Peak power output predicts maximal oxygen uptake and performance time in trained cyclists

The purposes of this study were firstly to determine the relationship between the peak power output (Wpeak) and maximal oxygen uptake (VO2max) attained during a laboratory cycling test to exhaustion, and secondly to assess the relationship between Wpeak and times in a 20-km cycling trial. One hundred trained cyclists (54 men, 46 women) participated in the first part of this investigation. Each cyclist performed a minimum of one maximal test during which Wmax and VO2max were determined. For the second part of the study 19 cyclists completed a maximal test for the determination of Wpeak, and also a 20-km cycling time trial. Highly significant relationships were obtained between Wpeak and VO2max (r = 0.97, P less than 0.0001) and between Wpeak and 20-km cycle time (r = -0.91, P less than 0.001). Thus, Wpeak explained 94% of the variance in measured VO2max and 82% of the variability in cycle time over 20 km. We concluded that for trained cyclists, the VO2max can be accurately predicted from Wpeak, and that Wpeak is a valid predictor of 20-km cycle time.     

The influence of exercise duration at VO2 max on the off-transient pulmonary oxygen uptake phase during high intensity running activity

The purpose of this study was to examine the influence of time run at maximal oxygen uptake (VO2 max) on the off-transient pulmonary oxygen uptake phase after supra-lactate threshold runs. We hypothesised: 1) that among the velocities eliciting VO2 max there is a velocity threshold from which there is a slow component in the VO2-off transient, and 2) that at this velocity the longer the duration of this time at VO2 max (associated with an accumulated oxygen kinetics since VO2 can not overlap VO2 max), the longer is the off-transient phase of oxygen uptake kinetics. Nine long-distance runners performed five maximal tests on a synthetic track (400 m) while breathing through the COSMED K4b2 portable, telemetric metabolic analyser: i) an incremental test which determined VO2 max, the minimal velocity associated with VO2 max (vVO2 max) and the velocity at the lactate threshold (vLT), ii) and in a random order, four supra-lactate threshold runs performed until exhaustion at vLT + 25, 50, 75 and 100% of the difference between vLT and vVO2 max (vdelta25, vdelta50, vdelta75, vdelta100). At vdelta25, vdelta50 (= 91.0 +/- 0.9% vVO2 max) and vdelta75, an asymmetry was found between the VO2 on (double exponential) and off-transient (mono exponential) phases. Only at vdelta75 there was at positive relationship between the time run at VO2 max (%tlimtot) and the VO2 recovery time constant (Z = 1.8, P = 0.05). In conclusion, this study showed that among the velocities eliciting VO2 max, vdelta75 is the velocity at which the longer the duration of the time at VO2 max, the longer is the off-transient phase of oxygen uptake kinetics. It may be possible that at vdelta50 there is not an accumulated oxygen deficit during the plateau of VO2 at VO2 max and that the duration of the time at VO2 max during the exhaustive runs at vdelta100, could be too short to induce an accumulating oxygen deficit affecting the oxygen recovery.     

The energetics of middle-distance running

In order to assess the relative contribution of aerobic processes to running velocity (v), 27 male athletes were selected on the basis of their middle-distance performances over 800, 1500, 3000 or 5000 m, during the 1987 track season. To be selected for study, the average running velocity (v) corresponding to their performances had to be superior to 90% of the best French v of the season. Maximum O2 consumption (VO2max) and energy cost of running (C) had been measured within the 2 months preceding the track season, which, together with oxygen consumption at rest (VO2rest) allowed us to calculate the maximal v that could be sustained under aerobic conditions: vamax = (VO2max - VO2rest) x C-1. The treadmill running v corresponding to a blood lactate of 4 mmol.l-1 (vla4), was also calculated. In the whole group, C was significantly related to height (r = -0.43; P less than 0.03). Neither C nor VO2max (with, in this case, the exception of the 3000 m athletes) were correlated to v. On the other hand, vamax was significantly correlated to v over distances longer than 800 m. These v were also correlated to vla4. However vla4 occurred at 87.5% SD 3.3% of vamax, this relationship was interpreted as being an expression of the correlation between vamax and v. Calculation of vamax provided a useful means of analysing the performances. At the level of achievement studied, v sustained over 3000 m corresponded to vamax.(ABSTRACT TRUNCATED AT 250 WORDS)     

Performance of runners and swimmers after four weeks of intermittent hypobaric hypoxic exposure plus sea level training.

This double-blind, randomized, placebo-controlled trial examined the effects of 4 wk of resting exposure to intermittent hypobaric hypoxia (IHE, 3 h/day, 5 days/wk at 4,000-5,500 m) or normoxia combined with training at sea level on performance and maximal oxygen transport in athletes. Twenty-three trained swimmers and runners completed duplicate baseline time trials (100/400-m swims, or 3-km run) and measures for maximal oxygen uptake (VO(2max)), ventilation (VE(max)), and heart rate (HR(max)) and the oxygen uptake at the ventilatory threshold (VO(2) at VT) during incremental treadmill or swimming flume tests. Subjects were matched for sex, sport, performance, and training status and divided randomly between hypobaric hypoxia (Hypo, n = 11) and normobaric normoxia (Norm, n = 12) groups. All tests were repeated within the first (Post1) and third weeks (Post2) after the intervention. Time-trial performance did not improve in either group. We could not detect a significant difference between groups for a change in VO(2max), VE(max), HR(max), or VO(2) at VT after the intervention (group x test interaction P = 0.31, 0.24, 0.26, and 0.12, respectively). When runners and swimmers were considered separately, Hypo swimmers appeared to increase VO(2max) (+6.2%, interaction P = 0.07) at Post2 following a precompetition taper and increased VO(2) at VT (+8.9 and +12.1%, interaction P = 0.007 and 0.006, at Post1 and Post2). We conclude that this "dose" of IHE was not sufficient to improve performance or oxygen transport in this heterogeneous group of athletes. Whether there are potential benefits of this regimen for specific sports or training/tapering strategies may require further study.     

Oxygen uptake during high-intensity running: response following a single bout of interval training

Elevated oxygen uptake (VO2) during moderate-intensity running following a bout of interval running training has been studied previously. To further investigate this phenomenon, the VO2 response to high-intensity exercise was examined following a bout of interval running. Well-trained endurance runners were split into an experimental group [maximum oxygen uptake, VO2max 4.73 (0.39)l x min(-1)] and a reliability group [VO2max 4.77 (0.26)l x min(-1)]. The experimental group completed a training session (4 x 800 m at 1 km x h(-1) below speed at VO2max, with 3 min rest between each 800-m interval). Five minutes prior to, and 1 h following the training session, subjects completed 6 min 30 s of constant speed, high-intensity running designed to elicit 40% delta (where delta is the difference between VO2 at ventilatory threshold and VO2max; tests 1 and 2, respectively). The slow component of VO2 kinetics was quantified as the difference between the VO2 at 6 min and the VO2 at 3 min of exercise, i.e. deltaVO2(6-3). The deltaVO2(-3) was the same in two identical conditions in the reliability group [mean (SD): 0.30 (0.10)l x min(-1) vs 0.32 (0.13)l x min(-1)]. In the experimental group, the magnitude of the slow component of VO2 kinetics was increased in test 2 compared with test 1 by 24.9% [0.27 (0.14)l x min(-1) vs 0.34 (0.08)l x min(-1), P < 0.05]. The increase in deltaVO2(6-3) in the experimental group was observed in the absence of any significant change in body mass, core temperature or blood lactate concentration, either at the start or end of tests 1 or 2. It is concluded that similar mechanisms may be responsible for the slow component of VO2 kinetics and for the fatigue following the training session. It has been suggested previously that this mechanism may be linked primarily to changes within the active limb, with the recruitment of alternative and/or additional less efficient fibres.     

Cardiovascular changes associated with decreased aerobic capacity and aging in long-distance runners

Fifty-five male runners aged between 30 to 80 years were examined to determine the relative roles of various cardiovascular parameters which may account for the decrease in maximal oxygen uptake (VO2max) with aging. All subjects had similar body fat composition and trained for a similar mileage each week. The parameters tested were VO2max, maximal heart rate (HRmax), cardiac output (Q), and arteriovenous difference in oxygen concentration (Ca-Cv)O2 during graded, maximal treadmill running. Average body fat and training mileage were roughly 12% and 50 km.week-1, respectively. The average 10-km run-time slowed significantly by 6.0%.decade-1 [( 10-km run-time (min) = 0.323 x age (years) + 24.4] (n = 49, r = 0.692, p less than 0.001]. A strong correlation was found between age and VO2max [( VO2max (ml.kg-1.min-1) = -0.439 x age + 76.5] (n = 55, r = -0.768, p less than 0.001]. Thus, VO2max decreased by 6.9%.decade-1 along with reductions of HRmax (3.2%.decade-1, p less than 0.001) and Q (5.8%.decade-1, p less than 0.001), while no significant change with age was observed in estimated (Ca-Cv)O2. It was concluded that the decline of VO2max with aging in runners was mainly explained by the central factors (represented by the decline of HR and Q in this study), rather than by the peripheral factor (represented by (Ca-Cv)O2).     

Calculation of record-time in the 800-meter run: predictive value of Margaria's equation

Margaria's equation (1976)--describing the relationship between the minimum time necessary to cover a distance equal or longer than 1,000 m (record-time TR) and the maximal oxygen consumption (VO2 max)--has been modified in order to be applied to the calculation of TR in the 800 m foot race. Fifteen subjects participated in this study (VO2 max = 63 +/- 3.5 ml O2 X kg-1 X min-1, measured TR = 131 +/- 10 seconds). It has been found the TR calculated from Margaria's equation (TRc) are underestimated (TRc = 104 +/- 10 seconds). By taking into account the actual energy cost of running (0.19 ml O2 X kg-1 X m-1) and the kinetics of VO2 at the onset of exercise, TRc averaged 133 +/- 8.5 seconds. Moreover, the relationship between TRc and measured TR (TRm) is highly significant (TRc = 50.4 + 0.65 TRm; r = 0.75; P less than 0.01). These results validate Margaria's equation modifications.     

Physiological correlates of middle-distance running performance. A comparative study between men and women.

To compare the relative contributions of their functional capacities to performance in relation to sex, two groups of middle-distance runners (24 men and 14 women) were selected on the basis of performances over 1500-m and 3000-m running races. To be selected for the study, the average running velocity (v) in relation to performances had to be superior to a percentage (90% for men and 88% for women) of the best French v achieved during the season by an athlete of the same sex. Maximal O2 consumption (VO2max) and energy cost of running (CR) were measured in the 2 months preceding the track season. This allowed us to calculate the maximal v that could be sustained under aerobic conditions, va,max. A v:va,max ratio derived from 1500-m to 3000-m races was used to calculate the maximal duration of a competitive race for which v = va,max (tva,max). In both groups va,max was correlated to v. The relationships calculated for each distance were similar in both sexes. The CR [0.179 (SD 0.010) ml.kg-1 x m-1 in the women versus 0.177 (SD 0.010) in the men] and tva,max [7.0 (SD 2.0) min versus 8.4 (SD 2.1)] also showed no difference. The relationships between VO2max and body mass (mb) calculated in the men and the women were different. At the same mb the women had a 10% lower CR than the men; their lower mb thus resulted in an identical CR.(ABSTRACT TRUNCATED AT 250 WORDS)     

Explosive-strength training improves 5-km running time by improving running economy and muscle power.

To investigate the effects of simultaneous explosive-strength and endurance training on physical performance characteristics, 10 experimental (E) and 8 control (C) endurance athletes trained for 9 wk. The total training volume was kept the same in both groups, but 32% of training in E and 3% in C was replaced by explosive-type strength training. A 5-km time trial (5K), running economy (RE), maximal 20-m speed (V20 m), and 5-jump (5J) tests were measured on a track. Maximal anaerobic (MART) and aerobic treadmill running tests were used to determine maximal velocity in the MART (VMART) and maximal oxygen uptake (VO2 max). The 5K time, RE, and VMART improved (P < 0.05) in E, but no changes were observed in C. V20 m and 5J increased in E (P < 0.01) and decreased in C (P < 0.05). VO2 max increased in C (P < 0.05), but no changes were observed in E. In the pooled data, the changes in the 5K velocity during 9 wk of training correlated (P < 0.05) with the changes in RE [O2 uptake (r = -0.54)] and VMART (r = 0.55). In conclusion, the present simultaneous explosive-strength and endurance training improved the 5K time in well-trained endurance athletes without changes in their VO2 max. This improvement was due to improved neuromuscular characteristics that were transferred into improved VMART and running economy.     

Maximal aerobic capacity for repetitive lifting: comparison with three standard exercise testing modes

A multi-stage, repetitive lifting maximal oxygen uptake (VO2max) test was developed to be used as an occupational research tool which would parallel standard ergometric VO2max testing procedures. The repetitive lifting VO2max test was administered to 18 men using an automatic repetitive lifting device. An intraclass reliability coefficient of 0.91 was obtained with data from repeated tests on seven subjects. Repetitive lifting VO2max test responses were compared to those for treadmill, cycle ergometer and arm crank ergometer. The mean +/- SD repetitive lifting VO2max of 3.20 +/- 0.42 l.min-1 was significantly (p less than 0.01) less than treadmill VO2max (delta = 0.92 l.min-1) and cycle ergometer VO2max (delta = 0.43 l.min-1) and significantly greater than arm crank ergometer VO2max (delta = 0.63 l.min-1). The correlation between repetitive lifting oxygen uptake and power output was r = 0.65. VO2max correlated highly among exercise modes, but maximum power output did not. The efficiency of repetitive lifting exercise was significantly greater than that for arm cranking and less than that for leg cycling. The repetitive lifting VO2max test has an important advantage over treadmill or cycle ergometer tests in the determination of relative repetitive lifting intensities. The individual curves of VO2 vs. power output established during the multi-stage lifting VO2max test can be used to accurately select work loads required to elicit given percentages of maximal oxygen uptake.     

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.     

Day-to-day changes in oxygen uptake kinetics at the onset of exercise during strenuous endurance training.

The aim of this study was to assess the effect of strenuous endurance training on day-to-day changes in oxygen uptake (VO2) on-kinetics (time constant) at the onset of exercise. Four healthy men participated in strenuous training for 30 min.day-1, 6 days.week-1 for 3 weeks. The VO2 was measured breath-by-breath every day except Sunday at exercise intensities corresponding to the lactate threshold (LT) and the onset of blood lactate accumulation (OBLA) which were obtained before training. Furthermore, an incremental exercise test was performed to determine LT, OBLA and maximal oxygen uptake (VO2max) before and after the training period and every weekend. The 30-min heavy endurance training was performed on a cycle ergometer 5 days.week-1 for 3 weeks. Another six men served as the control group. After training, significant reductions of the VO2 time constant for exercise at the pretraining LT exercise intensity (P less than 0.05) and at OBLA exercise intensity (P less than 0.01) were observed, whereas the VO2 time constants in the control group did not change significantly. A high correlation between the decrease in the VO2 time constant and training day was observed in exercise at the pretraining LT exercise intensity (r = -0.76; P less than 0.001) as well as in the OBLA exercise intensity (r = -0.91; P less than 0.001). A significant reduction in the blood lactate concentration during submaximal exercise and in the heart rate on-kinetics was observed in the training group.(ABSTRACT TRUNCATED AT 250 WORDS)     

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

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

Longitudinal associations between anaerobic threshold and distance running performance

Longitudinal alterations in anaerobic threshold (AT) and distance running performance were assessed three times within a 4-month period of intensive training, using 20 male, trained middle-distance runners (19-23 yr). A major effect of the high intensity regular intensive training together with 60- to 90-min AT level running training (2 d X wk-1) was a significant increase in the amount of O2 uptake corresponding to AT (VO2 AT; ml O2 X min-1 X kg-1) and in maximal oxygen uptake (VO2max; ml O2 X min-1 X kg-1). Both VO2 AT and VO2max showed significant correlations (r = -0.69 to -0.92 and r = -0.60 to -0.85, respectively) with the 10,000 m run time in every test. However, further analyses of the data indicate that increasing VO2 AT (r = -0.63, P less than 0.05) rather than VO2max (r = -0.15) could result in improving the 10,000 m race performance to a larger extent, and that the absolute amount of change (delta) in the 10,000 m run time is best accounted for by a combination of delta VO2 AT and delta 5,000 m run time. Our data suggest that, among runners not previously trained over long distances, training-induced alterations in AT in response to regular intensive training together with AT level running training may contribute significantly to the enhancement of AT and endurance running performance, probably together with an increase in muscle respiratory capacity.     

Determinants of maximal oxygen uptake in severe acute hypoxia

To unravel the mechanisms by which maximal oxygen uptake (VO2 max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2 (hypoxia, approximately 5,300 m above sea level). With hypoxia, exercise PaO2 dropped to 31-34 mmHg and arterial O2 content (CaO2) was reduced by 35% (P < 0.001). Forty-one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (PiO2) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia (P < 0.05). Hypoxia caused a 47% decrease in VO2 max (a greater fall than accountable by reduced CaO2). Peak cardiac output decreased by 17% (P < 0.01), due to equal reductions in both peak heart rate and stroke VOlume (P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia (P < 0.001) correlating closely with VO2 max (r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction of VO2 max in severe acute hypoxia: 1) reduction of PiO2, 2) impairment of pulmonary gas exchange, and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss in VO2 max.     

Metabolic and cardiovascular adjustment to arm training

Maximal and submaximal metabolic and cardiovascular measures and work capacity were studied in control (n = 7) and experimental (n = 9) subjects (S's) during arm work prior to and following 10 wk of interval arm training. These measures were oxygen uptake (VO2), minute ventilation (VE), heart rate (HR), respiratory exchange ratio (R), cardiac output (Q), stroke volume (SV), and arteriovenous oxygen difference ((a--v)O2 diff). In addition, maximal oxygen uptake (VO2max) was measured in both groups during treadmill running. Experimental S's showed significant increases (P less than 0.01) in peak VO2 (438 ml.min-1), max VE (17.7 l.min-1), max (a--v)O2 diff (20.8 ml.l-1), and work time (9.2 min) during arm ergometry, while maximum values of Q, SV, HR, and R remained unchanged. In addition, submaximal heart rates were significantly lower during arm ergometry after training. VO2max during treadmill running remained essentially unchanged. No changes in metabolic and physiological measures were noted for the controls after the 10-wk training period. The results support the concept of training specificity for VO2max, and indicate that the improvement in peak VO2 in arm ergometry reflects enhanced oxygen utilization due to an expanded (a--v)O2 diff.     

Energetics of kayaking at submaximal and maximal speeds

The energy cost of kayaking per unit distance (C(k), kJ x m(-1)) was assessed in eight middle- to high-class athletes (three males and five females; 45-76 kg body mass; 1.50-1.88 m height; 15-32 years of age) at submaximal and maximal speeds. At submaximal speeds, C(k) was measured by dividing the steady-state oxygen consumption (VO(2), l x s(-1)) by the speed (v, m x s(-1)), assuming an energy equivalent of 20.9 kJ x l O(-1)(2). At maximal speeds, C(k) was calculated from the ratio of the total metabolic energy expenditure (E, kJ) to the distance (d, m). E was assumed to be the sum of three terms, as originally proposed by Wilkie (1980): E = AnS + alphaVO(2max) x t-alphaVO(2max) x tau(1-e(-t x tau(-1))), were alpha is the energy equivalent of O(2) (20.9 kJ x l O(2)(-1)), tau is the time constant with which VO(2max) is attained at the onset of exercise at the muscular level, AnS is the amount of energy derived from anaerobic energy utilization, t is the performance time, and VO(2max) is the net maximal VO(2). Individual VO(2max) was obtained from the VO(2) measured during the last minute of the 1000-m or 2000-m maximal run. The average metabolic power output (E, kW) amounted to 141% and 102% of the individual maximal aerobic power (VO(2max)) from the shortest (250 m) to the longest (2000 m) distance, respectively. The average (SD) power provided by oxidative processes increased with the distance covered [from 0.64 (0.14) kW at 250 m to 1.02 (0.31) kW at 2000 m], whereas that provided by anaerobic sources showed the opposite trend. The net C(k) was a continuous power function of the speed over the entire range of velocities from 2.88 to 4.45 m x s(-1): C(k) = 0.02 x v(2.26) (r = 0.937, n = 32).     

The relationship between maximal oxygen uptake and glucose tolerance/insulin response ratio in normal young men.

Maximal oxygen uptake (VO2max.), glucose tolerance (K-value), and insulin response (IRI-area) were studied in seventeen young, non-obese, non-diabetic males. The ratio between K-value and IRI-area correlated significantly with VO2 max. (r = 0.70, p less than 0.01) also when differences in body fat mass were eliminated by partial correlation analysis (r = 0.56, p less than 0.05). Subjects with a high VO2 max. thus maintained a given glucose tolerance with a lower insulin response than did subjects in whom VO2 max. was low.     

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.     

Fat-free mass and excess post-exercise oxygen consumption in the 40 minutes after short-duration exhaustive exercise in young male Japanese athletes

The relationship between fat-free mass (FFM) and excess post-exercise oxygen consumption (EPOC) has not been well researched because of the relatively small number of subjects studied. This study investigated the effects of FFM on EPOC and EPOC/maximum oxygen consumption. 250 Japanese male athletes between 16 and 21 years old from Nagasaki prefecture had their EPOC measured up to 40 minutes after short-duration exhaustive exercise. The value was named as EPOC40 min. The proportions of EPOC up to 1, 3, 6, 10, and 25 minutes to EPOC40 min were calculated and named as P1, P3, P6, P10, and P25, respectively. Body size and composition, VO2max and resting metabolic rate (RMR) were also measured. Mean EPOC40 min was 9.04 L or 158 ml/kg FFM. EPOC40 min was related to FFM (r=0.55, p<0.001) and VO2max (r=0.37, p<0.001). The ratio of EPOC40 min to VO2max was related to FFM (r=0.28, p<0.001). P1, P3, P6, P10, and P25 were negatively related to EPOC40 min/FFM, EPOC40 min/VO2max, and FFM. Athletes who had larger FFM had larger EPOC40 40 min and EPOC40 40 min/VO2max, and smaller P1, P3, P10, and P25.