Effects of hyperthermia on cerebral blood flow and metabolism during prolonged exercise in humans.

The development of hyperthermia during prolonged exercise in humans is associated with various changes in the brain, but it is not known whether the cerebral metabolism or the global cerebral blood flow (gCBF) is affected. Eight endurance-trained subjects completed two exercise bouts on a cycle ergometer. The gCBF and cerebral metabolic rates of oxygen, glucose, and lactate were determined with the Kety-Schmidt technique after 15 min of exercise when core temperature was similar across trials, and at the end of exercise, either when subjects remained normothermic (core temperature = 37.9 degrees C; control) or when severe hyperthermia had developed (core temperature = 39.5 degrees C; hyperthermia). The gCBF was similar after 15 min in the two trials, and it remained stable throughout control. In contrast, during hyperthermia gCBF decreased by 18% and was therefore lower in hyperthermia compared with control at the end of exercise (43 +/- 4 vs. 51 +/- 4 ml. 100 g(-1). min(-1); P < 0.05). Concomitant with the reduction in gCBF, there was a proportionally larger increase in the arteriovenous differences for oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared with control. The hyperthermia-induced lowering of gCBF did not alter cerebral lactate release. The hyperthermia-induced reduction in exercise cerebral blood flow seems to relate to a concomitant 18% lowering of arterial carbon dioxide tension, whereas the higher cerebral metabolic rate of oxygen may be ascribed to a Q(10) (temperature) effect and/or the level of cerebral neuronal activity associated with increased exertion.     

Cerebral metabolic response to submaximal exercise.

We studied cerebral oxygenation and metabolism during submaximal cycling in 12 subjects. At two work rates, middle cerebral artery blood velocity increased from 62 +/- 3 to 63 +/- 3 and 70 +/- 5 cm/s as did cerebral oxygenation determined by near-infrared spectroscopy. Oxyhemoglobin increased by 10 +/- 3 and 25 +/- 3 micromol/l (P < 0. 01), and there was no significant change in brain norepinephrine spillover. The arterial-to-internal-jugular-venous (a-v) difference for O(2) decreased at low-intensity exercise (from 3.1 +/- 0.1 to 2. 9 +/- 0.1 mmol/l; P < 0.05) and recovered at moderate exercise (to 3. 3 +/- 0.1 mmol/l). The profile for glucose was similar: its a-v difference tended to decrease at low-intensity exercise (from 0.55 +/- 0.05 to 0.50 +/- 0.02 mmol/l) and increased during moderate exercise (to 0.64 +/- 0.04 mmol/l; P < 0.05). Thus the molar ratio (a-v difference, O(2) to glucose) did not change significantly. However, when the a-v difference for lactate (0.02 +/- 0.03 to 0.18 +/- 0.04 mmol/l) was taken into account, the O(2)-to-carbohydrate ratio decreased (from 6.1 +/- 0.4 to 4.7 +/- 0.3; P < 0.05). The enhanced cerebral oxygenation suggests that, during exercise, cerebral blood flow increases in excess of the O(2) demand. Yet it seems that during exercise not all carbohydrate taken up by the brain is oxidized, as brain lactate metabolism appears to lower the balance of O(2)-to-carbohydrate uptake.     

Effect of carbohydrate ingestion on exercise metabolism

Five male cyclists were studied during 2 h of cycle ergometer exercise (70% VO2 max) on two occasions to examine the effect of carbohydrate ingestion on muscle glycogen utilization. In the experimental trial (CHO) subjects ingested 250 ml of a glucose polymer solution containing 30 g of carbohydrate at 0, 30, 60, and 90 min of exercise; in the control trial (CON) they received an equal volume of a sweet placebo. No differences between trials were seen in O2 uptake or heart rate during exercise. Venous blood glucose was similar before exercise in both trials, but, on average, was higher during exercise in CHO [5.2 +/- 0.2 (SE) mmol/l] compared with CON (4.8 +/- 0.1, P less than 0.05). Plasma insulin levels were similar in both trials. Muscle glycogen levels were also similar in CHO and CON both before and after exercise; accordingly, there was no difference between trials in the amount of glycogen used during the 2 h of exercise (CHO = 62.8 +/- 10.1 mmol/kg wet wt, CON = 56.9 +/- 10.1). The results of this study indicate that carbohydrate ingestion does not influence the utilization of muscle glycogen during prolonged strenuous exercise.     

The effect of face fanning during recovery from exercise hyperthermia

Hyperthermia was induced in nine subjects on two separate occasions by a progressive treadmill run, which resulted in an average esophageal temperature (Tes) of 39.77 +/- 0.07 degree C after 30-57 min. Fanning the face during exercise to simulate conditions during running (wind at 3.75 m X s-1) maintained a tympanic temperature (Tty) that was lower than Tes; the difference was 1.5 degrees C at the end of exercise. In one session, face fanning was interrupted at the end of running, whereas in the other it was maintained for 15 min after exercise stopped. Face fanning had no significant influence on the fall of Tes during recovery, but it markedly influenced the course of Tty during this period. When face fanning was stopped at the end of the run, Tty rose by nearly 0.5 degree C, peaked after 4.5 min, and thereafter decreased slowly to a value close to Tes. In contrast, when face fanning was maintained throughout the recovery period, Tty rose only slightly (0.1 degree C) and remained significantly lower than Tes at all times. The results suggest that following hyperthermic exercise, face fanning could be helpful in preventing acute cerebral hyperthermia.     

Effects of L-tyrosine and carbohydrate ingestion on endurance exercise performance.

To test the effects of tyrosine ingestion with or without carbohydrate supplementation on endurance performance, nine competitive cyclists cycled at 70% peak oxygen uptake for 90 min under four different feeding conditions followed immediately by a time trial. At 30-min intervals, beginning 60 min before exercise, each subject consumed either 5 ml/kg body wt of water sweetened with aspartame [placebo (Pla)], polydextrose (70 g/l) (CHO), L-tyrosine (25 mg/kg body wt) (Tyr), or polydextrose (70 g/l) and L-tyrosine (25 mg/kg body wt) (CHO+Tyr). The experimental trials were given in random order and were carried out by using a counterbalanced double-blind design. No differences were found between treatments for oxygen uptake, heart rate, or rating of perceived exertion at any time during the 90-min ride. Plasma tyrosine rose significantly from 60 min before exercise to test termination (TT) in Tyr (means +/- SE) (480 +/- 26 micromol) and CHO+Tyr (463 +/- 34 micromol) and was significantly higher in these groups from 30 min before exercise to TT vs. CHO (90 +/- 3 micromol) and Pla (111 +/- 7 micromol) (P < 0.05). Plasma free tryptophan was higher after 90 min of exercise, 15 min into the endurance time trial, and at TT in Tyr (10.1 +/- 0.9, 10.4 +/- 0.8, and 12.0 +/- 0.9 micromol, respectively) and Pla (9.7 +/- 0.5, 10.0 +/- 0.3, and 11.7 +/- 0.5 micromol, respectively) vs. CHO (7.8 +/- 0.5, 8.6 +/- 0.5, and 9.3 +/- 0.6 micromol, respectively) and CHO+Tyr (7.8 +/- 0.5, 8.5 +/- 0.5, 9.4 +/- 0.5 micromol, respectively) (P < 0.05). The plasma tyrosine-to-free tryptophan ratio was significantly higher in Tyr and CHO+Tyr vs. CHO and Pla from 30 min before exercise to TT (P < 0.05). CHO (27.1 +/- 0.9 min) and CHO+Tyr (26.1 +/- 1.1 min) treatments resulted in a reduced time to complete the endurance time trial compared with Pla (34.4 +/- 2.9 min) and Tyr (32.6 +/- 3.0 min) (P < 0.05). These findings demonstrate that tyrosine ingestion did not enhance performance during a cycling time trial after 90 min of steady-state exercise.     

Effect of carbohydrate ingestion on glucose kinetics during exercise in the heat.

Six endurance-trained men [peak oxygen uptake (V(O(2))) = 4.58 +/- 0.50 (SE) l/min] completed 60 min of exercise at a workload requiring 68 +/- 2% peak V(O(2)) in an environmental chamber maintained at 35 degrees C (<50% relative humidity) on two occasions, separated by at least 1 wk. Subjects ingested either a 6% glucose solution containing 1 microCi [3-(3)H]glucose/g glucose (CHO trial) or a sweet placebo (Con trial) during the trials. Rates of hepatic glucose production [HGP = glucose rate of appearance (R(a)) in Con trial] and glucose disappearance (R(d)), were measured using a primed, continuous infusion of [6,6-(2)H]glucose, corrected for gut-derived glucose (gut R(a)) in the CHO trial. No differences in heart rate, V(O(2)), respiratory exchange ratio, or rectal temperature were observed between trials. Plasma glucose concentrations were similar at rest but increased (P < 0.05) to a greater extent in the CHO trial compared with the Con trial. This was due to the absorption of ingested glucose in the CHO trial, because gut R(a) after 30 and 50 min (16 +/- 5 micromol. kg(-1). min(-1)) was higher (P < 0.05) compared with rest, whereas HGP during exercise was not different between trials. Glucose R(d) was higher (P < 0.05) in the CHO trial after 30 and 50 min (48.0 +/- 6.3 vs 34.6 +/- 3.8 micromol. kg(-1). min(-1), CHO vs. Con, respectively). These results indicate that ingestion of carbohydrate, at a rate of approximately 1.0 g/min, increases glucose R(d) but does not blunt the rise in HGP during exercise in the heat.     

Effect of carbohydrate supplements and water on exercise metabolism in the heat

Carbohydrate (CHO) supplements of different concentrations were compared with water to determine their effects on thermal regulation and plasma volume maintenance while subjects exercised for 2 h in the heat and to determine their impact on carbohydrate utilization. Trained cyclists (n = 12) rode at 48.8 +/- 0.8% maximal O2 consumption in an environmental chamber maintained at 33.0 +/- 0.1 degree C and 51.7 +/- 1.4% relative humidity on three separate occasions. During each exercise bout the subjects received 3 ml/kg body wt of H2O, a 2.0% glucose polymer (LC) solution, or an 8.5% glucose polymer (HC) solution every 15 min. Muscle biopsies from the vastus lateralis were obtained before and after the H2O and HC trials only. Rectal temperature and heart rate, but not O2 consumption, rose from the 10- to 120-min period of exercise. No differences among treatments were found for these variables. There were also no significant differences among treatments for percent changes in plasma volume and blood volume. Plasma glucose and insulin were unchanged during the H2O and LC trials but were significantly elevated during the HC trial. In addition, CHO oxidation was significantly greater during the HC trial than during the H2O trial from 60 to 120 min of exercise. However, the reduction in muscle glycogen during the HC trial (206.5 +/- 23.6 mumol/g protein) was significantly less (P less than 0.05) than during the H2O trial (342.3 +/- 41.9 mumol/g protein).(ABSTRACT TRUNCATED AT 250 WORDS)     

Early postexercise muscle glycogen recovery is enhanced with a carbohydrate-protein supplement.

In the present study, we tested the hypothesis that a carbohydrate-protein (CHO-Pro) supplement would be more effective in the replenishment of muscle glycogen after exercise compared with a carbohydrate supplement of equal carbohydrate content (LCHO) or caloric equivalency (HCHO). After 2.5 +/- 0.1 h of intense cycling to deplete the muscle glycogen stores, subjects (n = 7) received, using a rank-ordered design, a CHO-Pro (80 g CHO, 28 g Pro, 6 g fat), LCHO (80 g CHO, 6 g fat), or HCHO (108 g CHO, 6 g fat) supplement immediately after exercise (10 min) and 2 h postexercise. Before exercise and during 4 h of recovery, muscle glycogen of the vastus lateralis was determined periodically by nuclear magnetic resonance spectroscopy. Exercise significantly reduced the muscle glycogen stores (final concentrations: 40.9 +/- 5.9 mmol/l CHO-Pro, 41.9 +/- 5.7 mmol/l HCHO, 40.7 +/- 5.0 mmol/l LCHO). After 240 min of recovery, muscle glycogen was significantly greater for the CHO-Pro treatment (88.8 +/- 4.4 mmol/l) when compared with the LCHO (70.0 +/- 4.0 mmol/l; P = 0.004) and HCHO (75.5 +/- 2.8 mmol/l; P = 0.013) treatments. Glycogen storage did not differ significantly between the LCHO and HCHO treatments. There were no significant differences in the plasma insulin responses among treatments, although plasma glucose was significantly lower during the CHO-Pro treatment. These results suggest that a CHO-Pro supplement is more effective for the rapid replenishment of muscle glycogen after exercise than a CHO supplement of equal CHO or caloric content.     

Combined ingestion of protein and carbohydrate improves protein balance during ultra-endurance exercise

The aims of this study were to compare different tracer methods to assess whole body protein turnover during 6 h of prolonged endurance exercise when carbohydrate was ingested throughout the exercise period and to investigate whether addition of protein can improve protein balance. Eight endurance-trained athletes were studied on two different occasions at rest (4 h), during 6 h of exercise at 50% of maximal O2 uptake (in sequential order: 2.5 h of cycling, 1 h of running, and 2.5 h of cycling), and during subsequent recovery (4 h). Subjects ingested carbohydrate (CHO trial; 0.7 g CHO.kg(-1.)h(-1)) or carbohydrate/protein beverages (CHO + PRO trial; 0.7 g CHO.kg(-1).h(-1) and 0.25 g PRO.kg(-1).h(-1)) at 30-min intervals during the entire study. Whole body protein metabolism was determined by infusion of L-[1-13C]leucine, L-[2H5]phenylalanine, and [15N2]urea tracers with sampling of blood and expired breath. Leucine oxidation increased from rest to exercise [27 +/- 2.5 vs. 74 +/- 8.8 (CHO) and 85 +/- 9.5 vs. 200 +/- 16.3 mg protein.kg(-1).h(-1) (CHO + PRO), P < 0.05], whereas phenylalanine oxidation and urea production did not increase with exercise. Whole body protein balance during exercise with carbohydrate ingestion was negative (-74 +/- 8.8, -17 +/- 1.1, and -72 +/- 5.7 mg protein.kg(-1).h(-1)) when L-[1-13C]leucine, L-[2H5]phenylalanine, and [15N2]urea, respectively, were used as tracers. Addition of protein to the carbohydrate drinks resulted in a positive or less-negative protein balance (-32 +/- 16.3, 165 +/- 4.6, and 151 +/- 13.4 mg protein.kg(-1).h(-1)) when L-[1-13C]leucine, L-[2H5]phenylalanine, and [15N2]urea, respectively, were used as tracers. We conclude that, even during 6 h of exhaustive exercise in trained athletes using carbohydrate supplements, net protein oxidation does not increase compared with the resting state and/or postexercise recovery. Combined ingestion of protein and carbohydrate improves net protein balance at rest as well as during exercise and postexercise recovery.     

Hyperthermia and central fatigue during prolonged exercise in humans.

The present study investigated the effects of hyperthermia on the contributions of central and peripheral factors to the development of neuromuscular fatigue. Fourteen men exercised at 60% maximal oxygen consumption on a cycle ergometer in hot (40 degrees C; hyperthermia) and thermoneutral (18 degrees C; control) environments. In hyperthermia, the core temperature increased throughout the exercise period and reached a peak value of 40.0 +/- 0.1 degrees C (mean +/- SE) at exhaustion after 50 +/- 3 min of exercise. In control, core temperature stabilized at approximately 38.0 +/- 0.1 degrees C, and exercise was maintained for 1 h without exhausting the subjects. Immediately after the cycle trials, subjects performed 2 min of sustained maximal voluntary contraction (MVC) either with the exercised legs (knee extension) or with a "nonexercised" muscle group (handgrip). The degree of voluntary activation during sustained maximal knee extensions was assessed by superimposing electrical stimulation (EL) to nervus femoralis. Voluntary knee extensor force was similar during the first 5 s of contraction in hyperthermia and control. Thereafter, force declined in both trials, but the reduction in maximal voluntary force was more pronounced in the hyperthermic trial, and, from 30 to 120 s, the force was significantly lower in hyperthermia compared with control. Calculation of the voluntary activation percentage (MVC/MVC + EL) revealed that the degree of central activation was significantly lower in hyperthermia (54 +/- 7%) compared with control (82 +/- 6%). In contrast, total force of the knee extensors (MVC + force from EL) was not different in the two trials. Force development during handgrip contraction followed the same pattern of response as was observed for the knee extensors. In conclusion, these data demonstrate that the ability to generate force during a prolonged MVC is attenuated with hyperthermia, and the impaired performance is associated with a reduction in the voluntary activation percentage.     

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).     

Exercise performance following a carbohydrate load in chronic airflow obstruction

We evaluated the effects of a large (920 cal) liquid carbohydrate (CHO) load on the maximum exercise capacity of 18 patients with chronic airflow obstruction [forced expiratory volume at at 1 s (FEV1) = 1.27 +/- 0.48 liters; FEV1/forced vital capacity = 0.41 +/- 0.11]. Patients underwent duplicate incremental cycle ergometer exercise tests to a symptom-limited maximum following CHO and a liquid placebo in single-blind fashion. Expired gas measurements were obtained during each power output. In 12 patients arterial blood gases were measured, and in six patients venous blood was obtained for measurement of glucose, electrolytes, and osmolality. With CHO, the maximum power output decreased from 86 +/- 30 to 76 +/- 31 W (P less than 0.001), whereas the ventilation at exhaustion was nearly identical (47.6 +/- 13.2 and 46.8 +/- 12.5 l/min). Arterial partial pressure of CO2 (PaCO2) at exhaustion decreased (P less than 0.025), arterial partial pressure of O2 (PaO2) increased (P less than 0.01), and the ventilatory equivalent for CO2 (VE/VCO2) increased (P less than 0.005) with CHO. At equivalent power outputs, CHO resulted in significant increases in VE (P less than 0.001) and VCO2 (P less than 0.001); PaCO2 was unchanged, whereas PaO2 increased (P less than 0.01). CHO increased the serum glucose at rest and during exercise. No changes in serum osmolality or electrolytes occurred during exercise following CHO. After CHO loading, the majority of patients appeared to reach their limiting level of ventilation at a lower power output. In contrast, there was no significant difference in the mean maximum power output with CHO in six normal control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Attenuated hepatosplanchnic uptake of lactate during intense exercise in humans.

We evaluated whether the increase in blood lactate with intense exercise is influenced by a low hepatosplanchnic blood flow as assessed by indocyanine green dye elimination and blood sampling from an artery and the hepatic vein in eight men. The hepatosplanchnic blood flow decreased from a resting value of 1.6 +/- 0.1 to 0.7 +/- 0.1 (SE) l/min during exercise. Yet the hepatosplanchnic O2 uptake increased from 67 +/- 3 to 93 +/- 13 ml/min, and the output of glucose increased from 1.1 +/- 0.1 to 2.1 +/- 0.3 mmol/min (P < 0.05). Even at the lowest hepatosplanchnic venous hemoglobin O2 saturation during exercise of 6%, the average concentration of glucose in arterial blood was maintained close to the resting level (5.2 +/- 0.2 vs. 5.5 +/- 0.2 mmol/l), whereas the difference between arterial and hepatic venous blood glucose increased to a maximum of 22 mmol/l. In arterial blood, the concentration of lactate increased from 1.1 +/- 0.2 to 6.0 +/- 1.0 mmol/l, and the hepatosplanchnic uptake of lactate was elevated from 0.4 +/- 0.06 to 1.0 +/- 0.05 mmol/min during exercise (P < 0.05). However, when the hepatosplanchnic venous hemoglobin O2 saturation became low, the arterial and hepatosplanchnic venous blood lactate difference approached zero. Even with a marked reduction in its blood flow, exercise did not challenge the ability of the liver to maintain blood glucose homeostasis. However, it appeared that the contribution of the Cori cycle decreased, and the accumulation of lactate in blood became influenced by the reduced hepatosplanchnic blood flow.     

Role of lungs and inactive muscle in acid-base control after maximal exercise

The pulmonary responses and changes in plasma acid-base status occurring across the inactive forearm muscle were examined after 30 s of intense exercise in six male subjects exercising on an isokinetic cycle ergometer. Arterial and deep forearm venous blood were sampled at rest and during 10 min after exercise; ventilation and pulmonary gas exchange variables were measured breath by breath during exercise and recovery. Immediately after exercise, ventilation and CO2 output increased to 124 +/- 17 1/min and 3.24 +/- 0.195 l/min, respectively. The subsequent decrease in CO2 output was slower than the decrease in O2 intake (half time of 105 +/- 15 and 47 +/- 4 s, respectively); the respiratory exchange ratio was greater than 1.0 throughout the 10 min of recovery. Arterial plasma concentrations of Na+, K+, and Ca2+ increased transiently after exercise. Arterial lactate ion concentration ([La-]) increased to 14-15 meq/l within 1.5 min and remained at this level for the rest of the study. Throughout recovery there was a positive arteriovenous [La-] difference of 4-5 meq/l, associated with an increase in the arteriovenous strong ion difference ([SID]) and by a large increase in the venous Pco2 and [HCO3-]. These findings were interpreted as indicating uptake of La- by the inactive muscle, leading to a fall in the muscle [SID] and increase in plasma [SID], associated with an increase in muscle PCO2. The venoarterial CO2 content difference was 38% greater than could be accounted for by metabolism of La- alone, suggesting liberation of CO2 stored in muscle, possibly as carbamate.(ABSTRACT TRUNCATED AT 250 WORDS)     

MCA Vmean and the arterial lactate-to-pyruvate ratio correlate during rhythmic handgrip.

Regulation of cerebral blood flow during physiological activation including exercise remains unknown but may be related to the arterial lactate-to-pyruvate (L/P) ratio. We evaluated whether an exercise-induced increase in middle cerebral artery mean velocity (MCA Vmean) relates to the arterial L/P ratio at two plasma lactate levels. MCA Vmean was determined by ultrasound Doppler sonography at rest, during 10 min of rhythmic handgrip exercise at approximately 65% of maximal voluntary contraction force, and during 20 min of recovery in seven healthy male volunteers during control and a approximately 15 mmol/l hyperglycemic clamp. Cerebral arteriovenous differences for metabolites were obtained by brachial artery and retrograde jugular venous catheterization. Control resting arterial lactate was 0.78 +/- 0.09 mmol/l (mean +/- SE) and pyruvate 55.7 +/- 12.0 micromol/l (L/P ratio 16.4 +/- 1.0) with a corresponding MCA Vmean of 46.7 +/- 4.5 cm/s. During rhythmic handgrip the increase in MCA Vmean to 51.2 +/- 4.6 cm/s was related to the increased L/P ratio (23.8 +/- 2.5; r2 = 0.79; P < 0.01). Hyperglycemia increased arterial lactate and pyruvate to 1.9 +/- 0.2 mmol/l and 115 +/- 4 micromol/l, respectively, but it did not significantly influence the L/P ratio or MCA Vmean at rest or during exercise. Conversely, MCA Vmean did not correlate significantly, neither to the arterial lactate nor to the pyruvate concentrations. These results support that the arterial plasma L/P ratio modulates cerebral blood flow during cerebral activation independently from the plasma glucose concentration.     

Muscle glycogen resynthesis during recovery from cycle exercise: no effect of additional protein ingestion.

In the present study, we have investigated the effect of carbohydrate and protein hydrolysate ingestion on muscle glycogen resynthesis during 4 h of recovery from intense cycle exercise. Five volunteers were studied during recovery while they ingested, immediately after exercise, a 600-ml bolus and then every 15 min a 150-ml bolus containing 1) 1.67 g. kg body wt(-1). l(-1) of sucrose and 0.5 g. kg body wt(-1). l(-1) of a whey protein hydrolysate (CHO/protein), 2) 1.67 g. kg body wt(-1). l(-1) of sucrose (CHO), and 3) water. CHO/protein and CHO ingestion caused an increased arterial glucose concentration compared with water ingestion during 4 h of recovery. With CHO ingestion, glucose concentration was 1-1.5 mmol/l higher during the first hour of recovery compared with CHO/protein ingestion. Leg glucose uptake was initially 0.7 mmol/min with water ingestion and decreased gradually with no measurable glucose uptake observed at 3 h of recovery. Leg glucose uptake was rather constant at 0.9 mmol/min with CHO/protein and CHO ingestion, and insulin levels were stable at 70, 45, and 5 mU/l for CHO/protein, CHO, and water ingestion, respectively. Glycogen resynthesis rates were 52 +/- 7, 48 +/- 5, and 18 +/- 6 for the first 1.5 h of recovery and decreased to 30 +/- 6, 36 +/- 3, and 8 +/- 6 mmol. kg dry muscle(-1). h(-1) between 1.5 and 4 h for CHO/protein, CHO, and water ingestion, respectively. No differences could be observed between CHO/protein and CHO ingestion ingestion. It is concluded that coingestion of carbohydrate and protein, compared with ingestion of carbohydrate alone, did not increase leg glucose uptake or glycogen resynthesis rate further when carbohydrate was ingested in sufficient amounts every 15 min to induce an optimal rate of glycogen resynthesis.     

Cardiovascular response to cycle exercise during and after pregnancy

Our purpose was to determine if pregnancy alters the cardiovascular response to exercise. Thirty-nine women [29 +/- 4 (SD) yr], performed submaximal and maximal exercise cycle ergometry during pregnancy (antepartum, AP, 26 +/- 3 wk of gestation) and postpartum (PP, 8 +/- 2 wk). Neither maximal O2 uptake (VO2max) nor maximal heart rate (HR) was different AP and PP (VO2 = 1.91 +/- 0.32 and 1.83 +/- 0.31 l/min; HR = 182 +/- 8 and 184 +/- 7 beats/min, P greater than 0.05 for both). Cardiac output (Q, acetylene rebreathing technique) averaged 2.2 to 2.8 l/min higher AP (P less than 0.01) at rest and at each exercise work load. Increases in both HR and stroke volume (SV) contributed to the elevated Q at the lower exercise work loads, whereas an increased SV was primarily responsible for the higher Q at higher levels. The slope of the Q vs. VO2 relationship was not different AP and PP (6.15 +/- 1.32 and 6.18 +/- 1.34 l/min Q/l/min VO2, P greater than 0.05). In contrast, the arteriovenous O2 difference (a-vO2 difference) was lower at each exercise work load AP, suggesting that the higher Q AP was distributed to nonexercising vascular beds. We conclude that Q is greater and a-vO2 difference is less at all levels of exercise in pregnant subjects than in the same women postpartum but that the coupling of the increase in Q to the increase in systemic O2 demand (VO2) is not different.(ABSTRACT TRUNCATED AT 250 WORDS)     

Epinephrine-induced changes in muscle carbohydrate metabolism during exercise in male subjects

Epinephrine increases glycogenolysis in resting skeletal muscle, but less is known about the effects of epinephrine on exercising muscle. To study this, epinephrine was given intraarterially to one leg during two-legged cycle exercise in nine healthy males. The epinephrine-stimulated (EPI) and non-stimulated (C) legs were compared with regard to glycogen, glucose, glucose 6-phosphate (G6P), alpha-glycerophosphate (alpha-GP), and lactate contents in muscle biopsies taken before and after the 45-min submaximal exercise, as well as brachial arterial-femoral venous (a-fv) differences for epinephrine, norepinephrine, lactate, glucose, and O2 during exercise. During exercise the arterial plasma epinephrine concentration was 4.8 +/- 0.8 nmol/l and the femoral venous epinephrine concentrations were 10.3 +/- 2.1 and 3.9 +/- 0.6 nmol/l, respectively, in the EPI and C leg. During exercise the a-fv difference for lactate was greater (-0.41 +/- 0.14 vs. -0.21 +/- 0.14 mmol/l; P less than 0.001), and the a-fv difference for glucose was smaller (0.07 +/- 0.12 vs. 0.24 +/- 0.12 mmol/l; P less than 0.01) in the EPI than in the C leg, but the a-fv differences for O2 were similar. Muscle glycogen depletion (137 +/- 63 vs. 99 +/- 43 mmol/kg dry muscle; P less than 0.1) and the muscle concentrations of glucose (P less than 0.05), alpha-GP (P less than 0.1), G6P (P greater than 0.1), and lactate (P greater than 0.1) tended to be higher in the EPI than the C leg after exercise. These findings suggest that physiological concentrations of epinephrine may enhance muscle glycogenolysis during submaximal exercise in male subjects.     

Aging attenuates vascular and metabolic plasticity but does not limit improvement in muscle VO(2) max

The interactions between exercise, vascular and metabolic plasticity, and aging have provided insight into the prevention and restoration of declining whole body and small muscle mass exercise performance known to occur with age. Metabolic and vascular adaptations to normoxic knee-extensor exercise training (1 h 3 times a week for 8 wk) were compared between six sedentary young (20 +/- 1 yr) and six sedentary old (67 +/- 2 yr) subjects. Arterial and venous blood samples, in conjunction with a thermodilution technique facilitated the measurement of quadriceps muscle blood flow and hematologic variables during incremental knee-extensor exercise. Pretraining, young and old subjects attained a similar maximal work rate (WR(max)) (young = 27 +/- 3, old = 24 +/- 4 W) and similar maximal quadriceps O(2) consumption (muscle Vo(2 max)) (young = 0.52 +/- 0.03, old = 0.42 +/- 0.05 l/min), which increased equally in both groups posttraining (WR(max), young = 38 +/- 1, old = 36 +/- 4 W, Muscle Vo(2 max), young = 0.71 +/- 0.1, old = 0.63 +/- 0.1 l/min). Before training, muscle blood flow was approximately 500 ml lower in the old compared with the young throughout incremental knee-extensor exercise. After 8 wk of knee-extensor exercise training, the young reduced muscle blood flow approximately 700 ml/min, elevated arteriovenous O(2) difference approximately 1.3 ml/dl, and increased leg vascular resistance approximately 17 mmHg x ml(-1) x min(-1), whereas the old subjects revealed no training-induced changes in these variables. Together, these findings indicate that after 8 wk of small muscle mass exercise training, young and old subjects of equal initial metabolic capacity have a similar ability to increase quadriceps muscle WR(max) and muscle Vo(2 max), despite an attenuated vascular and/or metabolic adaptation to submaximal exercise in the old.     

Perceived exertion is associated with an altered brain activity during exercise with progressive hyperthermia.

The present study tested the hypothesis that perceived exertion during prolonged exercise in hot environments is associated with changes in cerebral electrical activity rather than changes in the electromyogram (EMG) of the exercising muscles. Therefore, electroencephalogram (EEG) in three positions (frontal, central, and occipital cortex), EMG, rating of perceived exertion (RPE), and core temperature were measured in 14 subjects during submaximal exercise in normal (18 degrees C, control) and hot (40 degrees C, hyperthermia) environments. RPE increased from 11 +/- 1 units at 5 min to 20 +/- 0 units at exhaustion (50 +/- 3 min) in the trial with progressive hyperthermia, whereas exercise in the control trial was maintained with a stable core temperature for 1 h without exhausting the subjects. Altered EEG activity was observed in all electrode positions, and stepwise forward-regression analysis identified core temperature and a frequency index of the EEG over the frontal cortex as the best predictors of RPE. In contrast, there were no significant correlations between RPE and any of the measured EMG parameters (median spectral frequency, root mean square, or amplitude), and the EMG parameters were not different in hyperthermia compared with control. Thus hyperthermia does not seem to affect the activation pattern of the muscles. Rather, the linear correlation among core temperature, EEG frequency index, and RPE indicates that alterations in cerebral activity may be associated with the hyperthermia-induced development of fatigue during prolonged exercise in hot environments.