit and possibly earlier fatigue in response to even light exercise in older individuals.