Substrate turnover and oxidation during moderate-intensity exercise following acute plasma volume expansion.

In previous work using prolonged, light cycle exercise, we were unable to demonstrate an effect of acute plasma volume (PV) expansion on glucose kinetics or substrate oxidation, despite a decline in whole-body lipolysis (Phillips et al., 1997). However, PV is known to decrease arterial O2 content. The purpose of this study was to examine whether substrate turnover and oxidation would be altered with heavier exercise where the challenge to O2 delivery is increased. Eight untrained males (VO2max = 3.52 +/- 0.12 l/min) twice performed 90 min of cycle ergometry at 62 % VO2peak, both prior to (CON) and following induced plasma volume expansion (Dextran [6 %] or Pentaspan [10 %]) (6.7 ml/kg) (PVX). Glucose and glycerol kinetics were determined with primed constant infusions of [6.6-(2)H2] glucose and [(2)H5] glycerol, respectively. PVX resulted in a 15.8 +/- 2.2 % increase (p < 0.05) in PV. Glucose and glycerol appearance (Ra) and utilization (Rd), although increasing progressively (p < 0.05) with exercise, were not different between conditions. Similarly, no differences in substrate oxidation, either fat or carbohydrate, were observed between the two conditions. Prolonged exercise resulted in an increase (p < 0.05) in plasma glucagon and a decrease (p < 0.05) in plasma insulin during both conditions. With PVX, the exercise-induced increase in glucagon was diminished (p < 0.05). We conclude that impairment in O2 content mediated by an elevated PV does not alter glucose, and glycerol kinetics or substrate oxidation even at moderate exercise intensity.     

Aldosterone dynamics during graded exercise at sea level and high altitude.

Hormonal responses to graded exercise of eight low altitude residents were examined at sea level (SL) and after 1 (acute) and 11 (chronic) days at 4,300 m (HA). Caloric, water, and electrolyte intakes were controlled, as were temperature and humidity. Blood was sampled at rest and during light and moderate upright bicycle exercise (20 min at 40% and 75% of maximal O2 uptake, respectively). Mean VO2 max at HA was 27% lower than at SL. Resting plasma levels of aldosterone (Aldo), renin, and angiotensin II (A II) were significantly lower (P smaller than 0.05) on day 1 at HA compared to SL, but returned to SL values by day 11. Plasma cortisol values at rest were similar at SL and HA and were not significantly altered by light or moderate exercise. Renin, A II, and Aldo rose progressively with increasing workload in each environment. With acute HA, renin and Aldo were lower than at either SL or chronic HA. The chronic HA levels tended to approximate SL findings, implying adaptation. The data suggest that aldosterone is predominantly under the control of the renin-angiotensin system during graded exercise at sea level and that the response of this system is altered on acute high-altitude exposure.     

Altitude acclimatization attenuates plasma ammonia accumulation during submaximal exercise

This study examined the effects of acclimatization to 4,300 m altitude on changes in plasma ammonia concentrations with 30 min of submaximal [75% maximal O2 uptake (VO2max)] cycle exercise. Human test subjects were divided into a sedentary (n = 6) and active group (n = 5). Maximal uptake (VO2max) was determined at sea level and at high altitude (HA; 4,300 m) after acute (t less than 24 h) and chronic (t = 13 days) exposure. The VO2max of both groups decreased 32% with acute HA when compared with sea level. In the sedentary group, VO2max decreased an additional 16% after 13 days of continuous residence at 4,300 m, whereas VO2max in the active group showed no further change. In both sedentary and active subjects, plasma ammonia concentrations were increased (P less than 0.05) over resting levels immediately after submaximal exercise at sea level as well as during acute HA exposure. With chronic HA exposure, the active group showed no increase in plasma ammonia immediately after submaximal exercise, whereas the postexercise ammonia in the sedentary group was elevated but to a lesser extent than at sea level or with acute HA exposure. Thus postexercise plasma ammonia concentration was decreased with altitude acclimatization when compared with ammonia concentrations following exercise performed at the same relative intensity at sea level or acute HA. This decrease in ammonia accumulation may contribute to enhanced endurance performance and altered substrate utilization with exercise following acclimatization to altitude.     

Acute plasma volume expansion in the untrained alters the hormonal response to prolonged moderate-intensity exercise.

To investigate the role of an increase in plasma volume (PV), characteristically observed with short-term endurance training, on the endocrine response to prolonged moderate intensity exercise, eight untrained males (VO2 peak = 3.52 +/- 0.12 l x min(-1)) performed 90 min of cycle ergometry at approximately 60% VO2peak both before (CON) and following (PVX) PV expansion. Acute PV expansion, which was accomplished using a solution of Dextran (6%) or Pentispan (10%) (6.7 ml kg(-1)), resulted in a calculated 15.8+/-2.2% increase (p<0.05) in PV. The prolonged exercise resulted in increases (p<0.05) in plasma vasopressin (AVP), plasma rennin activity (PRA), aldosterone (ALD), atrial naturetic peptide (alpha-ANP), and the catecholamines norepinephrine (NE) and epinephrine (EPI). PVX blunted the increases (p<0.05) in AVP, PRA, ALD, NE and EPI, during the exercise itself. The concentration of alpha-ANP was also lower (p<0.05) during exercise following PVX, an effect that could be attributed to the lower resting levels. No differences in osmolality was observed between conditions. These results demonstrate that PVX alters the fluid regulatory hormonal response in untrained subjects to moderate intensity dynamic exercise in a manner similar to that observed following short-term training induced alterations in PV. The specific mechanisms responsible for these alterations remain unclear, but appear to be related directly to the increase in PV.     

Early adaptations in gas exchange, cardiac function and haematology to prolonged exercise training in man

In order to determine the effect of short-term training on central adaptations, gas exchange and cardiac function were measured during a prolonged submaximal exercise challenge prior to and following 10-12 consecutive days of exercise. In addition, vascular volumes and selected haematological properties were also examined. The subjects, healthy males between the ages of 19 and 30 years of age, cycled for 2 h per day at approximately 59% of pre-training peak oxygen consumption (VO2) i.e., maximal oxygen consumption (VO2max). Following the training, VO2max (l.min-1) increased (P less than 0.05) by 4.3% (3.94, 0.11 vs 4.11, 0.11; mean, SE) whereas maximal exercise ventilation (VE,max) and maximal heart rate (fc,max) were unchanged. During submaximal exercise, VO2 was unaltered by the training whereas carbon dioxide production (VE) and respiratory exchange ratio were all reduced (P less than 0.05). The altered activity pattern failed to elicit adaptations in either submaximal exercise cardiac output or arteriovenous O2 difference. fc was reduced (P less than 0.05). Plasma volume (PV) as measured by 125I human serum albumin increased by 365 ml or 11.8%, while red cell volume (RCV) as measured by 51chromium-labelled red blood cells (RBC) was unaltered. The increase in PV was accompanied by reductions (P less than 0.05) in haematocrit, haemoglobin concentration (g.100 ml-1), and RBCs (10(6) mm-3). Collectively these changes suggest only minimal adaptations in maximal oxygen transport during the early period of prolonged exercise training. However, as evidenced by the changes during submaximal exercise, both the ventilatory and the cardiodynamic response were altered.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of detraining on cardiovascular responses to exercise: role of blood volume

In this study we determined whether the decline in exercise stroke volume (SV) observed when endurance-trained men stop training for a few weeks is associated with a reduced blood volume. Additionally, we determined the extent to which cardiovascular function could be restored in detrained individuals by expanding blood volume to a similar level as when trained. Maximal O2 uptake (VO2max) was determined, and cardiac output (CO2 rebreathing) was measured during upright cycling at 50-60% VO2max in eight endurance-trained men before and after 2-4 wk of inactivity. Detraining produced a 9% decline in blood volume (5,177 to 4,692 ml; P less than 0.01) during upright exercise, due primarily to a 12% lowering (P less than 0.01) of plasma volume (PV; Evans blue dye technique). SV was reduced by 12% (P less than 0.05) and VO2max declined 6% (P less than 0.01), whereas heart rate (HR) and total peripheral resistance (TPR) during submaximal exercise were increased 11% (P less than 0.01) and 8% (P less than 0.05), respectively. When blood volume was expanded to a similar absolute level in the trained and detrained state (approximately 5,500 +/- 200 ml) by infusing a 6% dextran solution in saline, the effects of detraining on cardiovascular response were reversed. SV and VO2max were increased (P less than 0.05) by PV expansion in the detrained state to within 2-4% of trained values. Additionally, HR and TPR during submaximal exercise were lowered to near trained values. These findings indicate that the decline in cardiovascular function following a few weeks of detraining is largely due to a reduction in blood volume, which appears to limit ventricular filling during upright exercise.     

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.     

Acute plasma volume expansion alters cardiovascular but not thermal function during moderate intensity prolonged exercise

To investigate the hypothesis that the increase in plasma volume (PV) that typically occurs with training results in improved cardiovascular and thermal regulation during prolonged exercise, eight untrained males (V(O2)peak = 3.52 +/- 0.12 L x min(-1)) performed 90 min of cycle ergometry at 62% V(O2)peak before and after acute PV expansion. Subjects were infused with a PV-expanding solution (dextran (6%) or Pentaspan (10%)) equivalent to 6.7 mL x kg(-1) body mass (PVX) or acted as their own control (CON) in a randomized order. PVX resulted in a calculated 15.8% increase in resting PV, which relative to CON, was maintained throughout the exercise (P < 0.05). During PVX, heart rate was lower (P < 0.05) and stroke volume and cardiac output were higher (P < 0.05) during the exercise. Mean arterial pressure and total peripheral resistance, although altered by exercise (P < 0.05), were not different between the two conditions. Core temperature, which was progressively increased by the exercise (P < 0.01), was not affected by PVX. A similar decrease in body weight was observed between the conditions as a result of the exercise (P < 0.01). These results indicate that acute PVX alters cardiovascular performance without affecting the thermoregulatory response to prolonged cycle exercise.     

Alterations in blood volume following short-term supramaximal exercise

To investigate the role of high-intensity intermittent exercise on adaptations in blood volume and selected hematological measures, four male subjects aged 19-23 yr [peak O2 consumption (VO2max) = 53 ml X min-1 X kg-1] performed supramaximal (120% VO2max) cycle exercise on 3 consecutive days. Each exercise session consisted of intermittent work performed as bouts of 1-min work to 4-min rest until fatigue or until a maximum of 24 repetitions had been completed. Measurements on blood samples were made before the exercise period and 24 h after the last exercise session. Plasma volume (PV) estimated using 131I-human serum albumin increased by 11.6% (3,504 vs. 3,912 ml; P less than 0.05). Total blood volume (TBV) based on PV and hematocrit (Hct) values increased by 4.5% (5,798 vs. 6,059 ml; P less than 0.05), whereas red cell volume (RCV) decreased by 6.4% (2,294 vs. 2,147 ml; P less than 0.05). Measurements of hematological indices indicated significant reductions (P less than 0.05) in whole-blood Hct (39.7 vs. 35.5%), hemoglobin concentration (15.5 vs. 13.9 g/100 ml), hemoglobin content (897 vs. 839 g), and red blood cell count (5.15 vs. 4.55 X 10(6) X mm-3). The findings of this study suggest that exercise intensity is a major factor in promoting exercise-induced hypervolemia and that rapid elevations in PV can be induced early in training.     

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)     

Thermoregulatory and aerobic changes after endurance training in a hypobaric hypoxic and warm environment.

Plasma volume (PV) expansion by endurance training and/or heat acclimatization is known to increase aerobic and thermoregulatory capacities in humans. Also, higher erythrocyte volume (EV) fractions in blood are known to improve these capacities. We tested the hypothesis that training in a hypobaric hypoxic and warm environment would increase peak aerobic power (VO(2)(peak)) and forearm skin vascular conductance (FVC) response to increased esophageal temperature (T(es)) more than training in either environment alone, by increasing both PV and EV. Twenty men were divided into four training regimens (n = 5 each): low-altitude cool (610-m altitude, 20 degrees C ambient temperature, 50% relative humidity), high-altitude cool (2,000 m, 20 degrees C), low-altitude warm (610 m, 30 degrees C), and high-altitude warm (HW; 2,000 m, 30 degrees C). They exercised on a cycle ergometer at 60% VO(2)(peak) for 1 h/day for 10 days in a climate chamber. After training, PV increased in all trials, but EV increased in only high-altitude trials (both P < 0.05). VO(2)(peak) increased in all trials (P < 0.05) but without any significant differences among trials. FVC response to increased T(es) was measured during exercise at 60% of the pretraining VO(2)(peak) at 610 m and 30 degrees C. After the training, T(es) threshold for increasing FVC decreased in warm trials (P < 0.05) but not in cool trials and was significantly lower in HW than in cool trials (P < 0.05). The slope of FVC increase/T(es) increase increased in all trials (P < 0.05) except for high-altitude cool (P > 0.4) and was significantly higher in HW than in cool trials (P < 0.05). Thus, against our hypothesis, the VO(2)(peak) for HW did not increase more than in other trials. Moreover, slope of FVC increase/T(es) increase in HW increased most, despite the similar increase in blood volume, suggesting that factors other than blood volume were involved in the highest FVC response in HW.     

Plasma volume expansion does not increase maximal cardiac output or VO2 max in lowlanders acclimatized to altitude

With altitude acclimatization, blood hemoglobin concentration increases while plasma volume (PV) and maximal cardiac output (Qmax) decrease. This investigation aimed to determine whether reduction of Qmax at altitude is due to low circulating blood volume (BV). Eight Danish lowlanders (3 females, 5 males: age 24.0 +/- 0.6 yr; mean +/- SE) performed submaximal and maximal exercise on a cycle ergometer after 9 wk at 5,260 m altitude (Mt. Chacaltaya, Bolivia). This was done first with BV resulting from acclimatization (BV = 5.40 +/- 0.39 liters) and again 2-4 days later, 1 h after PV expansion with 1 liter of 6% dextran 70 (BV = 6.32 +/- 0.34 liters). PV expansion had no effect on Qmax, maximal O2 consumption (VO2), and exercise capacity. Despite maximal systemic O2 transport being reduced 19% due to hemodilution after PV expansion, whole body VO2 was maintained by greater systemic O2 extraction (P < 0.05). Leg blood flow was elevated (P < 0.05) in hypervolemic conditions, which compensated for hemodilution resulting in similar leg O2 delivery and leg VO2 during exercise regardless of PV. Pulmonary ventilation, gas exchange, and acid-base balance were essentially unaffected by PV expansion. Sea level Qmax and exercise capacity were restored with hyperoxia at altitude independently of BV. Low BV is not a primary cause for reduction of Qmax at altitude when acclimatized. Furthermore, hemodilution caused by PV expansion at altitude is compensated for by increased systemic O2 extraction with similar peak muscular O2 delivery, such that maximal exercise capacity is unaffected.     

Why is VO2 max after altitude acclimatization still reduced despite normalization of arterial O2 content?

Acute hypoxia (AH) reduces maximal O2 consumption (VO2 max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O2 saturation that can normalize arterial O2 concentration ([O2]), VO2 max remains low. To determine why, seven lowlanders were studied at VO2 max (cycle ergometry) at sea level (SL), after 9-10 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (FiO2 = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by approximately 15% in both AH and CH (P < 0.05). At maximal exercise, arterial [O2] in AH was 31% lower than at SL (P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O2 extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76% of the cardiac output perfused the legs, in CH the legs received only 67%. Pulmonary VO2 max (4.1 +/- 0.3 l/min at SL) fell to 2.2 +/- 0.1 l/min in AH (P < 0.05) and was only 2.4 +/- 0.2 l/min in CH (P < 0.05). These data suggest that the failure to recover VO2 max after acclimatization despite normalization of arterial [O2] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH.     

Prolonged exercise following diuretic-induced hypohydration: effects on cardiovascular and thermal strain

To examine the role of a reduction in plasma volume (PV) on the cardiovascular and thermoregulatory responses to submaximal exercise, ten untrained males (VO2 peak = 3.96 +/- 0.14 L x min(-1); mean +/- SE) performed 60 min of cycle exercise at -61% of VO2 peak while on a diuretic (DIU) and under control (CON) conditions. Participants consumed either Novotriamazide (100 mg triameterene + 50 mg hydrochlorothiazide, a diuretic) or a placebo, in random order, for 4 days prior to the exercise. Diuretic resulted in a calculated 14.6% reduction (P < 0.05) in resting PV. Heart rate was higher (P < 0.05) at rest and throughout exercise for DIU compared with CON. No differences were observed for cardiac output (Qc) and stroke volume (SV) at rest for the two conditions, but during exercise both Qc and SV were lower (P < 0.05) with DIU. Exercise VO2 (L x min(-1)) for CON and DIU at 30 min (2.39 +/- 0.09 vs 2.43 +/- 0.08) and 60 min (2.56 +/- 0.08 vs 2.53 +/- 0.12) were similar between conditions. Whole body a-vO2 difference was significantly greater (P < 0.05) for DIU both at rest and during exercise as compared with CON. Rectal temperature (Tre) was significantly higher (P < 0.05) during DIU from 15 min to the end of exercise. Blood concentrations of norepinephrine were higher (P < 0.05) with DIU compared to CON at 15 min of exercise and beyond. For blood epinephrine, no differences were observed between DIU and CON. These results suggest that reductions in PV led to greater circulating concentrations of norepinephrine which likely resulted from increased cardiac and thermoregulatory stresses. In addition, reductions in PV do not appear to increase cardiovascular instability during prolonged dynamic exercise.     

Expression of the cell adhesion molecules on leukocytes that demarginate during acute maximal exercise.

The pulmonary vascular bed is an important reservoir for the marginated pool of leukocytes that can be mobilized by exercise or catecholamines. This study was designed to determine the phenotypic characteristics of leukocytes that are mobilized into the circulation during exercise. Twenty healthy volunteers performed incremental exercise to exhaustion [maximal O2 consumption (VO2 max)] on a cycle ergometer. Blood was collected at baseline, at 3-min intervals during exercise, at VO2 max, and 30 min after exercise. Total white cell, polymorphonuclear leukocyte (PMN), and lymphocyte counts increased with exercise to VO2 max (P < 0.05). Flow cytometric analysis showed that the mean fluorescence intensity of L-selectin on PMN (from 14.9 +/- 1 at baseline to 9.5 +/- 1.6 at VO2 max, P < 0.05) and lymphocytes (from 11.7 +/- 1.2 at baseline to 8 +/- 0.8 at VO2 max, P < 0.05) decreased with exercise. Mean fluorescence intensity of CD11b on PMN increased with exercise (from 10.2 +/- 0.6 at baseline to 25 +/- 2.5 at VO2 max, P < 0.002) but remained unchanged on lymphocytes. Myeloperoxidase levels in PMN did not change with exercise. In vitro studies showed that neither catecholamines nor plasma collected at VO2 max during exercise changed leukocyte L-selectin or CD11b levels. We conclude that PMN released from the marginated pool during exercise express low levels of L-selectin and high levels of CD11b.     

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.     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

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.     

Influence of polycythemia on blood volume and thermoregulation during exercise-heat stress

We studied the effects of autologous erythrocyte infusion on blood volume and thermoregulation during exercise in the heat. By use of a double-blind design, nine unacclimated male subjects were infused with either 600 ml of a NaCl-glucose-phosphate solution containing a approximately 50% hematocrit (n = 6, reinfusion) or 600 ml of this solution only (n = 3, saline). A heat stress test (HST) was attempted approximately 2-wk pre- and 48-h postinfusion during the late spring months. After 30 min of rest in a 20 degrees C antechamber, the HST consisted of a 120-min exposure (2 repeats of 15 min rest and 45 min treadmill walking) in a hot (35 degrees C, 45% rh) environment while euhydrated. Erythrocyte volume (RCV, 51Cr) and plasma volume (PV, 125I) were measured 24 h before each HST, and maximal O2 uptake (VO2max) was measured 24 h after each HST. Generally, no significant effects were found for the saline group. For the reinfusion group, RCV (11%, P less than 0.01) and VO2max (11%, P less than 0.05) increased after infusion, and the following observations were made: 1) the increased RCV was associated with a reduction in PV to maintain the same blood volume as during the preinfusion measurements; 2) polycythemia reduced total circulating protein but did not alter F-cell ratio, plasma osmolality, plasma protein content, or plasma lactate at rest or during exercise-heat stress; 3) polycythemia did not change the volume of fluid entering the intravascular space from rest to exercise-heat stress; and 4) polycythemia tended to reduce the rate of heat storage during exercise-heat stress.     

Response of red cell and plasma volume to prolonged training in humans

To clarify the role of progressive heavy training on vascular volumes and hematologic status, seven untrained males [maximal O2 uptake (VO2max) = 45.1 +/- 1.1 (SE) ml.kg-1.min-1] cycled 2 h/day at an estimated 62% of VO2max. Training was conducted five to six times per week for approximately 8 wk. During this time, VO2max increased (P less than 0.05) by 17.2%. Plasma volume (PV) measured by 125I increased (P less than 0.05) from 3,068 +/- 104 ml at 0 wk to 3,490 +/- 126 ml at 4 wk and then plateaued during the remaining four wk (3,362 +/- 113 ml). Red cell (RBC) mass (RCM) measured by 51Cr-labeled RBC did not change during the initial 4 wk of training (2,247 +/- 66 vs. 2,309 +/- 128 ml). As well, no apparent change occurred in RCM during the final 4 wk of training when RCM was estimated using PV and hematocrit (Hct). Collectively, PV plus RCM, expressed as total blood volume (TBV), increased (P less than 0.05) by 10% at 4 wk and then stabilized for the final 4 wk. During the initial phase of training, reductions (P less than 0.05) were also noted in Hct (4.6%), hemoglobin (Hb, 4.0%), and RBC count (6.3%). In contrast, an increase in mean cell volume (MCV, 1.7%) and mean cell Hb (2.3%) was observed (P less than 0.05). From 4 to 8 wk, no further changes (P greater than 0.05) in Hb, RBC, and MCV were found, whereas both mean cell Hb and Hct returned to pretraining levels.(ABSTRACT TRUNCATED AT 250 WORDS)