Inspiratory muscle fatigue increases sympathetic vasomotor outflow and blood pressure during submaximal exercise

The purpose of this study was to elucidate the influence of inspiratory muscle fatigue on muscle sympathetic nerve activity (MSNA) and blood pressure (BP) response during submaximal exercise. We hypothesized that inspiratory muscle fatigue would elicit increases in sympathetic vasoconstrictor outflow and BP during dynamic leg exercise. The subjects carried out four submaximal exercise tests: two were maximal inspiratory pressure (PI(max)) tests and two were MSNA tests. In the PI(max) tests, the subjects performed two 10-min exercises at 40% peak oxygen uptake using a cycle ergometer in a semirecumbent position [spontaneous breathing for 5 min and with or without inspiratory resistive breathing for 5 min (breathing frequency: 60 breaths/min, inspiratory and expiratory times were each set at 0.5 s)]. Before and immediately after exercise, PI(max) was estimated. In MSNA tests, the subjects performed two 15-min exercises (spontaneous breathing for 5 min, with or without inspiratory resistive breathing for 5 min, and spontaneous breathing for 5 min). MSNA was recorded via microneurography of the right median nerve at the elbow. PI(max) decreased following exercise with resistive breathing, whereas no change was found without resistance. The time-dependent increase in MSNA burst frequency (BF) appeared during exercise with inspiratory resistive breathing, accompanied by an augmentation of diastolic BP (DBP) (with resistance: MSNA, BF +83.4%; DBP, +23.8%; without resistance: MSNA BF, +19.2%; DBP, -0.4%, from spontaneous breathing during exercise). These results suggest that inspiratory muscle fatigue induces increases in muscle sympathetic vasomotor outflow and BP during dynamic leg exercise at mild intensity.     

Maximal oxygen uptake is not limited by a central nervous system governor.

We tested the hypothesis that the work of the heart was not a limiting factor in the attainment of maximal oxygen uptake (VO2 max). We measured cardiac output (Q) and blood pressures (BP) during exercise at two different rates of maximal work to estimate the work of the heart through calculation of the rate-pressure product, as a part of the ongoing discussion regarding factors limiting VO2 max. Eight well-trained men (age 24.4 +/- 2.8 yr, weight 81.3 +/- 7.8 kg, and VO2 max 59.1 +/- 2.0 ml x min(-1) x kg(-1)) performed two maximal combined arm and leg exercises, differing 10% in watts, with average duration of time to exhaustion of 4 min 50 s and 3 min 40 s, respectively. There were no differences between work rates in measured VO2 max, maximal Q, and peak heart rate between work rates (0.02 l/min, 0.3 l/min, and 0.8 beats/min, respectively), but the systolic, diastolic, and calculated mean BP were significantly higher (19, 5, and 10 mmHg, respectively) in the higher than in the lower maximal work rate. The products of heart rate times systolic or mean BP and Q times systolic or mean BP were significantly higher (3,715, 1,780, 569, and 1,780, respectively) during the higher than the lower work rate. Differences in these four products indicate a higher mechanical work of the heart on higher than lower maximal work rate. Therefore, this study does not support the theory, which states that the work of the heart, and consequently VO2 max, during maximal exercise is hindered by a command from the central nervous system aiming at protecting the heart from being ischemic.     

Vascular and metabolic response to isolated small muscle mass exercise: effect of age

To determine the effect of age on quadriceps muscle blood flow (QMBF), leg vascular resistance (LVR), and maximum oxygen uptake (QVO2 max), a thermal dilution technique was used in conjunction with arterial and venous femoral blood sampling in six sedentary young (19.8 +/- 1.3 yr) and six sedentary old (66.5 +/- 2.1 yr) males during incremental knee extensor exercise (KE). Young and old attained a similar maximal KE work rate (WRmax) (young: 25.2 +/- 2.1 and old: 24.1 +/- 4 W) and QVO2 max (young: 0.52 +/- 0.03 and old: 0.42 +/- 0.05 l/min). QMBF during KE was lower in old subjects by approximately 500 ml/min across all work rates, with old subjects demonstrating a significantly lower QMBF/W (old: 174 +/- 20 and young: 239 +/- 46 ml. min-1. W-1). Although the vasodilatory response to incremental KE was approximately 142% greater in the old (young: 0.0019 and old: 0.0046 mmHg. min. ml-1. W-1), consistently elevated leg vascular resistance (LVR) in the old, approximately 80% higher LVR in the old at 50% WR and approximately 40% higher LVR in the old at WRmax (young: 44.1 +/- 3.6 and old: 31.0 +/- 1.7 mmHg. min. ml-1), dictated that during incremental KE the LVR of the old subjects was never less than that of the young subjects. Pulse pressures, indicative of arterial vessel compliance, were approximately 36% higher in the old subjects across all work rates. In conclusion, well-matched sedentary young and old subjects with similar quadriceps muscle mass achieved a similar WRmax and QVO2 max during incremental KE. The old subjects, despite a reduced QMBF, had a greater vasodilatory response to incremental KE. Given that small muscle mass exercise, such as KE, utilizes only a fraction of maximal cardiac output, peripheral mechanisms such as consistently elevated leg vascular resistance and greater pulse pressures appear to be responsible for reduced blood flow persisting throughout graded KE in the old subjects.     

Cardiopulmonary responses to exercise in obese girls and young women.

A study of exercise performance was carried out in 17 obese girls and young adults. During submaximal steady-state bicycle exercise oxygen intake (Vo2) for a given work output (W) was raised in obese subjects but minute ventilation at a fixed carbon dioxide output, gas exchange, blood gases, and cardiac output at a given VO2 were similar to the values previously found for normals. In obese subjects high levels of VO2 for fixed W were also obtained on the treadmill but when these were standardized for body weight (unlike the bicycle test) it was shown that the obese girls and women exercised within the normal (expected) range of aerobic energy expenditure. During maximal performance the absolute VO2 max was the same in obese and nonobese subjects but for a given body weight, lean body mass, and leg muscle (plus) bone volume, VO2max was reduced by 23.8, 16.3, and 24.5% respectively, in the former group. It was concluded that obesity though having minimal affect on responses to submaximal exercise is nevertheless associated with a marked reduction in physiological performance at or near maximal effort.     

Angiotensin-converting enzyme ID polymorphism and fitness phenotype in the HERITAGE Family Study.

It has been suggested that genetic variation in the angiotensin-converting enzyme (ACE) gene is associated with physical performance. We studied the association between the ACE insertion (I)/deletion (D) polymorphism and several fitness phenotypes measured before and after 20 wk of a standardized endurance training program in sedentary Caucasian (n = 476) and black (n = 248) subjects. Phenotypes measured were oxygen uptake (VO(2)), work rate, heart rate, minute ventilation, tidal volume, and blood lactate levels during maximal and submaximal [50 W and at 60 and 80% of maximal VO(2) (VO(2 max))] exercise and stroke volume and cardiac output during submaximal exercise (50 W and at 60% VO(2 max)). The ACE ID polymorphism was typed with the three-primer PCR method. Out of 216 association tests performed on 54 phenotypes in 4 groups of participants, only 11 showed significant (P values from 0.042 to 0. 0001) associations with the ACE ID polymorphism. In contrast to previous claims, in Caucasian offspring, the DD homozygotes showed a 14-38% greater increase with training in VO(2 max), VO(2) at 80% of VO(2 max), and all work rate phenotypes and a 36% greater decrease in heart rate at 50 W than did the II homozygotes. No associations were evident in Caucasian parents or black parents or offspring. Thus these data do not support the hypothesis that the ACE ID polymorphism plays a major role in cardiorespiratory endurance.     

Effects of short-term training using powercranks on cardiovascular fitness and cycling efficiency

Powercranks use a specially designed clutch to promote independent pedal work by each leg during cycling. We examined the effects of 6 wk of training on cyclists using Powercranks (n=6) or normal cranks (n=6) on maximal oxygen consumption (VO2max) and anaerobic threshold (AT) during a graded exercise test (GXT), and heart rate (HR), oxygen consumption (VO2), respiratory exchange ration (RER), and gross efficiency (GE) during a 1-hour submaximal ride at a constant load. Subjects trained at 70% of VO2max for 1 h.d(-1), 3 d.wk(-1), for 6 weeks. The GXT and 1-hour submaximal ride were performed using normal cranks pretraining and posttraining. The 1-hour submaximal ride was performed at an intensity equal to approximately 69% of pretraining VO2max with VO2, RER, GE, and HR determined at 15-minute intervals during the ride. No differences were observed between or within groups for VO2max or AT during the GXT. The Powercranks group had significantly higher GE values than the normal cranks group (23.6 +/- 1.3% versus 21.3 +/- 1.7%, and 23.9 +/- 1.4% versus 21.0 +/- 1.9% at 45 and 60 min, respectively), and significantly lower HR at 30, 45, and 60 minutes and VO2 at 45 and 60 minutes during the 1-hour submaximal ride posttraining. It appears that 6 weeks of training with Powercranks induced physiological adaptations that reduced energy expenditure during a 1-hour submaximal ride.     

Effects of respiratory muscle work on exercise performance.

The normal respiratory muscle effort at maximal exercise requires a significant fraction of cardiac output and causes leg blood flow to fall. We questioned whether the high levels of respiratory muscle work experienced in heavy exercise would affect performance. Seven male cyclists [maximal O(2) consumption (VO(2)) 63 +/- 5 ml. kg(-1). min(-1)] each completed 11 randomized trials on a cycle ergometer at a workload requiring 90% maximal VO(2). Respiratory muscle work was either decreased (unloading), increased (loading), or unchanged (control). Time to exhaustion was increased with unloading in 76% of the trials by an average of 1.3 +/- 0.4 min or 14 +/- 5% and decreased with loading in 83% of the trials by an average of 1.0 +/- 0.6 min or 15 +/- 3% compared with control (P < 0.05). Respiratory muscle unloading during exercise reduced VO(2), caused hyperventilation, and reduced the rate of change in perceptions of respiratory and limb discomfort throughout the duration of exercise. These findings demonstrate that the work of breathing normally incurred during sustained, heavy-intensity exercise (90% VO(2)) has a significant influence on exercise performance. We speculate that this effect of the normal respiratory muscle load on performance in trained male cyclists is due to the associated reduction in leg blood flow, which enhances both the onset of leg fatigue and the intensity with which both leg and respiratory muscle efforts are perceived.     

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.     

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.     

Vascular and metabolic response to cycle exercise in sedentary humans: effect of age

We measured leg blood flow (LBF), drew arterial-venous (A-V) blood samples, and calculated muscle O(2) consumption (VO(2)) during incremental cycle ergometry exercise [15, 30, and 99 W and maximal effort (maximal work rate, WR(max))] in nine sedentary young (20 +/- 1 yr) and nine sedentary old (70 +/- 2 yr) males. LBF was preserved in the old subjects at 15 and 30 W. However, at 99 W and at WR(max), leg vascular conductance was attenuated because of a reduced LBF (young: 4.1 +/- 0.2 l/min and old: 3.1 +/- 0.3 l/min) and an elevated mean arterial blood pressure (young: 112 +/- 3 mmHg and old: 132 +/- 3 mmHg) in the old subjects. Leg A-V O(2) difference changed little with increasing WR in the old group but was elevated compared with the young subjects. Muscle maximal VO(2) and cycle WR(max) were significantly lower in the old subjects (young: 0.8 +/- 0.05 l/min and 193 +/- 7 W; old: 0.5 +/- 0.03 l/min and 117 +/- 10 W). The submaximally unchanged and maximally reduced cardiac output associated with aging coupled with its potential maldistribution are candidates for the limited LBF during moderate to heavy exercise in older sedentary subjects.     

Effect of fatigue on maximal power output at different contraction velocities in humans.

The effect of fatigue as a result of a standard submaximal dynamic exercise on maximal short-term power output generated at different contraction velocities was studied in humans. Six subjects performed 25-s maximal efforts on an isokinetic cycle ergometer at five different pedaling rates (60, 75, 90, 105, and 120 rpm). Measurements of maximal power output were made under control conditions [after 6 min of cycling at 30% maximal O2 uptake (VO2max)] and after fatiguing exercise that consisted of 6 min of cycling at 90% VO2max with a pedaling rate of 90 rpm. Compared with control values, maximal peak power measured after fatiguing exercise was significantly reduced by 23 +/- 19, 28 +/- 11, and 25 +/- 11% at pedaling rates of 90, 105, and 120 rpm, respectively. Reductions in maximum peak power of 11 +/- 8 and 14 +/- 8% at 60 and 75 rpm, respectively, were not significant. The rate of decline in peak power during the 25-s control measurement was least at 60 rpm (5.1 +/- 2.3 W/s) and greatest at 120 rpm (26.3 +/- 13.9 W/s). After fatiguing exercise, the rate of decline in peak power at pedaling rates of 105 and 120 rpm decreased significantly from 21.5 +/- 9.0 and 26.3 +/- 13.9 W/s to 10.0 +/- 7.3 and 13.3 +/- 6.9 W/s, respectively. These experiments indicate that fatigue induced by submaximal dynamic exercise results in a velocity-dependent effect on muscle power. It is suggested that the reduced maximal power at the higher velocities was due to a selective effect of fatigue on the faster fatigue-sensitive fibers of the active muscle mass.     

Dynamic exercise training in foxhounds. I. Oxygen consumption and hemodynamic responses

Ten foxhounds were studied during maximal and submaximal exercise on a motor-driven treadmill before and after 8-12 wk of training. Training consisted of working at 80% of maximal heart rate 1 h/day, 5 days/wk. Maximal O2 consumption (VO2max) increased 28% from 113.7 +/- 5.5 to 146.1 +/- 5.4 ml O2 X min-1 X kg-1, pre- to posttraining. This increase in VO2max was due primarily to a 27% increase in maximal cardiac output, since maximal arteriovenous O2 difference increased only 4% above pretraining values. Mean arterial pressure during maximal exercise did not change from pre- to posttraining, with the result that calculated systemic vascular resistance (SVR) decreased 20%. There were no training-induced changes in O2 consumption, cardiac output, arteriovenous O2 difference, mean arterial pressure, or SVR at any level of submaximal exercise. However, if post- and pretraining values are compared, heart rate was lower and stroke volume was greater at any level of submaximal exercise. Venous lactate concentrations during a given level of submaximal exercise were significantly lower during posttraining compared with pretraining, but venous lactate concentrations during maximal exercise did not change as a result of exercise training. These results indicate that a program of endurance training will produce a significant increase in VO2max in the foxhound. This increase in VO2max is similar to that reported previously for humans and rats but is derived primarily from central (stroke volume) changes rather than a combination of central and peripheral (O2 extraction) changes.     

The effects of one- and two-legged exercise on the lactate and ventilatory threshold

The purpose of this investigation was to compare differences between one- and two-legged exercise on the lactate (LT) and ventilation (VT) threshold. On four separate occasions, eight male volunteer subjects (1-leg VO2max = 3.36 l X min-1; 2-leg VO2max = 4.27 l X min-1) performed 1- and 2-legged submaximal and maximal exercise. Submaximal threshold tests for 1- and 2-legs, began with a warm-up at 50 W and then increased every 3 minutes by 16 W and 50 W, respectively. Similar increments occurred every minute for the maximal tests. Venous blood samples were collected during the last 30 s of each work load, whereas noninvasive gas measures were calculated every 30 s. No differences in VO2 (l X min-1) were found between 1- and 2-legs at LT or VT, but significant differences (p less than 0.05) were recorded at a given power output. Lactate concentration ([LA]) was different (p less than 0.05) between 1- and 2-legs (2.52 vs. 1.97 mmol X l-1) at LT. This suggests it is VO2 rather than muscle mass which affects LT and VT. VO2max for 1-leg exercise was 79% of the 2-leg value. This implies the central circulation rather than the peripheral muscle is limiting to VO2max.     

Cardiorespiratory deconditioning with static and dynamic leg exercise during bed rest.

Bed rest deconditioning was assessed in seven healthy men (19-22 yr) following three 14-day periods of controlled activity during recumbency by measuring submaximal and maximal oxygen uptake (VO2), ventilation (VE), heart rate, and plasma volume. Exercise regimens were performed in the supine position and included a) two 30-min periods daily of intermittent static exercise at 21% of maximal leg extension force, and b) two 30-min periods of dynamic bicycle ergometer exercise daily at 68% of VO2max. No prescribed exercise was performed during the third bed rest period. Compared with their respective pre-bed rest control values, VO2max decreased (P less than 0.05) under all exercise conditions; -12.3% with no exercise, -9.2% with dynamic exercise, but only -4.8% with static exercise. Maximal heart rate was increased by 3.3% to 4.9% (P less than 0.05) under the three exercise conditions, while plasma volume decreased (P less than 0.05) -15.1% with no exercise and -10.1% with static, but only -7.8% (NS) with dynamic exercise. Since neither the static nor dynamic exercise training regimes minimized the changes in all the variables studied, some combination of these two types of exercise may be necessary for maximum protection from the effects of the bed deconditioning.     

Effect of exercise on cerebral perfusion in humans at high altitude.

The effects of submaximal and maximal exercise on cerebral perfusion were assessed using a portable, recumbent cycle ergometer in nine unacclimatized subjects ascending to 5,260 m. At 150 m, mean (SD) cerebral oxygenation (rSO2%) increased during submaximal exercise from 68.4 (SD 2.1) to 70.9 (SD 3.8) (P < 0.0001) and at maximal oxygen uptake (.VO2(max)) to 69.8 (SD 3.1) (P < 0.02). In contrast, at each of the high altitudes studied, rSO2 was reduced during submaximal exercise from 66.2 (SD 2.5) to 62.6 (SD 2.1) at 3,610 m (P < 0.0001), 63.0 (SD 2.1) to 58.9 (SD 2.1) at 4,750 m (P < 0.0001), and 62.4 (SD 3.6) to 61.2 (SD 3.9) at 5,260 m (P < 0.01), and at .VO2(max) to 61.2 (SD 3.3) at 3,610 m (P < 0.0001), to 59.4 (SD 2.6) at 4,750 m (P < 0.0001), and to 58.0 (SD 3.0) at 5,260 m (P < 0.0001). Cerebrovascular resistance tended to fall during submaximal exercise (P = not significant) and rise at .VO2(max), following the changes in arterial oxygen saturation and end-tidal CO(2). Cerebral oxygen delivery was maintained during submaximal exercise at 150 m with a nonsignificant fall at .VO2(max), but at high altitude peaked at 30% of .VO2(max) and then fell progressively at higher levels of exercise. The fall in rSO2 and oxygen delivery during exercise may limit exercise at altitude and is likely to contribute to the problems of acute mountain sickness and high-altitude cerebral edema.     

The effects of inspiratory intrathoracic pressure production on the cardiovascular response to submaximal exercise in health and chronic heart failure

We sought to determine whether the normal inspiratory intrathoracic pressures (P(ITP)) produced during exercise contribute to the blunted cardiac output and locomotor limb blood flow responses observed in chronic heart failure (CHF). Five chronically instrumented dogs exercised on a treadmill at 2.5 mile/h at 5% grade while healthy or after the induction of tachycardia-induced CHF. We observed several key differences in the cardiovascular responses to changes in the inspiratory P(ITP) excursion between health and CHF; namely, 1) removing approximately 70% of the normally produced inspiratory P(ITP) excursion during exercise (with 15 cmH(2)O inspiratory positive pressure ventilation) significantly reduced stroke volume (SV) in healthy animals by 5 +/- 2% (P < 0.05) but significantly increased SV and cardiac output (Q(TOT)) in animals with CHF by 5 +/- 1% (P < 0.05); 2) doubling the magnitude of the inspiratory P(ITP) excursion had no effect on SV or Q(TOT) in healthy animals but significantly reduced steady-state Q(TOT) and SV in animals with CHF by -4 +/- 3% and -10 +/- 3%, respectively; 3) removing the majority of the normally produced inspiratory P(ITP) excursion had no effect on blood flow distribution in healthy animals but increased hindlimb blood flow (9 +/- 3%, P < 0.05) out of proportion to the increases in Q(TOT); and 4) the only similarity between healthy and CHF animals was that increasing the inspiratory P(ITP) excursion significantly reduced steady-state locomotor limb blood flow by 5 +/- 2% and 6 +/- 3%, respectively (P < 0.05 for both). We conclude that 1) the normally produced inspiratory P(ITP) excursions are required for a maximal SV response to submaximal exercise in healthy animals but detrimental to the SV and Q(TOT) responses to submaximal exercise in CHF, 2) the respiratory muscle ergoreflex tonically restrains locomotor limb blood flow during submaximal exercise in CHF, and 3) excessive inspiratory muscle work further compromises cardiac function and blood flow distribution in both health and CHF.     

Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans

Our aim was to isolate the independent effects of 1) inspiratory muscle work (W(b)) and 2) arterial hypoxemia during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia [inspired O(2) fraction (Fi(O(2))) = 0.15, arterial hemoglobin saturation (Sa(O(2))) = 81 +/- 1%; 8.6 +/- 0.5 min, 273 +/- 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (Sa(O(2)) = 95 +/- 1%; Normoxia-Ctrl). These trials were repeated, but with a 35-80% reduction in W(b) achieved via proportional assist ventilation (PAV). Quadriceps twitch force was assessed via magnetic femoral nerve stimulation before and 2 min after exercise. The isolated effects of W(b) in hypoxia on quadriceps fatigue, independent of reductions in Sa(O(2)), were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of Sa(O(2)) (P = 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Q(tw,pot)) decreased by 30 +/- 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 +/- 4%; P = 0.0007). This effect of W(b) on quadriceps fatigue occurred at exercise work rates during which, in normoxia, reducing W(b) had no significant effect on fatigue. The isolated effects of reduced Sa(O(2)) on quadriceps fatigue, independent of changes in W(b), were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of W(b). Q(tw,pot) decreased by 15 +/- 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (-22 +/- 3%; P = 0.034). We conclude that both arterial hypoxemia and W(b) contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work rates during which, in normoxia, W(b) has no effect on peripheral fatigue.     

Cardiovascular responses of 70- to 79-yr-old men and women to exercise training

This study determined the effects of endurance or resistance exercise training on maximal O2 consumption (VO2max) and the cardiovascular responses to exercise of 70- to 79-yr-old men and women. Healthy untrained subjects were randomly assigned to a control group (n = 12) or to an endurance (n = 16) or resistance training group (n = 19). Training consisted of three sessions per week for 26 wk. Resistance training consisted of one set of 8-12 repetitions on 10 Nautilus machines. Endurance training consisted of 40 min at 50-70% VO2max and at 75-85% VO2max for the first and last 13 wk of training, respectively. The endurance training group increased its VO2max by 16% during the first 13 wk of training and by a total of 22% after 26 wk of training; this group also increased its maximal O2 pulse, systolic blood pressure, and ventilation, and decreased its heart rate and perceived exertion during submaximal exercise. The resistance training group did not elicit significant changes in VO2max or in other maximal or submaximal cardiovascular responses despite eliciting 9 and 18% increases in lower and upper body strength, respectively. Thus healthy men and women in their 70s can respond to prolonged endurance exercise training with adaptations similar to those of younger individuals. Resistance training in older individuals has no effect on cardiovascular responses to submaximal or maximal treadmill exercise.     

Cardiovascular response to cycle exercise during and after pregnancy

Our purpose was to determine if pregnancy alters the cardiovascular response to exercise. Thirty-nine women [29 +/- 4 (SD) yr], performed submaximal and maximal exercise cycle ergometry during pregnancy (antepartum, AP, 26 +/- 3 wk of gestation) and postpartum (PP, 8 +/- 2 wk). Neither maximal O2 uptake (VO2max) nor maximal heart rate (HR) was different AP and PP (VO2 = 1.91 +/- 0.32 and 1.83 +/- 0.31 l/min; HR = 182 +/- 8 and 184 +/- 7 beats/min, P greater than 0.05 for both). Cardiac output (Q, acetylene rebreathing technique) averaged 2.2 to 2.8 l/min higher AP (P less than 0.01) at rest and at each exercise work load. Increases in both HR and stroke volume (SV) contributed to the elevated Q at the lower exercise work loads, whereas an increased SV was primarily responsible for the higher Q at higher levels. The slope of the Q vs. VO2 relationship was not different AP and PP (6.15 +/- 1.32 and 6.18 +/- 1.34 l/min Q/l/min VO2, P greater than 0.05). In contrast, the arteriovenous O2 difference (a-vO2 difference) was lower at each exercise work load AP, suggesting that the higher Q AP was distributed to nonexercising vascular beds. We conclude that Q is greater and a-vO2 difference is less at all levels of exercise in pregnant subjects than in the same women postpartum but that the coupling of the increase in Q to the increase in systemic O2 demand (VO2) is not different.(ABSTRACT TRUNCATED AT 250 WORDS)     

Threshold effects of respiratory muscle work on limb vascular resistance

The purpose of this study was to determine whether the human diaphragm, like limb muscle, has a threshold of force output at which a metaboreflex is activated causing systemic vasoconstriction. We used Doppler ultrasound techniques to quantify leg blood flow (Q(L)) and utilized the changes in mouth twitch pressure (DeltaP(M)T) in response to bilateral phrenic nerve stimulation to quantify the onset of diaphragm fatigue. Six healthy male subjects performed four randomly assigned trials of identical duration (8 +/- 2 min) and breathing pattern [20 breaths/min and time spent on inspiration during the duty cycle (time spent on inspiration/total time of one breathing cycle) was 0.4] during which they inspired primarily with the diaphragm. For trials 1-3, inspiratory resistance and effort was gradually increased [30, 40, and 50% maximal inspiratory pressure (MIP)], diaphragm fatigue did not occur, and Q(L), limb vascular resistance (LVR), and mean arterial pressure remained unchanged from control (P > 0.05). The fourth trial utilized the same breathing pattern with 60% MIP and caused diaphragm fatigue, as shown by a 30 +/- 12% reduction in P(M)T with bilateral phrenic nerve stimulation. During the fatigue trial, Q(L) and LVR were unchanged from baseline at minute 1, but LVR rose 36% and Q(L) fell 25% at minute 2 and by 52% and 30%, respectively, during the final minutes of the trial. Both LVR and Q(L) returned to control within 30 s of recovery. In summary, voluntary increases in inspiratory muscle effort, in the absence of fatigue, had no effect on LVR and Q(L), whereas fatiguing the diaphragm elicited time-dependent increases in LVR and decreases in Q(L). We attribute the limb vasoconstriction to a metaboreflex originating in the diaphragm, which reaches its threshold for activation during fatiguing contractions.