Exercise and blood lymphocyte subset responses: intensity, duration, and subject fitness effects

This study examined the effect of exercise intensity and duration on the percent blood lymphocytes in men of low [LF; maximal O2 uptake (VO2max) less than 50 ml.kg-1.min-1 and sedentary], moderate (MF; VO2max = 50-60 ml.kg-1.min-1 and recreationally active), and high (HF; VO2max greater than 60 ml.kg-1.min-1 and recent training history) fitness. Thirty healthy adult men (aged 20-31 yr) participated in four randomly ordered cycle ergometer rides: ride 1 (65% VO2max, 30 min), ride 2 (30% VO2max, 60 min), ride 3 (75% VO2max, 60 min), and ride 4 (65% VO2max, 120 min). Blood samples were drawn at various times before and after the exercise sessions. Lymphocyte subsets were determined by flow cytometry using monoclonal antibodies for total T (CD3+), T-helper (CD4+), and T-suppressor (CD8+) lymphocytes and for a subset of cells expressing a natural killer (NK) cell antigen (Leu7+). Plasma catecholamines were assayed to determine exercise stress. There were sharp reductions (P less than 0.01) in the percentage of pan-T and T-helper lymphocytes immediately after exercise across all fitness levels; the magnitude of this reduction was greatest after the highest intensity (ride 3) or longest duration (ride 4) work. In contrast, the absolute number of T and T-helper cells tended to increase after exercise and significantly so in the HF subjects (P less than 0.005). There was no significant effect of exercise or subject fitness category on the percentage of T-suppressor lymphocytes, although the absolute numbers of this subset increased significantly after exercise in LF subjects. Marked increases (P less than 0.01) in the percentage of NK cells occurred immediately after exercise at all intensities and durations tested; numerical increases in total NK cells were significant in all fitness groups after the highest intensity work (ride 3; P less than 0.005). Irrespective of whether the changes were expressed as percentage or total numbers, recovery to base line occurred at 30 min after exercise. The results suggest that the exercise effect on blood lymphocyte subset percentages in men is transient and occurs across all fitness levels. Concomitant changes in plasma catecholamine concentrations are only weakly associated with these lymphocyte subset percentage responses to exercise. Furthermore, this study shows that the exercise-induced changes in lymphocyte percentages do not consistently reflect changes in the absolute numbers of cells.     

Exercise intensity and glucose tolerance in trained and nontrained subjects

The improved glucose tolerance and increased insulin sensitivity associated with regular exercise appear to be the result, in large part, of the residual effects of the last bout of exercise. To determine the effects of exercise intensity on this response, glucose tolerance and the insulin response to a glucose load were determined in seven well-trained male subjects [maximal O2 uptake (VO2max) = 58 ml.kg-1.min-1] and in seven nontrained male subjects (VO2max = 49 ml.kg-1.min-1) in the morning after an overnight fast 1) 40 h after the last training session (control), 2) 14 h after 40 min of exercise on a cycle ergometer at 40% VO2max, and 3) 14 h after 40 min of exercise at 80% VO2max. Subjects replicated their diets for 3 days before each test and ate a standard meal the evening before the oral glucose tolerance test. No differences in the 3-h insulin or glucose response were observed between the control trial and before exercise at either 40 or 80% VO2max in the trained subjects. In the nontrained subjects the plasma insulin response was decreased by 40% after a single bout of exercise at either 40 or 80% VO2max (7.0 X 10(3) vs. 5.0 X 10(3), P less than 0.05; 3.8 X 10(3) microU.ml-1.180 min-1, P less than 0.01). The insulin response after a single bout of exercise in the nontrained subjects was comparable with the insulin responses found in the trained subjects for the control and exercise trials.(ABSTRACT TRUNCATED AT 250 WORDS)     

The influence of cardiorespiratory fitness on the decrement in maximal aerobic power at high altitude

There are conflicting reports in the literature which imply that the decrement in maximal aerobic power experienced by a sea-level (SL) resident sojourning at high altitude (HA) is either smaller or larger for the more aerobically "fit" person. In the present study, data collected during several investigations conducted at an altitude of 4300 m were analyzed to determine if the level of aerobic fitness influenced the decrement in maximal oxygen uptake (VO2max) at HA. The VO2max of 51 male SL residents was measured at an altitude of 50 m and again at 4300 m. The subjects' ages, heights, and weights (mean +/- SE) were 22 +/- 1 yr, 177 +/- 7 cm and 78 +/- 2 kg, respectively. The subjects' VO2max ranged from 36 to 60 ml X kg -1 X min -1 (mean +/- SE = 48 +/- 1) and the individual values were normally distributed within this range. Likewise, the decrement in VO2max at HA was normally distributed from 3 ml X kg-1 X min-1 (9% VO2max at SL) to 29 ml X kg-1 X min-1 (54% VO2max at SL), and averaged 13 +/- 1 ml X kg-1 X min-1 (27 +/- 1% VO2max at SL). The linear correlation coefficient between aerobic fitness and the magnitude of the decrement in VO2max at HA expressed in absolute terms was r = 0.56, or expressed as % VO2max at SL was r = 0.30; both were statistically significant (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of incomplete pulmonary gas exchange on VO2 max

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of hyperoxia on substrate utilization during intense submaximal exercise

Six trained males [mean maximal O2 uptake (VO2max) = 66 ml X kg-1 X min-1] performed 30 min of cycling (mean = 76.8% VO2max) during normoxia (21.35 +/- 0.16% O2) and hyperoxia (61.34 +/- 1.0% O2). Values for VO2, CO2 output (VCO2), minute ventilation (VE), respiratory exchange ratio (RER), venous lactate, glycerol, free fatty acids, glucose, and alanine were obtained before, during, and after the exercise bout to investigate the possibility that a substrate shift is responsible for the previously observed enhanced performance and decreased RER during exercise with hyperoxia. VO2, free fatty acids, glucose, and alanine values were not significantly different in hyperoxia compared with normoxia. VCO2, RER, VE, and glycerol and lactate levels were all lower during hyperoxia. These results are interpreted to support the possibility of a substrate shift during hyperoxia.     

Rate of decline in blood lactate after cycling exercise in endurance-trained and -untrained subjects

The purpose of this study was to compare the rate of decline in blood lactate (La) levels in nine trained men [maximal O2 consumption (VO2max) 65.5 +/- 3.3 ml.kg-1.min-1] and eight untrained men (VO2max 42.2 +/- 2.8 ml.kg-1.min-1) during passive recovery from a 3-min exercise bout. Trained and untrained subjects cycled at 85 and 80% VO2max, respectively, to produce similar peak blood La concentrations. Twenty samples of arterialized venous blood were drawn from a heated hand vein during 60 min of recovery and analyzed in an automated La analyzer. The data were then fitted to a biexponential function, which closely described the observed data (r = 0.97-0.98). There was no difference in the coefficient expressing the rate of decline in blood La for trained and untrained groups (0.0587 +/- 0.0111 vs. 0.0579 +/- 0.0100, respectively). However, trained subjects demonstrated a faster time-to-peak La (P = 0.01), indicative of a faster efflux of La from muscle to blood. Thus the rate of decline in blood La after exercise does not appear to be affected by training. The faster decline previously reported for trained subjects may be due to the use of a linear rather than a biexponential curve fit.     

Oxygen consumption following exercise of moderate intensity and duration.

To study the effects of exercise intensity and duration on excess postexercise oxygen consumption (EPOC), 8 men [age = 27.6 (SD 3.8) years, VO2max = 46.1 (SD 8.5) ml min-1 kg-1] performed four randomly assigned cycle-ergometer tests (20 min at 60% VO2max, 40 min at 60% VO2max, 20 min at 70% VO2max, and 40 min at 70% VO2max). O2 uptake, heart rate and rectal temperature were measured before, during, and for 1 h following the exercise tests. Blood for plasma lactate measurements was obtained via cannulae before, and at selected times, during and following exercise. VO2 rapidly declined to preexercise levels following each of the four testing sessions, and there were no differences in EPOC between the sessions. Blood lactate and rectal temperature increased (P < 0.05) with exercise, but had returned to preexercise levels by 40 min of recovery. The results indicate that VO2 returned to resting levels within 40 min after the end of exercise, regardless of the intensity (60% and 70% VO2max) or duration (20 min and 40 min) of the exercise, in men with a moderate aerobic fitness level.     

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.     

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.     

Aerobic power and cardiovascular response to stress

The relationship between aerobic fitness as measured by maximal O2 uptake (VO2max) and the cardiovascular response to laboratory stressors was examined in two experiments. First, 34 male college students were screened on the basis of their heart rate (HR) response to a reaction time-shock avoidance (RT-AV) task. The six individuals showing an average HR increase of 45 beats/min (reactives) and the six subjects showing an average increase of 8 beats/min (nonreactives) did not differ in VO2max (47.7 +/- 2 vs. 48.7 +/- 1 ml.kg-1.min-1, respectively). However, a statistically significant association between a reported family history of hypertension and peak HR response to RT-AV was seen. In the second series of experiments, the plasma catecholamine and cardiovascular responses of eight elite endurance-trained athletes (VO2max 70.6 +/- 1 ml.kg-1.min-1) and eight untrained volunteers (VO2max 45.5 +/- 1 ml.kg-1.min-1) were compared on the following: RT-AV, reaction time for monetary reward (RT-AP), cold pressor, isometric handgrip, and orthostatic challenge (standing). The trained group exhibited a significantly lower mean HR at rest (P less than 0.05), otherwise there were no significant differences between the two groups. The results indicate that although individual differences (e.g., family history of hypertension and high resting HR) can be related to the potential for cardiovascular responses to novel laboratory challenges, the contribution of fitness to this characteristic is much less clear. Further exploration of questions pertaining to fitness and stress should focus on individuals with a predisposition to stress reactivity.     

Distribution of blood flow in muscles of miniature swine during exercise

The purpose of this study was to determine how the distribution of blood flow within and among the skeletal muscles of miniature swine (22 +/- 1 kg body wt) varies as a function of treadmill speed. Radiolabeled microspheres were used to measure cardiac output (Q) and tissue blood flows in preexercise and at 3-5 min of treadmill exercise at 4.8, 8.0, 11.3, 14.5, and 17.7 km/h. All pigs (n = 8) attained maximal O2 consumption (VO2max) (60 +/- 4 ml X min-1 X kg-1) by the time they ran at 17.7 km/h. At VO2max, 87% of Q (9.9 +/- 0.5 l/min) was to skeletal muscle, which constituted 36 +/- 1% of body mass. Average total muscle blood flow at VO2max was 127 +/- 14 ml X min-1 X 100 g-1; average limb muscle flow was 135 +/- 17 ml X min-1 X 100 g-1. Within the limb muscles, blood flow was distributed so that the deep red parts of extensor muscles had flows about two times higher than the more superficial white portions of the same muscles; the highest muscle blood flows occurred in the elbow flexors (brachialis: 290 +/- 44 ml X min-1 X 100 g-1). Peak exercise blood flows in the limb muscles were proportional (P less than 0.05) to the succinate dehydrogenase activities (r = 0.84), capillary densities (r = 0.78), and populations of oxidative (slow-twitch oxidative + fast-twitch oxidative-glycolytic) fiber types (r = 0.93) in the muscles. Total muscle blood flow plotted as a function of exercise intensity did not peak until the pigs attained VO2max, although flows in some individual muscles showed a plateau in this relationship at submaximal exercise intensities. The data demonstrate that blood flow in skeletal muscles of miniature swine is distributed heterogeneously and varies in relation to fiber type composition and exercise intensity.     

Sex difference in maximal oxygen uptake. Effect of equating haemoglobin concentration

Ten men and 11 women were studied to determine the effect of experimentally equating haemoglobin concentration ([Hb]) on the sex difference in maximal oxygen uptake (VO2max). VO2max was measured on a cycle ergometer using a continuous, load-incremented protocol. The men were studied under two conditions: 1) with normal [Hb] (153 g X L-1) and 2) two days following withdrawal of blood, which reduced their mean [Hb] to exactly equal the mean of the women (134 g X L-1). Prior to blood withdrawal, VO2max expressed in L X min-1 and relative to body weight and ride time on the cycle ergometer test were greater (p less than .01) in men by 1.11 L X min-1 (47%), 4.8 ml X kg-1 min-1 (11.5%) and 5.9 min (67%), respectively, whereas VO2max expressed relative to fat-free weight (FFW) was not significantly different. Equalizing [Hb] reduced (p less than .01) the mean VO2max of the men by 0.26 L X min-1 (7.5%), 3.2 ml X kg-1 min-1 (6.9%) or 4.1 ml X kg FFW-1 min-1 (7.7%), and ride time by 0.7 min (4.8%). Equalizing [Hb] reduced the sex difference for VO2max less than predicted from proportional changes in the oxygen content of the arterial blood and arteriovenous oxygen content difference during maximal exercise. It was concluded that the sex difference in [Hb] accounts for a significant, but relatively small portion of the sex difference in VO2max (L X min-1). Other factors such as the dimensions of the oxygen transport system and musculature are of greater importance.     

Does fitness level modulate the cardiovascular hemodynamic response to exercise?

Subjects with greater aerobic fitness demonstrate better diastolic compliance at rest, but whether fitness modulates exercise cardiac compliance and cardiac filling pressures remains to be determined. On the basis of maximal oxygen consumption (VO2max), healthy male subjects were categorized into either low (LO: VO2max=43+/-6 ml.kg-1.min-1; n=3) or high (HI: VO2max=60+/-3 ml.kg-1.min-1; n=5) aerobic power. Subjects performed incremental cycle exercise to 90% Vo(2max). Right atrial (RAP) and pulmonary artery wedge (PAWP) pressures were measured, and left ventricular (LV) transmural filling pressure (TMFP=PAWP-RAP) was calculated. Cardiac output (CO) and stroke volume (SV) were determined by direct Fick, and LV end-diastolic volume (EDV) was estimated from echocardiographic fractional area change and Fick SV. There were no between-group differences for any measure at rest. At a submaximal workload of 150 W, PAWP and TMFP were higher (P<0.05) in LO compared with HI (12 vs. 8 mmHg, and 9 vs. 4 mmHg, respectively). At peak exercise, CO, SV, and EDV were lower in LO (P<0.05). RAP was not different at peak exercise, but PAWP (23 vs. 15 mmHg) and TMFP (12 vs. 6 mmHg) were higher in LO (P<0.05). Compared with less fit subjects, subjects with greater aerobic fitness demonstrated lower LV filling pressures during exercise, whereas SV and EDV were either similar (submaximal exercise) or higher (peak exercise), suggesting superior diastolic function and compliance.     

Decline in VO2max with aging in master athletes and sedentary men

Fifteen well-trained master endurance athletes [62.0 +/- 2.3 (SE) yr] and 14 sedentary control subjects (61.4 +/- 1.4 yr) were reevaluated after an average follow-up period of approximately 8 yr to obtain information regarding the effects of physical activity on the age-related decline in maximal O2 uptake capacity (VO2max). The master athletes had been training for 10.2 +/- 2.9 yr before initial testing and continued to train during the follow-up period. The sedentary subjects' VO2max declined by an average of 3.3 ml.kg-1.min-1 (33.9 +/- 1.7 vs. 30.6 +/- 1.6, P less than 0.001) over the course of the study, a decline of 12% per decade. In these subjects maximal heart rate declined 8 beats/min (171 vs. 163) and maximal O2 pulse decreased from 0.20 to 0.18 ml.kg-1.beat (P less than 0.05). The master athletes' VO2 max decreased by an average of 2.2 ml.kg-1.min-1 (54.0 +/- 1.7 vs. 51.8 +/- 1.8, P less than 0.05), a 5.5% decline per decade. The master athletes' maximal heart rate was unchanged (171 +/- 3 beats/min) and their maximal O2 pulse decreased from 0.32 to 0.30 ml.kg-1.beat (P less than 0.05). These findings provide evidence that the age-related decrease in VO2max of master athletes who continue to engage in regular vigorous endurance exercise training is approximately one-half the rate of decline seen in age-matched sedentary subjects. Furthermore our results suggest that endurance exercise training may reduce the rate of decline in maximal heart rate that typically occurs as an individual ages.     

Linear relationship between VO2max and VO2max decrement during exposure to acute hypoxia

The purpose of these experiments is to test the hypothesis that exercise-induced hypoxemia at sea level in highly trained athletes might be exacerbated during acute hypoxia and therefore result in correspondingly larger decrements in maximal O2 uptake (VO2max) compared with less trained individuals. Thirteen healthy male volunteers were divided into two groups according to their level of fitness: 1) trained endurance athletes (T) (n = 7), with a VO2max range of 56-75 ml.kg-1.min-1 and 2) untrained individuals (UT) (n = 6), with a VO2max range of 33-49 ml.kg-1.min-1. Subjects performed two incremental cycle ergometry tests to determine VO2max under hypoxic conditions [14% O2-86% N2, barometric pressure (PB) = 760 Torr] and normoxic conditions (21% O2-79% N2, PB = 760 Torr). Tests were single blind, randomly administered, and separated by at least 72 h. Mean percent oxyhemoglobin saturation (%SaO2) during maximal exercise under hypoxic conditions was significantly (P less than 0.05) lower in the T group (77%) compared with the UT group (86%). Furthermore, the T group exhibited larger decrements (P less than 0.05) in VO2max (normoxic-hypoxic) compared with the UT group. Finally, a significant linear correlation (r = 0.94) existed between normoxic VO2max (ml.kg-1.min-1) and delta VO2max (normoxic-hypoxic). These data suggest that highly T endurance athletes suffer more severe gas exchange impairments during acute exposure to hypoxia than UT individuals, and this may explain a portion of the observed variance in delta VO2max among individuals during acute altitude or hypoxia exposure.     

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.     

Physical fitness of blind and sighted children

Twenty-seven children (age 7-17 years) with varying degrees of blindness but with no other known disorder were assessed for physical fitness. Twenty-seven randomly selected children with normal eyesight were also assessed. Maximum oxygen uptake (VO2max) was measured directly during a progressive exercise test on a treadmill. There was a significant and substantial reduction in VO2max in totally blind children (mean +/- standard deviation 35.0 +/- 7.5 ml X min-1 X kg-1) compared with normal children (45.9 +/- 6.6 ml X min-1 X kg-1). Partially sighted children had a significant but smaller reduction in VO2max. Fitness assessed by a step-test was significantly reduced in the visually impaired children, and skin-fold thickness was also significantly greater in totally blind children. The level of habitual physical activity for each child, as assessed by a questionnaire, correlated with VO2max (r = 0.53, p less than 0.0001). Blind children were significantly less active than normal children, and the difference between mean VO2max for blind and normal children became non-significant when their different activity levels were taken into account. It is concluded that totally blind children are less fit than other children at least partly because of their lower level of habitual activity.     

Voluntary exercise and its effects on young SHR and stroke-prone hypertensive rats

To determine whether voluntary exercise would lower resting blood pressure in spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SP-SHR), two separate but interrelated investigations were undertaken. The studies were initiated when the animals were 28-35 days of age and after they were assigned to either activity or sedentary cages. The activity cages were connected to transducers and recorders that allowed the monitoring and calculation of frequency, duration, and running speed. The SHR group ran 3-7 km/day intermittently for 12 wk at high speeds (48-68 m/min), which resulted in heart rates in excess of 500 beats/min. When the SHR exercised, they seldom exceeded 33 revolutions/bout (37 m) with the majority being less than 22 revolutions/bout. This type of exercise training significantly lowered, but did not normalize, resting blood pressure by approximately 20 mmHg [nontrained (NT) = 185 +/- 5; trained (T) = 163 +/- 5 mmHg] while increasing maximum O2 consumption (VO2max) (NT = 78 +/- 2.6; T = 95 +/- 2.2 ml X min-1 X kg-1) and endurance run time (NT = 62 +/- 9.0; T = 286 +/- 15.0 min), respectively. Although SP-SHR exhibited comparable patterns of voluntary activity, the effects were not similar. First, after approximately 5 wk of consuming a special Japanese rat chow and a 1% NaCl drinking solution, cerebrovascular lesions occurred and deaths ultimately resulted in both exercising and sedentary groups. Second, although there was statistical evidence for a training effect (higher VO2max, longer VO2 test run times), voluntary exercise had no advantage in either male or female runners in lowering resting blood pressures or in improving their life-spans. Whereas voluntary activity wheel exercise or moderate forced treadmill exercise will lower resting blood pressures in young SHR populations, similar generalizations cannot be made with young SP-SHR rats.     

The effect of citrate loading on exercise performance, acid-base balance and metabolism

Nine subjects (VO2max 65 +/- 2 ml.kg-1.min-1, mean +/- SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g.kg-1 body mass) or a sodium chloride placebo (P, 0.045 g.kg-1 body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% VO2max, followed by exercise to exhaustion at 95% VO2max. Pre-exercise arterialized-venous [H+] was lower in C (36.2 +/- 0.5 nmol.l-1; pH 7.44) than P (39.4 +/- 0.4 nmol.l-1; pH 7.40); the plasma [H+] remained lower and [HCO3-] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% VO2max was similar in C (310 +/- 69 s) and P (313 +/- 74 s). Cardiorespiratory variables (ventilation, VO2, VCO2, heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195 +/- 19 mumol.l-1; P, 81 +/- 7 mumol.l-1) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% VO2max. Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.