Exogenous carbohydrate oxidation from drinks ingested during prolonged exercise in a cold environment in humans.

Six healthy male volunteers performed four rides to exhaustion on a cycle ergometer at approximately 80% of maximal oxygen consumption. Subjects ingested a bolus volume of fluid (7.14 ml/kg) immediately before exercise and additional fluid volumes (1.43 ml/kg) every 10 min during exercise. The fluids ingested were either a flavored water control or glucose-electrolyte beverages with glucose concentrations of 2, 6, or 12%. The beverages were labeled with [U-(13)C]glucose (99.2%: 0.05 g/l). Exercise capacity was not different (P = 0.13) between trials; median (range) exercise time was 83.52 (79.85--89.68), 103.19 (78.82--108.22), 100.37 (80.60--124.07), and 94.76 (76.78--114.25) min in the 0, 2, 6, and 12% trials, respectively. The oxidation of exogenous glucose in each 15-min period was significantly lower in the 2% trial (P = 0.02) than in the 6 and 12% trials where oxidation rates were between 0.5 and 0.7 g/min. No difference in endogenous glucose oxidation was observed between trials (P = 0.71). These findings indicate that the oxidation of exogenous glucose during exercise of this intensity and duration in a cold environment is similar to that observed in warmer conditions. Thus a low oxidation of exogenous substrate is unlikely to be a factor limiting the effectiveness of carbohydrate-electrolyte drink ingestion on exercise capacity in a cold environment.     

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

We investigated whether a core temperature threshold for hyperthermic hyperventilation is seen during prolonged submaximal exercise in the heat when core temperature before the exercise is reduced and whether the evoked hyperventilatory response is affected by altering the initial core temperature. Ten male subjects performed three exercise trials at 50% of peak oxygen uptake in the heat (37°C and 50% relative humidity) after altering their initial esophageal temperature (T(es)). Initial T(es) was manipulated by immersion for 25 min in water at 18°C (Precooling), 35°C (Control), or 40°C (Preheating). T(es) after the water immersion was significantly higher in the Preheating trial (37.5 ± 0.3°C) and lower in the Precooling trial (36.1 ± 0.3°C) than in the Control trial (36.9 ± 0.3°C). In the Precooling trial, minute ventilation (Ve) showed little change until T(es) reached 37.1 ± 0.4°C. Above this core temperature threshold, Ve increased linearly in proportion to increasing T(es). In the Control trial, Ve increased as T(es) increased from 37.0°C to 38.6°C after the onset of exercise. In the Preheating trial, Ve increased from the initially elevated levels of T(es) (from 37.6 to 38.6°C) and Ve. The sensitivity of Ve to increasing T(es) above the threshold for hyperventilation (the slope of the T(es)-Ve relation) did not significantly vary across trials (Precooling trial = 10.6 ± 5.9, Control trial = 8.7 ± 5.1, and Preheating trial = 9.2 ± 6.9 L·min(-1)·°C(-1)). These results suggest that during prolonged submaximal exercise at a constant workload in humans, there is a clear core temperature threshold for hyperthermic hyperventilation and that the evoked hyperventilatory response is unaffected by altering initial core temperature.     

Influence of body temperature on the development of fatigue during prolonged exercise in the heat.

We investigated whether fatigue during prolonged exercise in uncompensable hot environments occurred at the same critical level of hyperthermia when the initial value and the rate of increase in body temperature are altered. To examine the effect of initial body temperature [esophageal temperature (Tes) = 35.9 +/- 0.2, 37.4 +/- 0. 1, or 38.2 +/- 0.1 (SE) degrees C induced by 30 min of water immersion], seven cyclists (maximal O2 uptake = 5.1 +/- 0.1 l/min) performed three randomly assigned bouts of cycle ergometer exercise (60% maximal O2 uptake) in the heat (40 degrees C) until volitional exhaustion. To determine the influence of rate of heat storage (0.10 vs. 0.05 degrees C/min induced by a water-perfused jacket), four cyclists performed two additional exercise bouts, starting with Tes of 37.0 degrees C. Despite different initial temperatures, all subjects fatigued at an identical level of hyperthermia (Tes = 40. 1-40.2 degrees C, muscle temperature = 40.7-40.9 degrees C, skin temperature = 37.0-37.2 degrees C) and cardiovascular strain (heart rate = 196-198 beats/min, cardiac output = 19.9-20.8 l/min). Time to exhaustion was inversely related to the initial body temperature: 63 +/- 3, 46 +/- 3, and 28 +/- 2 min with initial Tes of approximately 36, 37, and 38 degrees C, respectively (all P < 0.05). Similarly, with different rates of heat storage, all subjects reached exhaustion at similar Tes and muscle temperature (40.1-40.3 and 40. 7-40.9 degrees C, respectively), but with significantly different skin temperature (38.4 +/- 0.4 vs. 35.6 +/- 0.2 degrees C during high vs. low rate of heat storage, respectively, P < 0.05). Time to exhaustion was significantly shorter at the high than at the lower rate of heat storage (31 +/- 4 vs. 56 +/- 11 min, respectively, P < 0.05). Increases in heart rate and reductions in stroke volume paralleled the rise in core temperature (36-40 degrees C), with skin blood flow plateauing at Tes of approximately 38 degrees C. These results demonstrate that high internal body temperature per se causes fatigue in trained subjects during prolonged exercise in uncompensable hot environments. Furthermore, time to exhaustion in hot environments is inversely related to the initial temperature and directly related to the rate of heat storage.     

Immune changes in humans during cold exposure: effects of prior heating and exercise.

This study examined the immunological responses to cold exposure together with the effects of pretreatment with either passive heating or exercise (with and without a thermal clamp). On four separate occasions, seven healthy men [mean age 24.0 +/- 1.9 (SE) yr, peak oxygen consumption = 45.7 +/- 2.0 ml. kg(-1). min(-1)] sat for 2 h in a climatic chamber maintained at 5 degrees C. Before exposure, subjects participated in one of four pretreatment conditions. For the thermoneutral control condition, subjects remained seated for 1 h in a water bath at 35 degrees C. In another pretreatment, subjects were passively heated in a warm (38 degrees C) water bath for 1 h. In two other pretreatments, subjects exercised for 1 h at 55% peak oxygen consumption (once immersed in 18 degrees C water and once in 35 degrees C water). Core temperature rose by 1 degrees C during passive heating and during exercise in 35 degrees C water and remained stable during exercise in 18 degrees C water (thermal clamping). Subsequent cold exposure induced a leukocytosis and granulocytosis, an increase in natural killer cell count and activity, and a rise in circulating levels of interleukin-6. Pretreatment with exercise in 18 degrees C water augmented the leukocyte, granulocyte, and monocyte response. These results indicate that acute cold exposure has immunostimulating effects and that, with thermal clamping, pretreatment with physical exercise can enhance this response. Increases in levels of circulating norepinephrine may account for the changes observed during cold exposure and their modification by changes in initial status.     

Plasma hypoxanthine and ammonia in humans during prolonged exercise

In this study we examined the time course of changes in the plasma concentration of oxypurines [hypoxanthine (Hx), xanthine and urate] during prolonged cycling to fatigue. Ten subjects with an estimated maximum oxygen uptake (VO2(max)) of 54 (range 47-67) ml x kg(-1) x min(-1) cycled at [mean (SEM)] 74 (2)% of VO2(max) until fatigue [79 (8) min]. Plasma levels of oxypurines increased during exercise, but the magnitude and the time course varied considerably between subjects. The plasma concentration of Hx ([Hx]) was 1.3 (0.3) micromol/l at rest and increased eight fold at fatigue. After 60 min of exercise plasma [Hx] was >10 micromol/l in four subjects, whereas in the remaining five subjects it was <5 micromol/l. The muscle contents of total adenine nucleotides (TAN = ATP+ADP+AMP) and inosine monophosphate (IMP) were measured before and after exercise in five subjects. Subjects with a high plasma [Hx] at fatigue also demonstrated a pronounced decrease in muscle TAN and increase in IMP. Plasma [Hx] after 60 min of exercise correlated significantly with plasma concentration of ammonia ([NH(3)], r = 0.90) and blood lactate (r = 0.66). Endurance, measured as time to fatigue, was inversely correlated to plasma [Hx] at 60 min (r = -0.68, P < 0.05) but not to either plasma [NH(3)] or blood lactate. It is concluded that during moderate-intensity exercise, plasma [Hx] increases, but to a variable extent between subjects. The present data suggest that plasma [Hx] is a marker of adenine nucleotide degradation and energetic stress during exercise. The potential use of plasma [Hx] to assess training status and to identify overtraining deserves further attention.     

Carnitine metabolism during prolonged exercise and recovery in humans

Lennon et al. (J. Appl. Physiol. 55: 489-495, 1983) have recently reported a large loss of muscle total carnitine (TC) after 40 min of moderate exercise. These authors have also suggested that elevations in plasma esterified carnitine (EC) were due to the release of these carnitine esters from muscle during exercise. After 10 male subjects underwent 90 min of cycle egometry we found no alteration in muscle TC from preexercise values. Plasma EC progressively increased above resting values during exercise and remained elevated above rest at 0.75 and 1.5 h into recovery. Elevations of plasma EC were largely due to a decrement in free carnitine (FC) in both conditions. Immediately postexercise the urinary fractional reabsorbsion of EC and FC were similar to that at rest. These results suggest that a net loss of TC from exercising muscle does not occur. As in other conditions marked by falling insulin concentrations, elevations in plasma EC could result from an exchange of carnitine with the hepatic carnitine pool.     

Neurohumoral responses during prolonged exercise in humans.

This study examined neurohumoral alterations during prolonged exercise with and without hyperthermia. The cerebral oxygen-to-carbohydrate uptake ratio (O2/CHO = arteriovenous oxygen difference divided by arteriovenous glucose difference plus one-half lactate), the cerebral balances of dopamine, and the metabolic precursor of serotonin, tryptophan, were evaluated in eight endurance-trained subjects during exercise randomized to be with or without hyperthermia. The core temperature stabilized at 37.9 +/- 0.1 degrees C (mean +/- SE) in the control trial, whereas it increased to 39.7 +/- 0.2 degrees C in the hyperthermic trial, with a concomitant increase in perceived exertion (P < 0.05). At rest, the brain had a small release of tryptophan (arteriovenous difference of -1.2 +/- 0.3 micromol/l), whereas a net balance was obtained during the two exercise trials. Both the arterial and jugular venous dopamine levels became elevated during the hyperthermic trial, but the net release from the brain was unchanged. During exercise, the O2/CHO was similar across trials, but, during recovery from the hyperthermic trial, the ratio decreased to 3.8 +/- 0.3 (P < 0.05), whereas it returned to the baseline level of approximately 6 within 5 min after the control trial. The lowering of O2/CHO was established by an increased arteriovenous glucose difference (1.1 +/- 0.1 mmol/l during recovery from hyperthermia vs. 0.7 +/- 0.1 mmol/l in control; P < 0.05). The present findings indicate that the brain has an increased need for carbohydrates during recovery from strenuous exercise, whereas enhanced perception of effort as observed during exercise with hyperthermia was not related to alterations in the cerebral balances of dopamine or tryptophan.     

Physical performance and metabolic changes induced by combined prolonged exercise and different energy intakes in humans

The purpose of this study was to evaluate the effects on physical performance of three levels of energy intake during a 5-day period of prolonged physical exercise and relative sleep deprivation. A group of 27 male soldiers were randomly assigned to three groups receiving either 1800 kcal · 24 h^–1 (7560 kJ, LC), 3200 kcal · 24h^–1 (13440 kJ, MC) or 4200 kcal-24h^–1 (17640 kJ, HC). They took part in a 5-day combat course (CC) of heavy and continuous physical activities, with less than 4 h sleep per day. Performance capacity was tested just before and at the end of CC. Maximal oxygen uptake ( O_2max) was determined during an exhausting incremental exercise test on a cycle ergometer. Anaerobic performance was measured from the time during which exercise could be maintained at supra maximal loads on a cycle ergometer. After CC, the subjects receiving LC exhibited a 14% decrease in power output at exhaustion in the incremental exercise test [from 325 (SEM 8) to 278 (SEM 9) W,P < 0.001] and a significant decrease in O_2max of 8% [from 3.74 (SEM 0.06) to 3.45 (SEM 0.05) l · min^–1,P<0.05]. The remaining two experimental groups demonstrated the same mechanical and metabolic performances on days 1 and 5. Anaerobic performance was not influenced by energy intake and the field course. Blood samples were obtained at rest on days 1 and 5. At the end of CC, the data demonstrated a significant decrease in blood glucose concentrated ion (P<0.01) for LC diet only. Plasma free fatty acid, blood glycerol and -OH butyrate were significantly increased in all groups, from day 1, but the values observed for LC were higher than those for the MC and HC diets. The concentrations of the anabolic hormones, insulin and testosterone, decreased in the three groups, the lowest values being observed in the LG group (P < 0.05). In conclusion, we found that only a severe energy deficit decreased physical performance during submaximal exercise. A moderate deficit between energy intake and expenditure did not affect performance. Supramaximal exercise did not appear to be influenced by energy intake and CC.     

Changes in exercise and post-exercise core temperature under different clothing conditions

 This study evaluates the effect of different levels of insulation on esophageal (T _es) and rectal (T _re) temperature responses during and following moderate exercise. Seven subjects completed three 18-min bouts of treadmill exercise (75% VO_2max, 22°C ambient temperature) followed by 30 min of recovery wearing either: (1) jogging shoes, T-shirt and shorts (athletic clothing); (2) single-knit commercial coveralls worn over the athletic clothing (coveralls); or (3) a Canadian Armed Forces nuclear, bacteriological and chemical warfare protective overgarment with hood, worn over the athletic clothing (NBCW overgarment). T _es was similar at the start of exercise for each condition and baseline T _re was ∼0.4°C higher than T _es. The hourly equivalent rate of increase in T _es during the final 5 min of exercise was 1.8°C, 3.0°C and 4.2°C for athletic clothing, coveralls and NBCW overgarment respectively (P<0.05). End-exercise T _es was significantly different between conditions [37.7°C (SEM 0.1°C), 38.2°C (SEM 0.2°C and 38.5°C (SEM 0.2°C) for athletic clothing, coveralls and NBCW overgarment respectively)] (P<0.05). No comparable difference in the rate of temperature increase for T _re was demonstrated, except that end-exercise T _re for the NBCW overgarment condition was significantly greater (0.5°C) than that for the athletic clothing condition. There was a drop in T _es during the initial minutes of recovery to sustained plateaus which were significantly (P<0.05) elevated above pre-exercise resting values by 0.6°C, 0.8°C and 1.0°C, for athletic clothing, coveralls, and NBCW overgarment, respectively. Post-exercise T _re decreased very gradually from end-exercise values during the 30-min recovery. Only the NBCW overgarment condition T _re was significantly elevated (0.3°C) above the athletic clothing condition (P<0.05). In conclusion, T _es is far more sensitive in reflecting the heat stress of different levels of insulation during exercise and post-exercise than T _re. Physiological mechanisms are discussed as possible explanations for the differences in response. Received: 30 June 1998 / Accepted: 19 February 1999     

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.     

Adaptive responses to fescue toxicosis under thermoneutral and heat stress conditions

This study determined the potential for short-term adaptation to fescue toxicosis and heat stress in rats. Male CD outbred rats (n=24) were implanted with temperature transmitters (Respironics, Bend, OR) to measure core temperature (Tc) and general activity. All rats were initially fed diets with ground, uninfected tall fescue seed (E−) and exposed to 21 °C (thermoneutral, TN) to establish baseline values. In Period 1, all groups were maintained at TN for 7 days, with one group fed a diet containing ground, endophyte-infected tall fescue seed (E+, approximately 165 μg ergovaline/kg BW/d) and two groups fed E− diet. Ergovaline is thought to be the primary toxin responsible for many symptoms associated with fescue toxicosis. Period 1 was followed by 7 days at 31 °C (heat stress, HS, Period 2) on the same diets. All animals were fed E− diet during the second 7 day of HS (Period 3). In the final 7 day (Period 4), E+ diet was returned to the original group and fed to one of the previously E− groups, with the third group remaining on E− diet. A 40% decrease in FI occurred with E+ treatment at TN (P<0.05), with a comparable BW reduction (P<0.05) after 4 day. Both responses worsened during HS. Treatment with E+ in Period 4 indicated that FI and BW had not adapted to fescue toxicosis. A reduction in daily Tc occurred with E+ treatment at TN (P<0.05) followed by hyperthermia during the initial stage of HS (P<0.05). Although feed intake and growth rate showed no change over time, there was a reduction in fescue toxicosis-induced hyperthermia in the heat with repeat treatment. Conditioning animals to fescue toxicosis and heat stress prior to exposure may be beneficial in reducing impacts on thermal status of the animal.     

Early muscular and metabolic adaptations to prolonged exercise training in humans

A short-term training program involving 2 h of daily exercise at 59% of peak O2 uptake (VO2max) repeated for 10-12 consecutive days was employed to determine the significance of adaptations in energy metabolic potential on alterations in energy metabolism and substrate utilization in working muscle. The initial VO2max determined before training on the eight male subjects was 53.0 +/- 2.0 (SE) ml.kg-1.min-1. Analysis of samples obtained by needle biopsy from the vastus lateralis muscle before exercise (0 min) and at 15, 60, and 99 min of exercise indicated that on the average training resulted (P less than 0.05) in a 6.5% higher concentration of creatine phosphate, a 9.9% lower concentration of creatine, and a 39% lower concentration of lactate. Training had no effect on ATP concentration. These adaptations were also accompanied by a reduction in the utilization in glycogen such that by the end of exercise glycogen concentration was 47.1% higher in the trained muscle. Analysis of the maximal activities of representative enzymes of different metabolic pathways and segments indicated no change in potential in the citric acid cycle (succinate dehydrogenase, citrate synthase), beta-oxidation (3-hydroxyacyl CoA dehydrogenase), glucose phosphorylation (hexokinase), or potential for glycogenolysis (phosphorylase) and glycolysis (pyruvate kinase, phosphofructokinase, alpha-glycerophosphate dehydrogenase, lactate dehydrogenase). With the exception of increases in the capillary-to-fiber area ratio in type IIa fibers, no change was found in any fiber type (types I, IIa, and IIb) for area, number of capillaries, capillary-to-fiber area ratio, or oxidative potential with training.(ABSTRACT TRUNCATED AT 250 WORDS)     

L-Arginine infusion increases glucose clearance during prolonged exercise in humans

Nitric oxide synthase (NOS) inhibition has been shown in humans to attenuate exercise-induced increases in muscle glucose uptake. We examined the effect of infusing the NO precursor L-arginine (L-Arg) on glucose kinetics during exercise in humans. Nine endurance-trained males cycled for 120 min at 72+/-1% Vo(2 peak) followed immediately by a 15-min "all-out" cycling performance bout. A [6,6-(2)H]glucose tracer was infused throughout exercise, and either saline alone (Control, CON) or saline containing L-Arg HCL (L-Arg, 30 g at 0.5 g/min) was confused in a double-blind, randomized order during the last 60 min of exercise. L-Arg augmented the increases in glucose rate of appearance, glucose rate of disappearance, and glucose clearance rate (L-Arg: 16.1+/-1.8 ml.min(-1).kg(-1); CON: 11.9+/- 0.7 ml.min(-1).kg(-1) at 120 min, P<0.05) during exercise, with a net effect of reducing plasma glucose concentration during exercise. L-Arg infusion had no significant effect on plasma insulin concentration but attenuated the increase in nonesterified fatty acid and glycerol concentrations during exercise. L-Arg infusion had no effect on cycling exercise performance. In conclusion, L-Arg infusion during exercise significantly increases skeletal muscle glucose clearance in humans. Because plasma insulin concentration was unaffected by L-Arg infusion, greater NO production may have been responsible for this effect.     

Leg muscle metabolism during exercise in the heat and cold.

In an effort to assess the effects of environmental heat stress on muscle metabolism during exercise, 6 men performed work in the heat (Tdb = 44 degrees C, RH = 15%) and cold (Tdb = 9 degrees C, RH = 55%). Exercise consisted of three 15-min cycling bouts at 70 to 85% VO2max, with 10-min rest between each. Muscle biopsies obtained from the vastus lateralis before and after each work bout were analyzed for glycogen and triglyceride content. Venous blood samples drawn before and after exercise were assayed for lactate, glucose, free fatty acids, hemoglobin, and hematocrit. Oxygen uptake, heart rates and rectal temperatures were all significantly higher during exercise in the heat. Blood lactate concentration was roughly twice as great during the heat experiments as that measured in the 9 degrees C environment. Muscle glycogen utilization per 60 min was significantly greater in the heat ( - 74 m moles/kg-wet muscle) as compared to the cold exercise (- 42 m moles/kg-wet muscle). On the average, muscle triglyceride declined 23% during exercise in the cold and 11% in the heat. The findings of an enhanced glycolysis during exercise in the heat is compatible with earlier studies which demonstrate a decreased availability of oxygen due to a reduction in muscle blood flow.