Limited myogenic response to a single bout of weight-lifting exercise in old rats

The purpose of the present study was to compare themyogenic response of hindlimb muscles in young (14-20 wk of age)and old (>120 wk of age) rats with a single exhaustive bout of heavyresistance weight lifting. [³H]thymidine and[¹⁴C]leucine labeling were monitored for up to2 wk after the exercise bout to estimate serial changes in mitoticactivity and the level of amino acid uptake and myosin synthesis.Histological, histochemical, and immunohistochemical[anti-5-bromo-2'-deoxyuridine and myogenic determinationgenes (MyoD)] analyses of whole muscles and analysis ofmuscle-specific gene expression (MyoD) using Western blotting andRT-PCR were performed. Old rats showed significant muscle atrophy and alower exercise capacity than young rats. Exercise-induced muscledamage, as assessed in histological sections, and increases in serumcreatine kinase activity were evident in both young and old exercisedgroups. Mitotic activity was increased in young, but not old, rats 2 days after exercise. There was a biphasic increase in[¹⁴C]leucine uptake during the 14 dayspostexercise (peaks at 1-4 and 10 days) in young rats: only thefirst peak was observed in old rats. There was a lower uptake of[¹⁴C]leucine in the myosin fraction and animpaired expression of MyoD at the protein (immunohistochemistry andWestern blotting) and mRNA (RT-PCR) levels in old rats throughout thepostexercise period. These results demonstrate a reduced reparativecapability of muscle in response to a single bout of exercise in oldcompared with young rats.

     

Autophagic response to a single bout of moderate exercise in murine skeletal muscle

The effect of a single bout of exercise on autopahgy in murine gastrocnemius muscle was investigated. Autophagy is a process for the degradation system of cytoplasmic components, which may help maintain intracellular quality control of cell survival and turnover under normal conditions. The present study investigated the changes of autophagy-related proteins including microtubule-associated protein 1b light chain 3 (LC3), Beclin-1, Atg7 (autophagy-related gene 7), conjugation form of Atg12 to Atg5, lysosome-associated membrane protein (LAMP2a), and muscle-specific RING finger protein-1 (MURF-1) protein level in gastrocnemius muscle after a single bout of treadmill exercise. Mice exercised on a treadmill for 50 min at a speed of 12.3 m/min with a slope of 5°. The animals were sacrificed by cervical dislocation 0, 3, 6, or 12 h after exercise, and muscle samples were collected immediately. Western blot analysis demonstrated that the autophagy marker LC3-II was significantly decreased during the recovery period (3, 6, and 12 h) whereas there was no decrease immediately after exercise (0 h). To identify factors related to this decrease, autophagosome component proteins were examined in murine gastrocnemius muscle. A decrease in Beclin-1, Atg7, and LAMP2a during recovery period was concomitant with the decreased level of LC3-II. Additionally, MuRF-1 expression was significantly increased after a single bout of exercise. This study is the first to demonstrate autophasic related protein expression after a single bout of treadmill exercise and our results suggest that a single bout of treadmill exercise attenuates the autophagic response in murine skeletal muscle.     

大鼠一次性力竭跑台运动模型的建立及动态评价

目的跑台急性运动疲劳动物模型的建立及评价。方法选取清洁级雄性Wistar大鼠24只(8周龄)作为实验对象。采用多级递增负荷跑台运动方案(跑台坡度为0°,负荷分为三级)建立一次性力竭跑台运动动物模型。尾静脉取血,分别测定大鼠在安静、运动30 min、运动90 min、力竭、恢复30 min、恢复90 min各时间点外周血葡萄糖(GLU)、乳酸(LD)、尿素(BU)、丙二醛(MDA)浓度和肌酸激酶(CK)、超氧化物歧化酶(SOD)活性。结果一次性力竭运动过程中大鼠行为能力和运动能力、血液代谢产物及能量物质呈现阶段性的动态变化。外周血LD、BU、MDA浓度及CK活性均较安静时显著性增高(P<0.01,P<0.05);GLU浓度、SOD活性较安静时显著降低(P<0.01,P<0.05)。各指标的变化特征说明大鼠已达到运动疲劳状态。结论建立了大鼠一次性力竭跑台运动模型,并客观动态评价了大鼠在运动疲劳产生、发展、恢复等不同阶段各指标的变化特点及规律。该模型可用于后续运动疲劳机制的相关研究。     

Lipid metabolism response to a single, prolonged bout of endurance exercise in healthy young men

To discover the alterations in lipid metabolism linked to postexercise hypotriglyceridemia, we measured lipid kinetics, lipoprotein subclass distribution and lipid transfer enzymes in seven healthy, lean, young men the day after 2 h of cycling and rest. Compared with rest, exercise increased fatty acid rate of appearance and whole body fatty acid oxidation by approximately 65 and 40%, respectively (P < 0.05); exercise had no effect on VLDL-triglyceride (TG) secretion rate, increased VLDL-TG plasma clearance rate by 40 +/- 8%, and reduced VLDL-TG mean residence time by approximately 40 min and VLDL-apolipoprotein B-100 (apoB-100) secretion rate by 24 +/- 8% (all P < 0.05). Exercise also reduced the number of VLDL but almost doubled the number of IDL particles in plasma (P < 0.05). Muscle lipoprotein lipase content was not different after exercise and rest, but plasma lipoprotein lipase concentration increased by approximately 20% after exercise (P < 0.05). Plasma hepatic lipase and lecithin:cholesterol acyltransferase concentrations were not affected by exercise, whereas cholesterol ester transfer protein concentration was approximately 10% lower after exercise than after rest (P = 0.052). We conclude that 1) greater fatty acid availability after exercise does not stimulate VLDL-TG secretion, probably because of the increase in fatty acid oxidation and possibly also fatty acid use for restoration of tissue TG stores; 2) reduced secretion of VLDL-apoB-100 lowers plasma VLDL particle concentration; and 3) increased VLDL-TG plasma clearance maintains low plasma TG concentration but is not accompanied by similar increases in subsequent steps of the delipidation cascade. Acutely, therefore, the cardioprotective lowering of plasma TG and VLDL concentrations by exercise is counteracted by a proatherogenic increase in IDL concentration.     

Gender differences in insulin action after a single bout of exercise.

Effects of a single exercise bout on insulin action were compared in men (n = 10) and women (n = 10). On an exercise day, subjects cycled for 90 min at 85% lactate threshold, whereas on a rest (control) day, they remained semirecumbent. The period of exercise, or rest, was followed by a 3-h hyperinsulinemic-euglycemic clamp (30 mU.m(-2).min(-1)) and indirect calorimetry. Glucose kinetics were measured isotopically by using an infusion of [6,6-2H2]glucose. Glucose infusion rate (GIR) during the clamp on the rest day was not different between the genders. However, GIR on the exercise day was significantly lower in men compared with women (P = 0.01). This was mainly due to a significantly lower glucose rate of disappearance in men compared with women (P = 0.05), whereas no differences were observed in the endogenous glucose rate of appearance. Nonprotein respiratory quotient (NPRQ) increased significantly during the clamp from preclamp measurements in men and women on the rest day (P < 0.01). Exercise abolished the increase in NPRQ seen during the clamp on the rest day and tended to decrease NPRQ in men. Our results indicate the following: 1) exercise abolishes the usual increase in NPRQ observed during a hyperinsulinemic-euglycemic clamp in both genders, 2) men exhibit relatively lower whole body insulin action in the 3-4 h after exercise compared with women, and 3) gender differences in insulin action may be explained by a lower glucose rate of disappearance in the men after acute exercise. Together, these data imply gender differences in insulin action postexercise exist in peripheral tissues and not in liver.     

Thioredoxin induction of peripheral blood mononuclear cells in mice in response to a single bout of swimming exercise

Thioredoxin (TRX) is a stress-inducible protein with diverse intracellular functions, which is expressed under conditions of oxidative stress. Exercise is known to cause oxidative stress by the generation of oxygen radicals from various biological pathways. The purpose of this study was to determine the level of TRX induction of cellular extracts prepared from peripheral blood mononuclear cells after a 30-min swimming exercise in mice. Plasma corticosterone concentration, considered to be a marker for exercise-induced various stress, rose significantly (p < 0.05) 0.5 h after exercise and rapidly dropped down following recovery. The carbonyl proteins as a marker of oxidative stress were significantly (p < 0.05) higher after 6 and 12 h of recovery in cytosolic extracts. The cytoplasm and nucleus TRX expressions were slightly higher to resting values after 12 and 24 h of recovery. The nucleus TRX expression was significantly (p < 0.05) higher after 24 h of recovery. These findings demonstrate that exercise-induced oxidative stress may be associated with increased intracellular TRX expression after 12 and/or 24 h after exercise in peripheral blood mononuclear cells. It is implied that this delayed and prolonged over-expression of TRX may play some roles in response to exercise-induced oxidative stress.     

Oral arginine attenuates the growth hormone response to resistance exercise.

This study investigated the combined effect of resistance exercise and arginine ingestion on spontaneous growth hormone (GH) release. Eight healthy male subjects were studied randomly on four separate occasions [placebo, arginine (Arg), placebo + exercise (Ex), arginine + exercise (Arg+Ex)]. Subjects had blood sampled every 10 min for 3.5 h. After baseline sampling (30 min), subjects ingested a 7-g dose of arginine or placebo (blinded, randomly assigned). On the exercise days, the subject performed 3 sets of 9 exercises, 10 repetitions at 80% one repetition maximum. Resting GH concentrations were similar on each study day. Integrated GH area under the curve was significantly higher on the Ex day (508.7 +/- 169.6 min.ng/ml; P < 0.05) than on any of the other study days. Arg+Ex (260.5 +/- 76.8 min.ng/ml) resulted in a greater response than the placebo day but not significantly greater than the Arg day. The GH half-life and half duration were not influenced by the stimulus administered. The GH secretory burst mass was larger, but not significantly, on the Arg, Ex, and Arg+Ex day than the placebo day. Endogenous GH production rate (Ex > Arg+Ex > Arg > placebo) was greater on the Ex and Arg+Ex day than on the placebo day (P < 0.05) but there were no differences between the Ex and Arg+Ex day. Oral arginine alone (7 g) stimulated GH release, but a greater GH response was seen with exercise alone. The combined effect of arginine before exercise attenuates the GH response. Autonegative feedback possibly causes a refractory period such that when the two stimuli are presented there will be suppression of the somatotrope.     

Evidence for altered alpha-adrenoreceptor responsiveness after a single bout of maximal exercise.

We studied hemodynamic responses to alpha- and beta-receptor agonists in eight men to test the hypothesis that adrenoreceptor responsiveness is altered within 24 h of the performance of maximal exercise. Adrenoreceptor responsiveness was tested under two experimental conditions (with and without maximal exercise). Adrenoreceptor tests were performed 24 h after each subject performed graded upright cycle ergometry to volitional exhaustion. The 2 test days (experimental conditions) were separated by at least 1 wk, and the order of exercise and no-exercise conditions was counterbalanced. Steady-state graded infusions of phenylephrine (PE) and isoproterenol (Iso) were used to assess alpha- and beta-adrenoreceptor responsiveness, respectively. Slopes calculated from linear regressions between Iso and PE doses and changes in heart rate, blood pressure, and leg vascular resistance for each subject were used as an index of alpha- and beta-adrenoreceptor responsiveness. The slope of the relationship between heart rate and Iso with maximal exercise was 1773 +/- 164 beats x microm-1x kg-1x min-1 compared with 1987 +/- 142 beats x microg-1x kg-1x min-1 without exercise (P = 0.158), whereas the slopes of the relationship between vascular resistance to Iso were -438 +/- 123 peripheral resistance units (PRU) x microg-1x kg-1x min-1 with maximal exercise and -429 +/- 105 x microg-1x kg-1 x min-1 without exercise (P = 0.904). Maximal exercise was associated with greater (P < 0.05) vascular resistance (15.1 +/- 2.8 PRU x microg-1 kg-1x min-1) and mean arterial blood pressure (15.8 +/- 2.1 mmHg. microg-1x kg-1x min-1) responses to PE infusion compared with no exercise (9.0 +/- 2.0 PRU x microg-1 kg-1 x min-1 and 10.9 +/- 2.0 mmHg. microg-1x kg-1x min-1, respectively). These results provide evidence that a single bout of maximal exercise increases alpha1-adrenoreceptor responsiveness within 24 h without affecting beta-cardiac and vascular adrenoreceptor responses.     

Activation pattern of MAPK signaling in the hearts of trained and untrained rats following a single bout of exercise.

Since exercise training causes cardiac hypertrophy and a single bout induces mechanical stress to the heart, the present study aimed to characterize the activation patterns of multiple MAPK signaling pathways in the heart after a single bout of exercise or chronic exercises. The hearts of untrained rats received 5, 15, and 30 min of treadmill running exercise (Ex5 to Ex30) and rested for 0.5, 1, 3, 6, 12, and 24 h (PostEx0.5 to PostEx24) before subjecting them to the following different experiments. Activation of MAPKs (ERK, JNK, and p38) and MAPKKs (MEK1/2, SEK, and MKK3/6) increased immediately after acute exercise in a time-dependent manner, with ERK, JNK, and p38 peaking at Ex15, Ex15, and Ex30, respectively. Expression of immediate early genes (c-fos, c-jun, and c-myc) was augmented and activator protein-1 DNA binding activity was enhanced in untrained rats immediately after a single bout of exercise. The elevated levels of MAPKs declined to the resting levels within 24 h after exercise. In another set of experiments, following 4, 8, and 12 wk of exercise training, the rats exhibited significant cardiac hypertrophy by week 12. Activation of MAPKs in the 4-wk-trained rats increased after a 30-min single bout of exercise but decreased in the 8-wk group. Finally, the activity of MAPKs signaling in the 12-wk-trained rats exposed to an acute bout of exercise was unaltered. We conclude that exercise induces the activation of multiple MAPK (ERK, JNK, and p38) pathways in the heart, an effect that gradually declines with the development of exercise-induced cardiac hypertrophy.     

Human growth hormone response to repeated bouts of aerobic exercise

Kanaley, J. A., J. Y. Weltman, J. D. Veldhuis, A. D. Rogol,M. L. Hartman, and A. Weltman. Human growth hormone response torepeated bouts of aerobic exercise. J. Appl.Physiol. 83(5): 1756-1761, 1997.We examinedwhether repeated bouts of exercise could override growth hormone (GH)auto-negative feedback. Seven moderately trained men were studied onthree occasions: a control day (C), a sequential exercise day (SEB; at1000, 1130, and 1300), and a delayed exercise day (DEB; at 1000, 1400, and 1800). The duration of each exercise bout was 30 min at 70%maximal O₂ consumption (O_{2 max}) on a cycleergometer. Standard meals were provided at 0600 and 2200. GH wasmeasured every 5-10 min for 24 h (0800-0800). Daytime(0800-2200) integrated GH concentrations were ~150-160% greater during SEB and DEB than during C: 1,282 ± 345, 3,192 ± 669, and 3,389 ± 991 min · µg · l¹for C, SEB, and DEB, respectively [SEB > C(P < 0.06), DEB > C(P < 0.03)]. There were nodifferences in GH release during sleep (2300-0700). Deconvolutionanalysis revealed that the increase in 14-h integrated GH concentrationon DEB was accounted for by an increase in the mass of GH secreted perpulse (per liter of distribution volume,l_v): 7.0 ± 2.9 and 15.9 ± 2.6 µg/l_v for C and DEB,respectively (P < 0.01). Comparisonof 1.5-h integrated GH concentrations on the SEB and DEB days (30 minexercise + 60 min recovery) revealed that, with each subsequentexercise bout, GH release apparently increased progressively, with aslightly greater increase on the DEB day [SEB vs. DEB: 497 ± 162 vs. 407 ± 166 (bout 1), 566 ± 152 vs. 854 ± 184 (bout2), and 633 ± 149 vs. 1,030 ± 352 min · µg · l¹(bout 3),P < 0.05]. We conclude thatthe GH response to acute aerobic exercise is augmented with repeatedbouts of exercise.

     

A single bout of exercise improves motor memory

Regular physical activity has a positive impact on cognition and brain function. Here we investigated if a single bout of exercise can improve motor memory and motor skill learning. We also explored if the timing of the exercise bout in relation to the timing of practice has any impact on the acquisition and retention of a motor skill. Forty-eight young subjects were randomly allocated into three groups, which practiced a visuomotor accuracy-tracking task either before or after a bout of intense cycling or after rest. Motor skill acquisition was assessed during practice and retention was measured 1 hour, 24 hours and 7 days after practice. Differences among groups in the rate of motor skill acquisition were not significant. In contrast, both exercise groups showed a significantly better retention of the motor skill 24 hours and 7 days after practice. Furthermore, compared to the subjects that exercised before practice, the subjects that exercised after practice showed a better retention of the motor skill 7 days after practice. These findings indicate that one bout of intense exercise performed immediately before or after practicing a motor task is sufficient to improve the long-term retention of a motor skill. The positive effects of acute exercise on motor memory are maximized when exercise is performed immediately after practice, during the early stages of memory consolidation. Thus, the timing of exercise in relation to practice is possibly an important factor regulating the effects of acute exercise on long-term motor memory.     

Reduced vascular responsiveness after a single bout of dynamic exercise in the conscious rabbit.

We measured agonist-induced changes in the iliac artery blood flow velocity (IFV) independent of baroreflex-mediated compensatory mechanisms in chronically instrumented New Zealand White rabbits (n = 8). Animals were instrumented with a Doppler flow probe around the right common iliac artery. A Teflon catheter was inserted into the right iliolumbar artery for local infusion of the vasoactive agonists. Another Teflon catheter was inserted in the left femoral artery for the measurement of pulsatile and mean arterial (MAP) blood pressures and heart rate (HR). The alpha-adrenergic receptor agonist phenylephrine (PE, 1.32-10.0 micrograms), the beta 1- and beta 2-adrenergic receptor agonist isoproterenol (IP, 0.022-0.11 micrograms), and the purinergic receptor agonist adenosine (AD, 10.0-100.0 micrograms) were injected into the functionally isolated hindlimb, and dose-response curves were generated. Changes in IFV were obtained without changes in MAP or HR. Exercise increased HR, MAP, and IFV (65.3 +/- 7.1 beats/min, 11.1 +/- 2.2 mmHg, and 2.2 +/- 0.3 kHz, respectively). The maximum responses to PE, AD, and IP were reduced 29.0 +/- 6.7, 50.7 +/- 8.5, and 61.0 +/- 8.1%, respectively, after exercise. In conclusion, exercise attenuated adrenergic and purinergic receptor-mediated vascular responses in the intact conscious rabbit.