Effect of different muscle shortening velocities during prolonged incremental cycling exercise on the plasma growth hormone, insulin, glucose, glucagon, cortisol, leptin and lactate concentrations.

BACKGROUND: Strenuous exercise was reported to involve the alteration in the release of some "stress" hormones such as growth hormone (GH), cortisol, catecholamines and appropriate adjustment of energy metabolism but the relative contribution of these hormones to metabolic response, to cycling exercise performed at different muscle shortening velocities, has not been clarified. AIMS: The purpose of this experiment was to assess the effect of applying different pedalling rates during a prolonged incremental cycling exercise test on the changes in the plasma levels of growth hormone, cortisol, insulin, glucagon and leptin in humans. Material and METHODS: Fifteen healthy non-smoking men (means +/- SD: age 22.9 +/- 2.4 years; body mass 71.9 +/- 8.2 kg; height 178 +/- 6 cm; with VO2max of 3.896 +/- 0.544 1 x min(-1), assessed in laboratory tests, were subjects in this study. The subjects performed in two different days a prolonged incremental exercise tests at two different pedalling rates, one of them at 60 and another at 120 rev x min(-1). During this tests the power output has increased by 30 W every 6 minutes. The tests were stopped when the subject reached about 70 % of the VO2max. RESULTS AND CONCLUSIONS: We have found that choosing slow or fast pedalling rates (60 or 120 rev min(-1)), while generating the same external mechanical power output, had no effect on the pattern of changes in plasma cortisol, insulin, glucagon, glucose and leptin concentrations. But, generation of the same external mechanical power output at 120 rev min(-1) causes more stepper increase (p < 0.01) in the plasma growth hormone concentration [GH]pl and plasma lactate concentrations [La]pl when compared to that observed during cycling at 60 rev x min(-1). We have also found that the onset of a significant increase in [GH]pl during cycling at 60 rev x min(-1) was not accompanied by significant increase in [La]pl. While during cycling at 120 rev x min(-1) the onset of a significant increase in [La]pl occurred without increase in [GH]pl, but with continuation of exercise when plasma [La]pl increased, there was also a parallel rise in plasma [GH]pl, as reported before. This results indicates that the increase in [GH]pl during exercise is not closely related to the increase in [La]pl.     

Effect of different cycling frequencies during incremental exercise on the venous plasma potassium concentration in humans

The effect of different muscle shortening velocity was studied during cycling at a pedalling rate of 60 and 120 rev.min(-1) on the [K+]v in humans. Twenty-one healthy young men aged 22.5+/-2.2 years, body mass 72.7+/-6.4 kg, VO2 max 3.720+/-0.426 l. min(-1), performed an incremental exercise test until exhaustion. The power output increased by 30 W every 3 min, using an electrically controlled ergometer Ergoline 800 S (see Zoladz et al. J. Physiol. 488: 211-217, 1995). The test was performed twice: once at a cycling frequency of 60 rev.min(-1) (test A) and a few days later at a frequency of 120 rev. min(-1) (test B). At rest and at the end of each step (i.e. the last 15 s) antecubital venous blood samples for [K+]p were taken. Gas exchange variables were measured continuously (breath-by-breath) using Oxycon Champion Jaeger. The pre-exercise [K+]v in both tests was not significantly different amounting to 4.24+/-0.36 mmol.l(-1) in test A, and 4.37+/-0.45 mmol.l(-1) in test B. However, the [K+]p during cycling at 120 rev. min(-1) was significantly higher (p<0.001, ANOVA for repeated measurements) at each power output when compared to cycling at 60 rev.min(-1). The maximal power output reached 293+/-31 W in test A which was significantly higher (p<0.001) than in test B, which amounted to 223+/-40 W. The VO2max values in both tests reached 3.720+/-0.426 l. min(-1) vs 3.777+/-0.514 l. min(-1). These values were not significantly different. When the [K+]v was measured during incremental cycling exercise, a linear increase in [K+]v was observed in both tests. However, a significant (p<0.05) upward shift in the [K+]v and a % VO2max relationship was detected during cycling at 120 rev.min(-1). The [K+]v measured at the VO2max level in tests A and B amounted to 6.00+/-0.47 mmol.l-1 vs 6.04+/-0.41 mmol.l-1, respectively. This difference was not significant. It may thus be concluded that: a) generation of the same external mechanical power output during cycling at a pedalling rate of 120 rev.min(-1) causes significantly higher [K+]v changes than when cycling at 60 rev.min(-1), b) the increase of venous plasma potassium concentration during dynamic incremental exercise is linearly related to the metabolic cost of work expressed by the percentage of VO2max (increase as reported previously by Vollestad et al. J. Physiol. 475: 359-368, 1994), c) there is a tendency towards upward up shift in the [K+]v and % VO2max relation during cycling at 120 rev.min(-1) when compared to cycling at 60 rev.min(-1).     

High content of MYHC II in vastus lateralis is accompanied by higher VO2/power output ratio during moderate intensity cycling performed both at low and at high pedalling rates.

The aim of this study was to examine the relationship between the content of various types of myosin heavy chain isoforms (MyHC) in the vastus lateralis muscle and pulmonary oxygen uptake during moderate power output incremental exercise, performed at low and at high pedalling rates. Twenty one male subjects (mean +/- SD) aged 24.1 +/- 2.8 years; body mass 72.9 +/- 7.2 kg; height 179.1 +/- 4.8 cm; BMI 22.69 +/- 1.89 kg.m(-2); VO2max 50.6 +/- 5.3 ml.kg.min(-1), participated in this study. On separate days, they performed two incremental exercise tests at 60 rev.min(-1) and at 120 rev.min(-1), until exhaustion. Gas exchange variables were measured continuously breath by breath. Blood samples were taken for measurements of plasma lactate concentration prior to the exercise test and at the end of each step of the incremental exercise. Muscle biopsies were taken from the vastus lateralis muscle, using Bergstr?m needle, and they were analysed for the content of MyHC I and MyHC II using SDS--PAGE and two groups (n=7, each) were selected: group H with the highest content of MyHC II (60.7 % +/- 10.5 %) and group L with the lowest content of MyHC II (27.6 % +/- 6.1 %). We have found that during incremental exercise at the power output between 30-120 W, performed at 60 rev.min(-1), oxygen uptake in the group H was significantly greater than in the group L (ANCOVA, p=0.003, upward shift of the intercept in VO2/power output relationship). During cycling at the same power output but at 120 rev.min(-1), the oxygen uptake was also higher in the group H, when compared to the group L (i.e. upward shift of the intercept in VO2/power output relationship, ANCOVA, p=0.002). Moreover, the increase in pedalling rate from 60 to 120 rev.min(-1) was accompanied by a significantly higher increase of oxygen cost of cycling and by a significantly higher plasma lactate concentration in subjects from group H. We concluded that the muscle mechanical efficiency, expressed by the VO2/PO ratio, during cycling in the range of power outputs 30-120 W, performed at 60 as well as 120 rev.min(-1), is significantly lower in the individuals with the highest content of MyHC II, when compared to the individuals with the lowest content of MyHC II in the vastus lateralis.     

Effect of pedaling rates and myosin heavy chain composition in the vastus lateralis muscle on the power generating capability during incremental cycling in humans

In this study, we have determined power output reached at maximal oxygen uptake during incremental cycling exercise (P(I, max)) performed at low and at high pedaling rates in nineteen untrained men with various myosin heavy chain composition (MyHC) in the vastus lateralis muscle. On separate days, subjects performed two incremental exercise tests until exhaustion at 60 rev min(-1) and at 120 rev min(-1). In the studied group of subjects P(I, max) reached during cycling at 60 rev min(-1) was significantly higher (p=0.0001) than that at 120 rev min(-1) (287+/-29 vs. 215+/-42 W, respectively for 60 and 120 rev min(-1)). For further comparisons, two groups of subjects (n=6, each) were selected according to MyHC composition in the vastus lateralis muscle: group H with higher MyHC II content (56.8+/-2.79 %) and group L with lower MyHC II content in this muscle (28.6+/-5.8 %). P(I, max) reached during cycling performed at 60 rev min(-1) in group H was significantly lower than in group L (p=0.03). However, during cycling at 120 rev min(-1), there was no significant difference in P(I, max) reached by both groups of subjects (p=0.38). Moreover, oxygen uptake (VO(2)), blood hydrogen ion [H(+)], plasma lactate [La(-)] and ammonia [NH(3)] concentrations determined at the four highest power outputs completed during the incremental cycling performed at 60 as well as 120 rev min(-1), in the group H were significantly higher than in group L. We have concluded that during an incremental exercise performed at low pedaling rates the subjects with lower content of MyHC II in the vastus lateralis muscle possess greater power generating capabilities than the subjects with higher content of MyHC II. Surprisingly, at high pedaling rate, power generating capabilities in the subjects with higher MyHC II content in the vastus lateralis muscle did not differ from those found in the subjects with lower content of MyHC II in this muscle, despite higher blood [H(+)], [La(-)] and [NH(3)] concentrations. This indicates that at high pedaling rates the subjects with higher percentage of MyHC II in the vastus lateralis muscle perform relatively better than the subjects with lower percentage of MyHC II in this muscle.     

Growth hormone regulation in two types of aerobic exercise of equal oxygen uptake

Five normal men, aged 23 to 35 years, participated in two bouts of continuous aerobic cycling separated by five days. The first type of exercise (EI) was cycling at a pedalling frequency of 50 rev X min-1 with a load which produced a steady state O2 uptake of approximately 40% of the subjects' VO2max. The second type of exercise (EII) was cycling at a pedalling frequency of 90 rev X min-1 with a load such that an equal steady state VO2 was reached and maintained. Both EI and EII lasted 40 min. GH levels increased in EI and EII, reaching their maximum at 8 min of recovery (245 and 300% of resting values, respectively). No significant differences were observed between EI and EII in GH, lactate, glucagon, insulin, cortisol and glucose levels between the two exercises. While it has been reported earlier that GH levels were frequently related to lactate levels and/or decreased O2 availability (Sutton 1977; Raynaud et al. 1981; Kozlowski et al. 1983; VanHelder et al. 1984a, b), this study suggests that the opposite is also valid, that is, different types of exercise of equal VO2, duration and lactate production do not produce significantly different GH responses.     

Cycling efficiency and pedalling frequency in road cyclists

The purpose of this study was to determine the influence of pedalling rate on cycling efficiency in road cyclists. Seven competitive road cyclists participated in the study. Four separate experimental sessions were used to determine oxygen uptake (VO(2)) and carbon dioxide output (VCO(2)) at six exercise intensities that elicited a VO(2) equivalent to 54, 63, 73, 80, 87 and 93% of maximum VO(2) (VO(2max)). Exercise intensities were administered in random order, separated by rest periods of 3-5 min; four pedalling frequencies (60, 80, 100 and 120 rpm) were randomly tested per intensity. The oxygen cost of cycling was always lower when the exercise was performed at 60 rpm. At each exercise intensity, VO(2) showed a parabolic dependence on pedalling rate (r = 0.99-1, all P < 0.01) with a curvature that flattened as intensity increased. Likewise, the relationship between power output and gross efficiency (GE) was also best fitted to a parabola (r = 0.94-1, all P < 0.05). Regardless of pedalling rate, GE improved with increasing exercise intensity (P < 0.001). Conversely, GE worsened with pedalling rate (P < 0.001). Interestingly, the effect of pedalling cadence on GE decreased as a linear function of power output (r = 0.98, n = 6, P < 0.001). Similar delta efficiency (DE) values were obtained regardless of pedalling rate [21.5 (0.8), 22.3 (1.2), 22.6 (0.6) and 23.9 (1.0)%, for the 60, 80, 100 and 120 rpm, mean (SEM) respectively]. However, in contrast to GE, DE increased as a linear function of pedalling rate (r = 0.98, P < 0.05). The rate at which pulmonary ventilation increased was accentuated for the highest pedalling rate (P < 0.05), even after accounting for differences in exercise intensity and VO(2) (P < 0.05). Pedalling rate per se did not have any influence on heart rate which, in turn, increased linearly with VO(2). These results may help us to understand why competitive cyclists often pedal at cadences of 90-105 rpm to sustain a high power output during prolonged exercise.     

Pre-exercise hyperhydration delays dehydration and improves endurance capacity during 2 h of cycling in a temperate climate

Whether the use of pre-exercise hyperhydration could improve the performance of athletes who do not hydrate sufficiently during prolonged exercise is still unknown. We therefore compared the effects of pre-exercise hyperhydration and pre-exercise euhydration on endurance capacity, peak power output and selected components of the cardiovascular and thermoregulatory systems during prolonged cycling. Using a randomized, crossover experimental design, 6 endurance-trained subjects underwent a pre-exercise hyperhydration (26 ml of water x kg body mass(-1) with 1.2 g glycerol x kg body mass(-1)) or pre-exercise euhydration period of 80 min, followed by 2 h of cycling at 65% maximal oxygen consumption (VO(.)2max) (26-27 degrees C) that were interspersed by 5, 2-min intervals performed at 80% V(.)O2max. Following the 2 h cycling exercise, subjects underwent an incremental cycling test to exhaustion. Pre-exercise hyperhydration increased body water by 16.1+/-2.2 ml.kg body mass(-1). During exercise, subjects received 12.5 ml of sports drink x kg body mass(-1). With pre-exercise hyperhydration and pre-exercise euhydration, respectively, fluid ingestion during exercise replaced 31.0+/-2.9% and 37.1+/-6.8% of sweat losses (p>0.05). Body mass loss at the end of exercise reached 1.7+/-0.3% with pre-exercise hyperhydration and 3.3+/-0.4% with pre-exercise euhydration (p<0.05). During the 2 h of cycling, pre-exercise hyperhydration significantly decreased heart rate and perceived thirst, but rectal temperature, sweat rate, perceived exertion and perceived heat-stress did not differ between conditions. Pre-exercise hyperhydration significantly increased time to exhaustion and peak power output, compared with pre-exercise euhydration. We conclude that pre-exercise hyperhydration improves endurance capacity and peak power output and decreases heart rate and thirst sensation, but does not reduce rectal temperature during 2 h of moderate to intense cycling in a moderate environment when fluid consumption is 33% of sweat losses.     

Effects of previous exercise on the ventilatory determination of the aerobic threshold

To study the effects of previous submaximal exercise on the ventilatory determination of the Aerobic Threshold (AeT), 16 men were subjected to three maximal exercise tests (standard test = ST, retest = RT, and test with previous exercise = TPE ) on a cycle ergometer. The protocol for the three tests consisted of 3 min pedalling against 25 W, followed by increments of 25 W every minute until volitional fatigue. TPE was preceded by 10 min cycling at a power output corresponding to the AeT as determined in ST, followed by a recovery period pedalling against 25 W until VO2 returned to values consistent with the initial VO2 response to 25 W. AeT was determined from the gas exchange curves (ventilatory equivalent for O2, fraction of expired O2, excess of VCO2, ventilation, and respiratory gas exchange ratio) printed every 30 s. The results showed good ST X RT reliability (r = 0.89). TPE showed significantly higher AeT values (2.548 +/- 0.44 1 X min-1) when compared with ST (2.049 +/- 0.331 X min-1) and RT (2.083 +/- 0.30 1 X min-1). There were no significant differences for the sub-threshold respiratory gas exchange ratios among the trials. The sub-threshold VO2 response showed significantly higher values for TPE at power outputs above 50 W. It was concluded that the performance of previous exercise can increase the value for the ventilatory determination of the AeT due to a faster sub-threshold VO2 response.     

Pregnancy-induced changes in the maximal physiological responses during swimming.

The effect of pregnancy on peak O2 uptake (VO2 peak) during tethered swimming was evaluated in 10 women during their 25th and 35th wk of pregnancy, as well as 9-11 wk postpartum. The swim results were compared with cycle ergometry results obtained at similar times. The results indicated that exercise-induced maximal heart rates remained the same and were similar for the swim and cycle trials, approximately 184 +/- 4 beats/min. Cycling VO2 peak was not affected by pregnancy, averaging 1.94 +/- 0.11 l/min. Postpartum swim VO2 peak was similar to the cycle results; however, during pregnancy it was significantly lower than cycling VO2 peak (P less than 0.05; postpartum, 1.78 +/- 0.14 l/min; 25th wk, 1.64 +/- 0.12; 35th wk, 1.48 +/- 0.11). Hemoglobin concentrations and hematocrits were lower during pregnancy; however, changes in plasma volume (based on hematocrit and hemoglobin) were found to be significantly greater during cycling than during swimming and also greater during pregnancy for both modes of exercise. It was concluded that, unlike cycling, the VO2 peak of pregnant women during swimming is reduced. This reduction in VO2 peak was associated with a decreased peak ventilation (r = 0.864) but was not correlated to exercise-induced hemoconcentration (r = -0.29). Furthermore, pregnancy results in a greater-than-normal exercise-induced hemoconcentration, which may be related to pregnancy-induced changes in capillary dynamics.     

Estimation of oxygen cost of internal power during cycling exercise with changing pedal rate

It has been reported that oxygen uptake (VO2) increases exponentially with levels of the pedal rate during cycling. The purpose of this study was therefore to test the hypothesis that the O2 cost for internal power output (Pint) exerted in exercising muscle itself would be larger than for an external power output (Pext) calculated from external load and pedal rate during cycling exercise under various conditions of Pint and Pext in a large range of pedal rates. The O2 cost (DeltaVO2/ Deltapower output) was investigated in three experiments that featured different conditions on a cycle ergometer that were carried out at the same levels of total power output (Ptot; sum of Pint and Pext) (Exp. 1), Pext (Exp. 2) and load (Exp. 3). Each experiment consisted of three exercise tests with three levels of pedal rate (40 rpm for a lower pedal rate: LP; 70-80 rpm for a moderate pedal rate: MP; and 100-120 rpm for a higher pedal rate: HP) lasting for 2-3 min of unloaded cycling followed by 4-5 min of loaded cycling. Blood lactate accumulations (2.3-3.4 mmol l(-1)) at the HP were significantly higher compared with the LP (0.6-0.9 mmol l(-1)) and MP (0.9-1.0 mmol l(-1)) except for the LP in Exp. 1. The VO2 (360-432 ml min(-1) for LP, 479-644 ml min(-1) for MP, 960-1602 ml min(-1) for HP) during unloaded cycling in the three experiments increased exponentially with increasing pedal rates regardless of Pext=0. Moreover, the slope of the VO2-Pint (13.7 ml min(-1) W(-1)) relation revealed a steeper inclination than that of the VO2-Pext (10.2 ml min(-1) W(-1)) relation. We concluded that the O2 cost for Pint was larger than for Pext during the cycling exercises, indicating that the O2 cost for Ptot could be affected by the ratio of Pint to Ptot due to the levels of pedal rate.     

Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration

Five days of a high-fat diet while training, followed by 1 day of carbohydrate (CHO) restoration, increases rates of whole body fat oxidation and decreases CHO oxidation during aerobic cycling. The mechanisms responsible for these shifts in fuel oxidation are unknown but involve up- and downregulation of key regulatory enzymes in the pathways of skeletal muscle fat and CHO metabolism, respectively. This study measured muscle PDH and HSL activities before and after 20 min of cycling at 70% VO2peak and 1 min of sprinting at 150% peak power output (PPO). Estimations of muscle glycogenolysis were made during the initial minute of exercise at 70% VO2peak and during the 1-min sprint. Seven male cyclists undertook this exercise protocol on two occasions. For 5 days, subjects consumed in random order either a high-CHO (HCHO) diet (10.3 g x kg(-1) x day(-1) CHO, or approximately 70% of total energy intake) or an isoenergetic high-fat (FAT-adapt) diet (4.6 g x kg(-1) x day(-1) FAT, or 67% of total energy) while undertaking supervised aerobic endurance training. On day 6 for both treatments, subjects ingested an HCHO diet and rested before their experimental trials on day 7. This CHO restoration resulted in similar resting glycogen contents (FAT-adapt 873 +/- 121 vs. HCHO 868 +/- 120 micromol glucosyl units/g dry wt). However, the respiratory exchange ratio was lower during cycling at 70% VO2peak in the FAT-adapt trial, which resulted in an approximately 45% increase and an approximately 30% decrease in fat and CHO oxidation, respectively. PDH activity was lower at rest and throughout exercise at 70% VO2peak (1.69 +/- 0.25 vs. 2.39 +/- 0.19 mmol x kg wet wt(-1) x min(-1)) and the 1-min sprint in the FAT-adapt vs. the HCHO trial. Estimates of glycogenolysis during the 1st min of exercise at 70% VO2peak and the 1-min sprint were also lower after FAT-adapt (9.1 +/- 1.1 vs. 13.4 +/- 2.1 and 37.3 +/- 5.1 vs. 50.5 +/- 2.7 glucosyl units x kg dry wt(-1) x min(-1)). HSL activity was approximately 20% higher (P = 0.12) during exercise at 70% VO2peak after FAT-adapt. Results indicate that previously reported decreases in whole body CHO oxidation and increases in fat oxidation after the FAT-adapt protocol are a function of metabolic changes within skeletal muscle. The metabolic signals responsible for the shift in muscle substrate use during cycling at 70% VO2peak remain unclear, but lower accumulation of free ADP and AMP after the FAT-adapt trial may be responsible for the decreased glycogenolysis and PDH activation during sprinting.     

Effect of feeding and fasting on excess post-exercise oxygen consumption in juvenile southern catfish (Silurus meridionalis Chen)

The impact of feeding (fed to satiation, 13.85% body mass) on excess post-exercise oxygen consumption (EPOC, chasing for 2.5 min) was investigated in juvenile southern catfish (Silurus meridionalis Chen) (38.62-57.55 g) at 25. Cutlets of freshly killed loach species without viscera, head and tail were used as the test meal, and oxygen consumption (VO(2)) was adjusted to a standard body mass of 1 kg using a mass exponent of 0.75. Resting VO(2) increased significantly above fasting levels (49.89 versus 148.25 mg O(2) h(-)(1)) in 12 h postprandial catfish. VO(2) and ventilation frequency (V(f)) both increased immediately after exhaustive exercise and slowly returned to pre-exercise values in all experimental groups. The times taken for post-exercise VO(2) to return to the pre-exercise value were 20, 25 and 30 min in 12 h, 60 h and 120 h postprandial catfish, respectively. Peak VO(2) levels were 257.36+/-6.06, 219.32+/-6.32 and 200.91+/-5.50 mg O(2) h(-1) in 12 h, 60 h and 120 h postprandial catfish and EPOC values were 13.85+/-4.50, 27.24+/-3.15 and 41.91+/-3.02 mg O(2) in 12 h, 60 h and 120 h postprandial southern catfish, respectively. There were significant differences in both EPOC and peak VO(2) during the post-exercise recovery process among three experimental groups (p<0.05). These results showed that: (1) neither digestive nor exhaustive exercise could elicit maximal VO(2) in southern catfish, (2) both the digestive process and exercise (also the post-exercise recovery process) were curtailed under postprandial exercise, (3) the change of V(f) was smaller than that of VO(2) during the exhaustive exercise recovery process, (4) for a similar increment in VO(2), the change in V(f) was larger during the post-exercise process than during the digestive process.     

Exercise-induced prostacyclin release positively correlates with VO(2max) in young healthy men

In this study we have evaluated the effect of maximal incremental cycling exercise (IE) on the systemic release of prostacyclin (PGI(2)), assessed as plasma 6-keto-PGF(1alpha) concentration in young healthy men. Eleven physically active - untrained men (mean +/- S.D.) aged 22.7 +/- 2.1 years; body mass 76.3 +/- 9.1 kg; BMI 23.30 +/- 2.18 kg . m(-2); maximal oxygen uptake (VO(2max)) 46.5 +/- 3.9 ml . kg(-1) . min(-1), performed an IE test until exhaustion. Plasma concentrations of 6-keto-PGF(1alpha), lactate, and cytokines were measured in venous blood samples taken prior to the exercise and at the exhaustion. The net exercise-induced increase in 6-keto-PGF(1alpha) concentration, expressed as the difference between the end-exercise minus pre-exercise concentration positively correlated with VO(2max) (r=0.78, p=0.004) as well as with the net VO(2) increase at exhaustion (r=0.81, p=0.003), but not with other respiratory, cardiac, metabolic or inflammatory parameters of the exercise (minute ventilation, heart rate, plasma lactate, IL-6 or TNF-alpha concentrations). The exercise-induced increase in 6-keto-PGF(1alpha) concentration?? was significantly higher (p=0.008) in a group of subjects (n=5) with the highest VO(2max) when compared to the group of subjects with the lowest VO(2max), in which no increase in 6-keto-PGF(1alpha) concentration was found. In conclusion, we demonstrated, to our knowledge for the first time, that exercise-induced release of PGI(2) in young healthy men correlates with VO(2max), suggesting that vascular capacity to release PGI(2) in response to physical exercise represents an important factor characterizing exercise tolerance. Moreover, we postulate that the impairment of exercise-induced release of PGI(2) leads to the increased cardiovascular hazard of vigorous exercise.     

Effect of pedal cadence on the accumulated oxygen deficit, maximal aerobic power and blood lactate transition thresholds of high-performance junior endurance cyclists

In this study we investigated the effect of pedal cadence on the cycling economy, accumulated oxygen deficit (AOD), maximal oxygen consumption (VO2max) and blood lactate transition thresholds of ten high-performance junior endurance cyclists [mean (SD): 17.4 (0.4) years; 183.8 (3.5) cm, 71.56 (3.75) kg]. Cycling economy was measured on three ergometers with the specific cadence requirements of: 90-100 rpm for the road dual chain ring (RDCR90-100 rpm) ergometer, 120-130 rpm for the track dual chain ring (TDCR120-130 rpm) ergometer, and 90-130 rpm for the track single chain ring (TSCR90-130 rpm) ergometer. AODs were then estimated using the regression of oxygen consumption (VO2) on power output for each of these ergometers, in conjunction with the data from a 2-min supramaximal paced effort on the TSCR90-130 rpm ergometer. A regression of VO2 on power output for each ergometer resulted in significant differences (P<0.001) between the slopes and intercepts that produced a lower AOD for the RDCR90-100 rpm [2.79 (0.43) l] compared with those for the TDCR120-130 rpm [4.11 (0.78) l] and TSCR90-130 rpm [4.06 (0.84) l]. While there were no statistically significant VO2max differences (P = 0.153) between the three treatments [RDCR90-100 rpm: 5.31 (0.24) l x min(-1); TDCR120-130 rpm; 5.33 (0.25) 1 x min(-1); TSCR90-130 rpm: 5.44 (0.27) l x min(-1)], all pairwise comparisons of the power output at which VO2max occurred were significantly different (P<0.001). Statistically significant differences were identified between the RDCR90-100 rpm and TDCR120-130 rpm tests for power output (P = 0.003) and blood lactate (P = 0.003) at the lactate threshold (Thla-), and for power output (P = 0.005) at the individual anaerobic threshold (Thiat). Our findings emphasise that pedal cadence specificity is essential when assessing the cycling economy, AOD and blood lactate transition thresholds of high-performance junior endurance cyclists.     

Effect of maternal weight gain during pregnancy on exercise performance

We examined the effect of maternal weight gain during pregnancy on exercise performance. Ten women performed submaximal cycle (up to 60 W) and treadmill (4 km/h, up to 10% grade) exercise tests at 34 +/- 1.5 (SD) wk gestation and 7.6 +/- 1.7 wk postpartum. Postpartum subjects wearing weighted belts designed to equal their body weight during the antepartum tests performed two additional treadmill tests. Absolute O2 uptake (VO2) at the same work load was higher during pregnancy than postpartum during cycle (1.04 +/- 0.08 vs. 0.95 +/- 0.09 l/min, P = 0.014), treadmill (1.45 +/- 0.19 vs. 1.27 +/- 0.20 l/min, P = 0.0002), and weighted treadmill (1.45 +/ 0.19 vs. 1.36 +/- 0.20 l/min, P = 0.04) exercise. None of these differences remained, however, when VO2 was expressed per kilogram of body weight. Maximal VO2 (VO2max) estimated from the individual heart rate-VO2 curves was the same during and after pregnancy during cycling (1.96 +/- 0.37 to 1.98 +/- 0.39 l/min), whereas estimated VO2max increased postpartum during treadmill (2.04 +/- 0.38 to 2.21 +/- 0.36 l/min, P = 0.03) and weighted treadmill (2.04 +/- 0.38 to 2.19 +/- 0.38 l/min, P = 0.03) exercise. We conclude that increased body weight during pregnancy compared with the postpartum period accounts for 75% of the increased VO2 during submaximal weight-bearing exertion in pregnancy and contributes to reduced exercise capacity. The postpartum increase in estimated VO2max during weight-bearing exercise is the result of consistently higher antepartum heart rates during all submaximal work loads.     

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.     

Increases in submaximal cycling efficiency mediated by altitude acclimatization.

To investigate the hypothesis that respiratory gas exchange and, in particular, the O(2) consumption (VO(2)) response to exercise is altered after a 21-day expedition to 6,194 m, five male climbers (age 28.2 +/- 2 yr; weight 76.9 +/- 4.3 kg; means +/- SE) performed a progressive and prolonged two-step cycle test both before and 3-4 days after return to sea level. During both exercise tests, a depression (P < 0.05) in VO(2) (l/min) and an increase (P < 0.05) in minute ventilation (VE BTPS; l/min) and respiratory exchange ratio were observed after the expedition. These changes occurred in the absence of changes in CO(2) production (l/min). During steady-state submaximal exercise, net efficiency, calculated from the rates of the mechanical power output to the energy expended (VO(2)) above that measured at rest, increased (P < 0.05) from 25.9 +/- 1.6 to 31. 3 +/- 1.3% at the lighter power output and from 24.4 +/- 1.3 to 29.5 +/- 1.5% at the heavy power output. These changes were accompanied by a 4.5% reduction (P < 0.05) in peak VO(2) (3.99 +/- 0.17 vs. 3.81 +/- 0.18 l/min). After the expedition, an increase (P < 0.05) in hemoglobin concentration (15.0 +/- 0.49 vs. 15.8 +/- 0.41 g/100 ml) was found. It is concluded that, because resting VO(2) was unchanged, net efficiency is enhanced during submaximal exercise after a mountaineering expedition when the exercise is performed soon after return to sea level conditions.     

Electromyographic data do not support a progressive recruitment of muscle fibers during exercise exhibiting a VO2 slow component

The origin of the slow component (SC) of oxygen uptake kinetics, presenting during exercise above the ventilatory threshold (VT), remains unclear. Possible physiologic mechanisms include a progressive recruitment of type II muscle fibers. The purpose of this study was to examine alterations in muscle activity through electromyography (EMG) and mean power frequency (MPF) analysis during heavy cycling exercise. Eight trained cyclists (mean +/- S.E.; age = 30 +/- 3 years, height = 1771 +/- 4 cm, weight = 73.8 +/- 6.5 kg, VO2max = 4.33 +/- 0.28 l min(-1)) completed transitions from 20W to a workload equaling 50% of the difference between V(T) and VO2max. VO2 was monitored using a breath-by-breath measurement system, and EMG data were gathered from surface electrodes placed on the gastrocnemius lateralis and vastus lateralis oblique. Breath-by-breath data were time aligned, averaged, interpolated to 1-s intervals, and modeled with non-linear regression. Mean power frequency (MPF) and RMS EMG values were calculated for each minute during the exercise bout. Additionally, MPF was determined using both isolated EMG bursts and complete pedal revolutions. All subjects exhibited a VO2 SC (mean amplitude = 0.98 +/- 0.16 l min(-1)), yet no significant differences were observed during the exercise bout in MPF or RMS EMG data (p > 0.05) using either analysis technique. While it is possible that the sensitivity of EMG may be insufficient to identify changes in muscle activity theorized to affect the VO2 SC, the data indicated no relationship between MPF/EMG and the SC during heavy cycling.     

Disposal of blood [1-13C]lactate in humans during rest and exercise

Lactate irreversible disposal (RiLa) and oxidation (RoxLa) rates were studied in six male subjects during rest (Re), easy exercise [EE, 140 min of cycling at 50% of maximum O2 consumption (VO2max)] and hard exercise (HE, 65 min at 75% VO2max). Twenty minutes into each condition, subjects received a Na+-L(+)-[1-13C]lactate intravenous bolus injection. Blood was sampled intermittently from the contralateral arm for metabolite levels, acid-base status, and enrichment of 13C in lactate. Expired air was monitored continuously for determination of respiratory parameters, and aliquots were collected for determination of 13C enrichment in CO2. Steady-rate values for O2 consumption (VO2) were 0.33 +/- 0.01, 2.11 +/- 0.03, and 3.10 +/- 0.03 l/min for Re, EE, and HE, respectively. Corresponding values of blood lactate levels were 0.84 +/- 0.01, 1.33 +/- 0.05, and 4.75 +/- 0.28 mM in the three conditions. Blood lactate disposal rates were significantly correlated to VO2 (r = 0.78), averaging 123.4 +/- 20.7, 245.5 +/- 40.3, and 316.2 +/- 53.7 mg X kg-1 X h-1 during Re, EE, and HE, respectively. Lactate oxidation rate was also linearly related to VO2 (r = 0.81), and the percentage of RiLa oxidized increased from 49.3% at rest to 87.0% during exercise. A curvilinear relationship was found between RiLa and blood lactate concentration. It was concluded that, in humans, 1) lactate disposal (turnover) rate is directly related to the metabolic rate, 2) oxidation is the major fate of lactate removal during exercise, and 3) blood lactate concentration is not an accurate indicator of lactate disposal and oxidation.     

Supramaximal exercise after training-induced hypervolemia. I. Gas exchange and acid-base balance

The effect of an exercise-induced reduction in blood O2-carrying capacity on ventilatory gas exchange and acid-base balance during supramaximal exercise was studied in six males [peak O2 consumption (VO2peak), 3.98 +/- 0.49 l/min]. Three consecutive days of supramaximal exercise resulted in a preexercise reduction of hemoglobin concentration from 15.8 to 14.0 g/dl (P less than 0.05). During exercise (120% VO2peak) performed intermittently (1 min work to 4 min rest); a small but significant (P less than 0.05) increase was found for both O2 consumption (VO2) (l X min) and heart rate (beats/min) on day 2 of the training. On day 3, VO2 (l/min) was reduced 3.2% (P less than 0.05) over day 1 values. No changes were found in CO2 output and minute ventilation during exercise between training days. Similarly, short-term training failed to significantly alter the changes in arterialized blood PCO2, pH, and [HCO-3] observed during exercise. It is concluded that hypervolemia-induced reductions in O2-carrying capacity in the order of 10-11% cause minimal impairment to gas exchange and acid-base balance during supramaximal non-steady-state exercise.