Enhanced endothelium-dependent vasodilation in older endurance-trained men.

We hypothesized that abnormal endothelium-dependent vasodilation (EDD) found in older otherwise healthy subjects can be attenuated with long-term endurance training. Ten endurance-trained men, 68.5 +/- 2.3 yr old, and 10 healthy sedentary men, 64.7 +/- 1.4 yr old, were studied. Aerobic exercise capacity (VO(2 max)), fasting plasma cholesterol, insulin, and homocysteine concentrations were measured. Master athletes had higher VO(2 max) (42 +/- 2.3 vs. 27 +/- 1.4 ml. kg(-1). min(-1), P < 0.001), slightly higher total cholesterol (226 +/- 8 vs. 199 +/- 8 mg/dl, P = 0.05), similar insulin, and higher homocysteine (10.7 +/- 1.3 vs. 9.2 +/- 1.4 micromol/ml, p = 0.02) concentrations. Brachial arterial diameter, determined with vascular ultrasound, during the hyperemic response was greater in the master athletes than in controls (P = 0.005). Peak vasodilatory response was 109.1 +/- 2 vs. 103.6 +/- 2% (P < 0.05) in the athletes and controls, respectively. Endothelium-independent vasodilation in response to nitroglycerin was similar between the two groups. The increased arterial diameter during the hyperemic response correlated significantly with the VO(2 max) in the entire population (r = 0.66, P < 0.002). Our results suggest that long-term endurance exercise training in older men is associated with systemic enhanced EDD, which is even detectable in the conduit arteries of untrained muscle.     

Cardiovascular responses to lower body negative pressure in trained and untrained older men.

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59-73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.     

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment.

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial PO(2) (Pa(O(2))) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O(2) uptake (VO(2 max)) = 51 ml. kg(-1). min(-1)]. They were studied in random order (C or R), with a fast VO(2 max) protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% of VO(2 max) (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in VO(2 max) between R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of VO(2 max). At 90% of VO(2 max), Pa(O(2)) was lower during R (mean +/- SE = 94 +/- 2 Torr) than during C (105 +/- 2 Torr, P < 0.0001), as was ventilation (85.2 +/- 3.8 vs. 98.2 +/- 4.4 l/min BTPS, P < 0.0001) and cardiac output (19.1 +/- 0.6 vs. 21.1 +/- 1.0 l/min, P < 0.001). Arterial PCO(2) (32.0 +/- 0.5 vs. 30.0 +/- 0.6 Torr, P < 0.001) and alveolar-arterial O(2) difference (A-aDO(2); 22 +/- 2 vs. 16 +/- 2 Torr, P < 0.0001) were greater during R. Pa(O(2)) and A-aDO(2) were similar between slow and fast. Nadir Pa(O(2)) was 相似文献   

Aerobic training and cutaneous vasodilation in young and older men.

To determine the effect and underlying mechanisms of exercise training and the influence of age on the skin blood flow (SkBF) response to exercise in a hot environment, 22 young (Y; 18-30 yr) and 21 older (O; 61-78 yr) men were assigned to 16 wk of aerobic (A; YA, n = 8; OA, n = 11), resistance (R; YR, n = 7; OR, n = 3), or no training (C; YC, n = 7; OC, n = 7). Before and after treatment, subjects exercised at 60% of maximum oxygen consumption (VO2 max) on a cycle ergometer for 60 min at 36 degrees C. Cutaneous vascular conductance, defined as SkBF divided by mean arterial pressure, was monitored at control (vasoconstriction intact) and bretylium-treated (vasoconstriction blocked) sites on the forearm using laser-Doppler flowmetry. Forearm vascular conductance was calculated as forearm blood flow (venous occlusion plethysmography) divided by mean arterial pressure. Esophageal and skin temperatures were recorded. Only aerobic training (functionally defined a priori as a 5% or greater increase in VO2 max) produced a decrease in the mean body temperature threshold for increasing forearm vascular conductance (36.89 +/- 0.08 to 36.63 +/- 0.08 degrees C, P < 0.003) and cutaneous vascular conductance (36.91 +/- 0.08 to 36.65 +/- 0.08 degrees C, P < 0.004). Similar thresholds between control and bretylium-treated sites indicated that the decrease was mediated through the active vasodilator system. This shift was more pronounced in the older men who presented greater training-induced increases in VO2 max than did the young men (22 and 9%, respectively). In summary, older men improved their SkBF response to exercise-heat stress through the effect of aerobic training on the cutaneous vasodilator system.     

Fat energy use and plasma lipid changes associated with exercise intensity and temperature

The effect of 60 min of exercise at two intensities (50 and 60% VO2max) and temperatures (0 and 22 degrees C) on changes (delta) in plasma lipids [triglycerides (TG), glycerol (GLY), total cholesterol (TC), and HDL-cholesterol (HDL-C)] was examined. Subjects were 10 men aged 27 +/- 7 years (VO2max = 3.81 +/- 0.45 1 min, % fat = 12.2% +/- 7.1%). VO2 and respiratory exchange ratio results indicated that total energy and fat energy use were similar at the two temperatures. Changes in plasma volume (%delta PV) were different (P less than 0.05) at the two temperatures (22 degrees C: -2.3% vs 0 degrees C: 1.1%). Combining the data at each temperature revealed that the increases in concentrations were greater (P less than 0.05) at 22 degrees C (delta TG = 0.22, delta GLY = 0.20, delta TC = 0.14, delta HDL-C = 0.05 mmol l-1) vs 0 degrees C (delta TG = 0.10, delta GLY = 0.12, delta TC = 0.05, delta HDL-C = 0.02 mmol l-1). Combining the data for each intensity revealed that the increases in concentration were greater (P less than 0.05) at 60% VO2max for delta TG and delta HDL-C. The 60% VO2max/22 degrees C bout produced greater changes (P less than 0.05) than all other bouts for delta TC and delta HDL-C (0.21 and 0.08 mmol l-1, respectively). Only delta TG and delta GLY were greater at 22 degrees C when adjusted for %delta PV. These metabolic and plasma lipid results indicate that cold exposure does not act synergistically with exercise to further stimulate fat metabolism.     

Gender differences in the decline in aerobic capacity and its physiological determinants during the later decades of life.

We investigated the hemodynamic determinants of the age-associated decline in maximal oxygen uptake (V(O2 max)) and the influence of gender on the decline in V(O2 max) and its determinants in old and very old men and women. Sedentary, 60- to 92-yr-old women (n = 71) and men (n = 29), with no evidence of cardiovascular disease, underwent maximal treadmill exercise tests during which V(O2 max) and maximal cardiac output (Q(max)) were determined. V(O2 max) and age were inversely related in both women (-23 +/- 2 ml.min(-1).yr(-1); P < 0.0001) and men (-57 +/- 5 ml.min(-1).yr(-1); P < 0.0001). The absolute slope of the V(O2 max) vs. age relationship was twofold steeper in men than in women (P < 0.0001). Q(max) was also inversely related to age in a gender-specific manner (women = -87 +/- 25 ml.min(-1).yr(-1), P = 0.0009; men = -215 +/- 50 ml.min(-1).yr(-1), P = 0.0002; P = 0.01 women vs. men). Age-related changes in maximal exercise arteriovenous oxygen content difference (a-vD(O2)) were marginally different (P = 0.08) between women (-0.12 +/- 0.03 ml.dl(-1).yr(-1), P = 0.0003) and men (-0.22 +/- 0.04 ml.dl(-1).yr(-1), P < 0.0001). Age-associated decreases in Q(max) and a-vD(O2) contributed equally to the declines in V(O2 max) in both men and women. In the later stages of life, V(O2 max), Q(max), and a-vD(O2) decrease with age more rapidly in older men than they do in older women. As a result, the gender differences dissipate in the later decades of life. Declines in Q(max) and a-vD(O2) contribute equally to the age-related decrease in V(O2 max) in men and women.     

Enhanced protein breakdown after eccentric exercise in young and older men

The effects of eccentric exercise on whole body protein metabolism were compared in five young untrained [age 24 +/- 1 yr, maximal O2 uptake (VO2max) = 49 +/- 6 ml.kg-1.min-1] and five older untrained men (age 61 +/- 1 yr, VO2max = 34 +/- 2 ml.kg-1.min-1). They performed 45 min of eccentric exercise on a cycle ergometer at a power output equivalent to 80% VO2max (182 +/- 18 W). Beginning 5 days before exercise and continuing for at least 10 days after exercise, they consumed a eucaloric diet providing 1.5 g.kg-1.day-1 of protein. Leucine metabolism in the fed state was measured before, immediately after, and 10 days after exercise, with intravenous L-[1-13C]leucine as a tracer (0.115 mumol.kg-1.min-1). Leucine flux increased 9% immediately after exercise (P less than 0.011) and remained elevated 10 days later, with no effect of age. Leucine oxidation increased 19% immediately after exercise and remained 15% above baseline 10 days after exercise (P less than 0.0001), with no effect of age. In the young men, urinary excretion of 3-methylhistidine per gram of creatinine did not increase until 10 days postexercise (P less than 0.05), but in the older men, it increased 5 days after exercise and remained high through 10 days postexercise (P less than 0.05), averaging 37% higher than in the young men. These data suggest that eccentric exercise produces a similar increase in whole body protein breakdown in older and young men, but myofibrillar proteolysis may contribute more to whole body protein breakdown in the older group.     

Effect of maternal weight gain during pregnancy on exercise performance

We examined the effect of maternal weight gain during pregnancy on exercise performance. Ten women performed submaximal cycle (up to 60 W) and treadmill (4 km/h, up to 10% grade) exercise tests at 34 +/- 1.5 (SD) wk gestation and 7.6 +/- 1.7 wk postpartum. Postpartum subjects wearing weighted belts designed to equal their body weight during the antepartum tests performed two additional treadmill tests. Absolute O2 uptake (VO2) at the same work load was higher during pregnancy than postpartum during cycle (1.04 +/- 0.08 vs. 0.95 +/- 0.09 l/min, P = 0.014), treadmill (1.45 +/- 0.19 vs. 1.27 +/- 0.20 l/min, P = 0.0002), and weighted treadmill (1.45 +/ 0.19 vs. 1.36 +/- 0.20 l/min, P = 0.04) exercise. None of these differences remained, however, when VO2 was expressed per kilogram of body weight. Maximal VO2 (VO2max) estimated from the individual heart rate-VO2 curves was the same during and after pregnancy during cycling (1.96 +/- 0.37 to 1.98 +/- 0.39 l/min), whereas estimated VO2max increased postpartum during treadmill (2.04 +/- 0.38 to 2.21 +/- 0.36 l/min, P = 0.03) and weighted treadmill (2.04 +/- 0.38 to 2.19 +/- 0.38 l/min, P = 0.03) exercise. We conclude that increased body weight during pregnancy compared with the postpartum period accounts for 75% of the increased VO2 during submaximal weight-bearing exertion in pregnancy and contributes to reduced exercise capacity. The postpartum increase in estimated VO2max during weight-bearing exercise is the result of consistently higher antepartum heart rates during all submaximal work loads.     

Decreased maximal heart rate with aging is related to reduced {beta}-adrenergic responsiveness but is largely explained by a reduction in intrinsic heart rate.

A decrease in maximal exercise heart rate (HR(max)) is a key contributor to reductions in aerobic exercise capacity with aging. However, the mechanisms involved are incompletely understood. We sought to gain insight into the respective roles of intrinsic heart rate (HR(int)) and chronotropic beta-adrenergic responsiveness in the reductions in HR(max) with aging in healthy adults. HR(max) (Balke treadmill protocol to exhaustion), HR(int) (HR during acute ganglionic blockade with intravenous trimethaphan), and chronotropic beta-adrenergic responsiveness (increase in HR with incremental intravenous infusion of isoproterenol during ganglionic blockade) were determined in 15 older (65 +/- 5 yr) and 15 young (25 +/- 4 yr) healthy men. In the older men, HR(max) was lower (162 +/- 9 vs. 191 +/- 11 beats/min, P < 0.0001) and was associated with a lower HR(int) (58 +/- 7 vs. 83 +/- 9 beats/min, P < 0.0001) and chronotropic beta-adrenergic responsiveness (0.094 +/- 0.036 vs. 0.154 +/- 0.045 DeltaHR/[isoproterenol]: P < 0.0001). Both HR(int) (r = 0.87, P < 0.0001) and chronotropic beta-adrenergic responsiveness (r = 0.61, P < 0.0001) were positively related to HR(max). Accounting for the effects of HR(int) and chronotropic beta-adrenergic responsiveness reduced the age-related difference in HR(max) by 83%, rendering it statistically nonsignificant (P = 0.2). Maximal oxygen consumption was lower in the older men (34.9 +/- 8.1 vs. 48.6 +/- 6.7 ml x kg(-1) x min(-1), P < 0.0001) and was positively related to HR(max) (r = 0.62, P < 0.0001), HR(int) (r = 0.51, P = 0.002), and chronotropic beta-adrenergic responsiveness (r = 0.47, P = 0.005). Our findings indicate that, together, reductions in HR(int) and chronotropic responsiveness to beta-adrenergic stimulation largely explain decreases in HR(max) with aging, with the reduction in HR(int) playing by far the greatest role.     

Effect of carbohydrate feedings during high-intensity exercise

To determine the upper limits of steady-state exercise performance and carbohydrate oxidation late in exercise, seven trained men were studied on two occasions during prolonged cycling that alternated every 15 min between approximately 60% and approximately 85% of VO2max. When fed a sweet placebo throughout exercise, plasma glucose and respiratory exchange ratio (R) declined (P less than 0.05) from 5.0 +/- 0.1 mM and 0.91 +/- 0.01 after 30 min (i.e., at 85% VO2max) to 3.7 +/- 0.3 mM and 0.79 +/- 0.01 at fatigue (i.e., when the subjects were unable to continue exercise at 60% VO2max). Carbohydrate feeding throughout exercise (1 g/kg at 10 min, then 0.6 g/kg every 30 min) increased plasma glucose to approximately 6 mM and partially prevented this decline in carbohydrate oxidation, allowing the men to perform 19% more work (2.74 +/- 0.13 vs. 2.29 +/- 0.09 MJ, P less than 0.05) before fatiguing. Even when fed carbohydrate, however, by the 3rd h of exercise, R had fallen from 0.92 to 0.87, accompanied by a reduction in exercise intensity from approximately 85% to approximately 75% VO2max (both P less than 0.05). These data indicate that carbohydrate feedings enable trained cyclists to exercise at up to 75% VO2max and to oxidize carbohydrate at up to 2 g/min during the later stages of prolonged intense exercise.     

Rectal and rectal vs. esophageal temperatures in paraplegic men during prolonged exercise

This study investigated the rectal (Tre), esophageal (Tes), and skin (Tsk) temperature changes in a group of trained traumatic paraplegic men pushing their own wheelchairs on a motor-driven treadmill for a prolonged period in a neutral environment. There were two experiments. The first experiment (Tre and Tsk) involved a homogeneous group (T10-T12/L3) of highly trained paraplegic men [maximum O2 uptake (VO2max) 47.5 +/- 1.8 ml.kg-1.min-1] exercising for 80 min at 60-65% VO2max.Tre and Tsk (head, arm, thigh, and calf) and heart rate (HR) were recorded throughout. O2 uptake (VO2), minute ventilation (VE), CO2 production (VCO2), and heart rate (HR) were recorded at four intervals. During experiment 1 significant changes in HR and insignificant changes in VCO2, VE, and VO2 occurred throughout prolonged exercise. Tre increased significantly from 37.1 +/- 0.1 degrees C (rest) to 37.8 +/- 0.1 degrees C after 80 min of exercise. There were only significant changes in arm Tsk. Experiment 2 involved a nonhomogeneous group (T5-T10/T11) of active paraplegics (VO2max 39.9 +/- 4.3 ml.kg-1.min-1) exercising at 60-65% VO2max for up to 45 min on the treadmill while Tre and Tes were simultaneously recorded. Tes rose significantly faster than Tre during exercise (dT/dt 20 min: Tes 0.050 +/- 0.003 degrees C/min and Tre 0.019 +/- 0.005 degrees C/min), and Tes declined significantly faster than Tre at the end of exercise. Tes was significantly higher than Tre at the end of exercise. Our results suggest that during wheelchair propulsion by paraplegics, Tes may be a better estimate of core temperature than Tre.     

Endurance training of older men: responses to submaximal exercise.

The purpose of this study was to quantify the exercise response of older subjects on a time-to-fatigue (TTF) submaximal performance test before and after a training program. Eight older men (67.4 +/- 4.8 yr) performed two maximal treadmill tests to determine maximum oxygen uptake (VO2max) and ventilation threshold (TVE) and a constant-load submaximal exercise treadmill test that required an oxygen uptake (VO2) between TVE and VO2max. The submaximal test, performed at the same absolute work rate before and after the training program, was performed to volitional fatigue to measure endurance time. The men trained under supervision at an individualized pace representing approximately 70% of VO2max (80% maximum heart rate) for 1 h, four times per week for 9 wk. Significant increases were demonstrated for VO2max (ml.kg-1.min-1; 10.6%); maximal ventilation (VE, l/min; 11.6%), and TVE (l/min; 9.8%). Weight decreased 2.1%. Performance time on the TTF test increased by 180% (7.3 +/- 3.0 to 20.4 +/- 13.5 min). The similar end points for VO2, VE, and heart rate during the TTF and maximal treadmill tests established that the TTF test was stopped because of physiological limitations. The increase in performance time among the subjects was significantly correlated with improvements in VO2max and TVE, with the submaximal work rate representing a VO2 above TVE by 88% of the difference between TVE and VO2max pretraining and 73% of this difference on posttraining values.     

Stroke volume during exercise: interaction of environment and hydration

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O(2) consumption (VO(2 max)) 4.5 +/- 0.1 l/min; means +/- SE] cycled for 30 min (72% VO(2 max)) in the heat (H; 35 degrees C) or the cold (C; 8 degrees C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (T(es) 38. 2-38.3 degrees C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 +/- 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 +/- 1.3 ml (4.8%) in H and 3.4 +/- 0.4 ml (2.5%) in C, whereas T(es) increased 0.21 +/- 0.02 and 0. 10 +/- 0.02 degrees C in H and C, respectively (P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H (R = 0.96; P < 0.01) and C (R = 0. 85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.     

Effects of marked hyperthermia with and without dehydration on VO(2) kinetics during intense exercise.

This study determined whether marked hyperthermia alone or in combination with dehydration reduces the initial rate of rise in O(2) consumption (VO(2) on-kinetics) and the maximal rate of O(2) uptake (VO(2 max)) during intense cycling exercise. Six endurance-trained male cyclists completed four maximal cycle ergometer exercise tests (402 +/- 4 W) when euhydrated or dehydrated (4% body wt) with normal (starting esophageal temperature, 37.5 +/- 0.2 degrees C; mean skin temperature, approximately 31 degrees C) or elevated (+1 and +6 degrees C, respectively) thermal strain. In the euhydrated and normal condition, subjects reached VO(2 max) (4.7 +/- 0.2 l/min) in 228 +/- 34 s, with a mean response time of 42 +/- 2 s, and fatigued after 353 +/- 39 s. Hyperthermia alone or in combination with dehydration reduced mean response time (17-23%), VO(2 max) (16%), and performance time (51-53%) (all P < 0.01) but did not alter the absolute response time (i.e., the time to reach 63% response in the control trial, 3.2 +/- 0.1 l/min, 42 s). Reduction in VO(2 max) was accompanied by proportional decline in O(2) pulse and significantly elevated maximal heart rate (195 vs. 190 beats/min for hyperthermia vs. normal). Preventing hyperthermia in dehydrated subjects restored VO(2 max) and performance time by 65 and 50%, respectively. These results demonstrate that impaired high-intensity exercise performance with marked skin and internal body hyperthermia alone or in combination with dehydration is not associated with a diminished rate of rise in VO(2) but decreased VO(2 max).     

Physiological factors associated with the lower maximal oxygen consumption of master runners

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.     

Effect of inspiratory threshold loading on ventilatory kinetics during constant-load exercise

Humoral factors play an important role in the control of exercise hyperpnea. The role of neuromechanical ventilatory factors, however, is still being investigated. We tested the hypothesis that the afferents of the thoracopulmonary system, and consequently of the neuromechanical ventilatory loop, have an influence on the kinetics of oxygen consumption (VO2), carbon dioxide output (VCO2), and ventilation (VE) during moderate intensity exercise. We did this by comparing the ventilatory time constants (tau) of exercise with and without an inspiratory load. Fourteen healthy, trained men (age 22.6 +/- 3.2 yr) performed a continuous incremental cycle exercise test to determine maximal oxygen uptake (VO2max = 55.2 +/- 5.8 ml x min(-1) x kg(-1)). On another day, after unloaded warm-up they performed randomized constant-load tests at 40% of their VO2max for 8 min, one with and the other without an inspiratory threshold load of 15 cmH2O. Ventilatory variables were obtained breath by breath. Phase 2 ventilatory kinetics (VO2, VCO2, and VE) could be described in all cases by a monoexponential function. The bootstrap method revealed small coefficients of variation for the model parameters, indicating an accurate determination for all parameters. Paired Student's t-tests showed that the addition of the inspiratory resistance significantly increased the tau during phase 2 of VO2 (43.1 +/- 8.6 vs. 60.9 +/- 14.1 s; P < 0.001), VCO2 (60.3 +/- 17.6 vs. 84.5 +/- 18.1 s; P < 0.001) and VE (59.4 +/- 16.1 vs. 85.9 +/- 17.1 s; P < 0.001). The average rise in tau was 41.3% for VO2, 40.1% for VCO2, and 44.6% for VE. The tau changes indicated that neuromechanical ventilatory factors play a role in the ventilatory response to moderate exercise.     

Development of a submaximal test to predict elliptical cross-trainer VO2max

The purpose of this study was to develop an equation to predict VO2max from a submaximal elliptical cross-trainer test. Fifty-four apparently healthy subjects (25 men and 29 women, mean +/- SD age: 29.5 +/- 7.1 years, height: 173.3 +/- 12.6 cm, weight: 72.3 +/- 7.9 kg, percent body fat: 17.3 +/- 5.0%, and elliptical cross-trainer VO2max: 43.9 +/- 7.2 ml x kg(-1) x min(-1)) participated in the study and were randomly assigned to an original sample group (n = 40) and a cross-validation group (n = 14). Each subject completed an elliptical cross-trainer submaximal (3 5-minute submaximal stages) and a VO2max test on the same day, with a 15-minute rest period in between. Stepwise multiple regression analyses were used to develop an equation for estimating elliptical cross-trainer VO2max from the data of the original sample group. The accuracy of the equation was tested by using data from the cross-validation group. Because there was no shrinkage in R2 between the original sample group and the cross-validation group, data were combined in the final prediction equation (R2 = 0.732, standard error of the estimate = 3.91 ml x kg(-1) x min(-1), p < 0.05): VO2max = 73.676 + 7.383(gender) - 0.317(weight) + 0.003957(age x cadence) - 0.006452(age x heart rate at stage 2). The correlation coefficient between the predicted and measured VO2max values was r = 0.86. Dependent t-tests resulted in no significant differences (p > 0.05) between predicted (43.8 ml x kg(-1) x min(-1)) and measured (43.9 ml x kg(-1) x min(-1)) VO2max measurements. Results indicate that the protocol and equation developed in the current study can be used by exercise professionals to provide acceptably accurate estimates of VO2max in non-laboratory-based settings.     

Oxygen uptake kinetics during treadmill running in boys and men.

The purpose of this study was to compare the kinetics of the oxygen uptake (VO(2)) response of boys to men during treadmill running using a three-phase exponential modeling procedure. Eight boys (11-12 yr) and eight men (21-36 yr) completed an incremental treadmill test to determine lactate threshold (LT) and maximum VO(2). Subsequently, the subjects exercised for 6 min at two different running speeds corresponding to 80% of VO(2) at LT (moderate exercise) and 50% of the difference between VO(2) at LT and maximum VO(2) (heavy exercise). For moderate exercise, the time constant for the primary response was not significantly different between boys [10.2 +/- 1.0 (SE) s] and men (14.7 +/- 2.8 s). The gain of the primary response was significantly greater in boys than men (239.1 +/- 7.5 vs. 167.7 +/- 5.4 ml. kg(-1). km(-1); P < 0.05). For heavy exercise, the VO(2) on-kinetics were significantly faster in boys than men (primary response time constant = 14.9 +/- 1.1 vs. 19.0 +/- 1.6 s; P < 0.05), and the primary gain was significantly greater in boys than men (209.8 +/- 4.3 vs. 167.2 +/- 4.6 ml. kg(-1). km(-1); P < 0.05). The amplitude of the VO(2) slow component was significantly smaller in boys than men (19 +/- 19 vs. 289 +/- 40 ml/min; P < 0.05). The VO(2) responses at the onset of moderate and heavy treadmill exercise are different between boys and men, with a tendency for boys to have faster on-kinetics and a greater initial increase in VO(2) for a given increase in running speed.     

Early onset of pulmonary gas exchange disturbance during progressive exercise in healthy active men.

Some recent studies of competitive athletes have shown exercise-induced hypoxemia to begin in submaximal exercise. We examined the role of ventilatory factors in the submaximal exercise gas exchange disturbance (GED) of healthy men involved in regular work-related exercise but not in competitive activities. From the 38 national mountain rescue workers evaluated (36 +/- 1 yr), 14 were classified as GED and were compared with 14 subjects matched for age, height, weight, and maximal oxygen uptake (VO2 max; 3.61 +/- 0.12 l/min) and showing a normal response (N). Mean arterial PO2 was already lower than N (P = 0.05) at 40% VO2 max and continued to fall until VO2 max (GED: 80.2 +/- 1.6 vs. N: 91.7 +/- 1.3 Torr). A parallel upward shift in the alveolar-arterial oxygen difference vs. %VO2 max relationship was observed in GED compared with N from the onset throughout the incremental protocol. At submaximal intensities, ideal alveolar PO2, tidal volume, respiratory frequency, and dead space-to-tidal volume ratio were identical between groups. As per the higher arterial PCO2 of GED at VO2 max, subjects with an exaggerated submaximal alveolar-arterial oxygen difference also showed a relative maximal hypoventilation. Results thus suggest the existence of a common denominator that contributes to the GED of submaximal exercise and affects the maximal ventilatory response.     

Effects of prior exercise on muscle metabolism during sprint exercise in horses.

The effect of warm-up exercise on energy metabolism and muscle glycogenolysis during sprint exercise (Spr) was examined in six fit Standardbred horses exercised at 115% of maximal O(2) consumption (VO(2 max)) until fatigued, 5 min after each of three protocols: 1) no warm-up (NWU); 2) 10 min at 50% of VO(2 max) [low-intensity warm-up (LWU)]; and 3) 7 min at 50% VO(2 max) followed by 45-s intervals at 80, 90, and 100% VO(2 max) [high-intensity warm-up (HWU)]. Warm-up increased (P < 0.0001) muscle temperature (T(m)) at the onset of Spr in LWU (38.3 +/- 0.2 degrees C) and HWU (40.0 +/- 0. 3 degrees C) compared with NWU (36.6 +/- 0.2 degrees C), and the rate of rise in T(m) during Spr was greater in NWU than in LWU and HWU (P < 0.01). Peak VO(2) was higher and O(2) deficit lower (P < 0. 05) when Spr was preceded by warm-up. Rates of muscle glycogenolysis were lower (P < 0.05) in LWU, and rates of blood and muscle lactate accumulation and anaerobic ATP provision during Spr were lower in LWU and HWU compared with NWU. Mean runtime (s) in LWU (173 +/- 10 s) was greater than HWU (142 +/- 11 s) and NWU (124 +/- 4 s) (P < 0. 01). Warm-up was associated with augmentation of aerobic energy contribution to total energy expenditure, decreased glycogenolysis, and longer run time to fatigue during subsequent sprint exercise, with no additional benefit from HWU vs. LWU.