The purpose was to compare cardiorespiratory kinetics during exercise of different muscle groups (double-leg cycling vs treadmill walking and single-leg ankle plantar flexion) in old and young subjects. Oxygen uptake (VO2) during exercise transitions was measured breath by breath, and the phase 2 portion of the response was fit by a monoexponential for determination of the time constant (tau) of VO2. Two separate studies were performed: in study 1, 12 old (age 66.7 yr) and 16 young (aged 26.3 yr) subjects were compared during cycling and ankle plantar flexion exercise, and in the study 2, five old (aged 69.6 yr) and five young (24.4 yr) subjects were compared during cycling and treadmill walking. VO2 transients during square-wave cycling exercise were significantly slower in the old compared with the young groups. In contrast, VO2 kinetics did not differ between old and young groups during plantar flexion exercise. Heart rate (HR) kinetics followed the same pattern, with tau HR being significantly slower in the old vs young groups during transitions to cycling but not to plantar flexion. In study 2 tau VO2 and tau HR during on-transients to treadmill square-wave exercise were significantly slower in the old group compared with the young group, but tau VO2 was significantly faster during treadmill exercise than during cycling in the old group. The differences with aging between the modes of exercise may be related to the muscle mass involved and the circulatory demands. On the other hand, slowed VO2 kinetics with age appear to occur in a mode (cycling) in which the muscles are not accustomed to the activity, whereas in a mode of normal activity (walking) and with the muscle groups (plantar flexors) accustomed to the activity, VO2 kinetics are not slowed to the same degree with age.

Findings from studies of the effects of aging on the human respiratory controller are equivocal. This study assessed the ventilatory response to CO2 in hyperoxia and hypoxia in groups of younger (YS) and older (OS) humans. Two protocols were used. In the first, end-tidal PCO2 (PETCO2) was clamped at 1-2 Torr above rest (eucapnia), and, in the second, PETCO2 was clamped at 7-8 torr above resting PETCO2 (moderate hypercapnia). End-tidal PO2 was clamped at 100 Torr throughout except for two 2-min periods at 500 and 50 Torr. The ventilatory responses for each subject at each PO2 were fitted to the linear equation, VE = S(PETCO2 - B), where VE is minute ventilation, S is the response curve slope, and B is the response curve threshold. In eucapnia, there were no differences in hypoxic and hyperoxic VE between YS and OS. In hypercapnia, hypoxic VE was 24% lower in OS [39.93 +/- 2.71 (SE) l/min] than in YS (52.16 +/- 3.17 l/min). In hypoxia, S was significantly lower in OS (3.25 +/- 0.38 l.min-1.Torr-1) than in YS (4.76 +/- 0.37 l.min-1.Torr-1). We conclude that, in older humans, VE is lower in hypoxia during moderate hypercapnia, resulting mainly from a decreased peripheral chemoreflex CO2 sensitivity.

The critical power (CP) of a muscle group or individual may represent the highest rate of work which can be performed for an extended period. We investigated this concept in young (n = 13, 24.5 years) and elderly (n = 12, 70.7 years) active men by first determining CP and then comparing responses elicited by 24 min of cycle exercise at power outputs (omega) corresponding to CP. Values from the final 2 min of the 24-min ride were expressed relative to maximal values established in a ramp test. CP for the elderly was only 65% that for the young, but on a relative basis, it was significantly higher both in terms of omega (67 vs 62% of omega max) and oxygen consumption (VO2) (91.5 vs 85.2% of maximum oxygen consumption). There were no group differences in relative values for ventilation (VE), heart rate or respiratory exchange ratio (R). During the 24-min ride, VO2 and R achieved a plateau in both groups, while VE, blood lactate and arterial PCO2 continued to change in the young. It was concluded that CP can be determined in active elderly men, but that CP may not represent a true non-fatiguing work rate in either young or elderly men.

This study compared the ventilatory response to 20 min of acute isocapnic hypoxia (end‐tidal PO2, 50 mmHg) using the technique of dynamic end‐tidal forcing in young (Y) and old (O) men. Two groups of non‐smoking male subjects (mean ± s.d. age: Y, 29.8 ± 6.9 years; O, 73.4 ± 2.8 years) with similar body size, normal age‐predicted spirometry, and normal moderate levels of physical activity were studied. Compared with baseline ventilation in euoxia (10.79 ± 1.99 and 11.88 ± 0.91 l min−1) both groups responded to the abrupt onset of isocapnic hypoxia with peak ventilatory responses of 22.58 ± 2.60 and 24.56 ± 2.54 l min−1 for Y and O, respectively (not significant, n.s.). Both groups demonstrated a significant increment in neuromuscular drive (i.e. tidal volume (VT)/inspiratory time (TI); 0.46 ± 0.06 to 0.91 ± 0.15 and 0.48 ± 0.06 to 0.91 ± 0.12 l s−1 for Y and O, respectively) with a small (but also significant) change in central timing (TI/total ventilation time (Ttot); 0.38 ± 0.02 to 0.41 ± 0.02 and 0.42 ± 0.02 to 0.45 ± 0.02 for Y and O, respectively). Oxygen sensitivity was assessed using Weil's equation, and gave a hyperbolic factor (A) of 282 ± 75 and 317 ± 72, and using the linear equation: change in expiratory minute volume (ΔVE)/change in arterial O2 saturation (ΔSa,O2) which gave ‐1.17 ± 0.57 and ‐1.17 ± 0.42 l min−1%−1 (n.s.) for Y and O, respectively. After 20 min of sustained isocapnic hypoxia, ventilation declined to 14.29 ± 1.92 and 16.85 ± 2.34 l min−1 for Y and O, respectively (n.s.). The acute response to hypoxia was characterised by similar time constants (16.0 ± 5.4 and 18.5 ± 6.7 s) and time delays (4.8 ± 2.1 and 4.6 ± 1.9 s) for Y and O, respectively. Thus, the dynamic ventilatory response to acute isocapnic hypoxia is maintained into the eighth decade in a group of habitually active elderly men.

The rate and duration of peripheral chemoreceptor resensitization following sustained hypoxia was characterized in young and older (74-year-old) adults. In addition, cerebral blood velocity (CBV) was measured in young subjects during and following the relief from sustained hypoxia. Following 20 min of sustained eucapnic hypoxia (50 mmHg), subjects were re-exposed to brief (1.5 min) hypoxic pulses (50 mmHg), and the magnitude of the ventilatory response was used to gauge peripheral chemosensitivity. Five minutes after the relief from sustained hypoxia, ventilation (V E ) increased to 40.3 ± 4.5% of the initial hypoxic ventilatory response, and by 36 minV E increased to 100%, indicating that peripheral chemosensitivity to hypoxia was restored. TheV E response magnitude plotted versus time demonstrated thatV E , hence peripheral chemosensitivity, was restored at a rate of 1.9% per minute. Cerebral blood flow (CBF, inferred from CBV) remained constant during sustained hypoxia and increased by the same magnitude during the hypoxic pulses, suggesting that CBF has a small, if any, impact on the decline inV E during hypoxia and its subsequent recovery. To address the issue of whether hypoxic pulses affect subsequent challenges, series (continuous hypoxic pulses at various recovery intervals) and parallel (only 1 pulse per trial) methods were used. There were no differences in the ventilatory responses between the series and parallel methods. Older adults demonstrated a similar rate of recovery as in the young, suggesting that ageing in active older adults does not affect the peripheral chemoreceptor response.