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.     

Exercise training and "ventilation threshold" in elderly

Dynamic exercise training of the elderly increases maximal O2 uptake (VO2max); however, the effects of training on the ventilation threshold (VET) have not been studied. VET was identified as the final point before the ventilatory equivalent for O2 (VE/VO2) increased, without an increase in the ventilatory equivalent for CO2 (VE/VCO2). Inactive elderly males (mean age, 62 yr) were randomly assigned to a control (C, n = 44) or activity (A, n = 45) group. VO2max and VET were determined from an incremental treadmill test. Initial VO2max was not different between the C (2.34 +/- 0.42 l X min-1) and A (2.28 +/- 0.44 l X min-1) groups, nor was there a significant difference in the VO2 at the VET (C = 1.39 +/- 0.26 l X min-1; A = 1.31 +/- 0.23 l X min-1). The activity group trained for 30 min/day, 3 days/wk at an intensity of approximately 65-80% of VO2max. After 1 yr of training the activity group exhibited an 18% increase in VO2max (A = 2.70 +/- 0.54 l X min-1), but the change in VET was not significant (A = 1.39 +/- 0.28 l X min-1). There was no significant change in VO2max (C = 2.45 +/- 0.68 l X min-1) or VET (C = 1.38 +/- 0.31 l X min-1) in the control group. VET/VO2max declined significantly in the activity group (from 58 to 52% of VO2max). Change in VET/VO2max with training was not correlated with the initial VO2max value. We conclude that increases in aerobic capacity are more readily effected than alterations of the VET in elderly subjects.     

Lactate and ventilatory thresholds: disparity in time course of adaptations to training

We tested the hypothesis that the lactate threshold (Tlac) during incremental exercise could be increased significantly during the first 3 wk of endurance training without any concomitant change in the ventilatory threshold (Tvent). Tvent is defined as O2 uptake (VO2) at which ventilatory equivalent for O2 [expired ventilation per VO2 (VE/VO2)] increased without a simultaneous increase in the ventilatory equivalent for CO2 (VE/VCO2). Weekly measurements of ventilatory gas exchange and blood lactate responses during incremental and steady-rate exercise were performed on six subjects (4 male; 2 female) who exercised 6 days/wk, 30 min/session at 70-80% of pretraining VO2max for 3 wk. Pretraining Tlac and Tvent were not significantly different. After 3 wk of training, significant increases (P less than 0.05) occurred for mean (+/- SE) VO2max (392 +/- 103 ml/min) and Tlac (482 +/- 135 ml/min). Tvent did not change during the 3 wk of training, despite significant (P less than 0.05) reductions in VE responses to both incremental and steady-rate exercise. Thus ventilatory adaptations to exercise during the first 3 wk of exercise training were not accompanied by a detectable alteration in the ventilatory "threshold" during a 1-min incremental exercise protocol. The mean absolute difference between pairs of Tlac and Tvent posttraining was 499 ml/min. Despite the significant training-induced dissociation between Tlac and Tvent a high correlation between the two parameters was obtained posttraining (r = 0.86, P less than 0.05). These results indicate a coincidental rather than causal relationship.(ABSTRACT TRUNCATED AT 250 WORDS)     

Interactive effects of body posture and exercise training on maximal oxygen uptake

To determine the effect of posture on maximal O2 uptake (VO2 max) and other cardiorespiratory adaptations to exercise training, 16 male subjects were trained using high-intensity interval and prolonged continuous cycling in either the supine or upright posture 40 min/day 4 days/wk for 8 wk and 7 male subjects served as non-training controls. VO2 max measured during upright cycling and supine cycling, respectively, increased significantly (P less than 0.05) by 16.1 +/- 3.4 and 22.9 +/- 3.4% in the supine training group (STG) and by 14.6 +/- 2.0 and 6.0 +/- 2.0% in the upright training group (UTG). The increase in VO2 max measured during supine cycling was significantly greater (P less than 0.05) in the STG than in the UTG. The increase in VO2 max in the UTG was significantly greater (P less than 0.05) when measured during upright exercise than during supine exercise. However, there was no significant difference in posture-specific VO2 max adaptations in the STG. A postural specificity was also evident in other maximal cardiorespiratory variables (ventilation, CO2 production, and respiratory exchange ratio). In the UTG, maximal heart rate decreased significantly (P less than 0.05) only during supine cycling; there was no significant difference in maximal heart rate after training in the STG. We conclude that posture affects maximal cardiorespiratory adaptations to cycle training. Additionally, supine training is more effective than upright training in increasing maximal cardiorespiratory responses measured during supine exercise, and the effects of supine training generalize to the upright posture to a greater extent than the effects of upright training generalize to the supine posture.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of high intensity interval training on 2,3-diphosphoglycerate at rest and after maximal exercise

The purpose of this study was to examine the effect of intense interval training on erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels at rest and after maximal exercise. Eight normal men, mean +/- SE = 24.2 +/- 4.3 years, trained 4 days X week-1 for a period of 8 weeks. Each training session consisted of eight maximal 30-s rides on a cycle ergometer, with 4 min active rest between rides . Prior to and after training the subjects performed a maximal 45-s ride on an isokinetic cycle ergometer at 90 rev X min-1 and a graded leg exercise test ( GLET ) to exhaustion on a cycle ergometer. Blood samples were obtained from an antecubital vein before, during and after the GLET only. Training elicited significant increases in the amount of work done during the 45-s ride (P less than 0.05), and also in maximal oxygen uptake (VO2 max: Pre = 4.01 +/- 0.13; Post = 4.29 +/- 0.07 1 X min-1; P less than 0.05) during exercise and total recovery VO2 (Pre = 19.14 +/- 0.09; Post = 21.45 +/- 0.10 1 X 30 min-1; P less than 0.05) after the GLET . After training blood lactate was higher, base excess lower and pH lower during and following the GLET (P less than 0.05 for all variables).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Endurance training in older men and women II. Blood lactate response to submaximal exercise

Seven men and four women (age 63 +/- 2 yr, mean +/- SD, range 61-67 yr) participated in a 12-mo endurance training program to determine the effects of low-intensity (LI) and high-intensity (HI) training on the blood lactate response to submaximal exercise in older individuals. Maximal oxygen uptake (VO2max), blood lactate, O2 uptake (VO2), heart rate (HR), ventilation (VE), and respiratory exchange ratio (R) during three submaximal exercise bouts (65-90% VO2max) were determined before training, after 6 mo of LI training, and after an additional 6 mo of HI training. VO2max (ml X kg-1 X min-1) was increased 12% after LI training (P less than 0.05), while HI training induced a further increase of 18% (P less than 0.01). Lactate, HR, VE, and R were significantly lower (P less than 0.05) at the same absolute work rates after LI training, while HI training induced further but smaller reductions in these parameters (P greater than 0.05). In general, at the same relative work rates (ie., % of VO2max) after training, lactate was lower or unchanged, HR and R were unchanged, and VO2 and VE were higher. These findings indicate that LI training in older individuals results in adaptations in the response to submaximal exercise that are similar to those observed in younger populations and that additional higher intensity training results in further but less-marked changes.     

Endurance training reduces the magnitude of exercise-induced hyperammonemia in humans

The purpose of this study was to determine the influence of endurance-type exercise training on alterations of the ammonia content of blood in exercising humans. Seven females and four males trained 6 days/wk for 7 wk alternating days of continuous cycling (40 min) and interval running (five 5-min bouts). The NH3 content of blood was determined before and during cycle ergometer (CE) exercise (4 min) at power outputs (PO) of 119, 172, and 241 W pretraining and of 163, 230, and 271 W posttraining. These PO for each occasion represent relative work loads of approximately 65, 90, and 115% of peak CE maximum O2 uptake (PCE VO2), respectively. Training increased (P less than 0.05) PCE VO2 approximately 32% (2.72 +/- 0.25 to 3.56 +/- 0.29 l/min or 38.5 +/- 1.9 to 51.2 +/- 2.3 ml X kg-1 X min-1). Both pre- and posttraining the NH3 content of blood increased (P less than 0.05) with increasing intensity of exercise. Training did not influence the measure of these responses during exercise at the same relative intensity. During exercise at the same absolute PO, approximately 168 or 235 W, however, increases in blood NH3 were less (P less than 0.05) after training. The results indicate that the magnitude of increase in blood NH3 during exercise is determined by the energy requirement of the absolute work load, relative to an individual's aerobic power.     

Daily physical activity levels in preadolescent boys related to VO2max and lactate threshold

The purpose of this study was to investigate the physical activity levels in eleven 9-10 year old boys with reference to aerobic power or lactate threshold (LT). Daily physical activity levels were evaluated from a HR monitoring system for 12 h on three different days. VO2max, VO2-HR relationship and LT were determined by the progressive treadmill test. LT was 36.7 +/- 3.1 ml X kg-1 X min-1 and 71.0 +/- 6.6% VO2max. Mean total time of activities with HR above the level corresponding to 60% VO2max (T-60%) and that above LT (T-LT) were 34 +/- 7 and 18 +/- 7 min, respectively. VO2max (ml X kg-1 X min-1) correlated significantly with T-60% (p less than 0.01), while no significant relationship was found with LT in ml X kg-1 X min-1. In conclusion, longer daily physical activities at moderate to higher intensity for preadolescent children seem to increase VO2max rather than LT.     

31P nuclear magnetic resonance spectroscopy study of the anaerobic threshold in humans

The relationships among the lactate threshold (LT), ventilatory threshold (VT), and intracellular biochemical events in exercising muscle have not been well defined. Therefore 14 normal subjects performed incremental plantar flexion to exhaustion on 2 study days, the first for determination of LT and VT and the second for continuous 31P nuclear magnetic resonance spectroscopy of calf muscle. Exercising calf muscle pH fell precipitously at 66.4 +/- 3.4% (SE) of the maximum O2 uptake (VO2max) and was termed the intramuscular pH threshold. This did not occur at a significantly different metabolic rate from that at the LT (78.6 +/- 5.9% VO2max) or at the VT (75.0 +/- 4.1% VO2max, P = 0.15 by analysis of variance). Four subjects showed an intramuscular pH threshold and VT without a perceptible rise in forearm venous blood lactate. It is concluded that traditional markers of the "anaerobic threshold," the LT and VT, occur as intramuscular pH becomes acid for a group of normal subjects undergoing incremental exercise to exhaustion. It is speculated that neuronal pathways linking intramuscular biochemical events to the ventilatory control center may explain the intact VT in those subjects without an "intermediary" LT.     

Sweat lactate secretion during exercise in relation to women's aerobic capacity

The purpose of this investigation was to determine whether sweat lactate secretion during exercise [approximately 70% maximum O2 consumption (VO2max), 60 min] differed in active vs. sedentary female subjects. Sweat rate, total sweat lactate secretion, and sweat lactate concentration were monitored in a group of sedentary (VO2max = 41.0 +/- 1.62 ml X kg-1 X min-1) and active (VO2max = 51.2 +/- 3.20 ml X kg-1 X min-1) women. Sweat rate was significantly (P less than 0.05) greater in the active subjects. There was a significant difference between groups in total amount of sweat lactate secreted (P less than 0.05), with the active group secreting less lactate (29.8 +/- 5.03 mmol, mean +/- SE) than the sedentary group (50.2 +/- 6.61 mmol). Concomitant with the lower total sweat lactate secretion in the active subjects was a significantly (P less than 0.05) more dilute sweat lactate concentration (42.6 +/- 14.08 vs. 100.4 +/- 32.37 mM). In these female subjects, sweat lactate concentration was inversely correlated (r = -0.79, P less than 0.01, n = 10) to sweat rate. It is concluded that total sweat lactate loss is significantly less in active than in sedentary women and that the active subjects secrete a greater quantity of lactate dilute sweat.     

Effects of oral propranolol and exercise protocol on indices of aerobic function in normal man

The exercise responses to two different progressive, upright cycle ergometer tests were studied in nine healthy, young subjects either with no drug (ND) or following 48 h or oral propranolol (P) (40 mg q.i.d.). The ergometer tests increased work rate by 30 W either every 30 s or every 4 min. Propranolol caused a significant (p less than 0.05) reduction in peak oxygen uptake (VO2) during both the 30-s and 4-min tests (30-s ND, 3949 +/- 718 mL X min-1 (means +/- SD); 30-s P, 3408 +/- 778 mL X min-1; 4-min ND, 4058 +/- 409 mL X min-1; 4-min P, 3725 +/- 573 mL X min-1). There was no difference between 30-s ND and 4-min ND for peak VO2. The ventilatory anaerobic threshold was not significantly different between any test (30-s ND, 2337 +/- 434 mL O2 X min-1; 30-s P, 2174 +/- 406 mL O2 X min-1; ND, 2433 +/- 685 mL O2 X min-1; 4-min P, 2296 +/- 604 mL O2 X min-1). The VO2 at which blood lactate had increased by 0.5 mM above resting levels was significantly lower than the ventilatory anaerobic threshold for the 4-min ND (1917 +/- 489) and the 4-min P (1978 +/- 412) tests, but was not different for the 30-s ND and 30-s P tests. At exhaustion in the progressive tests, the blood PCO2 was higher (p less than 0.05) in both 30-s tests than 4-min tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

The relationship between lactate and ventilatory thresholds: coincidental or cause and effect?

To determine if blood lactate (LA) is the stimulus responsible for 'breakaway' ventilation (VE), the lactate (LT) and ventilation (VT) thresholds were monitored during one-legged cycling exercise. Ten healthy volunteer male subjects (Mean 2-legged VO2max = 4.27 l X min-1) performed prior exercise (PE) to reduce muscle glycogen stores by cycling at 75-85% of maximal heart rate (HR max) for 60-75 min, followed by a 30 h low carbohydrate diet. Pre- and post- LT and VT tests were performed on a cycle ergometer employing a continuous protocol with increments of 16 W every 3 min. Muscle biopsies were taken from the vastus lateralis muscle before the PE ride, prior to the threshold test 24 h later, and before testing the non-exercised (NE) leg. An I.V. catheter placed in the antecubital vein was used for serial blood samples taken at rest, and during the final 30 s of each progressive load. Gas analysis was calculated every 30 s (Beckman Metabolic Measurement Cart). Biopsies (N = 3) showed that the exercise and diet regimen elicited glycogen reduction which significantly (p less than 0.05) reduced R and the blood LA concentration in both the PE (2.62 to 1.99 mmol X l-1) and NE (2.87 to 2.26 mmol X l-1) legs at LT. At VT, LA concentrations were also significantly reduced in the PE (3.35 to 2.56 mmol X l-1) and NE (3.59 to 2.74 mmol X l-1) legs. VO2 and VE, however, were similar between pre- and post- tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of endurance exercise training on ventilatory function in older individuals

To evaluate the effect of endurance training on ventilatory function in older individuals, 1) 14 master athletes (MA) [age 63 +/- 2 yr (mean +/- SD); maximum O2 uptake (VO2max) 52.1 +/- 7.9 ml . kg-1 . min-1] were compared with 14 healthy male sedentary controls (CON) (age 63 +/- 3 yr; VO2max of 27.6 +/- 3.4 ml . kg-1 . min-1), and 2) 11 sedentary healthy men and women, age 63 +/- 2 yr, were reevaluated after 12 mo of endurance training that increased their VO2max 25%. MA had a significantly lower ventilatory response to submaximal exercise at the same O2 uptake (VE/VO2) and greater maximal voluntary ventilation (MVV), maximal exercise ventilation (VEmax), and ratio of VEmax to MVV than CON. Except for MVV, all of these parameters improved significantly in the previously sedentary subjects in response to training. Hypercapnic ventilatory response (HCVR) at rest and the ventilatory equivalent for CO2 (VE/VCO2) during submaximal exercise were similar for MA and CON and unaffected by training. We conclude that the increase in VE/VO2 during submaximal exercise observed with aging can be reversed by endurance training, and that after training, previously sedentary older individuals breathe at the same percentage of MVV during maximal exercise as highly trained athletes of similar age.     

Effects of training on lactate production and removal during progressive exercise in humans.

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.     

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)     

Effect of training on the rating of perceived exertion at the ventilatory threshold

The purpose of this study was to determine the effect of training on the rating of perceived exertion (RPE) at the ventilatory threshold. College students were assigned to either training (n = 17) or control (n = 10) groups. Trainers completed 18 interval training sessions (five X 5 min cycling at 90-100% VO2max) and 8 continuous training sessions (40 min running or cycling) in 6 weeks. Pre- and post-training, cardiorespiratory, metabolic, and perceptual variables were measured at the ventilatory threshold during graded exercise tests on a cycle ergometer. Ventilatory threshold was that point above which VE X VO2-1 increased abruptly relative to work rate. Post-training means of trained and control subjects were compared using analysis of covariance, with pre-training values as covariates. Following training, the adjusted means for the trained subjects were significantly greater (p less than 0.05) than for controls for VO2max (6%), and for work rate (20%), VO2 (23%), and %VO2max (13%) at the ventilatory threshold. However, adjusted means for RPE at the ventilatory threshold were not significantly different (2%). Both before and after training, exercise at the ventilatory threshold was perceived as 'somewhat hard' to 'hard' (RPE = 13-15) by both groups. The relationship between RPE and %VO2max was altered by training, with trained subjects having a lower RPE at a given %VO2max. It is concluded that RPE at the ventilatory threshold is not affected by training, despite that after training the ventilatory threshold occurs at a higher work rate and is associated with higher absolute and relative metabolic and cardiorespiratory demands.     

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.     

Comparison of body water turnover in endurance runners and age-matched sedentary men

This study compared the body water turnover in endurance athletes and age-matched sedentary men. Eight competitive endurance athletes (20.8+/-1.9 yr) and age-matched eight sedentary men (21.6+/-2.5 yr) participated in this study. Total body water and body water turnover were measured using the deuterium (D(2)O) dilution technique. Urine samples were obtained every day for 10 days after oral administration of D(2)O. The day-by-day concentrations were used to calculate the biological half-life of D(2)O and body water turnover. Maximal oxygen uptake (VO(2max)) and oxygen uptake corresponding to ventilatory threshold (VO(2VT)) as an index of aerobic capacity were determined during a graded exercise test. Both VO(2max) and VO(2VT) were higher in the exercise group than in the sedentary group (P<0.05). The biological half-life of D(2)O was significantly shorter in the exercise group than in the sedentary group (5.89+/-0.81 days vs. 7.52+/-0.77 days, P<0.05), and the percentage of the body water turnover was significantly higher in the exercise group than in the sedentary group (11.99+/-1.96% vs. 9.39+/-1.21%, P<0.05). The body water turnover was correlated with VO(2max) and VO(2VT), respectively (P<0.05). Based on these findings, this study speculates that a level of physical activity may induce a body water turnover higher in the healthy state, since the better trained subjects have a higher body water turnover.