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Biomedical subjects

D H Paterson

Publications and source records attributed to D H Paterson.

At least 37 records · Page 2Linked to original sources

Exercise gas transport determinants in elderly normotensive and hypertensive humans.

This study examined the effect of the phenylalkylamine calcium channel blocker verapamil, on resting left ventricular (LV) function and O2 uptake rate (VO2) during exercise at maximal and submaximal work rates. Nine older hypertensive (71 years; OH), 10 older sedentary normotensive (69 years; OS), 10 older active (71 years; OA) and 10 young (24 years; Y) individuals volunteered. Studies were completed in the control condition and 4-6 h following 240 mg verapamil SR per os. Resting LV systolic (fractional shortening; FS) and diastolic (early: late (E/A) flow velocity ratio and isovolumic relaxation time (IVRT) were measured by Doppler echocardiography. Maximal oxygen uptake (VO2,max) and, on subsequent test days, four transitions to and from a 6 min square wave exercise perturbation at a sub-anaerobic threshold intensity of 40 W (OH, OS, OA) or 100 W (Y) for determination of VO2 kinetics were performed on a cycle ergometer. Breath-by-breath VO2 transients were fitted with a monoexponential equation, starting at phase 2 of the response, while heart rate (HR) was fitted from phase 1, for the determination of the time constant of VO2 (tau VO2) and HR (tau HR). Baseline left ventricular FS was significantly greater in the OS (32%), OA (34%) and Y (34%) than in the OH (23%) groups, while E/A was significantly greater in the OA (1.16) and Y (2.34) than in the OH (0.9) and OS (0.82) groups (P < 0.05). Baseline VO2,max was higher and tau VO2 faster in the young (41.4 ml kg-1 min-1; 25.2 s) than in the older groups and in the OA (28.8 ml kg-1 min-1; 44.3 s) than in both OH (20.8 ml kg-1 min-1; 71.3 s) and OS (22.0 ml kg-1 min-1; 59.5 s) groups (P < 0.05). Heart rate kinetics showed similar differences to VO2 kinetics among the groups. After verapamil, no significant changes in FS, E/A or IVRT were observed in the OA and Y groups. In the OH group, FS (32%) and E/A (1.15) increased while IVRT decreased significantly (from 0.103 to 0.07; P < 0.05). In the OS group, only E/A increased significantly (0.82 to 1.0; P < 0.05). None of the exercise variables (VO2,max, tau VO2 or tau HR) were altered for the OA or Y groups. VO2,max increased (from 20.8 to 22.8 ml kg-1 min-1) in the OH and (from 22.0 to 24.1 ml kg-1 min-1) in the OS (P < 0.05). tau VO2 was accelerated from 71.3 to 49.2 s in the OH group and from 59.5 to 48.2 s in the OS group (P < 0.05). These results suggest that VO2 responses at maximal and submaximal work rates may be dependent upon the initial cardiac pump function of the study population.

Adult↗

The gas transporting systems: limits and modifications with age and training.

The interplay of cardiovascular and cellular oxygen uptake determinants of aerobic performance and the system adaptations to training in different population samples are examined in order to describe the limitation. With VO2max, a central limitation following myocardial infarction and ageing is modified with training. Peripheral adaptations occur and stroke volume may be increased primarily through improved diastolic filling. In submaximal perturbations, control of the increase in O2 uptake at exercise onset (O2 kinetics) is most often under peripheral metabolic control, but in exceptions may also be limited by central factors. In young and old the peripheral machinery is matched to the growth (puberty) and loss (ageing) of muscle mass. Cardiac stroke volume capacity may adjust following the changes in muscle mass. Submaximal endurance is closely influenced by the anaerobic threshold (theta(an)) and peripheral factors of oxidative metabolism. Relative to VO2max, the theta(an) is low in children and high in older adults, perhaps reflecting a slow time course in full development and loss of peripheral adaptations. Remarkable increases in endurance performance are related to relatively small changes in the maximal capacity and the relative intensity of performance.

Adaptation, Physiological↗

VCO2 and VE kinetics during moderate- and heavy-intensity exercise after acetazolamide administration.

The effect of carbonic anhydrase inhibition with acetazolamide (Acz) on CO2 output (VCO2) and ventilation (VE) kinetics was examined during moderate- and heavy-intensity exercise. Seven men [24 +/- 1 (SE) yr] performed cycling exercise during control (Con) and Acz (10 mg/kg body wt iv) sessions. Each subject performed step transitions (6 min) in work rate from 0 to 100 W [below ventilatory threshold ( VET)]. VE and gas exchange were measured breath by breath. The time constant (tau) was determined for exercise VET by using a three-component model (fit from the start of exercise). VCO2 kinetics were slower in Acz ( VET, MRT = 75 +/- 10 s) than Con ( VET, MRT = 54 +/- 7 s). During VET kinetics were faster in Acz (MRT = 85 +/- 17 s) than Con (MRT = 106 +/- 16 s). Carbonic anhydrase inhibition slowed VCO2 kinetics during both moderate- and heavy-intensity exercise, demonstrating impaired CO2 elimination in the nonsteady state of exercise. The slowed VE kinetics in Acz during exercise <VET is consistent with a mechanism coupling VE kinetics with the flow of CO2 to the lungs.

Acetazolamide↗

Peripheral chemoreceptor function after carbonic anhydrase inhibition during moderate-intensity exercise.

The effect of carbonic anhydrase inhibition with acetazolamide (Acz, 10 mg/kg) on the ventilatory response to an abrupt switch into hyperoxia (end-tidal PO2 = 450 Torr) and hypoxia (end-tidal PO2 = 50 Torr) was examined in five male subjects [30 +/- 3 (SE) yr]. Subjects exercised at a work rate chosen to elicit an O2 uptake equivalent to 80% of the ventilatory threshold. Ventilation (VE) was measured breath by breath. Arterial oxyhemoglobin saturation (%SaO2) was determined by ear oximetry. After the switch into hyperoxia, VE remained unchanged from the steady-state exercise prehyperoxic value (60.6 +/- 6.5 l/min) during Acz. During control studies (Con), VE decreased from the prehyperoxic value (52.4 +/- 5.5 l/min) by approximately 20% (VE nadir = 42.4 +/- 6.3 l/min) within 20 s after the switch into hyperoxia. VE increased during Acz and Con after the switch into hypoxia; the hypoxic ventilatory response was significantly lower after Acz compared with Con [Acz, change (Delta) in VE/DeltaSaO2 = 1.54 +/- 0.10 l. min-1. SaO2-1; Con, DeltaVE/DeltaSaO2 = 2.22 +/- 0.28 l. min-1. SaO2-1]. The peripheral chemoreceptor contribution to the ventilatory drive after acute Acz-induced carbonic anhydrase inhibition is not apparent in the steady state of moderate-intensity exercise. However, Acz administration did not completely attenuate the peripheral chemoreceptor response to hypoxia.

Acetazolamide↗

Anaerobic power of the arms and legs of young and older men.

The purpose of this study was to examine differences in the anaerobic exercise performance of young and older men. Eight healthy, active older (68.5 +/- 2.4 years old, mean S.D.) and eight healthy, active young (30.6 +/- 4.5 years old) subjects were assessed for peak and mean power output (PP and MP, respectively) of the legs and arms, during 30 s Wingate tests. PP during leg exercise was significantly (P < 0.05) higher in the young (14.6 +/- 1.6 W kg-1) compared with the older (10.7 +/- 1.0 W kg-1) group. MP of the legs was also greater in the young subjects (10.7 +/- 0.7 vs. 7.4 +/- 0.9 W kg-1). These differences in PP and MP remained significant when expressed relative to lean leg volume. PP during arm cranking was significantly greater in the young subjects (8.9 +/- 0.7 vs. 7.5 +/- 0.6 W kg-1) as was MP (6.4 +/- 0.7 vs. 5.0 +/- 0.7 W kg-1). Post-exercise blood lactate concentration in the older group (7.0 +/- 1.6 mmol l-1) was less (P < 0.05) than in the young group (10.6 +/- 2.0 mmol l-1), for leg work only. The significant loss of anaerobic power in the older group could not be explained by a difference in muscle mass. Power output was also lower in the arms, but to a lesser extent. The results of this study suggest that a reduction in the ability to perform high intensity exercise may be an inevitable consequence of ageing. The extent, however, of this decline varies with different muscle groups.

Adult↗

Oxygen uptake kinetics of older humans are slowed with age but are unaffected by hyperoxia.

Cross-sectional studies have compared the oxygen uptake (VO2) kinetics during the on-transient of moderate intensity exercise in older and younger adults. The slower values in the older adults may have been due to an age-related reduction in the capacity for O2 transport or alternatively a reduced intramuscular oxidative capacity. We studied: (1) the effects of ageing on VO2 kinetics in older adults on two occasions 9 years apart, and (2) the effect of hyperoxia on VO2 kinetics at the second test time. After a 9 year period, follow-up testing was undertaken on seven older adults (78 +/- 5 years, mean +/- S.D.). They each performed six repeats of 6 min bouts of constant-load cycle exercise from loadless cycling to 80% of their ventilatory threshold. They breathed one of two gas mixtures (euoxia: inspired O2 fraction, FI,O2, 0.21; hyperoxia: FI,O2, 0.70) on different trials determined on a random basis. Breath-by-breath VO2 data were time aligned and ensemble averaged. VO2 kinetics, modelled with a single exponential from phase 2 onset (+20 s) to steady state and described by the exponential time constant (tau) were compared with data collected from the same adults 9 years earlier. One-way repeated measures analysis of variance revealed that tau was slowed significantly with age (from 30 +/- 8 to 46 +/- 10 s), but was unaffected by hyperoxia (43 +/- 15 s). We concluded that: (1) in older adults studied longitudinally over a 9 year period, the on-transient VO2 kinetics are slowed, in agreement with, but to a greater extent, than from cross-sectional data; and (2) the phase 2 time constant (tau) for these older adults was not accelerated by hyperoxic breathing. Thus the expected hyperoxia-induced increase in the capacity for O2 transport was not associated with faster on-transient VO2 kinetics suggesting either that O2 transport may not limit VO2 kinetics during the 8th decade, or that O2 transport was not improved with hyperoxia.

Aged↗

The effects of caffeine on the kinetics of O2 uptake, CO2 production and expiratory ventilation in humans during the on-transient of moderate and heavy intensity exercise.

In order to test the hypothesis that glycogen sparing observed early during exercise following caffeine ingestion was a consequence of tighter metabolic control reflected in faster VO2 kinetics, we examined the effect of caffeine ingestion on oxygen uptake (VO2), carbon dioxide production (VCO2) and expiratory ventilation (VE) kinetics at the onset of both moderate (MOD) and heavy (HVY) intensity exercise. Male subjects (n = 10) were assigned to either a MOD (50% VO2,max, n = 5) or HVY (80% VO2,max, n = 5) exercise condition. Constant-load cycle ergometer exercise was performed as a step function from loadless cycling 1 h after ingestion of either dextrose (placebo, PLAC) or caffeine (CAFF; 6 mg (kg body mass)-1). Alveolar gas exchange was measured breath-by-breath. A 2- or 3-component exponential model, fitted through the entire exercise transient, was used to analyse gas exchange and ventilatory data for the determination of total lag time (TLT: the time taken to attain 63% of the total exponential increase). Caffeine had no effect on TLT for VO2 kinetics at either exercise intensity (MOD: 36 +/- 14 s (PLAC) and 41 +/- 10 s (CAFF); HVY: 99 +/- 30 s (PLAC) and 103 +/- 26 (CAFF) (mean +/- S.D.)). TLT for VE was increased with caffeine at both exercise intensities (MOD: 50 +/- 20 s (PLAC) and 59 +/- 21 s (CAFF); HVY: 168 +/- 35 s (PLAC) and 203 +/- 48 s (CAFF)) and for VCO2 during MOD only (MOD: 47 +/- 14 s (PLAC) and 53 +/- 17 s (CAFF); HVY: 65 +/- 13 s (PLAC) and 69 +/- 17 s (CAFF)). Contrary to our hypothesis, the metabolic effects of caffeine did not alter the on-transient VO2 kinetics in moderate or heavy exercise. VCO2 kinetics were slowed by a reduction in CO2 stores reflected in pre-exercise and exercise endtidal CO2 pressure (PET,CO2) and plasma PCO2 which, we propose, contributed to slowed VE kinetics.

Adult↗

Evaluation of muscle oxidative potential by 31P-MRS during incremental exercise in old and young humans.

The purpose of this study was to compare muscle oxidative capacity between moderately active young and old humans by measuring intracellular threshold (IT) during exercise with 31P-magnetic resonance spectroscopy (31P-MRS). Changes in phosphocreatine, inorganic phosphate, and intracellular pH were measured by 31P-MRS during a progressive unilateral ankle plantar flexion exercise protocol in groups of moderately active old (n = 12, mean age 66.7 years) and young (n = 13, mean age 26.2 years) individuals. From muscle biopsy samples of the lateral gastrocnemius, citrate synthase (CS) activity was determined in six subjects from each group, and fibre type composition was determined in nine old and ten young subjects. The old group had a lower IT for pH, as a percentage of peak work rate (P < 0.05), despite a similar CS activity compared to the young. IT was significantly correlated with CS activity (R = 0.59; P < 0.05), but not with fibre type composition. It was concluded that metabolic responses to exercise are affected by ageing, as indicated by a lower IT in old compared to young individuals.

Adult↗

The effects of age on kinetics of oxygen uptake and phosphocreatine in humans during exercise.

We compared the kinetics of oxygen uptake (VO2) and phosphocreatine (PCr) during the adjustment to and recovery from plantar flexion exercise in moderately active older (n = 10, 66.9 years) and younger (n = 10, 27.5 years) individuals. VO2 kinetics were similar in the two groups, with time constants (tau) averaging 46.3 +/- 10.2 s (younger, on-transient), 38.1 +/- 14.4 s (younger, off-transient), 46.3 +/- 17.8 (older, on-transient) and 40.7 +/- 19.2 s (older, off-transient). These were similar to corresponding PCr kinetics, measured by 31P nuclear magnetic resonance spectroscopy, which averaged 50.6 +/- 24.0 s (younger, on-transient), 42.0 +/- 16.1 s (younger, off-transient), 39.8 +/- 22.0 s (older, on-transient) and 37.6 +/- 21.6 s (older, off-transient). On-transient tau values for VO2 and PCr were correlated, for combined groups (r = 0.53; P = 0.015). We conclude that: (1) VO2 and PCr kinetics during exercise of a muscle group accustomed to daily activity are not compromised in physically active older humans, and (2) PCr kinetics reflect the kinetics of muscle O2 consumption, and are expressed at the lung (VO2 kinetics) after a transit delay.

Adult↗

O2 uptake kinetics after acetazolamide administration during moderate- and heavy-intensity exercise.

Inhibition of carbonic anhydrase (CA) is associated with a lower plasma lactate concentration ([La-]pl) during fatiguing exercise. We hypothesized that a lower [La-]pl may be associated with faster O2 uptake (V(O2)) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz, 10 mg/kg body wt iv). On 6 separate days, each subject performed 6-min step transitions in work rate from 0 to 100 W (below ventilatory threshold, VE(T). Gas exchange was measured breath by breath. Trials were interpolated at 1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- ( VE(T)). Arterialized venous blood was sampled from a dorsal hand vein and analyzed for [La-]pl. MRT was similar during Con (31.2 +/- 2.6 and 32.7 +/- 1.2 s for on and off, respectively) and Acz (30.9 +/- 3.0 and 31.4 +/- 1.5 s for on and off, respectively) for work rates VE(T), MRT was similar between Con (69.1 +/- 6.1 and 50.4 +/- 3.5 s for on and off, respectively) and Acz (69.7 +/- 5.9 and 53.8 +/- 3.8 s for on and off, respectively). On- and off-MRTs were slower for >VE(T) than for VE(T) exercise but was lower at the end of the transition during Acz (1.4 +/- 0.2 and 7.1 +/- 0.5 mmol/l for VE(T) respectively) than during Con (2.0 +/- 0.2 and 9.8 +/- 0.9 mmol/l for VE(T), respectively). CA inhibition does not affect O2 utilization at the onset of VE(T) exercise, suggesting that the contribution of oxidative phosphorylation to the energy demand is not affected by acute CA inhibition with Acz.

Acetazolamide↗

Effects of 5-day exercise training in elderly subjects on resting left ventricular diastolic function and VO2max.

We evaluated the effects of short-term, high-intensity exercise training and detraining on resting left ventricular diastolic function (LVDF) and maximal aerobic power (VO2max) in 7 sedentary older (age = 68 +/- 4 years) men (n = 5) and women (n = 2). Training consisted of cycling for 60 min with power output set at 70% (Day 1), 80% (Day 2), and 90% (Days 3-5) of the pretraining peak work rate. Detraining consisted of a return to regular exercise habits. LVDF increased 10% in the early (E) flow velocity, decreased 18% in the late (A) flow velocity wave, and decreased 31% in the isovolumic relaxation time. VO2max was increased 12% while plasma volume (PV) increased 10% following training and returned to baseline after detraining. The exercise-induced change in VO2max was directly related to the change in E/A (r = .52) and indirectly related to the change in IVRT (r = -.62). It was concluded that short-term, high-intensity exercise training improves LVDF and is tolerated well in older subjects, and that the calculated changes in PV and aerobic power are similar to those observed previously in a younger population.

Aged↗

Dynamics of the ventilatory response to step changes in end-tidal PCO2 in older humans.

The purpose of this study was to examine the ventilatory response to carbon dioxide (CO2) in young and older men. Six square-wave steps of end-tidal CO2 (PETCO2) were administered in euoxia (PETO2 = 100 torr), hyperoxia (PETO2 = 500 torr), and mild hypoxia (PETO2 = 60 torr). The peripheral and central chemoreflex loops were described by three parameters including a gain (gp and gc), time constant of the response (tau p, tau c), and a time delay (Tp, Tc), respectively. The young and older men showed similar characteristics for Tp and Tc, with Tp being 3 to 5 s shorter than Tc. In hypoxia, the ventilatory responses of the old group were characterised by a significantly smaller gc and a smaller gp. In hypoxia, tau c was significantly shortened from its euoxic value in the young group, but not in the old group. Thus, this study demonstrated that in older men, the ventilatory responses to CO2 in euoxia and hyperoxia are similar to younger men, while in hypoxia the ventilatory responses are characterised by smaller gain terms.

Adult↗

A model of oxygen transport capacity changes for independently living older men and women.

The purpose of the present investigation was to describe, for a subset of a large random survey of men and women, restricted to the ages of 55 to 85 years, the physiological decay pattern for aerobic fitness and contributing factors of cardiovascular and pulmonary function. The time course of the age-related changes in maximal oxygen uptake (VO2max), ventilatory threshold (TVE), maximal ventilation (VEmax), maximal heart rate (HRmax), and O2 pulse (VO2max/HRmax) were examined by fitting the data to a decaying exponential model by use of a least-squares parameter estimation technique. The time constant (tau) was used to describe the rate of decline. The women showed a much slower decline in VO2max (tau = 47.4 years) and TVE (tau = 83.3 years) than the men (tau = 20.8 and 15.4 years, respectively). There was a significant age-related decrease in body weight (0.45 kg.yr-1) in the men, whereas the women showed no change. Pulmonary function did not limit performance based on the very slow decline in VEmax and the normal FEV1.0. The decay in HRmax was better described by a linear model, resulting in an extremely slow tau. Maximal O2 pulse clearly exhibited an exponential decay, with a shorter tau (tau men = 13.5 years; tau women = 28.5 years) than any other variable.

Aged↗

Muscle capillarization O2 diffusion distance, and VO2 kinetics in old and young individuals.

The relationships between muscle capillarization, estimated O2 diffusion distance from capillary to mitochondria, and O2 uptake (VO2) kinetics were studied in 11 young (mean age, 25.9 yr) and 9 old (mean age, 66.0 yr) adults. VO2 kinetics were determined by calculating the time constants (tau) for the phase 2 VO2 adjustment to and recovery from the average of 12 repeats of a 6-min, moderate-intensity plantar flexion exercise. Muscle capillarization was determined from cross sections of biopsy material taken from lateral gastrocnemius. Young and old groups had similar VO2 kinetics (tau VO2-on = 44 vs. 48 s; tau VO2-off = 33 vs. 44 s, for young and old, respectively), muscle capillarization, and estimated O2 diffusion distances. Muscle capillarization, expressed as capillary density or average number of capillary contacts per fiber/average fiber area, and the estimates of diffusion distance were significantly correlated to VO2-off kinetics in the young (r = -0.68 to -0.83; P < 0.05). We conclude that 1) capillarization and VO2 kinetics during exercise of a muscle group accustomed to everyday activity (e.g., walking) are well maintained in old individuals, and 2) in the young, recovery of VO2 after exercise is faster, with a greater capillary supply over a given muscle fiber area or shorter O2 diffusion distances.

Adult↗

Nature of the interaction between central and peripheral chemoreceptor drives in human subjects.

The purpose of the current study was to investigate the nature of the interaction between the central and peripheral chemoreflex loops in humans, using the different speeds of response of the central and peripheral chemoreceptors to enable a temporal separation of their chemical stimulation. Subjects were exposed to an end-tidal Pco2 of 8-10 torr (1 torr = 1 mmHg = 133.3 Pa) above resting Pco2, with end-tidal Po2 = 100 torr, for 8 min. Thirty seconds after the hypercapnic stimulus was withdrawn, a 5-min hypoxic stimulus (end-tidal Po2 = 50 torr) was introduced. The 30-s interval was believed to be sufficient time for the peripheral chemoreceptors to adapt to the new level of carbon dioxide. Over the subsequent 5 min of hypoxia, however, the central chemoreceptors were exposed to diminishing hypercapnia. The response to the hypoxic step was compared with the effect of the same hypoxic step without the preceding period of hypercapnia. In 4 of the 5 subjects studied, the ventilatory response to hypoxia was unaffected by relative hypercapnia at the central chemoreceptor, suggesting that the central and peripheral chemoreflexes were independent of each other.

Adult↗

The influence of age and cardiorespiratory fitness on kinetics of oxygen uptake.

The purpose of this study was to determine the influences of ageing and cardiorespiratory fitness on kinetics of VO2 during the transition to exercise of moderate intensity. Subjects performed three transitions to and from a 6-minute square wave constant load, at an intensity corresponding to 90% of ventilatory threshold (VET), to determine VO2 kinetics. The young group had a significantly faster time constant of VO2 (tau VO2). Tau VO2 was significantly correlated with VO2max for both young and old groups; however, the slope of the tau VO2--VO2max regression equation was steeper for the old group, indicating that fit older subjects had VO2 kinetics that approached those of fit young. A multiple linear regression indicated that relative fitness was the strongest significant predictor of tau VO2, followed by sex and age. Although VO2 kinetics are definitely slowed with age, relative levels of cardiorespiratory fitness also have a great influence on the dynamic response of VO2.

Adult↗

Peripheral chemoreflex drive in moderate-intensity exercise.

The purpose of this study was to measure the contribution of the peripheral chemoreceptor (pR) to VE during the steady-state of moderate-intensity cycle ergometer exercise using continuous hyperoxic suppression of pRc drive, while stabilizing the drive from the central chemoreceptor by clamping end-tidal PCO2 (PETCO2) at the peak level attained during the hyperoxic period of a poikilocapnic ride. In the isocapnic protocol, the PETCO2 was maintained at a constant level by a negative feedback, open loop system. Five subjects completed four repetitions of each of the poikilocapnic and isocapnic protocols. In the poikilocapnic protocol, VE declines following the step into hyperoxia and then began to increase, whereas the decline in VE was maintained in the isocapnic protocol. However, the mean decrease in VE was not significantly different between the poikilocapnic (16.1 +/- 5.0%) and isocapnic (14.9 +/- 4.4%) protocols. These results suggest that the declining phase of VE is fully complete before the secondary central stimulating actions of hyperoxia on VE and that the pRc contributes about 15% of the drive to breathe in moderate intensity exercise.

Adult↗