Maximal oxygen uptake in Chilean workers of normal nutritional status

Maximum oxygen uptake (VO2max) was measured directly and predicted from cardiac frequency measurements in 54 healthy Chilean industrial workers aged 20 to 55 years, together with assessment of their dietary intake, body composition and blood chemistry. Measurement of VO2 was performed on a motor-driven treadmill. The predicted VO2max was obtained using a cycle ergometer by two methods: 1) the Astrand-Ryhming nomogram and 2) the linear relationship between "steady state" heart rate (HR) and submaximum work, with subsequent extrapolation to "maximum" heart rate. Extrapolation of the HR/load regression line to 170 bpm permitted determination of the physical working capacity at 170 bpm (W170). VO2max for the 20-29 year group (Group I) averaged 3624 ml.min-1 and decreased to 3066 ml.min-1 in the 50-55 year group (Group IV). Lower values were obtained using the Astrand-Ryhming nomogram and HR/load regression (-15% and -9% respectively). W170 was also affected by age (Group I: 190.6 W and Group IV: 158.5 W). No significant correlation were found between VO2max and plasma variables, with the exception of cholesterol (r = 0.59). On the contrary, anthropometric variables showed significant correlations with VO2max, which permitted the prediction of VO2max using multiple regression equations. The two best correlations were: 1. VO2max = 0.800 - 0.0225.(A) +0.0189.(W)+1.26.(H) (r = 0.87; p less than 0.001) 2. VO2max = 0.996 - 0.0176.(A) + 0.025.(W) + 0.838.(H) + 0.0255.(LBM) (r = 0.88; p less than 0.001) where A = years of age; W = body weight in kg; H = height in m and LBM = lean body mass in kg.     

Effects of human pregnancy and aerobic conditioning on alveolar gas exchange during exercise

This study examined the effects of aerobic conditioning during the second and third trimesters of human pregnancy on ventilatory responses to graded cycling. Previously sedentary pregnant women were assigned randomly to an exercise group (n = 14) or a nonexercising control group (n = 14). Data were collected at 15-17 weeks, 25-27 weeks and 34-36 weeks of pregnancy. Testing involved 20 W.min-1 increases in work rate to a heart rate of 170 beats.min-1 and (or) volitional fatigue. Breath-by-breath ventilatory and alveolar gas exchange measurements were compared at rest, a standard submaximal .VO2 and peak exercise. Within both groups, resting .V(E), .V(A), and V(T)/T(I) increased significantly with advancing gestation. Peak work rate, O2 pulse (.VO2/HR), .V(E), .V(A) respiratory rate, V(T)/T(I), .VO2, .VCO2, and the ventilatory threshold (T(vent)) were increased after physical conditioning. Chronic maternal exercise has no significant effect on pregnancy-induced changes in ventilation and (or) alveolar gas exchange at rest or during standard submaximal exercise. Training-induced increases in T(vent) and peak oxygen pulse support the efficacy of prenatal fitness programs to improve maternal work capacity.     

Oxygen uptake kinetics in trained athletes differing in VO2max

Previous work has shown that when VO2 kinetics are compared for endurance trained athletes and untrained subjects, the highly trained athletes have a faster response time. However, it remains to be determined whether the more rapid adjustment of VO2 toward steady state in athletes is due to VO2max differences or training adaptation alone. One approach to this problem is to study the time course of VO2 kinetics at the onset of work in athletes who differ in VO2max but have similar training habits. Therefore, the purpose of these experiments was to compare the time course of VO2 kinetics at the onset of exercise in athletes with similar training routines but who differ in VO2max. Ten subjects (VO2max range 50-70 ml . kg-1 . min-1) performed 6-minutes of cycle ergometer exercise at approximately 50% VO2max. Ventilation and gas exchange were monitored by open circuit techniques. The data were modeled with a single component exponential function incorporating a time delay, (TD); delta VO2t = delta VO2ss (1-e-t-TD/tau), where tau is the time constant delta VO2t is the increase in VO2 at time t and delta VO2ss is the steady-rate increment above resting VO2. Kinetic analysis revealed a range of VO2 half times from 21.6 to 36.0 s across subjects with a correlation coefficient of r = -0.80 (p less than 0.05) between VO2max and VO2 half time. These data suggest that in highly trained individuals with similar training habits, those with a higher VO2max achieve a more rapid VO2 adjustment at the onset of work.     

Human ventilatory responsiveness to hypoxia is unrelated to maximal aerobic capacity.

Ventilatory responsiveness to hypoxia (HVR) has been reported to be different between highly trained endurance athletes and healthy sedentary controls. However, a linkage between aerobic capacity and HVR has not been a universal finding. The purpose of this study was to examine the relationship between HVR and maximal oxygen consumption (VO2 max) in healthy men with a wide range of aerobic capacities. Subjects performed a HVR test followed by an incremental cycle test to exhaustion. Participants were classified according to their maximal aerobic capacity. Those with a VO2 max of >or=60 ml x kg(-1) x min(-1) were considered highly trained (n = 13); those with a VO2 max of 50-60 ml x kg(-1) x min(-1) were considered moderately-trained (n = 18); and those with a VO2 max of <50 ml x kg(-1) x min(-1) were considered untrained (n = 24). No statistical differences were detected between the three groups for HVR (P > 0.05), and the HVR values were variable within each group (range: untrained = 0.28-1.61, moderately trained = 0.23-2.39, and highly trained = 0.08-1.73 l x min.%arterial O2 saturation(-1)). The relationship between HVR and VO2 max was not statistically significant (r = -0.1723; P > 0.05). HVR was also unrelated to maximal minute ventilation and ventilatory equivalents for O2 and CO2. We found that a spectrum of hypoxic ventilatory control is present in well-trained endurance athletes and moderately and untrained men. We interpret these observations to mean that other factors are more important in determining hypoxic ventilatory control than physical conditioning per se.     

Effects of specific muscle training on VO2 on-response and early blood lactate

The relationship between half time of the O2 uptake on-response (t1/2 VO2on, seconds) and early blood lactate accumulation (delta Lab, mmol.1(-1) at the onset of submaximal arm and/or leg exercise was the object of a cross-sectional study of sedentary subjects (S,n = 3), and kayakers (K, n = 8), and of a longitudinal study on 11 untrained subjects of specific arm vs. leg training. In supine arm cranking (W = 125 watts) S had an average t1/2 VO2on of 82 s and a delta Aab of 9.2 mmol.1(-1) compared to 47 +/- 7 s and 4 +/- 1.4 mmol.1(-1), respectively, for K. In longitudinal trainees shorter t1/2 VO2on was accompanied by lower Lab for the trained limbs. Specific limb conditioning in swimmers and runners resulted in shorter t1/2 VO2on. A linear relationship was observed between delta Lab and t1/2 VO2on having an intercept on the time axis at congruent to 20 s and a slope proportional to muscle mass. Trained muscles were grouped closest to the intercept indicating local acceleration of the rate of O2 transfer approaching the t1/2 VO2on for isolated perfused muscle at the onset of work. Since t1/2 VO2on, we conclude that factors distal to the capillary are specifically involved in the local training response.     

Exercise intensity: effect on postexercise O2 uptake in trained and untrained women

Despite many reports of long-lasting elevation of metabolism after exercise, little is known regarding the effects of exercise intensity and duration on this phenomenon. This study examined the effect of a constant duration (30 min) of cycle ergometer exercise at varied intensity levels [50 and 70% of maximal O2 consumption (VO2max)] on 3-h recovery of oxygen uptake (VO2). VO2 and respiratory exchange ratios were measured by open-circuit spirometry in five trained female cyclists (age 25 +/- 1.7 yr) and five untrained females (age 27 +/- 0.8 yr). Postexercise VO2 measured at intervals for 3 h after exercise was greater (P less than 0.01) after exercise at 50% VO2max in trained (0.40 +/- 0.01 l/min) and untrained subjects (0.39 +/- 0.01 l/min) than after 70% VO2max in (0.31 +/- 0.02 l/min) and untrained subjects (0.29 +/- 0.02 l/min). The lower respiratory exchange ratio values (P less than 0.01) after 50% VO2max in trained (0.78 +/- 0.01) and untrained subjects (0.80 +/- 0.01) compared with 70% VO2max in trained (0.81 +/- 0.01) and untrained subjects (0.83 +/- 0.01) suggest that an increase in fat metabolism may be implicated in the long-term elevation of metabolism after exercise. This was supported by the greater estimated fatty acid oxidation (P less than 0.05) after 50% VO2max in trained (147 +/- 4 mg/min) and untrained subjects (133 +/- 9 mg/min) compared with 70% VO2max in trained (101 +/- 6 mg/min) and untrained subjects (85 +/- 7 mg/min).     

Effect of aerobic capacity on the T(2) increase in exercised skeletal muscle.

The increase in nuclear magnetic resonance transverse relaxation time (T(2)) of muscle water measured by magnetic resonance imaging after exercise has been correlated with work rate in human subjects. This study compared the T(2) increase in thigh muscles of trained (cycling VO(2 max) = 54.4 +/- 2.7 ml O(2). kg(-1). min(-1), mean +/- SE, n = 8, 4 female) vs. sedentary (31.7 +/- 0.9 ml O(2). kg(-1). min(-1), n = 8, 4 female) subjects after cycling exercise for 6 min at 50 and 90% of the subjects' individually determined VO(2 max). There was no significant difference between groups in the T(2) increase measured in quadriceps muscles within 3 min after the exercises, despite the fact that the absolute work rates were 60% higher in the trained group (253 +/- 15 vs. 159 +/- 21 W for the 90% exercise). In both groups, the increase in T(2) of vastus muscles was twofold greater after the 90% exercise than after the 50% exercise. The recovery of T(2) after the 90% exercise was significantly faster in vastus muscles of the trained compared with the sedentary group (mean recovery half-time 11.9 +/- 1.2 vs. 23.3 +/- 3.7 min). The results show that the increase in muscle T(2) varies with work rate relative to muscle maximum aerobic power, not with absolute work rate.     

The effect of fatigue and training status on firefighter performance

Firefighting is a strenuous occupation that requires optimal levels of physical fitness. The National Fire Protection Association suggests that firefighters should be allowed to exercise on duty to maintain adequate fitness levels. However, no research has addressed the effect of exercise-induced fatigue on subsequent fire ground performance. Therefore, the primary purpose of this study was to determine the effect that a single exercise session had on the performance of a simulated fire ground test (SFGT). Secondarily, this study sought to compare the effect of physical training status (i.e., trained vs. untrained firefighters) on the performance of an SFGT. Twelve trained (age: 31.8 ± 6.9 years; body mass index [BMI]: 27.7 ± 3.3 kg·m(-2); VO2peak: 45.6 ± 3.3 ml·kg(-1)·min(-1)) and 37 untrained (age: 31.0 ± 9.0 years; BMI: 31.3 ± 5.2 kg·m(-2); VO2peak: 40.2 ± 5.2 ml·kg(-1)·min(-1)) male career firefighters performed a baseline SFGT. The trained firefighters performed a second SFGT after an exercise session. Time to complete the SFGT, heart rate, and blood lactate were compared between baseline and exercise SFGT (EX-SFGT) conditions. In the trained firefighters, time to complete the SFGT (9.6% increase; p = 0.002) and heart rate (4.1% increase; p = 0.032) were greater during the EX-SFGT compared with baseline, with no difference in post-SFGT blood lactate (p = 0.841). The EX-SFGT time of the trained firefighters was faster than approximately 70% of the untrained firefighters' baseline SFGT time. In addition, the baseline SFGT time of the trained firefighters was faster than 81% of the untrained firefighters. This study demonstrated that on-duty exercise training reduced the work efficiency in firefighters. However, adaptations obtained through regular on-duty exercise training may limit decrements in work efficiency because of acute exercise fatigue and allow for superior work efficiency compared with not participating in a training program.     

Oxygen consumption and metabolic strain in rowing ergometer exercise

Oxygen consumption (VO2) when rowing was determined on a mechanically braked rowing ergometer (RE) with an electronic measuring device. VO2 was measured by an open spirometric system. The pneumotachograph valve was fixed to the sliding seat, thus reducing movement artefacts. A multi-stage test was performed, beginning with a work load of 150 W and increasing by 50 W every 2 minutes up to exhaustion. Serum lactate concentrations were determined in a 30 s break between the work stages. 61 examinations of oarsmen performing at maximum power of 5 W X kg-1 or more were analysed VO2 and heart rate (HR) for each working stage were measured and the regression line of VO2 on the work load (P) and an estimation error (Sxy) were calculated: VO2 = 12.5 X P + 415.2 (ml X min-1) (Sxy = +/- 337 ml, r = 0.98) Good reproducibility was found in repeated examinations. Similar spiroergometry was carried out on a bicycle ergometer (BE) with 10 well trained rowers and 6 trained cyclists. VO2 of rowing was about 600 ml X min-1 higher than for bicycling in the submaximal stages for both groups. The VO2max of RE exercise was 2.6% higher than for oarsmen on BE, and the cyclists reached a greater VO2 on BE than the oarsmen. No differences were found between RE and BE exercise heart rate. The net work efficiency when rowing was 19% for both groups, experienced and inexperienced: when cycling it was 25% for cyclists and 23% for oarsmen.     

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.     

Relation between the change of slope of heart rate and second lactic and ventilatory thresholds in muscular exercise with large load]

The time-course of heart rate, blood lactate, and ventilatory gas exchange was studied during an incremental exercise test on cycloergometer in order to ascertain whether heart rate deflection occurred at the same load as the second lactate S[La]2) and ventilatory (SV2) thresholds. Twelve moderately trained subjects, 22 to 30 years old, participated in the study. The initial power setting was 30 W for 3 min with successive increases of 30 W every min except at the end of the test where the increase was reduced to 20 and 10 W.min-1. Ventilatory flow (VE), oxygen uptake (VO2), carbon dioxide production (VCO2, ventilatory equivalents of O2 (EO2 = VE/VO2) and CO2 (ECO2 = VE/VCO2), and heart rate (HR) were determined during the last 20 s of every min. Venous blood samples were drawn at the end of each stage of effort and analyzed enzymatically for lactate concentration ([La]). The HR deflection, S[La]2, and SV2 were represented graphically by two investigators using a double blind procedure. Following the method proposed by Conconi et al. 1982, the deflection in HR was considered to begin at the point beyond which the increase in work intensity exceeded the increase in HR and the linearity of the work rate/HR relationship was lost. S[La]2 corresponded to the second breaking point of the lactate time-course curve (onset of blood lactate accumulation) and SV2 was identified at the second breaking point in the increase in VE and ventilatory equivalent for O2 uptake accompanied by a concomitant increase in ventilatory equivalent for CO2 output. We observed that the deflection point in HR was present only in 7 subjects. The work load, VO2, HR, and [La] levels at which heart rate departed from linearity did not differ significantly from those determined with S[La]2 ans SV2. The VO2 and HR values at HR deflection point were significantly correlated with those measured at S[La]2 and SV2. It is concluded that deflection in heart rate does not always occur, and when it does, it coincides with the second lactate and ventilatory gas exchange thresholds. It can thus be used for the determination of optimal intensity for individualized aerobic training.     

The effect of oral supplementation with L-carnitine on maximum and submaximum exercise capacity

Two trials were conducted to investigate the effects of L-carnitine supplementation upon maximum and submaximum exercise capacity. Two groups of healthy, untrained subjects were studied in double-blind cross-over trails. Oral supplementation of 2 g per day L-carnitine was used for 2 weeks in the first trial and the same dose but for 4 weeks in the second trial. Maximum and submaximum exercise capacity were assessed during a continuous progressive cycle ergometer exercise test performed at 70 rpm. In trial 1, plasma concentrations of lactate and beta-hydroxybutyrate were measured pre- and post-exercise. In trial 2, pre- and post-exercise plasma lactate were measured. The results of treatment with L-carnitine demonstrated no significant changes in maximum oxygen uptake (VO2max) or in maximum heart rate. In trial 1, there was a small improvement in submaximal performance as evidenced by a decrease in the heart-rate response to a work-load requiring 50% of VO2max. The more extensive trial 2 did not reproduce the significant result obtained in trial 1, that is, there was no significant decrease in heart rate at any given submaximal exercise intensity, under carnitine-supplemented conditions. Plasma metabolic concentrations were unchanged following L-carnitine, in both trials. It is concluded, that in contrast to other reports, carnitine supplementation may be of little benefit to exercise performance since the observed effects were small and inconsistent.     

Excess postexercise oxygen consumption is unaffected by the resistance and aerobic exercise order in an exercise session

The main purpose of this study was to compare the magnitude and duration of excess postexercise oxygen consumption (EPOC) after 2 exercise sessions with different exercise mode orders, resistance followed by aerobic exercise (R-A); aerobic by resistance exercise (A-R). Seven young men (19.6 ± 1.4 years) randomly underwent the 2 sessions. Aerobic exercise was performed on a treadmill for 30 minutes (80-85% of reserve heart rate). Resistance exercise consisted of 3 sets of 10 repetition maximum on 5 exercises. Previous to the exercise sessions, V(O2), heart rate, V(CO2), and respiratory exchange rate (RER) were measured for 15 minutes and again during recovery from exercise for 60 minutes. The EPOC magnitude was not significantly different between R-A (5.17 ± 2.26 L) and A-R (5.23 ± 2.48 L). Throughout the recovery period (60 minutes), V(O2) and HR values were significantly higher than those observed in the pre-exercise period (p < 0.05) in both exercise sessions. In the first 10 minutes of recovery, V(CO2) and RER declined to pre-exercise levels. Moreover, V(CO2) and RER values in A-R were significantly lower than in R-A. In conclusion, the main result of this study suggests that exercise mode order does not affect the EPOC magnitude and duration. Therefore, it is not necessary for an individual to consider the EPOC when making the decision as to which exercise mode is better to start a training session.     

Vascular volumes and hematology in male and female runners and cyclists

To examine the hypothesis that foot-strike hemolysis alters vascular volumes and selected hematological properties is trained athletes, we have measured total blood volume (TBV), red cell volume (RCV) and plasma volume (PV) in cyclists (n = 21) and runners (n = 17) and compared them to those of untrained controls (n = 20). TBV (ml x kg(-1)) was calculated as the sum of RCV (ml x kg(-1)) and PV (ml x kg(-1)) obtained using 51Cr and 125I-labelled albumin, respectively. Hematological assessment was carried out using a Coulter counter. Peak aerobic power (VO2peak) was measured during progressive exercise to fatigue using both cycle and treadmill ergometry. RCV was 15% higher (P < 0.05) in male cyclists [35.4 (1.0), mean (SE); n = 12] and runners [35.3 (0.98); n = 9] compared to the controls [30.7 (0.92); n = 12]. Similar differences existed between the female cyclists [28.2 (2.1); n = 9] and runners [28.4 (1.0); n = 8] compared to the untrained controls [24.9 (1.4); n = 8]. For the male athletes, PV was between 19% (cyclists) and 28% (runners) higher (P < 0.05) in the trained athletes compared to the untrained controls. The differences in PV between the female groups were not significant. Although the males had a higher (P < 0.05) TBV, RCV and PV than the females, no differences between cyclists and runners were found for either gender. Mean cell volume was not different between the athletic groups. VO2peak (ml x kg(-1) x min(-1)) was higher (P < 0.05) in both male [68.4 (1.5)] and female [54.8 (2.1)] runners when compared to the untrained males [47.1 (1.0)] and females [40.5 (2.1)]. Although differences existed between the genders in VO2peak for both cyclists and runners, no differences were found between the athletic groups within a gender. Since the vascular volumes were not different between cyclists and runners for either the males or females, foot-strike hemolysis would not appear to have an effect on that parameter. The significant correlations (P < 0.05) found between VO2peak and RCV (r = 0.64 and 0.64) and TBV (r = 0.82 and 0.63) for the males and females, respectively, suggests a role for the vascular system in realizing a high aerobic power.     

Adaptation of the left ventricle to exercise-induced hypertrophy

Cardiac functional and structural adaptations to exercise-induced hypertrophy were studied in 68 pigs. Pigs were exercise trained on a treadmill for 10 wk. Sequential measurements were made of cardiac dimensions, [left ventricular end-diastolic diameter (EDD), changes in diameter (delta D%), wall thickness (WTh), wall thickening (WTh%), left ventricular pressure (LVP), time derivative of pressure (dP/dt), stroke volume, total body O2 consumption (VO2), blood gases, and systemic hemodynamics] at rest and during moderate and severe exercise. Postmortem studies included morphometric measurements of capillary density, arteriolar density, mitochondria, and myofibrils. All of the exercise-trained pigs showed significant increases in aerobic capacity. Maximum O2 consumption (VO2 max) increased by 37.5% in group 1 (moderate exercise training) and 34% in group 3 (heavy exercise training). Cardiac hypertrophy ranged from less than 15% in a group (n = 8) subjected to moderate exercise training to greater than 30% in a group (n = 11) subjected to heavy exercise training. Before training, exercise was characterized by a decreasing EDD during progressive exercise; this was reversed after exercise training. Stroke volume and end-diastolic volumes during exercise showed a highly significant increase after exercise training and hypertrophy. Morphometric measurements showed that mitochondria and cell membranes increased with increasing myocyte growth in all exercise groups, but there was only a partially compensated adaptation of capillary proliferation. Arteriolar number and length increased in all exercise groups. Intrinsic contractility as measured by delta D%, WTh%, or left ventricular dP/dt did not increase with exercise training and in some instances decreased. Therefore, left ventricular adaptation to strenuous exercise in the pig heart is primarily one of changes in left ventricular dimensions and a compensated hypertrophy. Exercise-induced increases in EDD and stroke volume can be accounted for by decreases in peripheral resistance and increased cardiac dimensions.     

Effects of pregnancy and chronic exercise on maternal cardiac structure and function

This study examined the interactive effects of pregnancy and aerobic conditioning on maternal cardiac structure and function. Effects of closely monitored cycle ergometer conditioning were studied during the second (TM2) and third trimesters (TM3) in 22 previously sedentary pregnant women (exercised group, EG) and a nonexercising pregnant control group with similar characteristics (CG, n = 19). Subjects were studied in the resting state by two-dimensional echocardiography and during cycle ergometer exercise at three steady-state power outputs at the start of TM2 (ENTRY), at the end of TM2 and TM3 (postconditioning), and 3-4 months postpartum (NPR, nonpregnant reference, CG only). Aerobic conditioning did not increase left ventricular dimensions beyond those attributable to pregnancy itself. In addition, in contrast with previous studies of nonpregnant women, physical conditioning during pregnancy did not reduce heart rate (HR) in the resting state. During exercise, the slope of the HR versus oxygen uptake (VO2) regression decreased significantly between preconditioning and the end of TM3 in the EG, suggesting that training-induced reductions in HR become more evident with increasing exercise intensity. Also, significant reductions in oxygen pulse (VO2/HR) were observed at all three work rates in the CG, but not in the EG. These findings support the hypothesis that the cardiovascular effects of aerobic conditioning are obscured by more powerful effects of pregnancy in the resting state but become "unmasked" during strenuous exercise.     

Intersubject variability in cardiac output-O2 uptake relation of men during exercise

Intersubject variability in the relation between cardiac output (Q) and O2 uptake (VO2) was examined during supine cycling up to the maximum level in 40 normal untrained men age 27 +/- 4 (SD) yr. In individual subjects, Q increased linearly against VO2 in the submaximum exercise range. The SD of Q on VO2 was so small (0.47 +/- 0.25 l/min) that Q could be given by a linear function of VO2 as Q = K(VO2 - VO2 r) + Qr, where K, VO2 r, and Qr are the slope of the regression line, the resting VO2, and resting Q, respectively. K varied widely among the subjects studied, ranging from 5.5 to 10.3 and was independent of both physical characteristics and Qr, which ranged from 3.7 to 8.3 l/min. However, K correlated significantly with changes in heart rate, stroke volume, mean arterial pressure, and systemic vascular conductance. From these results, we concluded that the intersubject variability in the Q-VO2 relation was caused independently by individual variations in resting hemodynamics and in cardiovascular response to exercise.     

Plasma Met-enkephalin and catecholamine responses to intense exercise in humans.

Native and cryptic Met-enkephalin and catecholamines are coreleased in response to stress. However, it is not known whether Met-enkephalin and catecholamines exhibit concurrent temporal relationships in response to exercise. The purpose of this investigation was to examine the corelease of catecholamines and Met-enkephalin in endurance-trained (n = 6) and untrained (n = 6) male subjects during a 6-min bout of exercise: 4 min at 70% of maximal O2 uptake (VO2max) followed by 2 min at 120% VO2max. Peak catecholamine levels were found at 1 min of recovery. In trained subjects, native Met-enkephalin peaked during exercise at 70% VO2max, declined during exercise at 120% VO2max, and returned to basal levels by 1 min of recovery. In the untrained subjects, native Met-enkephalin peaked at 120% VO2max (6 min) and returned to baseline by 5 min of recovery. In both groups, cryptic Met-enkephalin peaked at 70% VO2max and returned to basal levels during exercise at 120% VO2max. These data demonstrate that during exercise there is a temporal dissociation in plasma levels of Met-enkephalin and catecholamines.     

Effects of age and physical performance capacity on distribution and composition of high-density lipoprotein subfractions in men

The influences of age and maximal aerobic capacity (VO2max) on serum lipoproteins with special regard to the concentration, composition and distribution of high density lipoprotein (HDL) subfractions were investigated in 51 healthy males of different characteristics: younger than 35 years, untrained (n = 14, mean age 28.2 years, SD 6.0; VO2max, 47.9 ml.kg-1.min-1, SD 5.8) and trained (n = 11, mean age 27.9 years, SD 4.3; VO2max, 61.1 ml.kg-1.min-1, SD 5.1), older than 50 years untrained (n = 14, mean age 58.9 years, SD 5.9, VO2max, 29.3 ml.kg-1.min-1, SD 5.3) and trained (n = 12, mean age 59.3 years, SD 7.2, VO2max, 45.7 ml.kg-1.min-1, SD 7.7). The fasting-state serum concentrations of total cholesterol, tri-acylglycerol and lipoprotein-cholesterol were measured. The HDL-subfractions were separated by density (rho) gradient ultracentrifugation. Concentrations of cholesterol, cholesterylester, tri-acylglycerol, phospholipids, apolipoprotein (apo) A-I and A-II were measured in the subfractions HDL2b: rho = 1.063-1.100 g.ml-1; HDL2al: rho = 1.00-1.110 g.ml-1; HDL2a2: rho = 1.110-1.150 g.ml-1; HDL3: rho = 1.150-1.210 g.ml-1. Elderly untrained subjects showed increased serum concentrations of total-, very low- and low density lipoprotein-cholesterol and elevated tri-acylglycerol levels. The HDL-cholesterol concentration was decreased, due to reduced concentrations of HDL2-subfractions. Significant changes in the composition of HDL2-subfractions were found in elderly untrained subjects. The HDL2-subfractions had more protein, a decreased apoA-I:A-II ratio and less phospholipids in comparison to HDL2-subfractions from younger untrained and trained, and elderly trained subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of inspiratory resistive loading on control of ventilation during progressive exercise

Eight healthy volunteers performed gradational tests to exhaustion on a mechanically braked cycle ergometer, with and without the addition of an inspiratory resistive load. Mean slopes for linear ventilatory responses during loaded and unloaded exercise [change in minute ventilation per change in CO2 output (delta VE/delta VCO2)] measured below the anaerobic threshold were 24.1 +/- 1.3 (SE) = l/l of CO2 and 26.2 +/- 1.0 l/l of CO2, respectively (P greater than 0.10). During loaded exercise, decrements in VE, tidal volume, respiratory frequency, arterial O2 saturation, and increases in end-tidal CO2 tension were observed only when work loads exceeded 65% of the unloaded maximum. There was a significant correlation between the resting ventilatory response to hypercapnia delta VE/delta PCO2 and the ventilatory response to VCO2 during exercise (delta VE/delta VCO2; r = 0.88; P less than 0.05). The maximal inspiratory pressure generated during loading correlated with CO2 sensitivity at rest (r = 0.91; P less than 0.05) and with exercise ventilation (delta VE/delta VCO2; r = 0.83; P less than 0.05). Although resistive loading did not alter O2 uptake (VO2) or heart rate (HR) as a function of work load, maximal VO2, HR, and exercise tolerance were decreased to 90% of control values. We conclude that a modest inspiratory resistive load reduces maximum exercise capacity and that CO2 responsiveness may play a role in the control of breathing during exercise when airway resistance is artificially increased.