Attenuated relationship between cardiac output and oxygen uptake during high-intensity exercise.

AIM: Recent findings have challenged the belief that the cardiac output (CO) and oxygen consumption (VO(2) ) relationship is linear from rest to maximal exercise. The purpose of this study was to determine the CO and stroke volume (SV) response to a range of exercise intensities, 40-100% of VO(2max), during cycling. METHODS: Ten well-trained cyclists performed a series of discontinuous exercise bouts to determine the CO and SV vs. VO(2) responses. RESULTS: The rate of increase in CO, relative to VO(2) , during exercise from 40 to 70% of VO(2max) was 4.4 ± 1.4 L L(-1). During exercise at 70-100% of VO(2max) , the rate of increase in CO was reduced to 2.1 ± 0.9 L L(-1) (P = 0.01). Stroke volume during exercise at 80-100% of VO(2max) was reduced by 7% when compared to exercise at 50-70% of VO(2max) (134 ± 5 vs. 143 ± 5 mL per beat, P = 0.02). Whole body arterial-venous O(2) difference increased significantly as intensity increased. CONCLUSION: The observation that the rate of increase in CO is reduced as exercise intensity increases suggests that cardiovascular performance displays signs of compromised function before maximal VO(2) is reached.

The effects of fasting on metabolism and performance.

An overnight fast of 8-10 h is normal for most people. Fasting is characterised by a coordinated set of metabolic changes designed to spare carbohydrate and increase reliance on fat as a substrate for energy supply. As well as sparing the limited endogenous carbohydrate, and increased rate of gluconeogenesis from amino acids, glycerol and ketone bodies help maintain the supply of carbohydrate. Many individuals undergo periodic fasts for health, religious or cultural reasons. Ramadan fasting, involving 1 month of abstention from food and fluid intake during daylight hours, is practised by a large part of the world population. This period involves a shift in the pattern of intake from daytime to the hours of darkness. There seems to be little effect on overall daily dietary intake and only small metabolic effects, but there may be implications for both physical and cognitive function. The limited evidence suggests that effects of Ramadan-style fasting on exercise performance are generally small. This needs to be balanced, however, against the observation that small differences in performance are critical in determining the outcomes of sporting events. Studies involving challenging sporting events (prolonged sustained or intermittent high-intensity events, hot and humid environments) are needed. Increases in subjective sensations of fatigue may be the result of loss of sleep or disruption of normal sleep patterns. Modifications to the competition timetable may minimise or even eliminate any effect on performance in sport, but there may be negative effects on performance in some events.

Maximal power and performance during a swim taper.

This study examined how altering training intensity during a taper impacts maximal mechanical power (Pmax), torque at power maximum (T), velocity at power maximum (V), and swim performance (m . sec (-1)). Using an arm ergometer with inertial loading, measurements of Pmax, T, and V were made for 7 consecutive weeks prior to the taper and during the taper in 7 female competitive collegiate swimmers. Subjects were tested over two consecutive years. Swim performance was obtained from 3 competitive meets; a conference meet (CM), the conference championship meet (CONF) and the national championship meet (NAT). A 50 to 60 % increase in the amount of "high-intensity training" during the taper of 2005 (High-Intensity Taper - HIT) resulted in Pmax values that were 8 to 14 % higher (40 to 60 Watts) at all but one time point when compared to the 2004 taper (Low-Intensity Taper - LIT). Swim performance was significantly worsened at the NAT following LIT. However, with the HIT, swim performance, Pmax, and T were maintained prior to and at NAT. A large reduction in high-intensity training during a taper reduces the length of time that Pmax, T, and swim performance can be maintained at peak levels.

Cardiovascular drift during prolonged exercise: new perspectives.

We propose that cardiovascular drift, characterized by a progressive decline in stroke volume after 10-20 min of exercise, is primarily due to increased heart rate rather tahn a progressive increase in cutaneous blood flow as body temperature rises.

Effects of beta-adrenergic receptor stimulation and blockade on substrate metabolism during submaximal exercise.

We used beta-adrenergic receptor stimulation and blockade as a tool to study substrate metabolism during exercise. Eight moderately trained subjects cycled for 60 min at 45% of VO(2 peak) 1) during a control trial (CON); 2) while epinephrine was intravenously infused at 0.015 microg. kg(-1) x min(-1) (beta-STIM); 3) after ingesting 80 mg of propranolol (beta-BLOCK); and 4) combining beta-BLOCK with intravenous infusion of Intralipid-heparin to restore plasma fatty acid (FFA) levels (beta-BLOCK+LIPID). beta-BLOCK suppressed lipolysis (i.e., glycerol rate of appearance) and fat oxidation while elevating carbohydrate oxidation above CON (135 +/- 11 vs. 113 +/- 10 micromol x kg(-1) x min(-1); P < 0.05) primarily by increasing rate of disappearance (R(d)) of glucose (36 +/- 2 vs. 22 +/- 2 micromol x kg(-1) x min(-1); P < 0.05). Plasma FFA restoration (beta-BLOCK+LIPID) attenuated the increase in R(d) glucose by more than one-half (28 +/- 3 micromol x kg(-1) x min(-1); P < 0.05), suggesting that part of the compensatory increase in muscle glucose uptake is due to reduced energy from fatty acids. On the other hand, beta-STIM markedly increased glycogen oxidation and reduced glucose clearance and fat oxidation despite elevating plasma FFA. Therefore, reduced plasma FFA availability with beta-BLOCK increased R(d) glucose, whereas beta-STIM increased glycogen oxidation, which reduced fat oxidation and glucose clearance. In summary, compared with control exercise at 45% VO(2 peak) (CON), both beta-BLOCK and beta-STIM reduced fat and increased carbohydrate oxidation, albeit through different mechanisms.

Low-fat diet alters intramuscular substrates and reduces lipolysis and fat oxidation during exercise.

We determined whether a low-fat diet reduces intramuscular triglyceride (IMTG) concentration, whole body lipolyis, total fat oxidation, and calculated nonplasma fatty acid (FA) oxidation during exercise. Seven endurance-trained cyclists were studied over a 3-wk period during which time they exercised 2 h/day at 70% of maximum O2 uptake VO(2 max) and consumed approximately 4,400 kcal/day. During the 1st wk, their fat intake provided 32% of energy. During the 2nd and 3rd wk, they were randomly assigned to eat 2 or 22% of energy from fat (2%FAT or 22%FAT). Compared with 22%FAT, 2%FAT lowered IMTG concentration and raised muscle glycogen concentration at rest (P < 0.05). Metabolism was studied during 1 h of exercise at 67% VO(2 max) performed in the fasted state. 2%FAT resulted in a 27% reduction (P < 0.05) in total fat oxidation vs. 22%FAT without altering the stable isotopically determined rates of plasma free fatty acid or glucose disappearance. Therefore, 2%FAT reduced calculated nonplasma FA oxidation by 40% in association with a 19% reduction in whole body lipolysis while increasing calculated minimal muscle glycogen oxidation compared with 22%FAT (all P < 0.05). In summary, an extremely low fat (2% of energy) and high-carbohydrate diet lowers whole body lipolysis, total fat oxidation, and nonplasma FA oxidation during exercise in the fasted state in association with a reduced concentration of intramuscular triglyceride.

Time course of learning to produce maximum cycling power.

The purpose of this investigation was to determine the time course and magnitude of learning effects associated with repeated maximum cycling power tests and to determine if cycle-trained men exhibit different learning effects than active men who are not cycle-trained. Cycle-trained (N = 13) and active men (N = 35) performed short maximal cycling bouts 4 times per day for 4 consecutive days. Inertial load cycle ergometry was used to measure maximum power and pedaling rate at maximum power. Maximum power of the cycle-trained men did not differ across days or bouts. Maximum power of the active men increased 7 % within the first day and 7 % from the mean of day one to day three. Pedaling rate at maximum power did not differ across days or bouts in either the cycle-trained or active men. These results demonstrate that valid and reliable results for maximum cycling power can be obtained from cycle-trained men in a single day, whereas active men require at least 2 days of practice in order to produce valid and reliable values.

Physical activity as a metabolic stressor.

Both physical activity and diet stimulate processes that, over time, alter the morphologic composition and biochemical function of the body. Physical activity provides stimuli that promote very specific and varied adaptations according to the type, intensity, and duration of exercise performed. There is further interest in the extent to which diet or supplementation can enhance the positive stimuli. Prolonged walking at low intensity presents little metabolic, hormonal, or cardiovascular stress, and the greatest perturbation from rest appears to be from increased fat oxidation and plasma free fatty acid mobilization resulting from a combination of increased lipolysis and decreased reesterification. More intense jogging or running largely stimulates increased oxidation of glycogen and triacylglycerol, both of which are stored directly within the muscle fibers. Furthermore, these intramuscular stores of carbohydrate and fat appear to be the primary substrates for the enhanced oxidative and performance ability derived from endurance training-induced increases in muscle mitochondrial density. Weightlifting that produces fatigue in brief periods (ie, in 15-90 s and after 15 repetitive contractions) elicits a high degree of motor unit recruitment and muscle fiber stimulation. This is a remarkably potent stimulus for altering protein synthesis in muscle and increasing neuromuscular function. The metabolic stress of physical activity can be measured by substrate turnover and depletion, cardiovascular response, hormonal perturbation, accumulation of metabolites, or even the extent to which the synthesis and degradation of specific proteins are altered, either acutely or by chronic exercise training.

Substrate metabolism during different exercise intensities in endurance-trained women.

We have studied eight endurance-trained women at rest and during exercise at 25, 65, and 85% of maximal oxygen uptake. The rate of appearance (R(a)) of free fatty acids (FFA) was determined by infusion of [(2)H(2)]palmitate, and fat oxidation rates were determined by indirect calorimetry. Glucose kinetics were assessed with [6,6-(2)H(2)]glucose. Glucose R(a) increased in relation to exercise intensity. In contrast, whereas FFA R(a) was significantly increased to the same extent in low- and moderate-intensity exercise, during high-intensity exercise, FFA R(a) was reduced compared with the other exercise values. Carbohydrate oxidation increased progressively with exercise intensity, whereas the highest rate of fat oxidation was during exercise at 65% of maximal oxygen uptake. After correction for differences in lean body mass, there were no differences between these results and previously reported data in endurance-trained men studied under the same conditions, except for slight differences in glucose metabolism during low-intensity exercise (Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, and Wolfe RR. Am J Physiol Endocrinol Metab 265: E380-E391, 1993). We conclude that the patterns of changes in substrate kinetics during moderate- and high-intensity exercise are similar in trained men and women.

Effects of plasma epinephrine on fat metabolism during exercise: interactions with exercise intensity.

This study determined the effects of elevated plasma epinephrine on fat metabolism during exercise. On four occasions, seven moderately trained subjects cycled at 25% of peak oxygen consumption (VO(2 peak)) for 60 min. After 15 min of exercise, subjects were intravenously infused with low (0.96 +/- 0.10 nM), moderate (1.92 +/- 0.24 nM), or high (3.44 +/- 0.50 nM) levels (all P < 0.05) of epinephrine to increase plasma epinephrine above control (Con; 0.59 +/- 0.10 nM). During the interval between 35 and 55 min of exercise, lipolysis [i.e., rate of appearance of glycerol] increased above Con (4.9 +/- 0.5 micromol. kg(-1). min(-1)) with low, moderate, and high (6.5 +/- 0.5, 7.1 +/- 0.8, and 10.6 +/- 1.2 micromol. kg(-1). min(-1), respectively; all P < 0.05) levels of epinephrine despite simultaneous increases in plasma insulin. The release of fatty acid into plasma also increased progressively with the graded epinephrine infusions. However, fatty acid oxidation was lower than Con (11.1 +/- 0.8 micromol. kg(-1). min(-1)) during moderate and high levels (8.7 +/- 0.7 and 8.1 +/- 0.9 micromol. kg(-1). min(-1), respectively; P < 0.05). In one additional trial, the same subjects exercised at 45% VO(2 peak) without epinephrine infusion, which produced a plasma epinephrine concentration identical to low levels. However, lipolysis was lower (i.e., 5.5 +/- 0.6 vs. 6.5 +/- 0.5 micromol. kg(-1). min(-1); P < 0.05). In conclusion, elevations in plasma epinephrine concentration during exercise at 25% of VO(2 peak) progressively increase whole body lipolysis but decrease fatty acid oxidation. Last, increasing exercise intensity from 25 to 45% VO(2 peak) attenuates the lipolytic actions of epinephrine.

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.

Water and carbohydrate ingestion during prolonged exercise increase maximal neuromuscular power.

This study investigated the individual and combined effects of water and carbohydrate ingestion during prolonged cycling on maximal neuromuscular power (P(max)), thermoregulation, cardiovascular function, and metabolism. Eight endurance-trained cyclists exercised for 122 min at 62% maximal oxygen uptake in a 35 degrees C environment (50% relative humidity, 2 m/s fan speed). P(max) was measured in triplicate during 6-min periods beginning at 26, 56, 86, and 116 min. On four different occasions, immediately before and during exercise, subjects ingested 1) 3.28 +/- 0.21 liters of water with no carbohydrate (W); 2) 3.39 +/- 0.23 liters of a solution containing 204 +/- 14 g of carbohydrate (W+C); 3) 204 +/- 14 g of carbohydrate in only 0.49 +/- 0.03 liter of solution (C); and 4) 0. 37 +/- 0.02 liter of water with no carbohydrate (placebo; Pl). These treatments were randomized, disguised, and presented double blind. At 26 min of exercise, P(max) was similar in all trials. From 26 to 116 min, P(max) declined 15.2 +/- 3.3 and 14.5 +/- 2.1% during C and Pl, respectively; 10.4 +/- 1.9% during W (W > C, W > Pl; P < 0.05); and 7.4 +/- 2.2% during W+C (W+C > W, W+C > C, and W+C > Pl; P < 0. 05). As an interesting secondary findings, we also observed that carbohydrate ingestion increased heat production, final core temperature, and whole body sweating rate. We conclude that, during prolonged moderate-intensity exercise in a warm environment, ingestion of W attenuates the decline in P(max). Furthermore, ingestion of W+C attenuates the decline in maximal power more than does W alone, and ingestion of C alone does not attenuate the decline in P(max) compared with Pl.

Cutaneous blood flow during exercise is higher in endurance-trained humans.

This study determined whether cutaneous blood flow during exercise is different in endurance-trained (Tr) compared with untrained (Untr) subjects. Ten Tr and ten Untr men (62.4 +/- 1.7 and 44.2 +/- 1.8 ml. kg(-1). min(-1), respectively; P < 0.05) underwent three 20-min cycling-exercise bouts at 50, 70, and 90% peak oxygen uptake in this order, with 30 min rest in between. The environmental conditions were neutral ( approximately 23-24 degrees C, 50% relative humidity, front and back fans at 2.5 m/s). Because of technical difficulties, only seven Tr and seven Untr subjects completed all forearm blood flow and laser-Doppler cutaneous blood flow (CBF) measurements. Albeit similar at rest, at the end of all three exercise bouts, forearm blood flow was approximately 40% higher in Tr compared with Untr subjects (50%: 4.64 +/- 0.50 vs. 3. 17 +/- 0.20, 70%: 6.17 +/- 0.61 vs. 4.41 +/- 0.37, 90%: 6.77 +/- 0. 62 vs. 5.01 +/- 0.37 ml. 100 ml(-1). min(-1), respectively; n = 7; all P < 0.05). CBF was also higher in Tr compared with Untr subjects at all relative intensities (n = 7; all P < 0.05). However, esophageal temperature was not different in Tr compared with Untr subjects at the end of any of the aforementioned exercise bouts (50%: 37.8 +/- 0.1 vs. 37.9 +/- 0.1 degrees C, 70%: 38.1 +/- 0.1 vs. 38.1 +/- 0.1 degrees C, and 90%: 38.8 +/- 0.1 vs. 38.6 +/- 0.1 degrees C, respectively). We conclude that a higher CBF may allow Tr subjects to achieve an esophageal temperature similar to that of Untr, despite their higher metabolic rates and thus higher heat production rates, during exercise at 50-90% peak oxygen uptake.

Preexercise medium-chain triglyceride ingestion does not alter muscle glycogen use during exercise.

This investigation determined whether ingestion of a tolerable amount of medium-chain triglycerides (MCT; approximately 25 g) reduces the rate of muscle glycogen use during high-intensity exercise. On two occasions, seven well-trained men cycled for 30 min at 84% maximal O(2) uptake. Exactly 1 h before exercise, they ingested either 1) carbohydrate (CHO; 0.72 g sucrose/kg) or 2) MCT+CHO [0.36 g tricaprin (C10:0)/kg plus 0.72 g sucrose/kg]. The change in glycogen concentration was measured in biopsies taken from the vastus lateralis before and after exercise. Additionally, glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the rate of glucose disappearance from plasma (R(d) glucose), as measured by stable isotope dilution techniques. The change in muscle glycogen concentration was not different during MCT+CHO and CHO (42.0 +/- 4.6 vs. 38.8 +/- 4.0 micromol glucosyl units/g wet wt). Furthermore, calculated glycogen oxidation was also similar (331 +/- 18 vs. 329 +/- 15 micromol. kg(-1). min(-1)). The coingestion of MCT+CHO did increase (P < 0.05) R(d) glucose at rest compared with CHO (26.9 +/- 1.5 vs. 20.7 +/- 0. 7 micromol.kg(-1). min(-1)), yet during exercise R(d) glucose was not different during the two trials. Therefore, the addition of a small amount of MCT to a preexercise CHO meal did not reduce muscle glycogen oxidation during high-intensity exercise, but it did increase glucose uptake at rest.

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia.

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (VO(2 max)) 4.7 +/- 0. 4 l/min (mean +/- SE)] cycled for 30 min in the heat (35 degrees C) in the upright and in the supine positions (VO(2) 2.93 +/- 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (T(es)) was 37. 8-38.0 degrees C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (T(es) = 38. 7-38.8 degrees C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 +/- 6 ml, 3.0 +/- 0.7 l/min, 6 +/- 2 mmHg, 22 +/- 8%, 14 +/- 2 beats/min, and 50-96%, respectively; all P < 0. 05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 +/- 2 vs. 9 +/- 1%) and the reductions in SV (13 +/- 4 vs. 21 +/- 3%) and cardiac output (8 +/- 3 vs. 14 +/- 3%) (all P < 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

Substrate metabolism when subjects are fed carbohydrate during exercise.

This study determined the effect of carbohydrate ingestion during exercise on the lipolytic rate, glucose disappearance from plasma (Rd Glc), and fat oxidation. Six moderately trained men cycled for 2 h on four separate occasions. During two trials, they were fed a high-glycemic carbohydrate meal during exercise at 30 min (0.8 g/kg), 60 min (0.4 g/kg), and 90 min (0.4 g/kg); once during low-intensity exercise [25% peak oxygen consumption (VO2 peak)] and once during moderate-intensity exercise (68% VO2 peak). During two additional trials, the subjects remained fasted (12-14 h) throughout exercise at each intensity. After 55 min of low-intensity exercise in fed subjects, hyperglycemia (30% increase) and a threefold elevation in plasma insulin concentration (P < 0.05) were associated with a 22% suppression of lipolysis compared with when subjects were fasted (5.2 +/- 0.5 vs. 6.7 +/- 1.2 micromol. kg-1. min-1, P < 0.05), but fat oxidation was not different from fasted levels at this time. Fat oxidation when subjects were fed carbohydrate was not reduced below fasting levels until 80-90 min of exercise, and lipolysis was in excess of fat oxidation at this time. The reduction in fat oxidation corresponded in time with the increase in Rd Glc. During moderate-intensity exercise, the very small elevation in plasma insulin concentration (approximately 3 microU/ml; P < 0.05) during the second hour of exercise when subjects were fed vs. when they were fasted slightly attenuated lipolysis (P < 0.05) but did not increase Rd Glc or suppress fat oxidation. These findings indicate that despite a suppression of lipolysis after carbohydrate ingestion during exercise, the lipolytic rate remained in excess and thus did not limit fat oxidation. Under these conditions, a reduction in fat oxidation was associated in time with an increase in glucose uptake.

Stroke volume decline during prolonged exercise is influenced by the increase in heart rate.

This study determined whether the decline in stroke volume (SV) during prolonged exercise is related to an increase in heart rate (HR) and/or an increase in cutaneous blood flow (CBF). Seven active men cycled for 60 min at approximately 57% peak O2 uptake in a neutral environment (i.e., 27 degrees C, <40% relative humidity). They received a placebo control (CON) or a small oral dose (i.e., approximately 7 mg) of the beta1-adrenoceptor blocker atenolol (BB) at the onset of exercise. At 15 min, HR and SV were similar during CON and BB. From 15 to 55 min during CON, a 13% decline in SV was associated with an 11% increase in HR and not with an increase in CBF. CBF increased mainly from 5 to 15 min and remained stable from 20 to 60 min of exercise in both treatments. However, from 15 to 55 min during BB, when the increase in HR was prevented by atenolol, the decline in SV was also prevented, despite a normal CBF response (i.e., similar to CON). Cardiac output was similar in both treatments and stable throughout the exercise bouts. We conclude that during prolonged exercise in a neutral environment the decline in SV is related to the increase in HR and is not affected by CBF.

Physiological determinants of endurance exercise performance.

Performance in endurance events is typically evaluated by the power or velocity that can be maintained for durations of 30 min. to four hours. The two main by-products of intense and prolonged oxidative metabolism that can limit performance are the accumulation of hydrogen ion (i.e. lactic acidosis) and heat (i.e. hyperthermia). A model for endurance performance is presented that revolves around identification of the lactate threshold velocity which is presented as a function of numerous morphological components as well as gross mechanical efficiency. When cycling at 80 RPM, gross mechanical efficiency is positively related to Type I muscle fiber composition, which has great potential to improve endurance performance. Endurance performance can also be influenced by altering the availability of oxygen and blood glucose during exercise. The latter need forms the basis for ingesting carbohydrate at 30-60 grams per hour during exercise. In laboratory simulations of performance, athletes fatigue due to hyperthermia when esophageal is approximately 40 degrees C, in association with near maximal heart rate and perceived exertion. It is likely that the central nervous system is involved in the aetiology of fatigue from hyperthermia. Dehydration during exercise promotes hyperthermia by reducing skin blood flow, sweating rate and thus heat dissipation. The combination of dehydration and hyperthermia during exercise causes large reductions in cardiac output and blood flow to the exercising musculature, and thus has a large potential to impair endurance performance. Endurance performance is optimized when training is aimed specifically at developing individual components of the model presented and nutritional supplementation prevents hypoglycemia and attenuates dehydration and hyperthermia. Indeed, the challenge at the transition to a new millennium is to synergistically integrate these physiological factors in training and competition.

Cardiovascular drift during prolonged exercise and the effects of dehydration.

Reductions in SV are the most striking component of "classic" CV drift as well as "dehydration induced" CV drift. Direct data for the widespread notion that increased skin blood flow causes SV to be reduced during "classic" CV drift is rather scarce. Reductions in SV due to dehydration and concomitant hyperthermia are clearly not due to increases in skin blood flow. Instead, skin blood flow declines as skin and systemic vascular resistance increase as the CV system attempts to cope with the severe challenge of large reductions in cardiac output. Approximately one-half of the reduction in SV is due to reduced blood volume from dehydration during exercise which produces hyperthermia. The remaining reduction in SV with dehydration and hyperthermia appears to be related to additional factors such as hyperthermia and their interaction with factors that further reduce ventricular filling, such as heart rate acceleration.