Effects of fasting and carbohydrate consumption on voluntary resting apnea duration

Breath holding is normally terminated due to the urge to breathe, mainly caused by the increasing carbon dioxide level. It was recently shown that a combination of 18 h of carbohydrate-free diet and prolonged exercise prior to breath holding lowered the respiratory exchange ratio (RER) and end-expiratory PO₂ at maximal breath-hold break-point (MBP). Current hypothesis: fasting will result in longer breath-hold duration than will fasting followed by carbohydrate intake. It was also hypothesized that breath-holds during carbohydrate supplementation would be ended at a higher alveolar PO₂. Ten male non-divers performed multiple breath-holds either to the first diaphragmatic contraction (PBP), or to MBP. The breath-holds were performed during normal diet (control; C), twice during fasting (F14 h, F18 h), followed by post fasting carbohydrate consumption (PFCC) and a repetition of the breath-hold testing 1–2 h after ingestion of carbohydrates. Duration, RER, end-tidal PO₂ and PCO₂, SaO₂ and blood glucose were determined. RER and blood glucose increased after PFCC compared with fasting and control conditions (P < 0.001). PBP breath-hold duration increased from 129 ± 34 s at C to 148 ± 33 s at F18 h, and was reduced during PFCC to 122 ± 30 s (P < 0.001). End-tidal PO₂ was higher at PFCC compared to F18 h (10.4 ± 1.2 vs. 9.5 ± 1.2 kPa at PBP, P < 0.05). Similar trends in breath-hold duration and physiology were seen in breath-holds that were terminated at MBP. Dietary restriction can affect breath-hold duration. The lower O₂ level at breakpoint during fasting suggests that breath holding may be less safe during fasting; the increased risk may be mitigated by ingestion of carbohydrates before breath holding.     

Arterial hypoxemia and performance during intense exercise

In order to determine the level of hypoxemia which is sufficient to impair maximal performance, seven well-trained male cyclists [maximum oxygen consumption (VO_2max)51·min^–1 or 60 ml·kg^–1·min^–1] performed a 5-min performance cycle test to exhaustion at maximal intensity as controlled by the subject, under three experimental conditions: normoxemia [percentage of arterial oxyhemoglobin saturation (%S _a O₂)>94%], and artificially induced mild (%S _aO₂=90±1%) and moderate (%S _aO₂=87±1%) hypoxemia. Performance, evaluated as the total work output (Work_tot) performed in the 5-min cycle test, progressively decreased with decreasing %S _aO₂ [mean (SE) Work_tot=107.40 (4.5) kJ, 104.07 (5.6) kJ, and 102.52 (4.7) kJ, under normoxemia, mild, and moderate hypoxemia, respectively]. However, only performance in the moderate hypoxemia condition was significantly different than in normoxemia (P=0.02). Mean oxygen consumption and heart rate were similar in the three conditions (P=0.18 andP=0.95, respectively). End-tidal partial pressure of CO₂ was significantly lower (P=0.005) during moderate hypoxemia compared with normoxemia, and ventilatory equivalent of CO₂ was significantly higher (P=0.005) in both hypoxemic conditions when compared with normoxemia. It is concluded that maximal performance capacity is significantly impaired in highly trained cyclists working under an %S _aO₂ level of 87% but not under a milder desaturation level of 90%.     

Posture control after prolonged exercise

The perturbations of equilibrium after prolonged exercise were investigated by dynamic posturography on nine well-trained subjects (four athletes and five triathletes). A sensory organization test, where the platform and visual surround were either stable or referenced to the subject's sway with eyes open or closed, was performed before and after a 25-km run (average time 1h 44 min) by the nine subjects. In addition, the same test was performed on the five triathletes only, before and after ergocycle exercise of identical duration (i.e. ergocycle time = running time). The results showed that the ability to maintain postural stability during conflicting sensory conditions decreased after exercise, with some differences depending on the kind of exercise. Sensory analysis revealed that the subjects made less effective use of vestibular inputs after running than after cycling (P?相似文献   

The effect of hypoxia on performance during 30 s or 45 s of supramaximal exercise

Summary The purpose of this study was to evaluate the effect of hypoxia (10.8±0.6% oxygen) on performance of 30 s and 45 s of supramaximal dynamic exercise. Twelve males were randomly allocated to perform either a 30 s or 45 s Wingate test (WT) on two occasions (hypoxia and room air) with a minimum of 1 week between tests. After a 5-min warm-up at 120 W subjects breathed the appropriate gas mixture from a wet spirometer during a 5-min rest period. Resting blood oxygen saturation was monitored with an ear oximeter and averaged 97.8 ± 1.5% and 83.2 ± 1.9% for the air (normoxic) and hypoxic conditions, respectively, immediately prior to the WT. Following all WT trials, subjects breathed room air for a 10-min passive recovery period. Muscle biopsies from the vastus lateralis were taken prior to and immediately following WT. Arterialized blood samples, for lactate and blood gases, were taken before and after both the warm-up and the performance of WT, and throughout the recovery period. Opencircuit spirometry was used to calculate the total oxygen consumption (Vo₂), carbon dioxide production and expired ventilation during WT. Hypoxia did not impair the performance of the 30-s or 45-s WT.Vo₃ was reduced during the 45-s hypoxic WT (1.71±0.21 I) compared with the normoxic trial (2.16±0.261), but there was no change during the 30-s test (1.22±0.11 vs 1.04±0.171 for the normoxic and hypoxic conditions, respectively). Muscle lactate (LA) increased more during hypoxia following both the 30-s and 45-s WT (67.1±25.0 mmol· kg^–1 dry weight) compared with normoxia (30.8 ± 18.0 mmol · kg^–1 dry weight). Hypoxia did not influence the change in intramuscular adenosine triphosphate, creatine phosphate and glucose-6-phosphate. The performance of WT during hypoxia was associated with a greater decrease in muscle glycogen (P<0.06). Throughout the recovery period, blood LA was lower following the hypoxia (8.43±2.88 mmol · l^–1) comparedwith normoxia (9.15±3.06 mmol · 1^–1). Breathing the hypoxic gas mixture prior to the performance of WT increased blood pH to 7.44±0.03, compared with 7.39±0.03 for normoxia. Blood pH remained higher during the 10-min recovery period following the hypoxic WT trials (7.24±0.08) compared with the normoxic WT (7.22±0.06). BloodP _{CO 2} was reduced prior to and immediately following WT during hypoxia, but there were no differences between the normoxic and hypoxic trials during the 10 min recovery period. These data indicate that more energy was transduced from the catabolism of glycogen to lactate during the hypoxic WT trials, which offset the reduced O₂ availability and maintained performance comparable with normoxic conditions. It is suggested that the induced respiratory alkalosis associated with breathing the hypoxic gas could account for the increased rate of muscle LA accumulation.     

Effects of prolonged exercise to exhaustion on left-ventricular function and pulmonary gas exchange

The purpose of this study was to simultaneously examine left-ventricular (LV) function and pulmonary gas exchange during prolonged constant-rate cycling in an attempt to explain the exercise-induced impairment in gas exchange. Eleven competitive cyclists rode their racing bicycles on a computerized cycle trainer at 25 W below the lactate threshold until exhaustion (exercise time = 2.51 +/- 0.86 h). LV systolic function was evaluated with two-dimensional echocardiography while arterial blood gases were used to assess pulmonary gas exchange. All variables were assessed concurrently before, during, and after exercise. LV function and cardiac output increased at the onset of exercise and were maintained until exhaustion. The alveolar-arterial P(O(2)) difference (A-a D(O(2))) increased within 15 min of the onset of exercise, was unchanged through to exhaustion, and returned to baseline 5 min post-exercise. Gas exchange was not related to cardiovascular function at the onset, or at end exercise. The results indicate that the widening A-aD(O(2)) during exercise is due to a readily reversible change in gas exchange function.     

Metabolic consequences of reduced frequency breathing during submaximal exercise at moderate altitude

Summary The intention of this study was to determine the metabolic consequences of reduced frequency breathing (RFB) at total lung capacity (TLC) in competitive cyclists during submaximal exercise at moderate altitude (1520 m; barometric pressure, P _B=84.6 kPa; 635 mm Hg). Nine trained males performed an RFB exercise test (10 breaths · min ^–1) and a normal breathing exercise test at 75–85% of the ventilatory threshold intensity for 6 min on separate days. RFB exercise induced significant (P<0.05) decreases in ventilation (V _E), carbon dioxide production (VCO₂), respiratory exchange ratio. (RER), ventilatory equivalent for O₂ consumption (V _E/VO₂), arterial O₂ saturation and increases in heart rate and venous lactate concentration, while maintaining a similar OZ consumption (VO₂). During recovery from RFB exercise (spontaneous breathing) a significant (P< 0.05) decrease in blood pH was detected along with increases in V _E, VO₂, VCO₂, RER, and venous partial pressure of carbon dioxide. The results indicate that voluntary hypoventilation at TLC, during submaximal cycling exercise at moderate altitude, elicits systemic hypercapnia, arterial hypoxemia, tissue hypoxia and acidosis. These data suggest that RFB exercise at moderate altitude causes an increase in energy production from glycolytic pathways above that which occurs with normal breathing.     

Pulmonary gas exchange does not worsen during repeat exercise in women

The purposes were to determine (1) if repeat exercise worsens pulmonary gas exchange in women, and, (2) if the level of pulmonary edema obtained in these same women is related to the gas exchange impairment during exercise. Fourteen women (27 +/- 4 yrs; maximal oxygen uptake = 3.12 +/- 0.42 L/min) with minimal arterial PO2 (PaO2) ranging from 76 to 104 mmHg with a maximal alveolar-arterial PO2 difference (AaDO2) ranging from 7 to 35 mmHg performed three bouts of near-maximal exercise on a cycle ergometer (236 +/- 27 W) for 5 min each with 10 min of rest between sets. Cardiorespiratory parameters and oxygenation were measured at rest, throughout exercise and recovery. Chest radiographs were obtained before and 30 min after the interval training session (see Respir Physiol Neurobiol, 153 (2006) 181-190). Repeat exercise did not affect pulmonary gas exchange between sets 1 and 3 (change in PaO2 = 3 +/- 2 mmHg; change in AaDO2 = 1 +/- 2 mmHg P > 0.05). Arterial PCO2 decreased by 4 +/- 2 mmHg (P < 0.05) between sets 1 and 2, which did not reduce further in set 3. The level of PaO2 or AaDO2 was not related to the change in edema score or the post-exercise edema score (P > 0.05). In conclusion, pulmonary gas exchange is not worsened in women during interval training despite the mild edema triggered by exercise.     

The significance of an increased RQ after sucrose ingestion during prolonged aerobic exercise

Summary Four well-trained male subjects worked for periods of 6 h on bicycle ergometers at work loads requiring about 47% of their maximal aerobic capacity. In one series of studies they received only water; in a second series they received 100 g of sucrose containing 100 c U-C¹⁴-labelled sucrose at the beginning of the fourth hour of work. In a third series of experiments, the same subjects received 100 g of non-labelled sucrose at the beginning of the fourth hour. During the experiment without U-C¹⁴-labelled sucrose, blood samples were withdrawn and analysed for glucose, lactate and pyruvate content. Data from C¹⁴O₂ recovery in expired air showed a good correlation with the amount of carbohydrate oxidized during the sucrose experiment. Peak values for the respiratory exchange ratio showed the same time response as those observed for the C¹⁴O₂ in the expired air. It is concluded that the observed rise in RQ after sucrose ingestion, under the conditions studied, is of metabolic origin, resulting from a complete conversion of pyruvate to CO₂.     

Influence of glucose ingestion by humans during recovery from exercise on substrate utilisation during subsequent exercise in a warm environment

Carbohydrate (CHO) ingestion during short-term recovery from prolonged running has been shown to increase the capacity for subsequent exercise in a warm environment. The aim of this study was to examine the effects of the amount of glucose given during recovery on substrate storage and utilisation during recovery and subsequent exercise in a warm environment. A group of 11 healthy male volunteers took part in two experiments in a controlled warm environment (35°C, 40% relative humidity), 1 week apart. On each occasion the subjects completed two treadmill runs (T1 and T2) at a speed equivalent to 60% of maximal oxygen uptake, for 90 min, until they were fatigued, or until aural temperature (T _aur) reached 39°C. The two runs were separated by a 4 h recovery period (REC), during which subjects consumed 55 g of naturally enriched [U-¹³C]-glucose in the form of a 7.5% carbohydrate-electrolyte solution (CES, mass of solution 667 g) immediately after T1. The subjects then consumed either: the same quantity of CES, or an equivalent volume of an electrolyte placebo, at 60, 120 and 180 min during REC, providing a total of 220 g (C220) or 55 g (C55) of [U-¹³C]-glucose, respectively. Expired gases were collected at 15 min intervals during exercise and 60 min intervals during REC, for determination of total CHO and fat oxidation by indirect respiratory calorimetry, and orally ingested [U-¹³C]-glucose oxidation, estimated from the ¹³C:¹²C ratio of expired CO₂. Substrate metabolism did not differ between conditions during T1. Despite the fact that total CHO (P<0.05) and ingested glucose oxidation (P<0.01) were greater during REC of the C220 condition, glycogen synthesis was estimated to be approximately fivefold greater (P<0.01) than in the C55 condition. During T2 the rate of total CHO oxidation was higher (P<0.01) and total fat oxidation lower (P<0.01) at all times during the C220 compared to the C55 condition. The greater CHO oxidation during C220 appeared to be met from ingested sources, as the rate of [U-¹³C]-glucose oxidation was greater (P<0.01) at all times during T2, compared to C55. Whilst more of the ingested substrate remained unoxidised on completion of T2 during C220, exercise duration was similar in the two experimental conditions, and was limited by thermoregulatory incapacity (T _aur>39°C) rather than substrate availability per se. Electronic Publication     

Utilization of carbohydrates and free fatty acids by the gastrocnemius of the dog during long lasting rhythmical exercise

Summary Utilization of carbohydrates and free fatty acids (FFA) has been investigated in gastrocnemii of dogs during long lasting isotonic rhythmical exercise induced by supramaximal stimulation of the sciatic nerve. Uptake or output of gases and substrates was determined according to the Fick principle. The first measurements were done at about 2 min after the beginning of work when blood flow has reached a steady state, and the latest at about 100 min after the beginning of exercise.During the first 7 min when the work performed exceeded 5 kg/100g×min and O₂ consumption exceeded 11 ml/100g×min, uptake of arterial glucose and FFA was low, accounting for less than 40% of the total O₂ consumption. Since the RQ values at the same time were about 1.0, glycogen must have been oxidized as the major aerobic energy source.About 13 min after the beginning of exercise, the work the muscles could perform declined to about half of the initial value and remained so for the following 90 min. During this time the oxygen extraction ratio of FFA was about 50% and of arterial glucose was 40–50%, while the RQ value was about 0.8.During initial strong exercise an output of lactic acid (LA) of about 10 mg/100 g×min was measured. With the decrease of work as a consequence of fatigue, LA output became negligible, and in many experiments small amounts of LA were taken up by the working gastrocnemii.It is concluded that glycogen is the major aerobic energy source for strong muscular exercise which cannot be substituted for by the oxidation of arterial glucose or FFA.Supported by the Deutsche Forschungsgemeinschaft.     

Histochemical and morphological observations on rat myocardium after exercise

Effects of seven levels of chronic physical activity on the metabolic and morphologic characteristics of left ventricular myocardium of adult male albino rats were investigated.Treatments included sedentary control; voluntary running; short-duration, high-intensity running; medium-duration, moderate-intensity running; long-duration, low-intensity running; electric stimulus control; and endurance swimming. Excluding the controls, the animals were trained 5 days per week for 8 consecutive weeks. Food and water were providedad libitum to them. Fifty-six animals comprised the final sample.Histochemical techniques were used to evaluate the relative glycogen, fatty acid, SDH and LDH concentrations in the cardiac fibers. Each stain was measured objectively, using a photometer. A Hematoxylin and Eosin stain was employed to rate morphologic features. These sections were evaluated subjectively on the basis of presence or absence of lesions.Physical training for 8 weeks was sufficient to produce metabolic adaptations in the rats. The trained animals gained 37.4 % less body weight than did the sedentary controls (P < 0.05). However, neither histochemical nor morphological changes had occurred to the hearts of these animals consequent to the 8 weeks training programs. Apparently, the myocardial tissues examined, from the trained animals, contain the enzymes, SDH and LDH, and the substrates, glycogen and fatty acids, in amounts greater than that needed to cope with the exercise stress afforded by these training programs.     

Myocardial lactate release during prolonged exercise under hypoxaemia

The possible appearance of myocardial lactate production during exercise under hypoxaemia, simulating an altitude of about 4500 metres above sea-level (masl) was investigated. Twelve healthy men were studied, after coronary sinus catheterization, during prolonged exercise breathing 12% 0₂ compared with men breathing air. Coronary sinus blood flow was measured by thermodilution. Exercise duration under each breathing condition was 30 min and the order normoxaemia/hypoxaemia was varied between subjects so as to compensate for any influence of a preceding exercise period on a subsequent one. Work load was adjusted so as to produce a heart rate (HR) of 130–140 beats min^-1 during both hypoxaemia and normoxaemia. [¹⁴C]lactate was infused at a constant rate i.v. throughout the study to detect a possible myocardial lactate release simultaneously with a net uptake. Myocardial 0₂ uptake did not differ significantly between hypoxaemia and normoxaemia. The compensation for reduced blood oxygen content was achieved entirely by a greater coronary blood flow. Yet, the arterial-coronary sinus (a-cs) lactate difference was lower during hypoxaemia than normoxaemia and isotope data indicated that this was caused by a myocardial lactate release of approximately 90 μmol min^-1 which was at hand during hypoxaemia but not normoxaemia, whether hypoxaemic exercise preceded or succeeded normoxaemic exercise. In conclusion, A 27% reduction in arterial oxygen saturation is almost compensated for by an increased coronary blood flow. However, during hypoxaemic exercise cardiac energy demand is to a smaller part, about 1 %, covered by anaerobic metabolism.     

Hormonal responses during a prolonged military field exercise with variable exercise intensity

The purpose of the present study was to test the hypothesis that the magnitude of hormonal concentration alterations during a prolonged military field exercise with constant energy intake (EI) is influenced by changes in energy deficit (ED) induced by varying the exercise intensity. Basal serum hormone concentrations were measured in a group of healthy young male volunteers (n = 7) during a 20-day field exercise. During the first week of the exercise, the average ED was 4,000 kcal/day (P-I), in the second week only 450 kcal/day (P-II), and in the last week 1,000 kcal/day (P-III). During the first 5 days of the field exercise, significant increases in cortisol (COR, +32%) and growth hormone (GH, +616%) concentrations were observed, while insulin (INS, −70%), total testosterone (TES, −27%), free testosterone (TES_free, −26%) decreased. However, after these initial responses, COR and GH returned to the pre-exercise level by the beginning of P-II. Also TES and TES_free recovered to the pre-exercise level by the beginning of P-III, and INS by the end of P-III. The concentration of TES (+29%) increased above the pre-exercise level by the beginning of P-III. Serum thyroxin (T₄) concentration was significantly lesser (−12%) and urine urea concentration significantly higher (+78%) after the field exercise than before it. Therefore, it can be concluded that the lower levels of ED in the second and third phase (ED <1,000 kcal/day) allowed recovery of hormonal changes observed in the first phase with ED much greater than 1000 kcal/day.     

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.