Effects of exhaustive submaximal exercise on cardiovascular function during sleep

The influence of an afternoon bout of exhaustive submaximal exercise on cardiovascular function and catecholamine excretion during sleep was examined in five female and four male subjects. Subjects walked on a treadmill for successive 50-min periods at 50, 60, and 70% maximal O2 consumption, separated by 10-min rest periods. Exercise terminated with volitional exhaustion. Following an adaptation night, electroencephalographic and impedance cardiographic measures were obtained during three successive nights of sleep, with exercise preceding night 3. Relative to the base-line night (night 2), exhaustive exercise resulted in a sustained elevation of heart rate and cardiac output throughout the entire night's sleep. The magnitude of these elevations was unaffected by sleep stage but decreased over the night. The typical pattern of circadian decline in cardiac output was unaltered. However, the decline in heart rate with sleep onset was greater on the exercise night. Changes in impedance dZ/dt and R-Z interval suggested an enhanced myocardial contractility during the first 3 h of sleep postexercise. Analysis of morning urine samples revealed that in seven of nine subjects norepinephrine excretion increased, epinephrine excretion decreased, and dopamine excretion was unchanged during sleep on the exercise night. It is suggested that these cardiac changes reflect a sustained increase in myocardial beta-receptor activity.     

Effects of 7 wk of endurance training on human skeletal muscle metabolism during submaximal exercise.

This is the first study to examine the effects of endurance training on the activation state of glycogen phosphorylase (Phos) and pyruvate dehydrogenase (PDH) in human skeletal muscle during exercise. We hypothesized that 7 wk of endurance training (Tr) would result in a posttransformationally regulated decrease in flux through Phos and an attenuated activation of PDH during exercise due to alterations in key allosteric modulators of these important enzymes. Eight healthy men (22 +/- 1 yr) cycled to exhaustion at the same absolute workload (206 +/- 5 W; approximately 80% of initial maximal oxygen uptake) before and after Tr. Muscle biopsies (vastus lateralis) were obtained at rest and after 5 and 15 min of exercise. Fifteen minutes of exercise post-Tr resulted in an attenuated activation of PDH (pre-Tr: 3.75 +/- 0.48 vs. post-Tr: 2.65 +/- 0.38 mmol.min(-1).kg wet wt(-1)), possibly due in part to lower pyruvate content (pre-Tr: 0.94 +/- 0.14 vs. post-Tr: 0.46 +/- 0.03 mmol/kg dry wt). The decreased pyruvate availability during exercise post-Tr may be due to a decreased muscle glycogenolytic rate (pre-Tr: 13.22 +/- 1.01 vs. post-Tr: 7.36 +/- 1.26 mmol.min(-1).kg dry wt(-1)). Decreased glycogenolysis was likely mediated, in part, by posttransformational regulation of Phos, as evidenced by smaller net increases in calculated muscle free ADP (pre-Tr: 111 +/- 16 vs. post-Tr: 84 +/- 10 micromol/kg dry wt) and P(i) (pre-Tr: 57.1 +/- 7.9 vs. post-Tr: 28.6 +/- 5.6 mmol/kg dry wt). We have demonstrated for the first time that several signals act to coordinately regulate Phos and PDH, and thus carbohydrate metabolism, in human skeletal muscle after 7 wk of endurance training.     

Is exhaustive training adequate preparation for endurance performance?

Our purpose was to test the significance of exhaustive training in aerobic or endurance capacity. The extent of adaptations to endurance training was evaluated by assessing the increase in physical performance capability and oxidative markers in the organs of rats trained by various exercise programs. Rats were trained by treadmill running 5 days.week-1 at 30 m.min-1 for 8 weeks by one of three protocols: T1-60 min.day-1; T2-120 min.day-1; and T3-120 min.day-1 (3 days.week-1) and to exhaustion (2 days.week-1). Groups T2 and T3 ran for longer than T1 in an endurance exercise test (P less than 0.05), in which the animals ran at 30 m.min-1 to exhaustion; no difference was observed between groups T2 and T3. All 3 trained groups showed a similar increase (20-27%) in the fast-twitch oxidative-glycolytic (FOG) fibers with a concomitant decrease in the fast-twitch glycolytic (FG) fiber population in gastrocnemius (p less than 0.05). The capillary supply in gastrocnemius increased with the duration of exercise (p less than 0.05): no difference was found between groups T2 and T3. Likewise, no distinction was seen between groups T2 and T3 in the increase in succinate dehydrogenase activity in gastrocnemius and the heart. These results suggest that the maximal adaptive response to endurance training does not require daily exhaustive exercise.     

Creatine phosphate in fiber types of skeletal muscle before and after exhaustive exercise

Percutaneous muscle biopsies were obtained from the vastus lateralis of physically active men (n = 12) 1) at rest, 2) immediately after an exercise bout consisting of 30 maximal voluntary knee extensions of constant angular velocity (3.14 rad/s), and 3) 60 s after termination of exercise. Creatine phosphate (CP) content was analyzed in pools of freeze-dried fast-twitch (FT) and slow-twitch (ST) muscle fiber fragments, and ATP, CP, creatine, and lactate content were assayed in mixed pools of FT and ST fibers. CP content at rest was 82.7 +/- 11.2 and 73.1 +/- 9.5 (SD) mmol/kg dry wt in FT and ST fibers (P less than 0.05). After exercise the corresponding values were 25.4 +/- 19.8 and 29.7 +/- 14.4 mmol/kg dry wt. After 60 s of recovery CP increased (P less than 0.01) to 41.3 +/- 12.6 and 49.6 +/- 11.7 mmol/kg dry wt in FT and ST fibers, respectively. CP content after recovery, relative to initial level, was higher in ST compared with FT fibers (P less than 0.05). ATP content decreased (P less than 0.05) and lactate content rose to 67.4 +/- 28.3 mmol/kg dry wt (P less than 0.001) in response to exercise. It is concluded that basal CP content is higher in FT fibers than in ST fibers. CP content also appears to be higher in ST fibers after a 60-s recovery period after maximal short-term exercise. These data are consistent with the different metabolic profiles of FT and ST fibers.     

Increased submaximal insulin-stimulated glucose uptake in mouse skeletal muscle after treadmill exercise.

The primary purpose of this study was to determine the effect of prior exercise on insulin-stimulated glucose uptake with physiological insulin in isolated muscles of mice. Male C57BL/6 mice completed a 60-min treadmill exercise protocol or were sedentary. Paired epitrochlearis, soleus, and extensor digitorum longus (EDL) muscles were incubated with [3H]-2-deoxyglucose without or with insulin (60 microU/ml) to measure glucose uptake. Insulin-stimulated glucose uptake for paired muscles was calculated by subtracting glucose uptake without insulin from glucose uptake with insulin. Muscles from other mice were assessed for glycogen and AMPK Thr172 phosphorylation. Exercised vs. sedentary mice had decreased glycogen in epitrochlearis (48%, P < 0.001), soleus (51%, P < 0.001), and EDL (41%, P < 0.01) and increased AMPK Thr172 phosphorylation (P < 0.05) in epitrochlearis (1.7-fold), soleus (2.0-fold), and EDL (1.4-fold). Insulin-independent glucose uptake was increased 30 min postexercise vs. sedentary in the epitrochlearis (1.2-fold, P < 0.001), soleus (1.4-fold, P < 0.05), and EDL (1.3-fold, P < 0.01). Insulin-stimulated glucose uptake was increased (P < 0.05) approximately 85 min after exercise in the epitrochlearis (sedentary: 0.266 +/- 0.045 micromol x g(-1) x 15 min(-1); exercised: 0.414 +/- 0.051) and soleus (sedentary: 0.102 +/- 0.049; exercised: 0.347 +/- 0.098) but not in the EDL. Akt Ser473 and Akt Thr308 phosphorylation for insulin-stimulated muscles did not differ in exercised vs. sedentary. These results demonstrate enhanced submaximal insulin-stimulated glucose uptake in the epitrochlearis and soleus of mice 85 min postexercise and suggest that it will be feasible to probe the mechanism of enhanced postexercise insulin sensitivity by using genetically modified mice.     

Lactate transport activity in rat skeletal muscle sarcolemmal vesicles after acute exhaustive exercise.

The effect of a single bout of exhaustive exercise on muscle lactate transport capacity was studied in rat skeletal muscle sarcolemmal (SL) vesicles. Rats were assigned to a control (C) group (n = 14) or an acutely exercised (E) group (n = 20). Exercise consisted of treadmill running (25 m/min, 10% grade) to exhaustion. SL vesicles purified from C and E rats were sealed because of sensitivity to osmotic forces. The time course of 1 mM lactate uptake in zero-trans conditions showed that the equilibrium level in the E group was significantly lower than in the C group (P < 0.05). The initial rate of 1 mM lactate uptake decreased significantly from 2.44 +/- 0.22 to 1.03 +/- 0.08 nmol. min(-1). mg protein(-1) (P < 0.05) after exercise, whereas that of 50 mM lactate uptake did not differ significantly between the two groups. For 100 mM external lactate concentration ([lactate]), exhaustive exercise increased initial rates of lactate uptake (219.6 +/- 36.3 to 465.4 +/- 80.2 nmol. min(-1). mg protein(-1), P < 0.05). Although saturation kinetics were observed in the C group with a maximal transport velocity of 233 nmol. min(-1). mg protein(-1) and a Michealis-Menten constant of 24.5 mM, saturation properties were not seen after exhaustive exercise in the E group, because initial rates of lactate uptake increased linearly with external [lactate]. We conclude that a single bout of exhaustive exercise significantly modified SL lactate transport activity, resulting in a decrease in 1 mM lactate uptake and was associated with alterations in the saturable properties at [lactate] above 50 mM. These results suggest that changes in sarcolemmal lactate transport activity may alter lactate and proton exchanges after exhaustive exercise.     

耐力训练和急性力竭运行对大鼠组织金属硫蛋白含量的不同…

为探讨金属硫蛋白（ＭＴ）在运动提高机体自我贩作用,本文实验观察了游泳运动对大鼠心、肝、肺、脑、血管、因浆和骨骼肌等组织金属硫蛋白含量的影响。结果表明耐力训练组大鼠心、肝、肺和骨骼组织金属硫蛋白含量较政党对照组明显降低１３－３４％（Ｐ〈０．０５）;急性力竭运动组大鼠心、肝、脑、肺和骨骼肌组织其含量较正常对照则明显或高２１－７５％（Ｐ〈０．０５）;但两组大鼠血管和血浆ＭＴ含量变化与对照组大鼠要比无统计     

Metabolic and performance responses during endurance exercise after high-fat and high-carbohydrate meals

We studied the effects of preexercise mealcomposition on metabolic and performance-related variables duringendurance exercise. Eight well-trained cyclists (maximal oxygen uptake65.0 to 83.5 ml · kg¹ · min¹)were studied on three occasions after an overnight fast. They weregiven isoenergetic meals containing carbohydrate (CHO), protein (P),and fat (F) in the following amounts (g/70 kg body wt):high-carbohydrate meal, 215 CHO, 26 P, 3 F; high-fat meal, 50 CHO, 14 P, 80 F. On the third occasion subjects were studied after an overnightfast. Four hours after consumption of the meal, subjects startedexercise for 90 min at 70% of their maximal oxygen uptake, followed by a 10-km time trial. The high-carbohydrate meal compared with the high-fat meal resulted in significant decreases(P < 0.05) in blood glucose, plasmanonesterified fatty acids, plasma glycerol, plasmachylomicron-triacylglycerol, and plasma 3-hydroxybutyrate concentrations during exercise. This was accompanied by anincrease in plasma insulin (P < 0.01 vs. no meal), plasma epinephrine, and plasma growth hormoneconcentrations (each P < 0.05 vs.either of the other conditions) during exercise. Despite these large differences in substrate and hormone concentrations in plasma, substrate oxidation during the 90-min exercise period was similar inthe three trials, and there were no differences in performance on thetime trial. These results suggest that, although the availability offatty acids and other substrates in plasma can be markedly altered bydietary means, the pattern of substrate oxidation during enduranceexercise is remarkably resistant to alteration.

     

Acute muscle stretching inhibits muscle strength endurance performance

Since strength and muscular strength endurance are linked, it is possible that the inhibitory influence that prior stretching has on strength can also extend to the reduction of muscle strength endurance. To date, however, studies measuring muscle strength endurance poststretching have been criticized because of problems with their reliability. The purpose of this study was twofold: both the muscle strength endurance performance after acute static stretching exercises and the repeatability of those differences were measured. Two separate experiments were conducted. In experiment 1, the knee-flexion muscle strength endurance exercise was measured by exercise performed at 60 and 40% of body weight following either a no-stretching or stretching regimen. In experiment 2, using a test-retest protocol, a knee-flexion muscle strength endurance exercise was performed at 50% body weight on 4 different days, with 2 tests following a no-stretching regimen (RNS) and 2 tests following a stretching regimen (RST). For experiment 1, when exercise was performed at 60% of body weight, stretching significantly (p < 0.05) reduced muscle strength endurance by 24%, and at 40% of body weight, it was reduced by 9%. For experiment 2, reliability was high (RNS, intraclass correlation = 0.94; RST, intraclass correlation = 0.97). Stretching also significantly (p < 0.05) reduced muscle strength endurance by 28%. Therefore, it is recommended that heavy static stretching exercises of a muscle group be avoided prior to any performances requiring maximal muscle strength endurance.     

Lymphocyte apoptosis after exhaustive and moderate exercise.

Apoptosis or programmed cell death is a process of fundamental importance for regulation of the immune response. Several reasons suggest that apoptosis is involved in exercise-induced alterations of the immune system such as postexercise lymphocytopenia. Healthy volunteers performed two treadmill exercise tests; the first was performed at 80% maximal oxygen uptake until exhaustion (exhaustive exercise) and the second 2 wk later at 60% maximal oxygen uptake with the identical running time (moderate exercise). Blood samples were taken before, immediately after, and 1 h after the test. Lymphocytes were analyzed for apoptotic and necrotic cells by using FITC-labeled annexin V-antibodies and nuclear propidium iodide uptake, respectively. In addition, apoptotic/necrotic cells were measured after a 24-h incubation of lymphocytes in the presence of camptothecin or phytohemagglutinin. Finally, plasma membrane expression of CD95-receptor and CD95-receptor ligand was investigated. Immediately after the exhaustive exercise, the percentage of apoptotic cells increased significantly, whereas it remained unchanged after the moderate exercise. Similar results were obtained after 24-h incubation of lymphocytes in medium alone or in the presence of camptothecin, but not with phytohemagglutinin. We found an upregulation of CD95-receptor expression after both exercise tests. However, only after exhaustive exercise a characteristic shift in CD95 expression profile toward cells with a high receptor density was observed. Expression of the CD95-receptor ligand remained unchanged after both exhaustive and moderate exercise. These results suggest that apoptosis may contribute to the regulation of the immune response after exhaustive exercise. Whether this mechanism can be regarded either as beneficial, i.e., deletion of autoreactive cells, or harmful, i.e., suppression of the immune response, awaits further investigations.     

Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise.

We determined the effects of augmented expiratory intrathoracic pressure (P(ITP)) production on cardiac output (Q(TOT)) and blood flow distribution in healthy dogs and dogs with chronic heart failure (CHF). From a control expiratory P(ITP) excursion of 7 +/- 2 cmH2O, the application of 5, 10, or 15 cmH2O expiratory threshold loads increased the expiratory P(ITP) excursion by 47 +/- 23, 67 +/- 32, and 118 +/- 18% (P < 0.05 for all). Stroke volume (SV) rapidly decreased (onset <10 s) with increases in the expiratory P(ITP) excursion (-2.1 +/- 0.5%, -2.4 +/- 0.9%, and -3.6 +/- 0.7%, P < 0.05), with slightly smaller reductions in Q(TOT) (0.8 +/- 0.6, 1.0 +/- 1.1, and 1.8 +/- 0.8%, P < 0.05) owing to small increases in heart rate. Both Q(TOT) and SV were restored to control levels when the inspiratory P(ITP) excursion was augmented by the addition of an inspiratory resistive load during 15 cmH2O expiratory threshold loading. The highest level of expiratory loading significantly reduced hindlimb blood flow by -5 +/- 2% owing to significant reductions in vascular conductance (-7 +/- 2%). After the induction of CHF by 6 wk of rapid cardiac pacing at 210 beats/min, the expiratory P(ITP) excursions during nonloaded breathing were not significantly changed (8 +/- 2 cmH2O), and the application of 5, 10, and 15 cmH2O expiratory threshold loads increased the expiratory P(ITP) excursion by 15 +/- 7, 23 +/- 7, and 31 +/- 7%, respectively (P < 0.05 for all). Both 10 and 15 cmH2O expiratory threshold loads significantly reduced SV (-3.5 +/- 0.7 and -4.2 +/- 0.7%, respectively) and Q(TOT) (-1.7 +/- 0.4 and -2.5 +/- 0.4%, P < 0.05) after the induction of CHF, with the reductions in SV predominantly occurring during inspiration. However, the augmentation of the inspiratory P(ITP) excursion now elicited further decreases in SV and Q(TOT). Only the highest level of expiratory loading significantly reduced hindlimb blood flow (-4 +/- 2%) as a result of significant reductions in vascular conductance (-5 +/- 2%). We conclude that increases in expiratory P(ITP) production-similar to those observed during severe expiratory flow limitation-reduce cardiac output and hindlimb blood flow during submaximal exercise in health and CHF.     

Recovery following exhaustive dynamic exercise in the human biceps muscle

The aim of the study was to investigate the recovery of the maximum voluntary contraction force (MVC), the endurance time and electromyographical (EMG) parameters following exhaustive dynamic exercise of the m. biceps brachii. EMG recordings were made in ten healthy subjects using bipolar surface electrodes placed over the common belly of the left arm biceps muscle. Up to 25 h post-exercise, the maximum contraction force and the EMG signal were recorded alternately at regular intervals. The EMG signal was recorded during 30-s contractions at 40% of the pre-fatigued MVC. Four hours and 25 h post-exercise, the endurance time of a 40% pre-fatigued MVC was recorded. Up to 25 h after the exercise the maximum contraction force, the endurance time and the EMG parameters were significantly different from the pre-exercise values. Nine out of ten subjects complained that muscle soreness had developed. Thus, long-lasting changes are found after exhaustive dynamic exercise, not only in the MVC and the muscle's endurance capacity, but also in the EMG signal.     

Increased fatigue resistance of respiratory muscles during exercise after respiratory muscle endurance training

Respiratory muscle fatigue develops during exhaustive exercise and can limit exercise performance. Respiratory muscle training, in turn, can increase exercise performance. We investigated whether respiratory muscle endurance training (RMT) reduces exercise-induced inspiratory and expiratory muscle fatigue. Twenty-one healthy, male volunteers performed twenty 30-min sessions of either normocapnic hyperpnoea (n = 13) or sham training (CON, n = 8) over 4-5 wk. Before and after training, subjects performed a constant-load cycling test at 85% maximal power output to exhaustion (PRE(EXH), POST(EXH)). A further posttraining test was stopped at the pretraining duration (POST(ISO)) i.e., isotime. Before and after cycling, transdiaphragmatic pressure was measured during cervical magnetic stimulation to assess diaphragm contractility, and gastric pressure was measured during thoracic magnetic stimulation to assess abdominal muscle contractility. Overall, RMT did not reduce respiratory muscle fatigue. However, in subjects who developed >10% of diaphragm or abdominal muscle fatigue in PRE(EXH), fatigue was significantly reduced after RMT in POST(ISO) (inspiratory: -17 +/- 6% vs. -9 +/- 10%, P = 0.038, n = 9; abdominal: -19 +/- 10% vs. -11 +/- 11%, P = 0.038, n = 9), while sham training had no significant effect. Similarly, cycling endurance in POST(EXH) did not improve after RMT (P = 0.071), while a significant improvement was seen in the subgroup with >10% of diaphragm fatigue after PRE(EXH) (P = 0.017), but not in the sham training group (P = 0.674). However, changes in cycling endurance did not correlate with changes in respiratory muscle fatigue. In conclusion, RMT decreased the development of respiratory muscle fatigue during intensive exercise, but this change did not seem to improve cycling endurance.     

Operation Everest II: muscle energetics during maximal exhaustive exercise

To investigate the metabolic basis for the reduction in peak blood lactate concentration that occurs with maximal exercise after acclimatization to altitude, eight male subjects [maximal O2 uptake of 51.2 +/- 3.0 (SE) ml.kg-1.min-1] were acclimated to progressive hypobaria over a 40-day period. Before decompression (SL-1), at 380 and 282 Torr, and on return to sea level (SL-2) the subjects performed progressive cycle exercise to exhaustion. Analysis of muscle samples obtained from the vastus lateralis before exercise and at exhaustion indicated a pronounced reduction (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 282 Torr (39.2 +/- 11) compared with SL-1 (113 +/- 9.7), 380 Torr (94.6 +/- 18), and SL-2 (92.7 +/- 22). For the other glycolytic intermediates studied (glucose 1-phosphate, glucose 6-phosphate, fructose 6-phosphate, fructose 1,6-bisphosphate, and pyruvate) only the increase in glucose 1-phosphate, glucose 6-phosphate, and fructose 6-phosphate were blunted (P less than 0.05) at 282 Torr. The reduction in muscle glycogen concentration during exercise was similar (P less than 0.05) for all environmental conditions. Although exercise resulted in reductions (P less than 0.05) in ATP and creatine phosphate averaging 30 and 51%, respectively, the magnitude of the change was not dependent on the degree of hypobaria. Inosine monophosphate was elevated (P less than 0.05) approximately 11-fold with exercise at both SL-1 and SL-2. These findings support the hypothesis that the lower lactate concentration observed at 282 Torr after exhaustive exercise is due to a reduction in anaerobic glycolysis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum enzyme variations in men during an exhaustive "square-wave" endurance exercise test

The present study was designed to test if both the intensity and duration of the 45-min Square-Wave Endurance Exercise Test (SWEET) would produce changes in serum enzyme activities. Nine men, four sedentary (S) and five athletes (A), performed VO2 max and SWEET, at their Maximal Intensity of Endurance (MIE45) as defined by maximal heart rate and the impossibility of maintaining MIE 45 + 5% for 45 min. Arterial blood was sampled at rest (R), exercise (Ex) (45th min) and during recovery (15th min) for measurements of levels of Haemoglobin (Hb), Haematocrit (Hct), pH and seven serum enzymes: Creatine kinase (CPK), Hexose-phosphate isomerase (PHI), Aldolase (ALD), Lactate dehydrogenase (LDH), Malate dehydrogenase (MDH), Aspartate amino-transferase (ASAT or GOT), and Alanine aminotransferase (ALAT or GPT). Five enzymes increased significantly during exercise (MIE45), the delta % (Ex - R/R) increases were as follows: PHI (72%), MDH (28%), LDH (21%), CPK (17%), and GOT (13.5%), whilst only a 10% increase was observed for Hct and Hb and there was no significant change in the arterial pH. There was no correlation between the delta % of Hb, Hct, pH, and the results for the enzymes. Thus, it does not seem that haemoconcentration and arterial blood acidosis which occur during exercise are only at the origin of the observed increases in enzymes. A difference between "sedentary" and "athletes" subjects was found at rest and exercise (delta % = A - S/S) for CPK (R = 222%; Ex = 235%), GOT (R = 90%; Ex = 75%) and ALD (R = 99%; Ex = 54%). These results suggest that the MIE45, by measured increases in enzymatic activity, seems to require great muscular effort.