Human Biology

In these studies, we examined whether the rightward shift in steady-state minute ventilation ( $\dot V$ E) versus O2 uptake curves after training is more closely linked to the reduced CO2 production from carbohydrate oxidation (CHOOX) after training than to the attenuated increase in blood lactate concentration. Steady state $\dot V$ E values and gas exchange were measured in eight previously sedentary men who underwent exercise tests of 60 W + 40 W every 6 min before and after a 9 week training programme of cycling approximately 40 min a day. Following training, the slower rises in $\dot V$ E with increasing exercise intensities were associated with a reduced reliance on CHOOX, (P < 0.01). Both before and after training, $\dot V$ E values in litres per minute rose as a linear $\dot V$ E = 18 · CHOOX + 14, function of rates of CHOOX in grams per minute (r = 0.99), irrespective of a marked shift to the right in arterialized venous blood lactate concentration versus CHOOX curves following training (P < 0.01). Thus, slower increases in steady-state $\dot V$ E values with increasing exercise intensities following endurance training appeared to be more closely linked to the decreased reliance on CHOOX than to the attenuated increase in blood lactate concentration.

The purposes of this study were firstly to determine the relationship between the peak power output (W peak) and maximal oxygen uptake (VO2max) attained during a laboratory cycling test to exhaustion, and secondly to assess the relationship betweenW peak 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 whichW max andVO2max were determined. For the second part of the study 19 cyclists completed a maximal test for the determination ofW peak, and also a 20-km cycling time trial. Highly significant relationships were obtained betweenW peak andVO2max (r=0.97,P<0.0001) and betweenW peak and 20-km cycle time (r= −0.91,P<0.001). Thus,W peak explained 94% of the variance in measuredVO2max and 82% of the variability in cycle time over 20 km. We concluded that for trained cyclists, theVO2max can be accurately predicted fromW peak, and thatW peak is a valid predictor of 20-km cycle time.

To determine why black distance runners currently out-perform white distance runners in South Africa, we measured maximum oxygen consumption (V O2max), maximum workload during a V O2max test (L max), ventilation threshold (V Thr), running economy, inspiratory ventilation (V I), tidal volume (V T), breathing frequency (f) and respiratory exchange ratio (RER) in sub-elite black and white runners matched for best standard 42.2 km marathon times. During maximal treadmill testing, the black runners achieved a significantly lower (P<0.05) L max (17 km h−1, 2% grade, vs 17 km h−1, 4% grade) and V I max (6.21 vs 6.821 kg−2/3 min−1), which was the result of a lower V T (101 vs 119 ml kg−2/3 breath−1) as f max was the same in both groups. The lower V T in the black runners was probably due to their smaller body size. The V Thr occurred at a higher percentage V O2max in black than in white runners (82.7%, SD 7.7% vs 75.6%, SD 6.2% respectively) but there were no differences in the V O2max. However, during a 42.2-km marathon run on a treadmill, the black athletes ran at the higher percentage V O2max (76%, SD 7.9% vs 68%, SD 5.3%), RER (0.96, SD 0.07 vs 0.91, SD 0.04) and f (56 breaths min−1, SD 11 vs 47 breaths min−1, SD 10), and at lower V T (78 ml kg−2/3 breath−1, SD 15 vs 85 ml kg−2/3 breath−1, SD 19). The combination of higher f and lower V T resulted in an identical V I. Blood lactate levels were lower in black than in white runners (1.3 mmol l−1, SD 0.6 vs 1.59 mmol l−1, SD 0.2 respectively). It appeared that the only physiological difference that may account for the superior performance of the black runners was their ability to run at a higher percentage V O2max max during competition than white runners.

These studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake ( $\dot V$ O2max), high-intensity exercise (HIE)] and 50% of peak power output [60% $\dot V$ O2max, moderate intensity exercise (MIE)]. Exercise time to exhaustion during HIE was not significantly different between trials: nor were the rates of muscle glycogen utilization during HIE different between trials, although starting muscle glycogen content was lower [68.1 (SEM 3.9) vs 120.6 (SEM 3.8) mmol · kg −1 wet mass, P < 0.01] after the HIGH-FAT diet. Despite a lower muscle glycogen content at the onset of MIE [32 (SEM 7) vs 73 (SEM 6) mmol · kg −1 wet mass, HIGH-FAT vs HIGH-CHO, P < 0.01], exercise time to exhaustion during subsequent MIE was significantly longer after the HIGH-FAT diet [79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, HIGH-FAT vs HIGH-CHO, P<0.01]. Enhanced endurance during MIE after the HIGH-FAT diet was associated with a lower respiratory exchange ratio [0.87 (SEM 0.03) vs 0.92 (SEM 0.02), P<0.05], and a decreased rate of carbohydrate oxidation [1.41 (SEM 0.70) vs 2.23 (SEM 0.40) g CHO · min−1, P<0.05]. These results would suggest that 2 weeks of adaptation to a high-fat diet would result in an enhanced resistance to fatigue and a significant sparing of endogenous carbohydrate during low to moderate intensity exercise in a relatively glycogen-depleted state and unimpaired performance during high intensity exercise.

... Or filter your current search. Hawley JA, Find all citations by this author (default). ... Indeed, it wasnot until the reintroduction of the muscle biopsy technique into exercise physiology in the 1960s that a series of studies on CHO utilisation during exercise appeared. ...

The purpose of this study was to devise and evaluate a laboratory test of cycling performance that simulates the variable power demands of competitive road racing. The test is a 100-km time trial interspersed with four 1-km and four 4-km sprints. On three occasions separated by 5-7 d, eight endurance-trained cyclists (peak oxygen uptake 5.0 +/- 0.7 L.min-1, peak power output 411 +/- 43 W, mean +/- SD) performed the test on their own bikes mounted on an air-braked Kingcycle ergometer. Subjects were free to regulate their power output but were asked to complete each sprint and the full distance as quickly as possible. The only feedback given to the cyclists during each test was elapsed distance. In the first test, time for the 100 km and mean times for the 1-km and 4-km sprints were 151:42 +/- 10:36, 1:16 +/- 0:06, and 5:31 +/- 0:16 min:s, respectively; these times improved by 1.6-2.2% in the second test, but there was little further improvement in the third test (0.7 to -0.5%). The between-test correlation for 100-km time was 0.93 (95% CI 0.79 to 0.98), and the within-cyclist coefficient of variation was 1.7% (95% CI 1.1 to 2.5%). Mean sprint performance showed similar good reliability (within-subject variation and correlations for the 1-km and 4-km sprint times of 1.9%, 2.0%, 0.93, and 0.81, respectively). The high reliability of this laboratory test will make the test useful for research on performance of competitive road cyclists.

Skeletal muscle buffering capacity (βm), enzyme activities and exercise performance were measured before and after 4 weeks of high-intensity, sub maximal␣interval training (HIT) undertaken by six well-trained competitive cyclists [mean maximal oxygen consumption ( O2max) = 66.2 ml · kg−1 · min−1]. HIT replaced a portion of habitual endurance training and consisted of six sessions, each of six to eight repetitions of 5 min duration at 80% of peak sustained power output (PPO) separated by 1 min of recovery. βm increased from 206.6 (17.9) to 240.4 (34.1) μmol H+ · g muscle dw−1 · pH−1 after HIT (P = 0.05). PPO, time to fatigue at 150% PPO (TF150) and 40-km cycle time trial performance (TT40) all significantly improved after HIT (P < 0.05). In contrast, there was no change in the activity of either phosphofructokinase or citrate synthase. In addition, βm correlated significantly with TT40 performance before HIT (r = −0.82, P < 0.05) and the relationship between change in βm and change in TT40 was close to significance (r = −0.74). βm did not correlate with TF150. These results indicate that βm may be an important determinant of relatively short-duration (< 60 min) endurance cycling activity and responds positively to just six sessions of high-intensity, submaximal interval training.

In these studies, we examined whether the rightward shift in steady-state minute ventilation ( $\dot V$ E) versus O2 uptake curves after training is more closely linked to the reduced CO2 production from carbohydrate oxidation (CHOOX) after training than to the attenuated increase in blood lactate concentration. Steady state $\dot V$ E values and gas exchange were measured in eight previously sedentary men who underwent exercise tests of 60 W + 40 W every 6 min before and after a 9 week training programme of cycling approximately 40 min a day. Following training, the slower rises in $\dot V$ E with increasing exercise intensities were associated with a reduced reliance on CHOOX, (P < 0.01). Both before and after training, $\dot V$ E values in litres per minute rose as a linear $\dot V$ E = 18 · CHOOX + 14, function of rates of CHOOX in grams per minute (r = 0.99), irrespective of a marked shift to the right in arterialized venous blood lactate concentration versus CHOOX curves following training (P < 0.01). Thus, slower increases in steady-state $\dot V$ E values with increasing exercise intensities following endurance training appeared to be more closely linked to the decreased reliance on CHOOX than to the attenuated increase in blood lactate concentration.

The purposes of this study were firstly to determine the relationship between the peak power output (W peak) and maximal oxygen uptake (VO2max) attained during a laboratory cycling test to exhaustion, and secondly to assess the relationship betweenW peak 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 whichW max andVO2max were determined. For the second part of the study 19 cyclists completed a maximal test for the determination ofW peak, and also a 20-km cycling time trial. Highly significant relationships were obtained betweenW peak andVO2max (r=0.97,P<0.0001) and betweenW peak and 20-km cycle time (r= −0.91,P<0.001). Thus,W peak explained 94% of the variance in measuredVO2max and 82% of the variability in cycle time over 20 km. We concluded that for trained cyclists, theVO2max can be accurately predicted fromW peak, and thatW peak is a valid predictor of 20-km cycle time.

To determine why black distance runners currently out-perform white distance runners in South Africa, we measured maximum oxygen consumption (V O2max), maximum workload during a V O2max test (L max), ventilation threshold (V Thr), running economy, inspiratory ventilation (V I), tidal volume (V T), breathing frequency (f) and respiratory exchange ratio (RER) in sub-elite black and white runners matched for best standard 42.2 km marathon times. During maximal treadmill testing, the black runners achieved a significantly lower (P<0.05) L max (17 km h−1, 2% grade, vs 17 km h−1, 4% grade) and V I max (6.21 vs 6.821 kg−2/3 min−1), which was the result of a lower V T (101 vs 119 ml kg−2/3 breath−1) as f max was the same in both groups. The lower V T in the black runners was probably due to their smaller body size. The V Thr occurred at a higher percentage V O2max in black than in white runners (82.7%, SD 7.7% vs 75.6%, SD 6.2% respectively) but there were no differences in the V O2max. However, during a 42.2-km marathon run on a treadmill, the black athletes ran at the higher percentage V O2max (76%, SD 7.9% vs 68%, SD 5.3%), RER (0.96, SD 0.07 vs 0.91, SD 0.04) and f (56 breaths min−1, SD 11 vs 47 breaths min−1, SD 10), and at lower V T (78 ml kg−2/3 breath−1, SD 15 vs 85 ml kg−2/3 breath−1, SD 19). The combination of higher f and lower V T resulted in an identical V I. Blood lactate levels were lower in black than in white runners (1.3 mmol l−1, SD 0.6 vs 1.59 mmol l−1, SD 0.2 respectively). It appeared that the only physiological difference that may account for the superior performance of the black runners was their ability to run at a higher percentage V O2max max during competition than white runners.

These studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake ( $\dot V$ O2max), high-intensity exercise (HIE)] and 50% of peak power output [60% $\dot V$ O2max, moderate intensity exercise (MIE)]. Exercise time to exhaustion during HIE was not significantly different between trials: nor were the rates of muscle glycogen utilization during HIE different between trials, although starting muscle glycogen content was lower [68.1 (SEM 3.9) vs 120.6 (SEM 3.8) mmol · kg −1 wet mass, P < 0.01] after the HIGH-FAT diet. Despite a lower muscle glycogen content at the onset of MIE [32 (SEM 7) vs 73 (SEM 6) mmol · kg −1 wet mass, HIGH-FAT vs HIGH-CHO, P < 0.01], exercise time to exhaustion during subsequent MIE was significantly longer after the HIGH-FAT diet [79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, HIGH-FAT vs HIGH-CHO, P<0.01]. Enhanced endurance during MIE after the HIGH-FAT diet was associated with a lower respiratory exchange ratio [0.87 (SEM 0.03) vs 0.92 (SEM 0.02), P<0.05], and a decreased rate of carbohydrate oxidation [1.41 (SEM 0.70) vs 2.23 (SEM 0.40) g CHO · min−1, P<0.05]. These results would suggest that 2 weeks of adaptation to a high-fat diet would result in an enhanced resistance to fatigue and a significant sparing of endogenous carbohydrate during low to moderate intensity exercise in a relatively glycogen-depleted state and unimpaired performance during high intensity exercise.

... Or filter your current search. Hawley JA, Find all citations by this author (default). ... Indeed, it wasnot until the reintroduction of the muscle biopsy technique into exercise physiology in the 1960s that a series of studies on CHO utilisation during exercise appeared. ...

The purpose of this study was to devise and evaluate a laboratory test of cycling performance that simulates the variable power demands of competitive road racing. The test is a 100-km time trial interspersed with four 1-km and four 4-km sprints. On three occasions separated by 5-7 d, eight endurance-trained cyclists (peak oxygen uptake 5.0 +/- 0.7 L.min-1, peak power output 411 +/- 43 W, mean +/- SD) performed the test on their own bikes mounted on an air-braked Kingcycle ergometer. Subjects were free to regulate their power output but were asked to complete each sprint and the full distance as quickly as possible. The only feedback given to the cyclists during each test was elapsed distance. In the first test, time for the 100 km and mean times for the 1-km and 4-km sprints were 151:42 +/- 10:36, 1:16 +/- 0:06, and 5:31 +/- 0:16 min:s, respectively; these times improved by 1.6-2.2% in the second test, but there was little further improvement in the third test (0.7 to -0.5%). The between-test correlation for 100-km time was 0.93 (95% CI 0.79 to 0.98), and the within-cyclist coefficient of variation was 1.7% (95% CI 1.1 to 2.5%). Mean sprint performance showed similar good reliability (within-subject variation and correlations for the 1-km and 4-km sprint times of 1.9%, 2.0%, 0.93, and 0.81, respectively). The high reliability of this laboratory test will make the test useful for research on performance of competitive road cyclists.