Endurance-trained Male Cyclists Research Articles

Effects of marked hyperthermia with and without dehydration on VO(2) kinetics during intense exercise.

This study determined whether marked hyperthermia alone or in combination with dehydration reduces the initial rate of rise in O(2) consumption (VO(2) on-kinetics) and the maximal rate of O(2) uptake (VO(2 max)) during intense cycling exercise. Six endurance-trained male cyclists completed four maximal cycle ergometer exercise tests (402 +/- 4 W) when euhydrated or dehydrated (4% body wt) with normal (starting esophageal temperature, 37.5 +/- 0.2 degrees C; mean skin temperature, approximately 31 degrees C) or elevated (+1 and +6 degrees C, respectively) thermal strain. In the euhydrated and normal condition, subjects reached VO(2 max) (4.7 +/- 0.2 l/min) in 228 +/- 34 s, with a mean response time of 42 +/- 2 s, and fatigued after 353 +/- 39 s. Hyperthermia alone or in combination with dehydration reduced mean response time (17-23%), VO(2 max) (16%), and performance time (51-53%) (all P < 0.01) but did not alter the absolute response time (i.e., the time to reach 63% response in the control trial, 3.2 +/- 0.1 l/min, 42 s). Reduction in VO(2 max) was accompanied by proportional decline in O(2) pulse and significantly elevated maximal heart rate (195 vs. 190 beats/min for hyperthermia vs. normal). Preventing hyperthermia in dehydrated subjects restored VO(2 max) and performance time by 65 and 50%, respectively. These results demonstrate that impaired high-intensity exercise performance with marked skin and internal body hyperthermia alone or in combination with dehydration is not associated with a diminished rate of rise in VO(2) but decreased VO(2 max).

Stroke volume during exercise: interaction of environment and hydration.

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O(2) consumption (VO(2 max)) 4.5 +/- 0.1 l/min; means +/- SE] cycled for 30 min (72% VO(2 max)) in the heat (H; 35 degrees C) or the cold (C; 8 degrees C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (T(es) 38. 2-38.3 degrees C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 +/- 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 +/- 1.3 ml (4.8%) in H and 3.4 +/- 0.4 ml (2.5%) in C, whereas T(es) increased 0.21 +/- 0.02 and 0. 10 +/- 0.02 degrees C in H and C, respectively (P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H (R = 0.96; P < 0.01) and C (R = 0. 85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.

Metabolic and performance adaptations to interval training in endurance-trained cyclists.

This study examined the effects of sustained high-intensity interval training (HIT) on the athletic performances and fuel utilisation of eight male endurance-trained cyclists. Before HIT, each subject undertook three baseline peak power output Wpeak tests and two simulated 40-km time-trial cycling performance (TT40) tests, of which the variabilities were 1.5 (1.3)% and 1.0 (0.5)%, respectively [mean (SD)]. Over 6 weeks, the cyclists then replaced 15 (2)% of their 300 (66) km.week-1 endurance training with 12 HIT sessions, each consisting of six to nine 5-min rides at 80% of Wpeak, separated by a l-min recovery. HIT increased Wpeak from 404 (40) to 424 (53) W (P < 0.01) and improved TT40 speeds from 42.0 (3.6) to 43.0 (4.2) km.h-1 (P < 0.05). Faster TT40 performances were due to increases in both the absolute work rates from 291 (43) to 327 (51) W (P < 0.05) and the relative work rates from 72.6 (5.3)% of pre-HIT Wpeak to 78.1 (2.8)% of post-HIT Wpeak (P < 0.05). HIT decreased carbohydrate (CHO) oxidation, plasma lactate concentration and ventilation when the cyclists rode at the same absolute work rates of 60, 70 and 80% of pre-HIT Wpeak (P < 0.05), but not when they exercised at the same relative (% post-HIT Wpeak) work rates. Thus, the ability of the cyclists to sustain higher percentages of Wpeak in TT40 performances after HIT was not due to lower rates of CHO oxidation. Higher relative work rates in the TT40 rides following HIT increased the estimated rates of CHO oxidation from approximately 4.3 to approximately 5.1 g.min-1.

Influence of ingesting a solution of branched‐chain amino acids on perceived exertion during exercise

On two occasions, seven male endurance-trained cyclists performed exhaustive exercise on a cycle ergometer in the morning after they had performed a bout of exercise the preceding evening in an attempt to lower the muscle glycogen stores. The subjects exercised at a work rate corresponding to approximately 70% of their maximal oxygen uptake for 60 min, followed by another 20 min of maximal exercise. During exercise the subjects were given either a solution of branched-chain amino acids (BCAAs) or flavoured water (placebo). Every 10 min during exercise the subjects rated their perceived exertion and mental fatigue on two different Borg scales. During the 60 min exercise at a given work rate the subjects ratings of perceived exertion when they were given BCAAs were 7% lower, and their ratings of mental fatigue were 15% lower than when they were given placebo. In addition, the performance in the colour task of Stroops Colour Word Test performed after exercise was improved when BCAAs had been ingested during exercise, compared with the results from the placebo trial. There was no difference in the physical performance between the two trials measured as the amount of work done during the last 20 min of exercise when the subjects performed at their maximum. The plasma concentration ratio of free tryptophan/BCAAs, which increased by 45% during exercise and by 150% 5 min after exercise in the placebo trial, remained unchanged or even decreased when BCAAs were ingested.

The relationship between test protocol and the development of exercise-induced hypoxemia (EIH) in highly trained athletes.

Healthy male endurance-trained cyclists [n = 11, age = 27.3 (3.9) years; mass = 73.0 (9.3) kg; height = 180.5 (6.9) cm; maximal oxygen consumption (VO2max) = 71.1 (5.8) ml.kg-1.min-1, mean +/- (SD)] were recruited to assess the relationship between test protocol and the development of desaturation of arterial hemoglobin with oxygen, during incremental exercise tests to maximal aerobic capacity (VO2max). All subjects demonstrated resting pulmonary function within normal limits [forced vital capacity (FVC) = 6.0 (0.9); forced expiratory volume (FEV1.0) = 4.9 (0.6); FEV1.0/FVC = 0.8 (0.1)] and completed three ramped VO2max tests (Mijnhardt KEM-3 electronically braked cycle ergometer) beginning at 0 W with increments of either 20,30 or 40 W.min-1. All periods of testing were separated by a minimum of 72 h. VO2max, peak minute ventilation (VEpeak) (Medical Graphics, CPX-D), peak heart rate (fcpeak), peak power output (Wpeak), and minimum percentage arterial oxyhemoglobin saturation (% SaO2min) (Omeda Biox 3740 pulse oximeter) were determined. There were no significant differences (p > 0.05) in VEpeak [191.5 (26.2), 196.0 (24.4), 194.3 (23.9) l.min-1] fcpeak [191.4 (7.0), 190.3 (5.5), 187.8 (5.9) beats.min-1], VO2max [5.0 (0.5), 5.1 (0.4), 5.1 (0.5) l.min-1] or %SaO2min [89.5 (1.5), 89.6 (1.3), 90.0 (2.3)] between protocols. The 20-W protocol [417 (27) W] demonstrated significantly lower Wpeak (P < 0.05) than the 30-W [434 (36) W] and 40-W [453 (38) W] protocols, indicating that peripheral fatigue may play an important factor in response to these tests. The results of this study demonstrate that arterial desaturation occurs as a result of intense exercise in highly trained athletes independent of the rate of attainment of VO2max.

Influence of ingesting a solution of branched-chain amino acids on plasma and muscle concentrations of amino acids during prolonged submaximal exercise

On two occasions, seven male endurance-trained cyclists performed sustained exhaustive exercise with reduced muscle glycogen stores. During exercise, the subjects were supplied in random order with an aqueous solution of branched-chain amino acids (BCAA) or flavored water (placebo). Ingestion of BCAA caused the concentration of these amino acids to increase by 135% in the plasma and by 57% in muscle tissue during exercise, whereas in the placebo trial there was no change or a slight decrease in the concentration in plasma and a decrease of 18% in the muscle. The plasma concentration of alanine increased by 48% during exercise when BCAA were ingested, and the increase in the muscle concentration of alanine during exercise was larger (70% versus 31% in the placebo trial), suggesting an increased rate of alanine production. Also, the plasma concentration of arginine increased by 14% during exercise when BCAA were ingested, whereas there was no change during exercise in the placebo trial. There was a smaller decrease in the muscle glutamate concentration during exercise in the BCAA trial (32% versus 47% in the placebo trial; p < 0.05), but, for the remaining amino acids, there was no difference between the BCAA and placebo trials. There was a significant decrease in the muscle glycogen concentration during exercise in the placebo trial, whereas only a small decrease was found in the BCAA trial (28 and 9 mmol/kg wet wt [ p < 0.05] in the placebo and BCAA trial, respectively). This might indicate that an increased supply of BCAA has a sparing effect on muscle glycogen degradation during exercise.

Influence of carbohydrate loading on fuel substrate turnover and oxidation during prolonged exercise.

This study compared liver glucose turnover, blood glucose oxidation, and muscle glycogen utilization in 15 male endurance-trained cyclists who rode for 180 min at 70% of maximal O2 consumption in either a carbohydrate-(CHO) loaded (CL) or a non-CHO-loaded (NL) state. Total CHO oxidation during exercise was similar in the CL and NL subjects (492 +/- 77 vs. 448 +/- 43 g, respectively), as were blood glucose oxidation (103 +/- 19 vs. 99 +/- 7 g, respectively) and liver glucose appearance (110 +/- 15 vs. 127 +/- 16 g, respectively). However, total muscle glycogen utilization was greater in CL than NL subjects (134 +/- 11 vs. 95 +/- 12 mmol/kg wet wt; P < 0.05), the former of which had higher muscle glycogen content at the start (194 +/- 4 vs. 124 +/- 7 mmol/kg wet wt; P < 0.05) and throughout the trial. Whereas high rates of muscle glycogen breakdown were maintained throughout the trial in CL subjects, rates of muscle glycogenolysis in NL subjects decreased to 26 mmol.kg wet wt-1.h-1 after 60 min of exercise (P < 0.05) when their muscle glycogen content had declined to 70 mmol/kg wet wt. Comparable rates of blood glucose and overall CHO oxidation in CL and NL subjects, despite a slowing of muscle glycogenolysis in the NL group, could be explained by an accelerated breakdown of glycogen in the nonworking muscles to redistribute CHO (lactate) to the working muscles for oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilation and blood lactate increase exponentially during incremental exercise.

This study examined whether the ventilatory (V) compensation for metabolic acidosis with increasing O2 uptake (VO2) and CO2 output (VCO2) might be more in accord with the theoretical expectation of a progressive acceleration of proton production from carbohydrate oxidation rather than a sudden onset of blood lactate (BLa) accumulation. The interrelationships between V, VO2, VCO2 and BLa concentration, [BLa], were investigated in 10 endurance-trained male cyclists during incremental (120 +/- 15 W min-1) exercise tests to exhaustion. Regression analyses on the V, VCO2 and [BLa] vs VO2 data revealed that all were better fitted by continuous Y = A.exp.[B.VO2] + C rate laws than by threshold linear rate equations (P < 0.0001). Plots of V vs VCO2 and [BLa] were also non-linear. Ventilation increased as an exponential V = 27 +/- 4.exp.[0.37 +/- 0.03.VCO2] function of VCO2 and as a hyperbolic function of [BLa]. In opposition to the 'anaerobic (lactate) threshold' hypothesis, we suggest these data are more readily explained by a continuous development of acidosis, rather than a sudden onset of BLa accumulation, during progressive exercise.