Short-term High-intensity Exercise Research Articles

Patients with classic congenital adrenal hyperplasia have decreased epinephrine reserve and defective glucose elevation in response to high-intensity exercise.

Classic congenital hyperplasia (CAH) is characterized by impaired adrenocortical function with a decrease in cortisol and aldosterone secretion and an increase in androgen secretion. Adrenomedullary function is also compromised due to developmental defects in the formation of the adrenal medulla, leading to decreased production of epinephrine. To examine the response to a natural stressful stimulus in patients with classic CAH, we studied hormonal, metabolic, and cardiorespiratory parameters in response to a standardized high-intensity exercise protocol in nine adolescent patients with CAH and nine healthy controls matched for gender, age, and percent body fat. The same relative workload was applied, based on individual maximal aerobic capacity, and all patients received their usual glucocorticoid and mineralocorticoid replacement. When compared with their normal counterparts, patients with CAH had significantly lower epinephrine levels both at baseline and at peak exercise (P < 0.01), whereas norepinephrine levels did not differ. Blood glucose concentrations were similar at baseline, but the normal exercise-induced rise observed in the healthy controls was significantly blunted in the CAH patients (P < 0.01). Peak heart rate was also lower in CAH patients than healthy controls (P < 0.05). As expected, the normal exercise-induced increase in cortisol was not observed in patients with CAH. No significant differences were found in serum levels of insulin, glucagon, GH, lactate and free fatty acids, blood pressure, or ability to sustain exercise between the two groups. Patients with CAH replaced with glucocorticoids have decreased adrenomedullary reserve and impaired exercise-induced changes in glucose but normal short-term high-intensity exercise performance. Whether the combination of epinephrine and cortisol deficiency poses a risk for hypoglycemia and/or decreased endurance during long-term physical stress has to be determined.

Preexercise hypervolemia does not affect arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise.

It is reported that preexercise hyperhydration caused arterial O(2) tension of horses performing submaximal exercise to decrease further by 15 Torr (Sosa-Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, and Rose RJ. Equine Vet J Suppl 34: 425-429, 2002). Because hydration status is important to optimal athletic performance and thermoregulation during exercise, the present study examined whether preexercise induction of hypervolemia would similarly accentuate the arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise. Two sets of experiments (namely, control and hypervolemia studies) were carried out on seven healthy, exercise-trained Thoroughbred horses in random order, 7 days apart. In resting horses, an 18.0 +/- 1.8% increase in plasma volume was induced with NaCl (0.30-0.45 g/kg dissolved in 1,500 ml H(2)O) administered via a nasogastric tube, 285-290 min preexercise. Blood-gas and pH measurements as well as concentrations of plasma protein, hemoglobin, and blood lactate were determined at rest and during incremental exercise leading to maximal exertion (14 m/s on a 3.5% uphill grade) that induced pulmonary hemorrhage in all horses in both treatments. In both treatments, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but statistically significant differences between treatments were not found. Thus preexercise 18% expansion of plasma volume failed to significantly affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing maximal exercise. Although blood lactate concentration and arterial pH were unaffected, hemodilution caused in this manner resulted in a significant (P < 0.01) attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O(2) content gradient.

Effects of age and recovery duration on peak power output during repeated cycling sprints.

The aim of the present study was to investigate the effects of age and recovery duration on the time course of cycling peak power and blood lactate concentration ([La]) during repeated bouts of short-term high-intensity exercise. Eleven prepubescent boys (9.6 +/- 0.7 yr), nine pubescent boys (15.0 +/- 0.7 yr) and ten men (20.4 +/- 0.8 yr) performed ten consecutive 10 s cycling sprints separated by either 30 s (R30), 1 min (R1), or 5 min (R5) passive recovery intervals against a friction load corresponding to 50 % of their optimal force (50 % Ffopt). Peak power produced at 50 % Ffopt (PP50) was calculated at each sprint including the flywheel inertia of the bicycle. Arterialized capillary blood samples were collected at rest and during the sprint exercises to measure the time course of [La]. In the prepubescent boys, whatever recovery intervals, PP50 remained unchanged during the ten 10 s sprint exercises. In the pubescent boys, PP50 decreased significantly by 18.5 % (p < 0.001) with R30 and by 15.3 % (p < 0.01) with R1 from the first to the tenth sprint but remained unchanged with R5. In the men, PP50 decreased respectively by 28.5 % (p < 0.001) and 11.3 % (p < 0.01) with R30 and R1 and slightly diminished with R5. For each recovery interval, the increase in blood [La] over the ten sprints was significantly lower in the prepubescent boys compared with the pubescent boys and the men. To conclude, the prepubescent boys sustained their PP50 during the ten 10 s sprint exercises with only 30 s recovery intervals. In contrast, the pubescent boys and the men needed 5 min recovery intervals. It was suggested that the faster recovery of PP50 in the prepubescent boys was due to their lower muscle glycolytic activity and their higher muscle oxidative capacity allowing a faster resynthesis in phosphocreatine.

EFFECT OF AGE ON THE TIME COURSE OF CYCLING PEAK POWER DURING REPEATED SPRINTS

PURPOSE: To investigate the time course of cycling peak power during repeated bouts of short-term high-intensity exercise. METHODS: Eleven prepubertal boys (Pre: 9.6 ± 0.7 yrs, Tanner stage: 1, VO2max: 49.9 ± 7.0 ml.min-1.kg-1BM), nine pubertal boys (Pub: 15.0 ± 0.7 yrs, Tanner stage: 3–5, VO2max: 58.3 ± 6.4 ml.min-1.kg-1BM) and ten Men (20.4 ± 0.8 yrs, VO2max: 54.5 ± 5.6 ml.min-1.kg-1BM) performed ten consecutive 10 s sprints on a cycle ergometer separated by 30 s passive recovery intervals against a friction load corresponding to 50% of their optimal force which was previously calculated during a force-velocity test. Cycling peak power was calculated at each sprint including flywheel inertia of the device (CPPi). Capillary arterialized blood samples were collected at rest and after each sprint to measure the time course of lactate concentration ([La]). RESULTS: In Pre, CPPi remained unchanged during the ten 10 s sprints. The decrease in CPPi over the ten sprints was significantly lower in Pub compared with Men (p < 0.001). In Pub, CPPi decreased significantly by 1.5% at the second sprint (p < 0.05), by 14.8% at the fifth sprint (p < 0.01) and by 20.5% at the tenth sprint (p < 0.01). In Men, the loss in CPPi represented 6.9% at the second sprint (p < 0.01), 18.9% at the fifth sprint (p < 0.01) and 28.8% at the tenth sprint (p < 0.01). After the tenth sprint, [La] was significantly higher in Men (15.4 ± 2.0 mmol.1-1) compared with Pre (8.5 ± 2.1 mmol.1-1, p < 0.001) and Pub (10.9 ± 2.4 mmol.1-1, p < 0.05). CONCLUSION: During ten repeated sprints separated by short recovery intervals, CPPi did not decrease in prepubertal boys. The faster recovery of CPPi in prepubertal boys might be explained by their lower muscle glycolytic activity and their higher muscle oxidative capacity allowing a faster resynthesis of phosphocreatine.

Effects of exercise on nitrogen excretion, carbamoyl phosphate synthetase III activity and related urea cycle enzymes in muscle and liver tissues of juvenile rainbow trout ( Oncorhynchus mykiss)

The purpose of this study was to determine if carbamoyl phosphate synthetase III (CPSase III) and related urea cycle enzyme activities in skeletal muscle tissue of juvenile rainbow trout ( Oncorhynchus mykiss) increase during short- or long-term exercise, in parallel with changes in whole-body urea excretion rates. Urea excretion was elevated by 65% in fish that swam at high-speed (50 cm/s) vs. low-speed (20 cm/s) over a 2-h period, with no significant changes in CPSase III, ornithine transcarbamoylase or glutamine synthetase activities in muscle tissue. Fish that swam for 4 days at high-speed had higher rates of ammonia excretion and GSase activity in muscle and liver tissue relative to low-speed swimmers. Calculations showed that 47–53% of excreted urea, theoretically could be accounted for by total muscle CPSase III activity in juvenile and adult trout. The data indicate that increases in the rate of urea excretion during short-term high intensity exercise are not linked to higher activities of urea cycle enzymes in muscle tissue, but this does not rule out the possibility of increased flux through muscle CPSase III and related enzymes. Furthermore, these results indicate that urea cycle enzyme activities in skeletal muscle tissue can account for a significant portion of total urea excretion in juvenile and adult trout.

Effect of prior high-intensity exercise on exercise-induced arterial hypoxemia in Thoroughbred horses.

Strenuously exercising horses exhibit arterial hypoxemia and exercise-induced pulmonary hemorrhage (EIPH), the latter resulting from stress failure of pulmonary capillaries. The present study was carried out to examine whether the structural changes in the blood-gas barrier caused by a prior bout of high-intensity short-term exercise capable of inducing EIPH would affect the arterial hypoxemia induced during a successive bout of exercise performed at the same workload. Two sets of experiments, double- and single-exercise-bout experiments, were carried out on seven healthy, sound Thoroughbred horses. Experiments were carried out in random order, 7 days apart. In the double-exercise experiments, horses performed two successive bouts (each lasting 120 s) of galloping at 14 m/s on a 3.5% uphill grade, separated by an interval of 6 min. Exertion at this workload induced arterial hypoxemia within 30 s of the onset of galloping as well as desaturation of Hb, a progressive rise in arterial PCO2, and acidosis as exercise duration increased from 30 to 120 s. In the single-exercise-bout experiments, blood-gas/pH data resembled those from the first run of the double-exercise experiments, and all horses experienced EIPH. Thus, in the double-exercise experiments, before the horses performed the second bout of galloping at 14 m/s on a 3.5% uphill grade, stress failure of pulmonary capillaries had occurred. Although arterial hypoxemia developed during the second run, arterial PO2 values were significantly (P < 0.01) higher than in the first run. Thus prior exercise not only failed to accentuate the severity of arterial hypoxemia, it actually diminished the magnitude of exercise-induced arterial hypoxemia. The decreased severity of exercise-induced arterial hypoxemia in the second run was due to an associated increase in alveolar PO2, as arterial PCO2 was significantly lower than in the first run. Thus our data do not support a role for structural changes in the blood-gas barrier related to the stress failure of pulmonary capillaries in causing the exercise-induced arterial hypoxemia in horses.

Inhibition of nitric oxide synthase with L-NAME does not increase lactate production at rest or during short-term high-intensity exercise in Thoroughbred horses.

The present study was carried out to determine whether inhibition of nitric oxide (NO) synthase promotes anaerobic metabolism in exercising horses, resulting in a significantly increased blood lactate concentration. N(omega)-nitro-L-arginine methyl ester (L-NAME) is a potent inhibitor of NO synthase that has been tested in horses and other species. Two sets of experiments, namely placebo (saline control) and L-NAME (20 mg/kg, i.v.) studies, were carried out on seven healthy, sound, exercise-trained, Thoroughbred horses in random order, 6 to 7 days apart. In both experiments, an incremental exercise protocol was used and data were obtained at rest, during submaximal exercise performed at 8 m/s on a 4.5% uphill grade, and during galloping at 14 m/s on a 4.5% uphill grade--a workload that not only elicited maximal heart rate and induced exercise-induced pulmonary haemorrhage, but also could not be sustained for more than 90 s. Measurements were also made in the recovery period. Mixed-venous blood samples, obtained at matched intervals in the two sets of experiments, were analysed in triplicate for determining the lactate concentration. Following administration of L-NAME, significant bradycardia occurred at rest (27 +/- 1 vs 37 +/- 2 beats/min in the placebo trials; p<0.0001) as well as during submaximal exercise (183 +/- 4 vs 200 +/- 4 beats/min in the placebo trials; p<0.001), but the heart rate increased during galloping at 14 m/s on a 4.5% uphill grade to reach values observed in the placebo trials (215 +/- 2 beats/min) and significant differences were not found. At rest, the mixed-venous blood lactate concentration was similar in the two experiments. With exercise, the mixed-venous blood lactate concentration increased progressively as work intensity increased in both trials, but significant differences were not found between the placebo and the L-NAME experiments during submaximal exercise, near-maximal exercise or recovery. These experiments demonstrated that inhibition of NO synthase in Thoroughbred horses does not promote enhanced anaerobic metabolism at rest or during short-term incremental exercise leading to galloping at maximal heart rate.

Nutritional ergogenic aids and exercise performance

The use of nutritional supplements in sport is widespread and few serious athletes do not, at some stage in their career, succumb to the temptation to experiment with one or more nutritional supplements. Nutritional ergogenic aids are aimed primarily at enhancing performance (either by affecting energy metabolism or by an effect on the central nervous system), at increasing lean body mass or muscle mass by stimulation of protein synthesis and at reducing body fat content. Although not strictly ergogenic (i.e. capable of enhancing work performance), supplements aimed at increasing resistance to infection and improving general health are seen by athletes as important in reducing the interruptions to training that minor illness and infection can cause. Creatine is perhaps the most widely used supplement in sport at the moment. Supplementation can increase muscle creatine phosphate levels and, although not all published studies show positive results, there is much evidence that performance of short-term high-intensity exercise can be improved by supplementation. Ingestion of large doses of bicarbonate can enhance performance of exercise where metabolic acidosis may be a limiting factor, but there is a significant risk of adverse gastrointestinal side effects. Caffeine can also improve performance, in part by a stimulation of fatty acid mobilization and sparing of the body's limited carbohydrate stores, but also via direct effects on muscle and possibly by central nervous system effects on the perception of effort and fatigue. Carnitine plays an essential role in fatty acid oxidation in muscle but, although supplements are used by athletes, there is no good evidence of a beneficial effect of supplementation. None of these products contravenes the International Olympic Committee regulations on doping in sports, although caffeine is not permitted above a urine concentration of 12 mg/l. Supplementation is particularly prevalent among strength and power athletes, where an increase in muscle mass can benefit performance. Protein supplements have not been shown to be effective except in those rare cases where the dietary protein intake is otherwise inadequate. Individual amino acids, especially ornithine, arginine and glutamine, are also commonly used, but their benefit is not supported by documented evidence. Cr and hydroxymethylbutyrate are also used by strength athletes, but again there are no well-controlled studies to provide evidence of a beneficial effect. Athletes use a wide variety of supplements aimed at improving or maintaining general health and vitamin and mineral supplementation is widespread. There is a theoretical basis, and limited evidence, to support the use of antioxidant vitamins and glutamine during periods of intensive training, but further evidence is required before the use of these supplements can be recommended.

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This Month in the Journal

Effects of exercise intensity and environmental stress on indices of oxidative stress and iron homeostasis during exercise in the horse.

The effects of prolonged variable-intensity and short-term high-intensity exercise on indices of oxidative stress and iron homeostasis were compared in six fit horses under cool [20 degrees C, 40% relative humidity (RH)] or hot/humid (30 degrees C, 80% RH) environmental conditions. The exercise protocols were designed to simulate equine competition, including racing (intense exercise) or the speed and endurance phase of a 3-day event (prolonged exercise). Increased plasma concentrations of lipid hydroperoxides and haemolysate concentrations of oxidised glutathione (GSSG) were measured within 30 min of the completion of exercise, indicating production of reactive oxygen species (ROS) and lipid membrane peroxidation. The horses were unable to complete the prolonged exercise protocol at high temperature and humidity. This coincided with higher maximal values of lipid hydroperoxides [138.2 (17.7) microM and GSSG [110.6 (18.2) microM], compared to high-intensity [105.2 (14.9) microM and 63.6 (8.6) microM, respectively] or prolonged [100.7 (18.7) microM and 86.2 (9.1) microM, respectively] exercise performed under cooler environmental conditions. Significant correlations were found between the duration of the final stage of exercise during hot/humid environmental conditions and increased levels of lipid hydroperoxides (r = 0.85), GSSG (r = 0.94), xanthine (r = 0.92) and uric acid (r = 0.96). Exercise also decreased the iron (Fe)-binding antioxidant activity of the plasma and increased the total plasma Fe levels, although this was only significant for prolonged exercise in ambient conditions. There was no detectable free Fe in the plasma at any stage of exercise. Other changes in biochemical parameters had returned to pre-exercise levels within 24 h after exercise. The results show that exercise can induce changes in biochemical parameters that are indicative of oxidative stress in the fit horse and that this was, exacerbated during exercise at high temperature and humidity.

LEFT VENTRICULAR DIASTOLIC FUNCTION AND AEROBIC POWER AFTER EXERCISE TRAINING AND CALCIUM CHANNEL BLOCKADE 1023

Recent studies have shown that the calcium channel blocker verapamil improves left ventricular diastolic function (LVDF) in healthy elderly with diastolic dysfunction. Cross-sectional studies also suggest that physically fit elderly may have LVDF parameters similar to the young. The purpose of this study was to compare resting LVDF and the exercise performance of older men following:1. 12 weeks of daily oral 240mg verapamilSR (V) administration, and 2. short term high intensity exercise training (XT). Nine healthy sedentary older men (68 +/- 3y), with evidence of LVDF using Doppler echocardiography, participated in both the drug (1) and exercise (2) programs separated by 2 months. Before (pre) and after (post) both programs resting LVDF was assessed using Doppler echocardiography, and aerobic power (VO2max) assessed during cycle ergometry. Both XT and V produced significant increases in VO2max of 12% respectively (p<0.05) with no difference between the groups. Doppler studies showed a significant reduction in the isovolumic relaxation time (IVRT) following XT (pre=0.095s vs post=0.072s) and V(pre=0.095s and post=0.069), and a significant increase in the ratio of early to late flow velocity (E/A) after XT (pre=0.94 vs post=1.21) and V (pre=0.94 vs post=1.26). No differences were observed in Doppler studies between XT and V. The comparable results of XT and V on LVDF in healthy older men with pre-existing diastolic dysfunction suggest that repeated elevations of venous return and heart rate with high intensity XT may improve calcium handling and hence LV function.

No effect of glycogen level on glycogen metabolism during high intensity exercise

This study examined the effect of glycogen supercompensation on glycogen breakdown, muscle and blood lactate accumulation, blood-pH, and performance during short-term high-intensity exercise. Young healthy volunteers performed two supramaximal (125% of VO2max) exercise tests on a bicycle ergometer, either for 1 min 45 s (protocol 1; N = 18) or to exhaustion (protocol 2; N = 14). The exercise tests were preceded by either 5 d on a controlled normal (N) diet, or by 2 d of glycogen-depleting exercise accompanied by the normal diet followed by 3 d on a carbohydrate-rich (CHR) diet. In protocol 1, preexercise muscle glycogen concentrations were 364 +/- 23 and 568 +/- 35 mumol.g-1 d.w. in the N and CHR condition, respectively (P < 0.05). During the exertion, glycogen concentration in the M. quadriceps decreased to the same extent in both groups. Accordingly, the exercise-induced increases in muscle and blood-lactate, and the fall in blood-pH were similar during N and CHR. In protocol 2, time to exhaustion was identical for N and CHR. It is concluded that during short-term intense exercise during which muscle glycogen availability exceeds glycogen demand, rate of glycogen breakdown, lactate accumulation, and performance are regulated irrespective of the preexercise muscle glycogen level.

Skeletal muscle buffer value, fibre type distribution and high intensity exercise performance in man

Interrelationships between quadriceps femoris muscle buffer value (beta), fibre type distribution, and lactate concentration and pH following short-term high intensity exercise were examined in eighteen young healthy human volunteers. Muscle biopsy samples were taken from the lateral portion of the quadriceps femoris muscle at rest and after fatiguing dynamic or isometric exercise. Isometric exercise required the maintenance of 60% quadriceps maximum voluntary contraction, and dynamic exercise, the performance of a modified Wingate Test. The muscle buffer value displayed a positive, but non-significant correlation with the relative area of the muscle occupied by type II fibres (r = 0.42, P = 0.09). An elevated beta was associated with a lesser decrement in muscle pH during intensive exercise but did not permit the accumulation of a higher muscle lactate concentration or allow for an enhanced dynamic or isometric exercise performance. A superior performance during dynamic exercise was associated with a high concentration of muscle lactate and a low muscle pH post-exercise; in turn, each of these factors was positively dependent on the relative area of the muscle occupied by type II fibres. The converse was found for isometric exercise, where there was a tendency for an enhanced performance to be associated with a low muscle lactate and high muscle pH post-exercise. No significant relationship between the relative type II fibre area and isometric performance capacity could be established. It was concluded that the muscle buffer value is not a major limiting factor to the performance of high intensity exercise, suggesting that the involvement of intramuscular acidosis in the development of fatigue may be indirect. The most important determinant of high intensity exercise capacity appears to be the proportional area of the muscle occupied by type II fibres, where a high value provides for a superior dynamic but inferior isometric exercise performance.

Pulmonary interstitial edema in the pig after heavy exercise.

During exercise (especially in hypoxia), the alveolar-arterial O2 tension difference increases. This impairment of pulmonary gas exchange is caused partly by diffusion disequilibrium, but it has also been shown that an exercise-induced increase in ventilation-perfusion (VA/Q) inequality develops. Possible explanations of increased VA/Q mismatch include nonuniform pulmonary vasoconstriction, reduced gas mixing in the large airways, airway obstruction, and the development of interstitial pulmonary edema. To directly determine whether the latter develops in high-intensity short-term exercise, we exercised pigs on a motor-driven treadmill at the highest speed that they could sustain for 6-7 min. Heart rate reached 274 +/- 5 min-1 in the exercised group, confirming that the pigs reached a near-maximal level of exercise. While running, the pigs were killed by an intravenous overdose of pentobarbital. Postmortem, the lungs were immediately removed, drained of blood, weighed, and then airway fixed with 10% formaldehyde. Four tissue blocks of the right lung of each pig were taken from the ventral and dorsal areas of the upper and lower lobes, respectively. They were stained with hematoxylin and eosin and prepared for histological examination by light microscopy. There was no difference in the lung-to-body weight ratio between exercised pigs (7.72 +/- 0.87 g/kg) and a nonexercised control group (7.70 +/- 0.68 g/kg). However, we found a significantly higher percentage of pulmonary arteries with perivascular edema in exercised (33.8 +/- 3.4%) than in nonexercised pigs (20.0 +/- 4.0%; P < 0.02). Thus, perivascular edema (and thus possibly also parenchymal interstitial edema) can occur during short-term heavy exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory muscle function in trained and untrained adolescents during short-term high intensity exercise.

The breathing pattern and respiratory muscle function were investigated in ten trained and ten untrained adolescents (aged 15-16 years) while undergoing an incremental intensity exercise test on a cycle ergometer up to 80% maximal oxygen consumption (VO2max), maintained to exhaustion. Before and after exercise, maximal inspiratory (PImax) and expiratory (PEmax) pressures were measured at residual volume and total lung capacity, respectively. During exercise, the breathing pattern [tidal volume (VT), respiratory frequency (fR), ventilation] and the relative contribution of ribcage and abdomen to VT were assessed using inductance plethysmography. Electromyographic activities of transversus abdominis (EMGtr) and diaphragm (EMGdi) muscles were recorded and analysed during exercise. There was a difference in the change in the pattern of breathing between the trained and the untrained group; fR increased significantly (P < 0.05) at 40% VO2max for the untrained group. Before exercise there was no difference in the maximal respiratory pressures. Up to 60% and 80% VO2max, transversus abdominis and diaphragm muscle activity increased significantly in the trained adolescents. However in this group, no evidence of respiratory muscle fatigue appeared: PImax, PEmax and the frequency spectrum of EMGtr and EMGdi were not altered by exercise up to exhaustion. In the untrained group, who had high ventilatory responses, expiratory muscle function was unchanged at the end of the exercise, but signs of inspiratory muscle fatigue appeared in that PImax was significantly decreased after exercise.

Factors influencing excess postexercise oxygen consumption in trained and untrained women

This study investigated the effects of blood lactate and norepinephrine levels and rectal temperature on excess postexercise oxygen consumption (EPOC) following two different exercise intensities. Six trained and seven untrained women each performed two exercise tests, short-term high-intensity exercise ([HI] ∼80% maximum oxygen consumption [Vo 2max]) and long-term low-intensity exercise ([LOW] ∼65% Vo 2max) until 300 kcal were expended. Rectal temperature, oxygen consumption (Vo 2), and lactate and norepinephrine levels were monitored at rest, during exercise, and for 60 minutes into recovery. Exercise times averaged 30.0 ± 4.5 and 23.7 ± 0.9 minutes in trained women and 45 ± 3.6 and 30.0 ± 0.4 minutes in untrained women for LOW and HI, respectively. Rectal temperature, Vo 2, and lactate and norepinephrine levels were significantly elevated ( P < .05) during HI compared with LOW in both groups. Vo 2 was elevated throughout recovery following LOW and HI in untrained women only. Additionally, Vo 2 was elevated until minutes 50 and 40 following LOW and HI, respectively, in trained subjects. Rectal temperature returned to resting levels after 30 minutes of recovery following LOW, but remained significantly elevated throughout minute 50 of recovery following HI in trained women. However, values remained significantly elevated throughout recovery following both exercise bouts in untrained subjects. Norepinephrine levels remained elevated above resting levels throughout recovery following HI and until minute 50 following LOW in trained subjects, whereas levels remained elevated for 5 minutes following LOW and 50 minutes following HI in untrained subjects. Lactate levels remained elevated above baseline values throughout recovery following HI and LOW in both groups. It was concluded that in response to exercise requiring the same caloric expenditure, the magnitude of EPOC is greater during HI compared with LOW. Further, while many of the variables examined contribute to EPOC, these factors alone could not account completely for the EPOC observed.

Anaerobic Performance—Assessed by the Wingate Test—in Patients with Cystic Fibrosis

Cystic fibrosis (CF) patients were studied to investigate the muscles’ ability to produce and sustain high-intensity short-term exercise in this population. The patients, 17 males and 23 females, ranged from 10 to 39 years of age. Each patient performed a pulmonary function test followed by a Wingate Anaerobic Test (WAnT). Based on a pulmonary function scoring system, patients were classified as having severe, moderate, or mild lung dysfunction, or normal lung function. Percent ideal body weight was used to categorize the patients as nourished or malnourished. Two indices of anaerobic performance (peak power and mean power) were determined from the WAnT and normalized by actual weight or by ideal weight. Patients in the severe and moderate groups had lower peak power (PP) and lower mean power (MP) than those in the mild and normal groups. Similarly, malnourished patients showed a lower PP and MP than did nourished patients. These results were similar regardless of whether PP or MP were normalized by weight or ideal weight. It is concluded that the anaerobic performance (muscle power and endurance) of CF patients, as assessed by the WAnT, was related to the degree of severity of the overall disease process.

Anaerobic Power Responses to Amino Acid Nutritional Supplementation

To examine the effect of a nutritional supplement (ATP-E) on high intensity exercise performance, 23 physically active males volunteered to perform six Wingate Anaerobic Power tests. Tests were performed prior to and at 14 and 21 days during ATP-E or placebo ingestion. The experiment followed a double-blind and random-order design. Twelve subjects (responders, R) showed an increase in preexercise blood ATP on Day 14 of ATP-E ingestion compared to control measures. The remaining 11 subjects (nonresponders, NR) had no change in preexercise blood ATP. Peak power and mean power were unchanged for both R and NR subjects across the exercise tests, but R experienced a decrease (p < 0.05) in immediate post-exercise plasma lactate on Day 14 of ATP-E testing compared to their control measures. NR had no change in peak plasma lactate at any time during the study. The results suggest that short-term high intensity exercise performance was maintained in R with less reliance on anaerobic metabolism, and that response was evident following 14 days of ATP-E ingestion.

Diaphragm does not produce ammonia or lactate during high-intensity short-term exercise

To ascertain whether costal diaphragm engages in ammonia and lactate production (like limb muscles) during high-intensity short-term exercise, experiments were carried out on six healthy trained ponies in which phrenic venous catheters had been implanted 5-9 days earlier. Simultaneous anaerobically obtained blood samples from abdominal aorta and the phrenic vein at rest and during 4 min of exertion at 32 km/h and at a 7% grade were analyzed for blood-gas variables as well as lactate and ammonia concentrations using standard procedures. At rest, heart rate was 47 +/- 4 beats/min and the diaphragmatic O2 extraction was 26.5%. With exercise, heart rate rose to 218 +/- 6 beats/min, marked acidosis and hyperventilation occurred, and the diaphragmatic O2 extraction increased threefold (80.9%). Such exercise is known to dramatically increase the work of breathing as respiratory frequency and change in pleural pressure approach 138 +/- 4 breaths/min and 30 +/- 3 cmH2O, respectively. Despite the fact that phrenic-venous O2 tension of exercised ponies decreased to 15.5 +/- 0.6 Torr, the phrenic-venous lactate and ammonia concentrations did not exceed corresponding arterial values. These data thus revealed that the diaphragm is uniquely unlike limb muscles, which at high workloads readily engage in net ammonia and lactate production, and that the diaphragmatic energy needs during high-intensity short-term exercise are primarily met by aerobic metabolism.

Exercise-induced hypercapnia in the horse

The effects of exercise intensity and duration on blood gases in thoroughbred horses were studied to characterize the apparent exercise-induced failure in pulmonary gas exchange that occurs in these animals. In response to 2 min of exercise, arterial CO2 tension (PaCO2) decreased in mild and moderate exercise, returned to normocapnic levels in moderate to heavy exercise, and rose 5-10 Torr above resting values during very heavy exercise when CO2 production (VCO2) exceeded 20 times the resting value, and mixed venous CO2 tension approximated 140 Torr. Exercise-induced hypoxemia occurred at the onset of heavy exercise and was associated with the absence of a hyperventilatory response and an alveolar-arterial PO2 difference that increased four to six times above rest with very heavy exercise. PaCO2 was related to VCO2 but not fb, as changes in breathing frequency (fb) of 8-20 breaths/min at comparable VCO2 did not affect PaCO2. Prolonging very heavy exercise from 2 to 4 min caused a severe metabolic acidosis (arterial pH less than 7.15) and hypoxemia was maintained; however, CO2 was no longer retained, as PaCO2 gradually fell to below resting levels, due to an increased tidal volume at constant fb. We conclude that a truly compensatory hyperventilation to very heavy exercise in the horse is not achieved because of the excessive volumes and flow rates required by their extraordinarily high VCO2 and VO2. On the other hand, the frank CO2 retention during short-term high-intensity exercise occurs even though the horse is not apparently mechanically obligated to tolerate it.