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Biomedical subjects

T D Noakes

Publications and source records attributed to T D Noakes.

At least 109 records · Page 6Linked to original sources
PubMed1998

Carbohydrate ingestion immediately before exercise does not improve 20 km time trial performance in well trained cyclists.

This study examined the effects of carbohydrate ingestion on 20 km cycle time-trial (TT) performance in 14 well-trained cyclists (11 males, 3 females; peak oxygen uptake [VO2peak] 4.52 +/- 0.60 l/min; values are mean +/- SD). All subjects performed two experimental trials on their own bicycles mounted on an air-braked ergometry system (Kingcycle). Subjects were instructed to maintain the same training and dietary regimens before trials, which were conducted in a random order, 3-7 days apart, and at the same time of day for each subject. On the day of a trial, subjects reported to the laboratory and ingested an 8 ml/kg body mass bolus of either a 6.8 g/100 ml commercial carbohydrate-electrolyte (CHO) beverage (39 +/- 4 g of CHO), or a coloured, flavoured placebo. Ten min after finishing the drink, subjects commenced a 5 min warm-up at 150 W, before commencing the 20 km TT. The average power output (312 +/- 40 vs 311 +/- 38 W) and heart-rate (171 +/- 6 vs 171 +/- 5 beats/min for CHO and placebo, respectively) during the two rides did not differ between treatments. Accordingly, the performance times for the two TT's were the same (27:41 +/- 1:39 min:sec, for both CHO and placebo). We conclude that the ingestion of approximately 40 g of carbohydrate does not improve maximal cycling performance lasting approximately 30 min, and that carbohydrate availability, in the form of circulating blood glucose, does not limit high-intensity exercise of this duration.

Adolescent↗
PubMed1998

Fluid and electrolyte disturbances in heat illness.

Three exercise-related heat illnesses are described in the literature -- heat cramps, heat exhaustion or heat syncope, and heat stroke. Of these, only exercise-induced heat stroke, which occurs infrequently, is definitely a heat illness caused by an increased rate of heat production unmatched by adequate heat loss causing progressive heat retention with the body temperature rising to dangerously high levels (> 41 degrees C). The terms heat cramps and heat exhaustion are misleading as neither is caused by an elevated body temperature; nor is there evidence that either is caused by specific fluid or electrolyte abnormalities. Cramps occur during or after exercise regardless of whether the exercise is performed in the heat or the cold, or in water. Current evidence suggests that a spinal neural mechanism may induce cramping that is unrelated to biochemical changes in either blood or in the affected skeletal muscles. Historically, heat exhaustion has been described as a condition of postural hypotension that develops immediately on termination of exercise especially when performed in the heat by unacclimatised persons. No modern evidence conflicts with this historical interpretation. Nor have more modern studies shown that exercise-related heat exhaustion is necessarily caused by specific fluid or electrolyte abnormalities. Similarly, there is no published evidence that fluid and electrolyte abnormalities are critical determinants of exercise-related heat stroke. This does not negate firm evidence that dehydration has important physiological effects that impair heat loss and exercise performance especially in the heat. Rather, it shows that exercise-induced heat stroke requires powerful initiating factors, in addition to dehydration which occurs commonly during prolonged exercise, whereas heat stroke is an extremely rare event. The purpose of this review is to provide an alternate, more critical review of the conditions that are considered to be exercise-related heat disorders and to evaluate the aetiological role of fluid and electrolyte disturbances. There is a need to better understand these conditions so that their clinical management can be based on modern information rather than on dated ideas, many of which have survived unchallenged for more than 50 years.

Athletic Injuries↗
PubMed1998

Maximal oxygen uptake: "classical" versus "contemporary" viewpoints: a rebuttal.

Bassett and Howley contend that the 1996 J. B. Wolffe lecture is erroneous because: 1) A. V. Hill did establish the existence of the "plateau phenomenon," 2) the maximum oxygen consumption (VO2max) is limited by the development of anaerobiosis in the active muscle, and 3) endurance performance is also determined by skeletal muscle anaerobiosis because the VO2max is the best predictor of athletic ability. As a result, 4) cardiovascular and not skeletal muscle factors determine endurance performance. They further contend that Hill's "scientific hunches were correct," requiring "only relatively minor refinements" in the past 70 yr. But the evidence presented in this rebuttal shows that Hill neither sought nor believed in either the "plateau phenomenon" or the concept of the individual maximum oxygen consumption. These twin concepts were created by Taylor et al. (97) in 1955 and erroneously attributed to Hill. Rather Hill believed that there was a universal human VO2max of 4 L x min(-1). His error resulted from his incorrect belief that the real VO2 unmeasurable because it includes a large "anaerobic component," rose exponentially at running speeds greater than 13.2 km x h(-1). But Hill and his colleagues were indeed the first to realize the danger that a plateau in cardiac output (CO) and hence in VO2 would pose for the heart itself. For unlike skeletal muscle, the pumping capacity of the heart is both dependent on, but also the determinant of, its own blood supply. Thus, if the CO reaches a peak causing the "plateau phenomenon," the immediate cause of that peak will have been a plateau in myocardial oxygen delivery, causing a developing myocardial ischemia. The ischemia must worsen as exercise continues beyond the supposed VO2 "plateau." To accommodate this dilemma, Hill and his colleagues proposed a governor "either in the heart muscle or in the nervous system" necessary to prevent myocardial ischemia developing during maximal exercise. This governor would cause maximal exercise to terminate before the development of a plateau in either coronary flow, CO, or VO2, or the onset of skeletal muscle anaerobiosis. Accordingly, a new physiological model is proposed in which skeletal muscle recruitment is regulated by a central "governor" specifically to prevent the development of a progressive myocardial ischemia that would precede the development of skeletal muscle anaerobiosis during maximum exercise. As a result cardiovascular function "limits" maximum exercise capacity, probably as a result of a limiting myocardial oxygen delivery. The model is compatible with all the published findings of cardiovascular function during exercise in hypobaric hypoxia, in which there is a greater likelihood that myocardial hypoxia will develop.

Anaerobic Threshold↗
PubMed1998

A new reliable laboratory test of endurance performance for road cyclists.

PURPOSE: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: The high reliability of this laboratory test will make the test useful for research on performance of competitive road cyclists.

Adult↗
PubMed1998

Influence of muscle glycogen content on metabolic regulation.

Euglycemia was maintained in 13 subjects with low muscle glycogen [low glycogen, euglycemic (LGE), n = 8; low glycogen, euglycemic, hyperinsulinemic (LGEI), n = 5] and 6 subjects with normal muscle glycogen (NGE), whereas hyperglycemia was maintained in 8 low muscle glycogen subjects (LGH). All subjects cycled for 145 min at 70% of maximal oxygen uptake during the infusions. Insulin was infused in LGEI at 0.2 mU.kg-1.min-1. During exercise, respiratory exchange ratio (RER) was lower and norepinephrine higher in LGE than in NGE. In LGEI and LGH, RER at the start of exercise was the same as in LGE but did not decrease as in LGE. Free fatty acids (FFA) were higher and plasma insulin concentrations lower in LGE than NGE, LGEI, or LGH over the first 45 min of exercise. Rate of glucose infusion (Ri) and rate of glucose oxidation (Rox) were higher in LGH and LGEI than in NGE or LGE, and Ri matched Rox in all groups except LGH, in which Ri was greater than Rox. Muscle glycogen disappearance was greater in NGE than LGE, LGEI, or LGH, but the latter three groups did not differ. In conclusion, this study showed that low muscle glycogen content results in a decrease in RER, an increase in FFA, fat oxidation, and norepinephrine both at rest and during exercise, and does not affect Rox when euglycemia is maintained by infusion of glucose alone. Rox was increased only during insulin and hyperglycemia.

Adult↗
PubMed1998

Preexercise muscle glycogen content affects metabolism during exercise despite maintenance of hyperglycemia.

Trained cyclists with low muscle glycogen (LGH; n = 8) or normal glycogen (NGH; n = 5) exercised for 145 min at 70% of maximal oxygen uptake during a hyperglycemic clamp. Respiratory exchange ratio was higher in NGH than LGH, and free fatty acid concentrations were lower in NGH than LGH. Areas under the curve for insulin and lactate were lower in LGH than NGH. Total glucose infusion and total glucose oxidation were not different between NGH and LGH, and total glucose oxidation amounted to 65 and 66% of total glucose infusion in NGH and LGH, respectively. Rates of glucose oxidation rose during exercise, reaching peaks of 9.2 +/- 1.7 and 8.3 +/- 1.1 mmol/min in NGH and LGH, respectively. Muscle glycogen disappearance was greater in NGH than LGH. Thus 1) low muscle glycogen content does not cause increased glucose oxidation, even during hyperglycemia; instead there is an increase in fat oxidation, 2) there is an upper limit to the rate of glucose oxidation during exercise with hyperglycemia irrespective of muscle glycogen status, and 3) net muscle glycogen utilization is determined by muscle glycogen content at the start of exercise, even during hyperglycemia.

Adult↗
PubMed1998

Carbohydrate intake during prolonged cycling minimizes effect of glycemic index of preexercise meal.

We studied the effects of the glycemic index (GI) of preexercise meals on metabolism and performance when carbohydrate (CHO) was ingested throughout exercise. Six well-trained cyclists performed three counterbalanced trials of 2-h cycling at approximately 70% of maximal oxygen uptake, followed by a performance ride of 300 kJ. Meals consumed 2 h before exercise consisted of 2 g CHO/kg body mass of either high-GI potato (HGI trial) or low-GI pasta (LGI trial), or of a low-energy jelly (Con trial). Immediately before and throughout exercise, subjects ingested a 10 g/100 ml [U-14C]glucose solution for a total of 24 ml/kg body mass. Despite differences in preexercise glucose, insulin, and free fatty acids concentrations among trials, both total CHO oxidation for HGI, LGI, and Con trials, respectively, during steady-state exercise [403 +/- 16, 376 +/- 29, and 373 +/- 24 (SE) g/2 h] and oxidation of the ingested CHO (65 +/- 6, 57 +/- 6, and 63 +/- 5 g/2 h) were similar. There was no difference in time to complete the subsequent performance ride (946 +/- 23, 954 +/- 35, and 970 +/- 26 s for HGI, LGI, and Con trials, respectively). When CHO is ingested during exercise in amounts presently recommended by sports nutrition guidelines, preexercise CHO intake has little effect on metabolism or on subsequent performance during prolonged cycling (approximately 2.5 h).

Adult↗
PubMed1998

A high rate of injury during the 1995 Rugby World Cup.

OBJECTIVE: To determine the frequency and nature of injuries sustained by the 416 players from 16 countries participating in the 1995 Rugby World Cup played in South Africa in May/June 1995. METHODS: The study was a prospective analysis of all injuries requiring medical attention during that competition. Data were collected by the match doctors on duty at each of the venues at which the matches were played. Data were collated and analysed. RESULTS: There were 48 preliminary and 7 final-round matches. Of a total of 70 injuries during the tournament, 58 occurred during the preliminary matches (frequency 30 injuries per 1000 player hours); the frequency was somewhat higher during the 7 final-round matches (43 injuries per 1000 player hours). Overall injury frequency was 1 injury every 0.8 matches during the preliminary and 1 every 0.6 matches during the final-round matches. Thirty per cent of injuries were to ligaments, 27% were lacerations and 14% were muscle strains. The lower limb accounted for 42% of all injuries, the upper limb for 29% and the face for 17%. Fifty-six per cent of injuries occurred during the tackle phase of play, 23% during the ruck and maul, 11% during open play and 9% during foul play. The scrum and line-out together contributed only 1% of all injuries. Loose forwards suffered 25% of all injuries; centres and wings 20%; prop forwards and half-backs 16% each; locks 14%; hookers 7% and fullbacks 3%. One player suffered a paralysing spinal cord injury during a preliminary match. The incidence of catastrophic neck injuries in the tournament was therefore 4.6 per 10,000 player hours. CONCLUSIONS: The frequency of injury in this competition is the highest yet recorded in any group of rugby players. The risk of rugby injury is therefore greatest in the best players in the game, challenging the view that superior fitness, skill and experience can reduce the risk of rugby injury. In contrast, the larger size, greater speed and superior competitiveness and commitment of the best rugby players in the world would explain why they are at the highest risk of injury. The high frequency of injury in international rugby has implications for: (i) the frequency with which such matches should be played; and (ii) the number of players needed to complete a season of international rugby.

Athletic Injuries↗
PubMed1997

Skeletal muscle buffering capacity and endurance performance after high-intensity interval training by well-trained cyclists.

Skeletal muscle buffering capacity (beta m), enzyme activities and exercise performance were measured before and after 4 weeks of high-intensity, submaximal interval training (HIT) undertaken by six well-trained competitive cyclists [mean maximal oxygen consumption (VO2max) = 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. beta m increased from 206.6 (17.9) to 240.4 (34.1) mumol 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, beta m correlated significantly with TT40 performance before HIT (r = -0.82, P < 0.05) and the relationship between change in beta m and change in TT40 was close to significance (r = -0.74). beta m did not correlate with TF150. These results indicate that beta m 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.

Adult↗
PubMed1997

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.

Adaptation, Physiological↗
PubMed1997

Effects of 3 days of carbohydrate supplementation on muscle glycogen content and utilisation during a 1-h cycling performance.

This study compared the effects of supplementing the normal diets of six trained cyclists [maximal oxygen uptake (VO2max) 4.5 (0.36) l.min-1; values are mean (SD)] with additional carbohydrate (CHO) on muscle glycogen utilisation during a 1-h cycle time-trial (TT). Using a randomised crossover design, subjects consumed either their normal diet (NORM) for 3 days, which consisted of 426 (137) g.day-1 CHO [5.9 (1.4) g. kg-1 body mass (BM)], or additional CHO (SUPP) to increase their intake to 661 (76) g.day-1 [9.3 (0.7) g. kg-1 BM]. The SUPP diet elevated muscle glycogen content from 459 (83) to 565 (62) mmol.kg-1 dry weight (d.w.) (P < 0.05). However, despite the increased pre-exercise muscle glycogen stores, there was no difference in the distance cycled during the TT [40.41 (1.44) vs 40.18 (1.76) km for NORM and SUPP, respectively]. With NORM, muscle glycogen declined from 459 (83) to 175 (64) mmol.kg-1 d.w., whereas with SUPP the corresponding values were 565 (62) and 292 (113) mmol.kg-1 d.w. Accordingly, both muscle glycogen utilisation [277 (64) vs 273 (114) mmol.kg-1 d.w.] and total CHO oxidation [169 (20) vs 165 (30) g.h-1 for NORM and SUPP, respectively] were similar. Neither were there any differences in plasma glucose or lactate concentrations during the two experimental trials. Plasma glucose concentration averaged 5.5 (0.5) and 5.6 (0.6) mmol.l-1, while plasma lactate concentration averaged 4.4 (1.9) and 4.4 (2.3) mmol.l-1 for NORM and SUPP, respectively. The results of this study show that when well-trained subjects increase the CHO content of their diet for 3 days from 6 to 9 g.kg-1 BM there is only a modest increase in muscle glycogen content. Since supplementary CHO did not improve TT performance, we conclude that additional CHO provides no benefit to performance for athletes who compete in intense, continuous events lasting 1 h. Furthermore, the substantial muscle CHO reserves observed at the termination of exercise indicate that whole-muscle glycogen depletion does not determine fatigue at this exercise intensity and duration.

Adult↗
PubMed1997

Time course of the effects of a high-fat diet and voluntary exercise on muscle enzyme activity in Long-Evans rats.

This study examined the time course of the effects of a high-fat diet and voluntary running exercise on rat skeletal muscle carnitine acyltransferase (CAT), beta-hydroxy-acyl-CoA dehydrogenase (HAD), and citrate synthase (CS) activities. Sixty male Long-Evans rats were randomly allocated to receive either a standard (12% fat by energy) laboratory chow diet (CHOW) or a high-fat (76% by energy) diet (HFD) and placed in running wheels for up to 6 weeks. Energy intakes and weekly voluntary running distances were similar in the CHOW and HFD rats. In both groups, weekly training distance more than doubled from week 4 to week 6. However, increased training had little influence on soleus (s) CAT(s), HAD(s), and CS(s) activities. CAT(s) and HAD(s) activities were higher in the HFD rats than in the CHOW rats from 2 weeks onward (p < 0.005), and CS(s) activities were not different between groups and remained constant over time. In contrast, increased training distance after 4 weeks in the CHOW rats resulted in an increase in deep vastus (v) CAT(v) activities to values similar to those in HFD rats prior to increases in training volume (p < 0.005) but had no effect on their HAD(v) and CS(v) activities. Increases in HAD(v) and CS(v) activities with increased training volume were only seen in the HFD rats (p < 0.005). HAD(v) activities and HAD/CS(v) activity ratios correlated with training distance in the HFD rats only (p < 0.001 and p < 0.01, respectively). These results suggest that a high-fat diet improves the beta-oxidation capacity of rat predominantly slow-twitch soleus muscle and enhances the effects of modest levels of training on the mitochondrial density and beta-oxidation capacity of rat deep vastus mixed fast- and slow-twitch muscles.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1997

Clinical assessment of the low-cost VariCom isokinetic knee exerciser.

A low-cost isokinetic knee exerciser, known as the VariCom and developed with the emphasis on fulfilling the rehabilitation needs of developing countries, was subjected to a clinical evaluation. The evaluation was motivated by successful laboratory assessment of the exerciser as well as encouraging qualitative data acquired recently from a developing world hospital. The principal aim of this study was to demonstrate that the exerciser, employing a simple shock-absorber and lever mechanism, was capable of fulfilling the major criteria required from isokinetic equipment. Amongst the most important of these were attainment of a 'spectrum of velocities', patient safety, reliability, ease-of-use, patient comfort and estimation of the torque generated by the patient's knee-joint. It was ultimately demonstrated that the combination of design simplicity, durability and functionality renders the VariCom knee-exerciser technologically appropriate for use in developing countries. More generally, the success of the exerciser, combined with its low manufacturing cost, renders it a viable alternative to traditional up-market equipment.

Biomedical Engineering↗
PubMed1997

Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis.

The aetiology of exercise-associated muscle cramps (EAMC), defined as 'painful, spasmodic, involuntary contractions of skeletal muscle during or immediately after physical exercise', has not been well investigated and is therefore not well understood. This review focuses on the physiological basis for skeletal muscle relaxation, a historical perspective and analysis of the commonly postulated causes of EAMC, and known facts about EAMC from recent clinical studies. Historically, the causes of EAMC have been proposed as (1) inherited abnormalities of substrate metabolism ('metabolic theory') (2) abnormalities of fluid balance ('dehydration theory'), (3) abnormalities of serum electrolyte concentrations ('electrolyte theory') and (4) extreme environmental conditions of heat or cold ('environmental theory'). Detailed analyses of the available scientific literature including data from recent studies do not support these hypothesis for the causes of EAMC. In a recent study, electromyographic (EMG) data obtained from runners during EAMC revealed that baseline activity is increased (between spasms of cramping) and that a reduction in the baseline EMG activity correlates well with clinical recovery. Furthermore, during acute EAMC the EMG activity is high, and passive stretching is effective in reducing EMG activity. This relieves the cramp probably by invoking the inverse stretch reflex. In two animal studies, abnormal reflex activity of the muscle spindle (increased activity) and the Golgi tendon organ (decreased activity) has been observed in fatigued muscle. We hypothesize that EAMC is caused by sustained abnormal spinal reflex activity which appears to be secondary to muscle fatigue. Local muscle fatigue is therefore responsible for increased muscle spindle afferent and decreased Golgi tendon organ afferent activity. Muscles which cross two joints can more easily be placed in shortened positions during exercise and would therefore decrease the Golgi tendon organ afferent activity. In addition, sustained abnormal reflex activity would explain increased baseline EMG activity between acute bouts of cramping. Finally, passive stretching invokes afferent activity from the Golgi tendon organ, thereby relieving the cramp and decreasing EMG activity.

Electromyography↗
PubMed1997

Nutritional strategies to minimize fatigue during prolonged exercise: fluid, electrolyte and energy replacement.

While the presence of palatable (20 mmol l-1) concentrations of NaCl in drinks containing carbohydrate consumed during intense exercise would not be expected to promote absorption or significantly help maintain fluid balance, there is no doubt that athletes should ingest some from of carbohydrate (other than fructose) during moderate-intensity exercise lasting > 90 min. As only approximately 20 g of ingested carbohydrate is oxidized in the first hour of exercise, athletes should probably consume 100 ml every 10 min of a dilute (3-5 g 100 ml-1) carbohydrate solution and thereafter increase the carbohydrate concentration to approximately 10 g 100 ml-1 to match the peak (approximately 1 g min-1) rates of plasma glucose oxidation. Drinking more than those amounts of carbohydrate may increase muscle glycogen oxidation by attenuating the fall in plasma insulin concentration and thereby delaying fat mobilization, especially at relatively low (55% of peak oxygen consumption) intensity exercise. As carbohydrate ingestion does not slow the rate of glycogen utilization in working muscle, it is also advisable for endurance athletes to start exercise with an adequate supply of muscle glycogen, irrespective of whether or not they ingest carbohydrate during exercise. While carbohydrate ingestion 'spares' conversion of liver glycogen to plasma glucose and prevents hypoglycemia, it does not delay the fatigue associated with a low (approximately 20 mmol kg-1) glycogen content in working muscle. Conversely, increases in glycogen content of working muscle at the start of exercise have no effect on the rates of plasma glucose oxidation. Higher initial rates of glycogen utilization by active muscles in 'carbohydrate-loaded' subjects decrease the indirect oxidation (via lactate) of non-working muscle glycogen, rather than the conversion of liver glycogen to plasma glucose. Hence, athletes should ingest carbohydrate during endurance exercise even if they have 'carbohydrate-loaded' before exercise.

Dietary Carbohydrates↗
PubMed1997

Nutritional strategies for promoting fat utilization and delaying the onset of fatigue during prolonged exercise.

Carbohydrate ingestion before and during endurance exercise delays the onset of fatigue (reduced power output). Therefore, endurance athletes are recommended to ingest diets high in carbohydrate (70% of total energy) during competition and training. However, increasing the availability of plasma free fatty acids has been shown to slow the rate of muscle and liver glycogen depletion by promoting the utilization of fat. Ingested fat, in the form of long-chain (C16-22) triacylglycerols, is largely unavailable during acute exercise, but medium-chain (C8-10) triacylglycerols are rapidly absorbed and oxidized. We have shown that the ingestion of medium-chain triacylglycerols in combination with carbohydrate spares muscle carbohydrate stores during 2 h of submaximal (< 70% VO2 peak) cycling exercise, and improves 40 km time-trial performance. These data suggest that by combining carbohydrate and medium-chain triacylglycerols as a pre-exercise supplement and as a nutritional supplement during exercise, fat oxidation will be enhanced, and endogenous carbohydrate will be spared. We have also examined the chronic metabolic adaptations and effects on substrate utilization and endurance performance when athletes ingest a diet that is high in fat (> 70% by energy). Dietary fat adaptation for a period of at least 2-4 weeks has resulted in a nearly two-fold increase in resistance to fatigue during prolonged, low- to moderate-intensity cycling (< 70% VO2 peak). Moreover, preliminary studies suggest that mean cycling 20 km time-trial performance following prolonged submaximal exercise is enhanced by 80 s after dietary fat adaptation and 3 days of carbohydrate loading. Thus the relative contribution of fuel substrate to prolonged endurance activity may be modified by training, pre-exercise feeding, habitual diet, or by artificially altering the hormonal milieu or the availability of circulating fuels. The time course and dose-response of these effects on maximizing the oxidative contribution of fat for exercise metabolism and in exercise performance have not been systematically studied during moderate- to high-intensity exercise in humans.

Adipose Tissue↗
PubMed1997

Training techniques to improve fatigue resistance and enhance endurance performance.

Despite their best efforts, sports scientists have found it difficult to persuade elite athletes to experiment with their training regimens. Thus, until recently, exercise physiologists have had limited impact on the training practices of successful athletes, with most of the innovations in the training patterns of the best athletes coming from the empirical observations of top-level coaches. One form of training recognized by sports scientists and used by athletes for several decades in interval/transition training. Such training consists of a number of exercise bouts alternated with short rest intervals of more slowly paced activity and is thought to improve the fatigue resistance of the active muscles by exposing them to sustained, high-intensity exercise at the athlete's maximal steady-state pace. Few scientific studies, however, have examined the effects of transition training on the performances of competitive athletes. This paper identifies the physiological factors associated with successful endurance performance, and summarizes the results of investigations on competitive endurance cyclists which examined the time-course of changes in performance in response to a sustained, high-intensity interval training programme.

Adult↗