This study examined six- and 12-month levels of adherence to physical activity, functional changes, and psychosocial determinants of physical activity in 176 older adults who participated in the “Get Fit for Active Living (GFAL)” pilot program. Functional and psychosocial measures were conducted in person at six months; psychosocial measures and physical activity participation were assessed by telephone interview at 12 months. Ninety-five per cent were retained in the study at the six-month follow-up, and 88 per cent at 12 months. The self-reported adherence rate to exercise at 12 months was 66 per cent. The main reason for continued exercise participation was to maintain health (45%). Reasons for nonadherence were illness (38%) and lack of motivation (32%). Results identify factors associated with positive behaviour change that health promoters can utilize when targeting the older adult population. The GFAL project results can serve as a model for sustainable, community-based older-adult exercise programs.

We hypothesised that the observed acceleration in the kinetics of exercise on-transient oxygen uptake (V˙O2) of five older humans (77 ± 7 years (mean ± S.D.) following 9 weeks of single-leg endurance exercise training was due to adaptations at the level of the muscle cell. Prior to, and following training, subjects performed constant-load single-limb knee extension exercise. Following training V˙O2 kinetics (phase 2, τ) were accelerated in the trained leg (week 0, 92 ± 44 s; week 9, 48 ± 22 s) and unchanged in the untrained leg (week 0, 104 ± 43 s; week 9, 126 ± 35 s). The kinetics of mean blood velocity in the femoral artery were faster than the kinetics of V˙O2, but were unchanged in both the trained (week 0, 19 ± 10 s; week 9, 26 ± 11 s) and untrained leg (week 0, 20 ± 18 s; week 9, 18 ± 10 s). Maximal citrate synthase activity, measured from biopsies of the vastus lateralis muscle, increased (P < 0.05) in the trained leg (week 0, 6.7 ± 2.0 µmol (g wet wt)-1 min-1; week 9, 11.4 ± 3.6 µmol (g wet wt)-1 min-1) but was unchanged in the untrained leg (week 0, 5.9 ± 0.5 µmol (g wet wt)-1 min-1; week 9, 7.9 ± 1.9 µmol (g wet wt)-1 min-1). These data suggest that the acceleration of V˙O2 kinetics was due to an improved rate of O2 utilisation by the muscle, but was not a result of increased O2 delivery. Experimental Physiology (2001) 86.5, 659-665.

We compared estimates for the phase 2 time constant (τ) of oxygen uptake (V˙O2) during moderate- and heavy-intensity exercise, and the slow component of V˙O2 during heavy-intensity exercise using previously published exponential models. Estimates for τ and the slow component were different (P < 0.05) among models. For moderate-intensity exercise, a two-component exponential model, or a mono-exponential model fitted from 20 s to 3 min were best. For heavy-intensity exercise, a three-component model fitted throughout the entire 6 min bout of exercise, or a two-component model fitted from 20 s were best. When the time delays for the two- and three-component models were equal the best statistical fit was obtained; however, this model produced an inappropriately low ΔV˙O2/ΔWR (WR, work rate) for the projected phase 2 steady state, and the estimate of phase 2 τ was shortened compared with other models. The slow component was quantified as the difference between V˙O2 at end-exercise (6 min) and at 3 min (ΔV˙O2 (6-3 min); 259 ml min-1), and also using the phase 3 amplitude terms (truncated to end-exercise) from exponential fits (409-833 ml min-1). Onset of the slow component was identified by the phase 3 time delay parameter as being of delayed onset ~2 min (vs. arbitrary 3 min). Using this delay ΔV˙O2 (6-2 min) was ~400 ml min-1. Use of valid consistent methods to estimate τ and the slow component in exercise are needed to advance physiological understanding. Experimental Physiology (2001) 86.5, 667-676.

The purpose of this study was to use an allometric model (maximal oxygen uptake (VO2,max) = FFMb1 × PAb2 × exp(b0 + b3 age + b4 sex) × ) to determine the influence of fat-free mass (FFM), physical activity (PA), sex and age on VO2,max in older men (n = 152) and women (n = 146) aged 55-86 years. VO2,max was measured during a fatigue-limited treadmill test, FFM was determined from skinfold thickness and physical activity by the Minnesota Leisure Time Physical Activity questionnaire. The model was linearised by taking the natural logarithm of VO2,max, FFM and physical activity. Variables were selected using multiple linear regression (P < 0.05). The sex variable was not significant (P = 0.062). The model explained 72.1 % of the variance in VO2,max. Significant individual coefficients were incorporated into the model yielding the following expression: VO2,max = FFM0.971 × PA0.026 × exp(-2.48 - 0.015age). Therefore, FFM and physical activity were significant factors contributing to the changes in VO2,max with age. In addition, controlling for FFM and physical activity abolished sex differences in VO2,max. The rate of decline in VO2,max (after accounting for FFM and physical activity) with age, was approximately 15 % per decade.

The effect of carbonic anhydrase (CA) inhibition with acetazolamide (ACZ, 10 mg kg-1 I.V.) on the peripheral and central chemosensitivity and breathing pattern was investigated in four women and three men aged 25 ± 3 years using a modified version of Read's rebreathing technique. Subjects were exposed to dynamic increases in CO2> in hypoxic and hyperoxic backgrounds during control conditions and following acute CA inhibition. All manoeuvres were repeated twice and averaged for data analysis. The central chemoreflex sensitivities, estimated from the slopes of the ventilatory response to CO2 during hyperoxic rebreathing, increased following acute CA inhibition (control vs. ACZ treatment: 1.87 ± 0.66 vs. 4.07 ± 1.03 l min-1 (mmHg CO2)-1, P < 0.05). The increased slope was reflected by an increase in the rate of rise of tidal volume and breathing frequency. Furthermore with ACZ, there was a left-ward shift of the ventilation vs. end-tidal PCO2 curve during hyperoxic hypercapnia but not hypoxic hypercapnia. The peripheral chemoreflex sensitivity was isolated by subtracting the hyperoxic slope (central only) from the hypoxic slope (central and peripheral). Following ACZ administration, the peripheral chemosensitivity was blunted (control vs. ACZ treatment: 3.66 ± 0.92 vs. 1.33 ± 0.46 l min-1 (mmHg CO2)-1, P < 0.05). In conclusion, acute CA inhibition enhanced the central chemosensitivity to CO2 but diminished the peripheral chemosensitivity.

We investigated anaerobic threshold (thetaL) gas exchange kinetics and maximal oxygen uptake (VO2,max) among older men with reduced left ventricular end-diastolic filling (LVDF). Ten men (mean age, 73 years) with LVDF impairment and low fitness, but without other cardiovascular dysfunction were studied. Treatments compared to control included: 5 days, high intensity exercise training protocol; 5 days, calcium channel blockade (240 mg verapamil); 21 days, detraining/washout; and 5 days, combined treatments. Results indicated no changes in resting left ventricular systolic function with any treatment. Significant resting diastolic function changes included increased early:late flow velocity (control, 0.87; training, 1.28; verapamil, 1.32), and a decreased isovolumic relaxation time (control, 0.10 s; training, 0.08 s; verapamil, 0.08 s). The combined treatments were not additive. Sub-threshold oxygen uptake kinetics (tauVO2, s) were significantly faster following either training or verapamil (tauVO2,control, 62 ± 12; tauVO2,training, 44 ± 9; tauVO2,verapamil, 48 ± 10) and combined treatments (tauVO2, 41 ± 8). V O2,max (ml kg-1 min-1) was significantly increased (control, 21.8 ± 2.2; training, 27.3 ± 2.2; verapamil, 25.2 ± 3.4; combined treatments, 26.9 ± 2.3). Increasing ventricular preload with either exercise training or calcium channel blockade was coincident with faster tauVO2 and increased VO2,max. Experimental Physiology (2000) 85.5, 547-555.

Neural mediation of the human cardiac response to isocapnic (IC) steady-state hypoxaemia was investigated using coarse-graining spectral analysis of heart rate variability (HRV). Six young adults were exposed in random order to a hypoxia or control protocol, in supine and sitting postures, while end-tidal PCO2 (PET,CO2) was clamped at resting eucapnic levels. An initial 11 min period of euoxia (PET,O2 100 mmHg; 13.3 kPa) was followed by a 22 min exposure to hypoxia (PET,O2 55 mmHg; 7.3 kPa), or continued euoxia (control). Harmonic and fractal powers of HRV were determined for the terminal 400 heart beats in each time period. Ventilation was stimulated (P < 0.05) and cardiac dynamics altered only by exposure to hypoxia. The cardiac interpulse interval was shortened (P < 0.001) similarly during hypoxia in both body positions. Vagally mediated high-frequency harmonic power (Ph) of HRV was decreased by hypoxia only in the supine position, while the fractal dimension, also linked to cardiac vagal control, was decreased in the sitting position (P < 0.05). However, low-frequency harmonic power (Pl) and the HRV indicator of sympathetic activity (Pl/Ph) were not altered by hypoxia in either position. These results suggest that, in humans, tachycardia induced by moderate IC hypoxaemia (arterial O2 saturation Sa,O2 85 %) was mediated by vagal withdrawal, irrespective of body position and resting autonomic balance, while associated changes in HRV were positionally dependent.

In discussions of the history of real estate markets a key role clearly must be assigned to financial institutions, yet our knowledge of their various structures, particularly before the late nineteenth century, remains sketchy. One organization created to facilitate real estate purchases in the absence of other institutional sources of mortgage loans was the building society, either permanent or terminating. This article gathers together the information available about terminating building societies in mid-nineteenth century Quebec City. After an explanation of the societies' objectives and regulations, the article examines the difficulties that these societies faced as a result of general economic fluctuations and of the changing desires of members, who often wished to use the societies to place savings at interest rather than for home purchase.

Biased technical change, scale economies, and factor substitution were part of U.S. manufacturing's technical response to factor price movements during the period 1850 to 1919. In this article we employ the cost dual of a Generalized Leontief production function to test directly for the presence of these three effects for nineteen two-digit manufacturing sectors. Biased technical change is found in all but one sector; scale economies in all but two; factor substitutability, in all but five. Estimates of scale and bias effects for labor, capital, and materials are presented by sector, and the results are compared with other recent work.

This paper examines the proposition that U.S. manufacturing experienced biased technical change during the period 1850–1919. Tests for bias, in Hicksian terms, are conducted using the translog cost dual. Redefined census data permit these tests to be made at the two-digit level of industry classification and with four inputs considered—labor, capital, materials, and a residual factor input. The tests demonstrate that labor-saving and capital-using biases existed, but material-using biases also were present. Furthermore, the patterns of bias varied considerably from industry to industry and often were of such a magnitude as to overpower ordinary substitution effects.