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1.
The aim of this study was to monitor muscle contractile performance in vivo, using an electrical stimulation protocol, immediately following an acute high and low intensity exercise session conducted at the same average intensity performed on a cycle ergometer. Eighteen healthy males (25.1 ± 4.5 years, 81.6 ± 9.8 kg, 1.83 ± 0.06 m; mean ± SD) participated in the study. On two occasions, separated by 1 week, subjects completed a high and low intensity exercise session in a random order on a cycle ergometer, performing equal total work in each. At the end of each test, a muscle performance test using electrical stimulation was performed within 120 s. Post-exercise muscle data were compared to the subjects’ rested muscle. We found a reduction in muscle contractile performance following both high and low intensity exercise protocols but a greater reduction in maximal voluntary contraction (MVC) (P < 0.01), rate of torque development (RTD) (P < 0.001), rate of relaxation (RR?), (P < 0.001) the 60 s slope of the fatigue protocol (P < 0.01) and torque frequency response (P < 0.05) following the high intensity bout. Importantly muscle performance remained reduced 1 h following high intensity exercise but was recovered following low intensity exercise. Muscle function was significantly reduced following higher intensity intermittent exercise in comparison to lower intensity exercise even when the average overall intensity was the same. This study is the first to demonstrate the sensitivity of muscle contractile characteristics to different exercise intensities and the impact of higher intensity bursts on muscle performance.  相似文献   

2.
Our purposes were (1) to examine resting arterial blood pressure following an acute bout of resistance exercise and submaximal dynamic exercise, (2) to examine the effects of these exercises on the plasma concentrations of atrial natriuretic peptide ([ANP]), and (3) to evaluate the potential relationship between [ANP] and post-exercise blood pressure. Thirteen males [24.3 ± (2.4) years] performed 15 min of unilateral leg press exercise (65% of their one-repetition maximum) and, 1 week later, ≈15 min of cycle ergometry (at 65% of their maximum oxygen consumption). Intra-arterial pressure was monitored during exercise and for 1 h post-exercise. Arterial blood was drawn at rest, during exercise and at intervals up to 60 min post-exercise for analysis of haematocrit and [αANP]. No differences occurred in blood pressure between trials, but significant decrements occurred following exercise in both trials. Systolic pressure was ≈20 mmHg lower than before exercise after 10 min, and mean pressure was ≈7 mmHg lower from 30 min onwards. Only slight (non-significant) elevations in [αANP] were detected immediately following exercise, with the concentrations declining to pre-exercise values by 5 min post-exercise. We conclude that post-exercise hypotension occurs following acute bouts of either resistance or submaximal dynamic exercise and, in this investigation, that this decreased blood pressure was not directly related to the release of αANP. Accepted: 29 July 1998  相似文献   

3.
This study examined how single bouts of exercise may differentially modulate neuroelectric correlates of attentional orienting and processing. Using a within‐participants design, ERPs and task performance were assessed in response to a perceptually challenging three‐stimulus oddball task prior to and following a bout of exercise or seated rest during two separate, counterbalanced sessions. Findings revealed that, following a single bout of exercise, attentional processing was sustained relative to pretest whereas prolonged sitting resulted in attentional decrements. Focal attention resulting from attentional orienting, in contrast, does not appear to be sensitive to the influences of single bouts of physical activity. These findings suggest that acute exercise‐induced changes in cognition do not originate from an overall modulation of attention but instead are specific to aspects of attentional processing.  相似文献   

4.
Summary Rapid depletion of muscle glycogen occurs during activities greater than 100% of maximal oxygen uptake. While carbohydrate ingestion prior to an endurance event has been shown to be beneficial, the effects of carbohyrate ingestion on repeated bouts of high-intensity exercise are not known. Therefore, the purpose of this study was to determine if carbohydrate ingestion prior to repeated bouts of high-intensity, short-duration exercise would improve performance. Ten well-trained male cyclists performed two experimental rides, one 15 min after consumption of 5.0 ml·kg–1 body weight of a 19.7% carbohydrate drink and one following a placebo. The experimental ride consisted of four 1.6 km timed performance rides separated by 4.8 km steadystate rides at 80% of maximal oxygen uptake (between the last two performance rides the steady-state rides were 1.6 km at 80% and 1.6 km at 90%). Blood glucose levels were significantly increased following both the ingestion of the carbohydrate beverage and the performance of the exercise bout. Total exercise time following ingestion of the experimental drink [mean (SD); 25.6 (3.3) min] was not different from that following ingestion of the placebo [25.2 (3.3) min]. Similarly, the sum of all four timed performance rides following ingestion of the experimental drink [6.8 (0.9) min] was not different from that following ingestion of the placebo [6.6 (0.9) min]. In the present study, carbohydrate ingestion 15 min prior to exercise increased blood glucose levels, although performance time was not affected.  相似文献   

5.
Using a damaging eccentric exercise regime of the mouse tibialis anterior (TA) muscle we have investigated the extent and time course of protection afforded by one bout of exercise against damage resulting from a second bout of activity. Maximal force and fibre morphology were preserved if the exercise was repeated within 21 days, but by 84 days muscles once again became susceptible to damage. Low-frequency force loss had a shorter time course of protection against repeated exercise, lasting less than 21 days. The results provide evidence for different mechanisms contributing to the development of muscle damage following eccentric exercise and provide a basis for characterizing the adaptive response of muscle to damaging exercise.  相似文献   

6.
Evidence indicates that repeated-bouts of eccentric exercise (EE) do not exacerbate the extent of muscle damage indices, as compared to a single-bout. We hypothesized that molecular adaptations, under repeated-bouts of EE, would include suppression of muscle repair inhibitory factors such as myostatin and up-regulation of muscle repair positive regulatory factors such as myogenic regulatory factors (MRFs). Fifteen males were recruited for this study. The exercise group (n = 9) successfully completed six sets of 15 reps of maximum voluntary eccentric contractions, for six consecutive days, using a dynamometer (Multicont-II). Blood and muscle biopsy samples were obtained from each subject 1 week prior to exercise, 2 days post the first training session, and 24 h after the last training session. Gene expression levels were determined using real-time RT-PCR. Blood samples were analyzed for creatine kinase (CK) and lactate-dehydrogenase (LDH) activity. Repeated-bouts of EE induced a large down-regulation of myostatin mRNA (−73%) which persisted throughout the study. The responses of MRFs were mild. At day 3 only myogenin increased significantly (1.9 fold) while MyoD decreased by 45%. Surprisingly, at day 7, despite the presence of muscle damage indices, all MRFs returned to the pre-exercise levels. The results of the present study showed that repeated-bouts of EE, for six consecutive days, dramatically decreased Myostatin mRNA expression but impaired the expression patterns of MRFs such that, with the exception of myogenin that showed a moderate non-sustained increase, MyoD and MYf5 response was minimal. Grants: Funding was provided by the Ministry of Health of the Hungarian Government. Grant number: ETT 388/2003.  相似文献   

7.
In rat muscle, faster dynamics of microvascular P(O2) (approximately blood flow (Q(m) to O2 uptake (V(O2) ratio) after prior contractions that did not alter blood [lactate] have been considered to be a consequence of faster V(O2) kinetics. However, in humans, prior exercise below the lactate threshold does not affect the pulmonary V(O2) kinetics. To clarify this apparent discrepancy, we examined the effects of prior moderate exercise on the kinetics of muscle oxygenation (deoxyhaemoglobin, [HHb] alpha V(O2m)/Q(m)) and pulmonary V(O2) (V(O2p) in humans. Eight subjects performed two bouts (6 min each) of moderate-intensity cycling separated by 6 min of baseline pedalling. Muscle (vastus lateralis) oxygenation was evaluated by near-infrared spectroscopy and V(O2p) was measured breath-by-breath. The time constant (tau) of the primary component of V(O2p) was not significantly affected by prior exercise (21.5 +/- 9.2 versus 25.6 +/- 9.7 s; Bout 1 versus 2, P= 0.49). The time delay (TD) of [HHb] decreased (11.6 +/- 2.6 versus 7.7 +/- 1.5 s; Bout 1 versus 2, P < 0.05) and tau[HHb] increased (7.0 +/- 3.5 versus 10.2 +/- 4.6 s; Bout 1 versus 2, P < 0.05), while the mean response time (TD + tau) did not change (18.6 +/- 2.7 versus 17.9 +/- 3.9 s) after prior moderate exercise. Thus, prior moderate exercise resulted in shorter onset and slower rate of increase in [HHb] during subsequent exercise. These data suggest that prior exercise altered the dynamic interaction between V(O2m)and Q(m) following the onset of exercise.  相似文献   

8.
It is well established that exercise-induced muscle damage (EIMD) has a detrimental effect on endurance exercise performed in the days that follow. However, it is unknown whether such effects remain after a repeated bout of EIMD. Therefore, the purpose of this study was to examine the effects of repeated bouts of muscle-damaging exercise on sub-maximal running exercise. Nine male participants completed baseline measurements associated with a sub-maximal running bout at lactate turn point. These measurements were repeated 24–48 h after EIMD, comprising 100 squats (10 sets of 10 at 80 % body mass). Two weeks later, when symptoms from the first bout of EIMD had dissipated, all procedures performed at baseline were repeated. Results revealed significant increases in muscle soreness and creatine kinase activity and decreases in peak knee extensor torque and vertical jump performance at 24–48 h after the initial bout of EIMD. However, after the repeated bout, symptoms of EIMD were reduced from baseline at 24–48 h. Significant increases in oxygen uptake $ (\dot{V}{\text{O}}_{2} ) $ , minute ventilation $ (\dot{V}_{\text{E}} ) $ , blood lactate ([BLa]), rating of perceived exertion (RPE), stride frequency and decreases in stride length were observed during sub-maximal running at 24–48 h following the initial bout of EIMD. However, following the repeated bout of EIMD, $ \dot{V}{\text{O}}_{2} ,\;\dot{V}_{\text{E}} , $ [BLa], RPE and stride pattern responses during sub-maximal running remained unchanged from baseline at all time points. These findings confirm that a single resistance session protects skeletal muscle against the detrimental effects of EIMD on sub-maximal running endurance exercise.  相似文献   

9.
The purpose of this study was to examine the effects of a succession of fatiguing stages, on ratings of perceived exertion (RPE) and estimated time limits (ETL) during an incremental exercise test. Twenty-seven cyclists performed a continuous incremental test and a discontinuous test with randomized workloads. A linear mixed model was used to compare the RPE, ETL, respiratory gas, heart rate, and blood data obtained during the two exercise tests. RPE and ETL were not significantly different between the tests. Ventilation, breathing frequency, heart rate, and blood lactate concentration were significantly higher during the last incremental test workloads. In conclusion, although the incremental exercise test generated higher cardiorespiratory and muscular workloads than observed during the randomized exercise test, most likely due to a greater fatiguing process, these higher workloads did not influence the perceptual response.  相似文献   

10.
The purpose of this study was to examine the kinetics of phosphocreatine (PCr) breakdown in repeated bouts of heavy-intensity exercise separated by three different durations of resting recovery. Healthy young adult male subjects (n = 7) performed three protocols involving two identical bouts of heavy-intensity dynamic plantar flexion exercise separated by 3, 6, and 15 min of rest. Muscle high-energy phosphates and intracellular acid-base status were measured using phosphorus-31 magnetic resonance spectroscopy. In addition, the change in concentration of total haemoglobin (Delta[Hb(tot)]) and deoxy-haemoglobin (Delta[HHb]) were monitored using near-infrared spectroscopy. Prior exercise resulted in an elevated (P < 0.05) intracellular hydrogen ion ([H(+)](i)) after 3 min (182 +/- 72 (SD) nM; pH 6.73) and 6 min (112 +/- 19 nM; pH 6.95) but not after 15 min (93 +/- 8 nM; pH 7.03) compared to pre-exercise in Con (90 +/- 3 nM; pHi 7.05). The on-transient time constant (tau) of the PCr primary component was not different amongst the exercise bouts. However, in each of the subsequent bouts the amplitude of the PCr slow component, total PCr breakdown, and rise in [H(+)](i) were reduced (P < 0.05). At exercise onset, Delta[Hb(tot)] was increased (P < 0.05) and the Delta[HHb] kinetic response was slowed (P < 0.05) in the exercise after 3 min, consistent with improved muscle perfusion. In summary, neither the level of acidosis or muscle perfusion at the onset of exercise appeared to be directly related to the time course of the on-transient PCr primary component or the magnitude of the PCr slow component during subsequent bouts of exercise.  相似文献   

11.
Chronic resistance training induces increases in muscle fibre cross-sectional area (CSA), otherwise known as hypertrophy. This is due to an increased volume percentage of myofibrillarproteins within a given fibre. The exact time-course for muscle fibre hypertrophy is not well-documented but appears to require at least 6-7 weeks of regular resistive training at reasonably high intensity before increases in fibre CSA are deemed significant. Proposed training-induced changes in neural drive are hypothesized to increase strength due to increased synchrony of motor unit firing, reducedant agonist muscle activity, and/or a reduction in any bilateral strength deficit. Nonetheless, increases in muscle protein synthesis were observed following an isolated bout of resistance exercise. In addition, muscle balance was positive, following resistance exercise when amino acids were infused/ingested. This showed that protein accretion occurred during the postexercise period. The implications of this hypothesis for training-induced increases in strength are discussed.  相似文献   

12.
It is known that chronic endurance training leads to improvements in the lipoprotein profile, but less is known about changes that occur during postexercise recovery acutely. We analyzed triglyceride (TG), cholesterol classes and apolipoproteins in samples collected before, during and after individual moderate- and hard-intensity exercise sessions in men and women that were isoenergetic between intensities. Young healthy men (n = 9) and young healthy women (n = 9) were studied under three different conditions with diet unchanged between trials: (1) before, during and 3 h after 90 min of exercise at 45% VO2peak (E45); (2) before, during and 3 h after 60 min of exercise at 65% VO2peak (E65), and (3) in a time-matched sedentary control trial (C). At baseline, high-density lipoprotein cholesterol (HDL-C) was higher in women than men (P < 0.05). In men and in women, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), HDL-C, apolipoprotein A-I (apoA-I), apolipoprotein B (apoB), and LDL peak particle size were unaltered by exercise either during exertion or after 3 h of recovery. In women, but not in men, average plasma TG was significantly reduced below C at 3 h postexercise by approximately 15% in E45 and 25% in E65 (P < 0.05) with no significant difference between exercise intensities. In summary, plasma TG concentration rapidly declines following exercise in women, but not in men. These results demonstrate an important mechanism by which each individual exercise session may incrementally reduce the risk for cardiovascular disease (CVD) in women.  相似文献   

13.
The purpose of this study was to determine the electrolyte concentration changes in arterial plasma from high-intensity repeated bouts of cycling exercise in well-trained females and to determine the relationships between arterial plasma lactate, potassium (K+), bicarbonate (HCO3), and pH with minute ventilation. Fourteen female subjects (mean age = 27 ± 4 years; mean height = 170 ± 7 cm; mean weight = 62 ± 7 kg; maximal oxygen uptake = 50 ± 6 ml/kg/min) were recruited to perform 3 × 5 min bouts of exercise at 236 ± 27 W with 10 min recovery between each set. Minute ventilation, arterial plasma lactate, potassium, calcium, chloride, and sodium ion concentrations were measured a minute 0, 1, 2, 3, 4, 5 of each set and midway through recovery (21 sampling points total per subject). The results showed that the strongest relationship was between arterial plasma K+ concentration and minute ventilation (r 2 = 0.91), and, that arterial plasma lactate mirrored both arterial plasma HCO3 and pH. In conclusion, this study demonstrates that women exhibit similar electrolyte responses as reported elsewhere in men, and support the idea that K+ may partly contribute to controlling ventilation during high-intensity exercise and recovery.  相似文献   

14.
15.
We tested the hypothesis that measurement of plasma catecholamine sulphate concentration after exercise reflects the overall activation of the sympathoadrenergic system during the whole period of repeated bouts of short-term exercise. A group of 11 male athletes performed two exercise tests at similar average power outputs consisting of three sets each. The tests either started with one set of three very intense sprints (95% of maximal running speed) followed by two sets of three less intense sprints (85% of maximal running speed; HLX) or vice versa (LHX). Similar mean areas under the curve of free noradrenaline (NA) during HLX and LHX [622 (SEM 13) vs 611 (SEM 14) nmol?·?l?1?·?min) as well as similar mean heart rates [143 (SEM 9) vs 143 (SEM 8) beats?·?min?1] indicated comparable sympathetic activation during both exercise tests. Even so, plasma concentration of free NA was still significantly higher at the end of LHX than of HLX [35.7 (SEM 3.5) vs 22.5 (SEM 2.1) nmol?·?l?1, respectively], i.e. when exercise ended with the more intense set of sprints. Plasma noradrenaline sulphate (NA-S) increased with exercise intensity showing higher mean increments after the first set of HLX compared to LHX [1.83 (SEM 0.42) vs 1.18 (SEM 0.29) nmol?·?l?1; P?0.05]. However, after the end of HLX and LHX, increments in plasma NA-S were similar [4.52 (SEM 0.76) vs 4.06 (SEM 0.79) nmol?·?l?1], suggesting that NA-S response changed in parallel with the overall activation of the sympathetic nervous system during repeated bouts of short-term exercise. The results supported the hypothesis that measurement of plasma NA-S immediately after repeated bouts of short-term exercise reflects overall activation of the sympathetic nervous system during prolonged periods of this type of exercise.  相似文献   

16.
The purpose of this study was to examine the acute immune response (circulating levels of leukocytes, cytokines and adipocytokines) to maximal resistance (MAX, 15 × 1RM) and hypertrophic resistance (HYP, 5 × 10RM) exercise bouts. Twelve healthy men (age = 28.2 ± 3.5 years, weight = 78.6 ± 10.4 kg, height 178.8 ± 5.0 cm, fat percentage = 16.5 ± 3.5 %) participated in the study. Blood was sampled before, immediately after and 15 and 30 min after exercise. Leukocytes (WBC) significantly increased immediately after HYP (p < 0.01), whereas in MAX, increases in WBC became significant after 30 min (p < 0.05). Lymphocytes increased only after HYP (p < 0.001), while MAX induced lymphopenia during recovery (p < 0.01). Monocyte chemoattractant protein-1 (MCP-1) decreased (p < 0.05) and interleukin-1 receptor antagonist (IL-1ra) increased after HYP, which were not observed after MAX. Adipsin and resistin decreased after both exercise bouts (p < 0.05), which suggest that heavy resistance exercise is at least transiently beneficial for adipocytokine profile. Immediate mechanical stress seemed similar as no differences in myoglobin response were observed. The higher magnitude of metabolic demand reflected in higher lactate response in HYP could be the reason for the significantly high responses in WBC, IL-1ra and decrease in MCP-1.  相似文献   

17.
Our aim was to examine the effect of betaine supplementation on selected circulating hormonal measures and Akt muscle signaling proteins after an acute exercise session. Twelve trained men (age 19.7 ± 1.23 years) underwent 2 weeks of supplementation with either betaine (B) (1.25 g BID) or placebo (P). Following a 2-week washout period, subjects underwent supplementation with the other treatment (B or P). Before and after each 2-week period, subjects performed an acute exercise session (AES). Circulating GH, IGF-1, cortisol, and insulin were measured. Vastus lateralis samples were analyzed for signaling proteins (Akt, p70 S6k, AMPK). B (vs. P) supplementation approached a significant increase in GH (mean ± SD (Area under the curve, AUC), B: 40.72 ± 6.14, P: 38.28 ± 5.54, p = 0.060) and significantly increased IGF-1 (mean ± SD (AUC), B: 106.19 ± 13.45, P: 95.10 ± 14.23, p = 0.010), but significantly decreased cortisol (mean ± SD (AUC), B: 1,079.18 ± 110.02, P: 1,228.53 ± 130.32, p = 0.007). There was no difference in insulin (AUC). B increased resting Total muscle Akt (p = 0.003). B potentiated phosphorylation (relative to P) of Akt (Ser473) and p70 S6 k (Thr389) (p = 0.016 and p = 0.005, respectively). Phosphorylation of AMPK (Thr172) decreased during both treatments (both p = 0.001). Betaine (vs. placebo) supplementation enhanced both the anabolic endocrine profile and the corresponding anabolic signaling environment, suggesting increased protein synthesis.  相似文献   

18.
To determine which active-recovery protocol would reduce faster the high blood H+ and lactate concentrations produced by repeated bouts of high-intensity exercise (HIE). On three occasions, 11 moderately trained males performed 4 bouts (1.5 min) at 163% of their respiratory compensation threshold (RCT) interspersed with active-recovery: (1) 4.5 min pedalling at 24% RCT (SHORT); (2) 6 min at 18% RCT (MEDIUM); (3) 9 min at 12% RCT (LONG). The total work completed during recovery was the same in all three trials. Respiratory gases and arterialized-blood samples were obtained during exercise. At the end of exercise, LONG in comparison to SHORT and MEDIUM increased plasma pH (7.32 ± 0.02 vs. ~7.22 ± 0.03; P < 0.05), while reduced lactate concentration (8.5 ± 0.9 vs. ~10.9 ± 0.8 mM; P < 0.05). Ventilatory equivalent for CO2 was higher in LONG than SHORT and MEDIUM (31.4 ± 0.5 vs. ~29.6 ± 0.5; P < 0.05). Low-intensity prolonged recovery between repeated bouts of HIE maximized H+ and lactate removal likely by enhancing CO2 unloading.  相似文献   

19.
We investigated the effects of cryotherapy followed by sequential exercise bouts on concentric and eccentric strength of the quadriceps. Nineteen males (18-27 years) participated in a two-stage design involving four sequences: ice and exercise, ice and rest, no ice and exercise, and no ice and rest. We gathered concentric and eccentric strength measures (torque) using a kinetic communicator (KIN-COM) prior to exercise, immediately following treatment, and 20- and 40-minutes post-treatment. There were significant decreases in concentric and eccentric strength immediately following the 25-minute cryotherapy treatment. This suggests that applying ice immediately prior to participation or returning an athlete to competition immediately following cryotherapy treatment may adversely affect his/her ability to perform. It appears that the reduction in strength following cryotherapy is of short duration (less than 20 minutes). The delayed effect of the ice treatment and sequential exercise appears to affect concentric and eccentric strength differently. Ice did not have a delayed effect on concentric strength, but there was a significant difference in eccentric values. This difference was a failure to improve during post-tests at the rate of those not treated with ice. Exercise did not have a significant effect on eccentric strength recovery, but there was a significant difference in concentric values. Moderate exercise following cryotherapy appears to help the recovery of concentric strength.  相似文献   

20.
In this study nine elite athletes each participated in three different 24- h trials, as follows: (1) complete bed rest (REST), (2) one bout of exercise at 1515 hours (ONE-EX), (3) two exercise bouts, one at 1100 hours and one at 1515 hours (TWO-EX-3 h), and (4) two exercise bouts, one at 0800 hours and one at 1515 hours (TWO-EX-6 h). Exercise was performed on a cycle ergometer with 10 min of warm-up and then 65 min at an exercise intensity of 75% of maximum oxygen uptake (V˙O2max). The polymorphonuclear neutrophil (PMN) counts increased consistently in response to exercise, and more in trial TWO-EX-3 h than in the two other exercise trials (P<0.01). The respiratory burst of PMN was measured as chemiluminescence (CL), obtained with phorbol myristate (PMA) and serum-opsonised zymosan (SOZ) as stimulators. Exercise triggered the CL response for a defined number of PMN, significantly above baseline (REST) values (P<0.05) for ONE-EX and TWO-EX-3 h, but not for TWO-EX-6 h. The strongest response was observed for TWO-EX-3 h, but the difference between exercise procedures was not significant. However, as a novel approach, a comparison was made using total oxidative potentials per litre of blood, as obtained by combining CL values and PMN numbers. TWO-EX-3 h yielded significantly higher values than the other experimental treatments. Thus, by this measure the total oxidative potential of PMN·l–1 blood remains at a higher level with short intervals between exercise bouts (i.e. 3 h instead of 6 h), possibly due to a combined effect of cell number increase and the priming state of PMN. This may suggest that for intensive training twice a day, a recovery phase of 5–6 h is preferable. The elevation in cell number is best explained by a combined effect of catecholamines and cortisol. Growth hormone is one probable candidate as a stimulator of CL, but other molecular participants that respond to exercise may exert roles as either stimulators or inhibitors of CL. Electronic Publication  相似文献   

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