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[The effects of an extreme endurance exercise event on autonomic nervous system activity].

UNLABELLED: Initial response of human body to exercise consists of a decrease in vagal tone, followed by an increase in sympathetic activity. After exercise cessation, the parasympathetic component quickly regains its pre-exercise level, whereas signs of sympathetic activation have been reported to persist as long as 24 hours after intense exercise. AIM: To verify in a group of young marathon runners whether extreme endurance exercise may induce an increase of sympathetic activity for up to 48 hours during recovery. MATERIAL AND METHODS: Twelve athletes aged 32+/-12 years, taking part in a marathon (42 km) were studied. We measured baroreflex sensitivity using the transfer function method (BRS-WBA), as well as standard spectral indexes of short-term heart rate variability (LF and HF power, LFnu, LF/HF). These parameters were measured before the marathon and on the second day (about 48 hours) following the event. Comparisons were made between the two measurements (after vs. before). RESULTS: We found a statistically significant decrease in BRS-WBA (15.1+/-4.5 vs. 10.5+/-3.5 ms/mmHg, p=0.013), as well as a trend towards higher values of LF/HF (1.0+/-1.0 vs. 1.4+/-1.4, p=0.09). An increase in LF (from 1048+/-874 to 1427+/-1678 ms2) was observed, but it did not reach statistical significance. CONCLUSIONS: These results suggest that increased sympathetic activity can persist for up to 24 hours after an extreme endurance exercise such as a marathon. It is thus likely that in less trained and less physically active people exposed to excessive amounts of strenuous exercise, the autonomic nervous system response can be similar. Further studies are needed, however, to verify this inference.

Adult↗

Effects of ischemic training on leg exercise endurance.

This study tested whether ischemic exercise training (Tr(IS+EX)) would increase endurance of ischemic (Ex(IS)) and ramp exercise (Ex(RA)) knee-extension tests more than exercise training (Tr(EX)) alone. Ten healthy subjects performed pre- and posttraining tests with each leg. For Ex(RA), after subjects warmed up, a weight was added each minute until they were exhausted. Ex(IS) was similar, but after warm-up, we inflated a thigh cuff to 150 mmHg instead of adding weights. One leg was chosen for Tr(IS+EX) (cuff inflated to 150 mmHg during exercise) and the other for Tr(EX), both with a small weight on each leg, four to six times per daily session for 3 to 5 min each, 5 days per week for 6 weeks. Ex(IS) duration increased 120% more (p = 0.002) in the Tr(IS+EX) leg than in the contralateral Tr(EX) leg, whereas Ex(RA) duration increased only 16% (nonsignificant). Tr(IS+EX )and Tr(EX) significantly attenuated the ventilation increase (ergoreflex) during Ex(IS). TheO(2) debt for Ex(IS )was significantly lower and systolic blood pressure recovery was faster after Tr(IS+EX) than after Tr(EX). Heart rate recovery after Ex(RA )andEx(IS )was faster after Tr(IS+EX). Apparently, Tr(IS+EX) with low-intensity resistance increases exercise endurance and attenuates the ergoreflex and therefore may be a useful tool to increase regional muscle endurance to improve systemic exercise capacity in patients.

Adult↗

Dynamic changes of deleted mitochondrial DNA in human leucocytes after endurance exercise.

We examined the time course of the appearance and disappearance of deleted mitochondrial DNA (mtDNA) in human leucocytes after endurance exercise. Five untrained healthy females [aged 20.2 (0.4) years] exercised for 30 min at 50-60 W at 60 rpm on a cycle ergometer for 2 or 3 consecutive days. Blood samples were collected immediately before exercise, and on three occasions after the end of the last exercise bout. Levels of mtDNA were analyzed using the nested polymerase chain reaction method. Prior to exercise, a common mtDNA deletion was identified in all subjects. This common deletion was again identified in all subjects 1 day after completion of the exercise regime. However, mtDNA with this common deletion was found to have disappeared 2 days after exercise in three subjects, and after 4 days in the other two subjects. The deletion then reappeared 5 or 6 days after the final exercise bout in three of the five subjects. These findings demonstrate that a common deletion in leucocytes disappears over a period of several days after endurance exercise and reappears a number of days thereafter. Therefore, the status of the appearance and disappearance of common mtDNA deletion in leucocytes is highly dynamic.

Adult↗

Effect of long-term diltiazem treatment on central haemodynamics and exercise endurance in essential hypertension.

The effects of long-term treatment with diltiazem on blood pressure, central haemodynamics and exercise endurance were studied in 16 men (mean age 52 years) with essential hypertension. Intra-arterial pressure and heart rate (HR) were monitored continuously. Cardiac output (CO) was measured by Cardiogreen at rest (supine and sitting) and during 50 W, 100 W and 150 W bicycle exercise. Haemodynamic measurements were repeated after continuous bicycling at 150 W for 20 min or until exhaustion. After 1 year on diltiazem (mean daily dose 278 mg) intra-arterial pressure was reduced (P less than 0.001) in all situations (at rest sitting from 183/108 mmHg to 157/92 mmHg (14%] due to reduction in total peripheral resistance. HR was reduced at rest (7%) and during exercise (10%). Stroke volume tended to increase while CO was unchanged. Exercise time at constant workload increased by 25%. After a peak level, intra-arterial pressure fell by 3% to 5% (P less than 0.05) due to a decrease in total peripheral resistance both before and during diltiazem treatment. Stroke volume and CO remained unchanged during endurance exercise while HR showed a small increase. Thus, there was no reduction in the overall cardiac pump function after long-term diltiazem treatment, and blood flow during exercise was maintained.

Body Weight↗

Relationship of chronic endurance exercise to the somatotropic and sex hormone status of older men.

To investigate putative abrogating effects of habitual endurance exercise on age-related changes in endocrine function and body composition, we compared insulin-like growth factor-I (IGF-I), sex hormonal status and body composition in 15 Masters runners and 15 minimally exercising men (MEM) aged 60-70 years. A higher maximal oxygen uptake (VO2 max.) in the runners (41.4+/-1.6 compared with 27.3+/-1.4 ml/kg/min, P=0.0001; mean+/-S.E.M.) reflected our group allocations. Analysis of body composition and bone mineral density (BMD) by dual energy X-ray absorptiometry showed no group differences in lean tissue mass or in regional or whole body BMD, but MEM were heavier, reflecting greater adiposity. Of nine muscle groups tested, only quadriceps strength differed significantly, being greater in runners (60.3+/-2.8 compared with 51.1+/-2.3 kg, P=0.02). Total IGF-I (129+/-10 compared with 124+/-11 ng/ml, P=0.72) and IGF-binding protein-3 (2854+/-94 compared with 2623+/-128ng/ml, P=0.16), were similarly depressed compared with young adult norms in both groups. There was no relationship between total or bioavailable IGF-I and any body composition, BMD or muscle strength variable. In the runners, concentrations of total testosterone (19.1+/-0.8 compared with 15.0+/-0.9 nmol/l, P=0.002) and sex hormone binding globulin (SHBG) (124.4+/-21.6 compared with 67.7+/-11.6 nmol/l, P=0.03) were significantly greater, but the free androgen index was significantly lower (20.7+/-2.7 compared with 31.4+/-4.1, P=0.04). Directly measured free testosterone, however, was similar between the runners and MEM (47.9+/-1.8 compared with 47.1+/-2.0 nmol/l P=0.80). Therefore the group differences in total testosterone and free androgen index were due to their different SHBG concentrations. Although estrone concentration was higher in MEM (85.1+/-5.2 compared with 108+/-6.7 pmol/l, P=0.03), estradiol concentration was similar between groups (73.0+/-6.3 compared with 81.8+/-8.0 pmol/l, P=0.18), indicating that estrogens were not responsible for the increased SHBG in runners. These results indicate that even high levels of regular endurance exercise do not prevent the decline in the somatotropic axis that occurs with aging. Furthermore, the somatic effects of exercise in older men (reduced adiposity and increased regional muscle strength) occurred independently of somatotropic or androgen status. Although habitual exercise does not influence free testosterone concentrations in older men, it appears to enhance the age-associated increase in SHBG synthesis.

Aged↗

Effects of intensive endurance exercise on DNA damage in leucocytes.

OBJECTIVE: It has been shown that highly intensive anaerobic exercise induces DNA damage in leucocytes (LEU). The present study was designed to investigate whether intensive endurance exercise is capable of inducing comparable effects. EXPERIMENTAL DESIGN: A prospective study. PARTICIPANTS: Twelve men (aged 27.3 +/- 4.1 years) who undertook a regular training of different extent (running volume 45 +/- 25 km.week-1) volunteered in the study. INTERVENTIONS: The subjects competed in a half marathon (HM) of 21.1 km, 93.0 +/- 10.4 min. MEASUREMENTS: Blood was taken at rest, 1 and 24 hrs after HM for determination of creatine kinase, neutrophil (PMN), lymphocyte and monocyte counts. DNA damage in LEU at rest and 24 hrs after HM was quantified using the single cell gel-electrophoresis (SCG) assay. RESULTS: PMN increased from 2.81 +/- 0.69 to 13.13 +/- 2.91 1 hrs after HM (p < 0.01) and returned to 3.26 +/- 0.47 10(9) cells.l-1 by 24 hr recovery. DNA migration (image length, IL) reflecting the extent of DNA damage was elevated significantly in 10 of 12 subjects one day after HM. IL rose from 32.7 +/- 2.2 to 40.7 +/- 3.9 microns (p < 0.01). Correlation analysis revealed a relationship between DNA migration 24 hrs after HM and PMN count 1 hr post-exercise (r = 0.67, p < 0.05). CONCLUSIONS: The results confirm the hypothesis that DNA damage in LEU occurs after intensive endurance exercise. We suppose our observation of exercise-induced DNA damage in LEU is affected by reactive oxygen species which are released from PMN. It is quite unclear whether DNA damage in LEU is causal involved in exercise-induced modifications of the immune system.

Adult↗

Fluid balance and endurance exercise performance.

Dehydration alters cardiovascular, thermoregulatory, central nervous system, and metabolic functions. One or more of these alterations will degrade endurance exercise performance when dehydration exceeds 2% of body weight. These performance decrements are accentuated by heat stress. To minimize the adverse consequences of body water deficits on endurance exercise performance, it is recommended that fluid intake be sufficient to minimize dehydration to less than 2% of body weight loss. This can usually be achieved with fluid intakes of under 1 L x h(-1).

Body Water↗

Endurance exercise capacity in adults with cystic fibrosis.

We have compared the maximal and endurance exercise capacities in 22 (15 male) adult cystic fibrosis (CF) patients with a resting oxygen saturation (SaO2) > or = 90%, with age and sex matched controls (CON). The maximum oxygen uptake (VO2max) and heart-rate were lower for the CF group whereas the maximum ventilation reached a higher percentage of predicted. Furthermore, for the CF group there was a relationship between the % predicted VO2max and measures of lung function, confirming a ventilatory limit to maximum exercise in patients with more severe disease and a near normal maximum exercise capacity in those with mild disease. Endurance capacity, defined as the duration of exercise at 80% of each individuals VO2max, was however similar for the two groups [CF: 22.21 (15.82) vs. CON: 24.94 (13.05) min]; despite the CF group exercising under less efficient ventilatory conditions. Endurance capacity was not related to the measurements of lung function. Of the seven CF patients desaturating at maximal exercise (SaO2 < 90%), five desaturated at a work load of 80% VO2max, whereas only one desaturated at 50% VO2max. This study confirms that with increasing severity of disease, maximal exercise capacity may be limited in adult CF patients, whereas endurance capacity (at the same relative work load) is unimpaired. Furthermore, CF patients who desaturate during a progressive maximal exercise test are likely to desaturate during constant work load exercise if the intensity is high but unlikely to do so if the intensity is low. The information from these exercise tests would be of value for prescribing individual training programmes and for evaluating the effects.

Adolescent↗

Serum cardiac troponin T after repeated endurance exercise events.

Recently Dr. Rowe made a hypothesis according to which small areas of myocardial necrosis can be caused by microvascular spasm, related to high catecholamine concentrations and other mechanisms, following extraordinary unremitting endurance exercises or due to the cumulative effect of several endurance events. It was this last suggestion which prompted us to investigate 25 top cyclists, taking part in the 77th Giro d'Italia. Blood samples were obtained the day before the start of the competition and once a week thereafter until the end. We measured myoglobin, lactic dehydrogenase, total creatine kinase, creatine kinase isoenzyme MB and serum cardiac troponin T (Tn-T), a highly sensitive and specific method for the detection of myocardial injury. While at measuring time points which followed we found a significant increase in the serum indicators of muscle damage, compared with their values at the beginning of the race, creatine kinase isoenzyme MB did not rise significantly and cardiac Tn-T was found in the serum of only 5 athletes, repeatedly in some cases, but always below the cut off values considered as indicating myocardial ischemia. On the basis of the behaviour of creatine kinase isoenzyme MB and, above all, of cardiac Tn-T, we can conclude that heavy endurance exercises, repeated daily for 22 days, as was the case in our study, do not seem able to produce, in top athletes, permanent heart damage by means of acute myocardial injury.

Adult↗

Body fat and exercise endurance in trained rats adapted to a high-fat and/or high-carbohydrate diet.

To study how diet composition affects exercise endurance and body composition, 48 male Sprague-Dawley rats were treadmill trained for 8 wk while consuming either a high-fat (F) diet or high-carbohydrate (C) diet. The diets were switched for one-half the number of rats in each group 3 days before the animals were killed, during which feeding time the rats did not exercise. One-half of rats receiving each of the four diet combinations were taken at rest (R) or exhaustion (E), resulting in eight groups: CCR, CFR, FFR, FCR, CCE CFE, FFE, and FCE. An analysis of variance revealed that resting glycogen in the FCR group was enhanced in muscle (19-33%) and liver (23%) compared with controls. Each F group's exercise time to exhaustion [CFE, 322.9 +/- 25.0; FFE, 356.8 +/- 37.8; FCE, 467.0 +/- 32.6 (SE) min] was different (P < 0.05) from control (CCE, 257.5 +/- 29.2 min). Postexercise glycogen was equivalent among all dietary groups, were muscle triglycerides. The FF and FC groups had higher 3-hydroxyacyl-CoA dehydrogenase activity in soleus muscle than either CC or CF animals. After training, body weights were similar between the two dietary groups; however, percent body fat was 17% greater after the F diet, even though F diet animals voluntarily consumed 12% less energy than did C diet animals. These data suggest that exercise endurance time is optimized in trained rats that receive a carbohydrate load after adaptation to a F diet. However, despite intense exercise training, the F diet promotes body fat deposition, and the health consequences of following such a regimen are still unknown.

Animals↗

The effect of endurance exercise training on plasma lipoprotein AI and lipoprotein AI:AII concentrations in sedentary adults.

The effect of 6 months of endurance exercise training on plasma concentrations of lipoprotein (Lp)AI and LpAI:AII was determined in 39 sedentary subjects (17 men, 22 women, average age, 57 years) with abnormal cholesterol concentrations (total cholesterol [TC] > 200 mg/dL, or high-density lipoprotein-cholesterol [HDL-C] < 35 mg/dL). Following exercise training, plasma LpAI concentrations increased (+5.9 +/- 1.2 mg/dL; P <.001), but there was no change in total apolipoprotein (apo) A-I or LpAI:AII concentrations. The change in plasma LpAI concentration was positively correlated to changes in total HDL-C (r =.495, P =.001), the sum of HDL4-C(nmr) + HDL5-C(nmr) (r =.417, P =.008), and average HDL particle size (r =.415, P =.009), but not to changes in body composition or Vo2max. In the 8 subjects with the greatest change in LpAI concentration following training, the size distribution of LpAI and LpAI:AII particles in plasma also was measured before and after training. In these subjects, the size distribution of LpAI:AII particles did not change with training, but there was a significant increase (0.1 nm; P =.048) in the peak size of the "medium" (7.8 to 9.8 nm) LpAI particles after training. In 7 subjects who served as age- and weight-matched sedentary controls, plasma concentrations of total apo A-I, the LpAI and LpAI:AII subfractions, and plasma lipoprotein-lipids did not differ significantly between baseline and final testing. These data indicate that endurance exercise training increases the average size and plasma concentrations of LpAI, but not LpAI:AII, particles, which may represent possible enhancements of reverse cholesterol transport and may provide insight into the role that exercise plays in reducing cardiovascular disease risk.

Aged↗

Differential mobilization of leucocyte and lymphocyte subpopulations into the circulation during endurance exercise.

A total of 14 healthy subjects [means (SD): 27.6 (3.8) years; body mass 77.8 (6.6) kg; height 183 (6) cm] performed endurance exercise to exhaustion at 100% of the individual anaerobic threshold (Th(an)) on a cycle ergometer (mean workload 207 (55) W; lactate concentrations 3.4 (1.2) mmol.l-1; duration 83.8 (22.2) min, including 5 min at 50% of individual Th(an)). Leucocyte subpopulations were measured by flow cytometry and catecholamines by radioimmunological methods. Blood samples were taken before and several times during exercise. Values were corrected for plasma volume changes and analysed using ANOVA for repeated measures. During the first 10 min of exercise, of all cell subpopulations the natural killer cells (CD3-CD16/CD56+) increased the most (229%). Also CD3+CD16/CD56+ (84%), CD8+CD45RO- (69%) cells, eosinophils (36%) and monocytes (62%) increased rapidly during that time. CD3+, CD3+HLA-DR+, CD4+CD45RO+, CD4+CD45RO-, CD8+CD45RO+ and CD19+ cells either did not increase or increased only slightly during exercise. Adrenaline and noradrenaline increased nearly linearly by 36% and 77% respectively at 10 min exercise. The increase of natural killer cells and heart rates between rest and 10 min of exercise correlated significantly (r = 0.576, P = 0.031). We conclude that natural killer cells, cytotoxic, non-MHC-restricted T-cells, monocytes and eosinophils are mobilized rapidly during the first minutes of endurance exercise. Both catecholamines and increased blood flow are likely to contribute this effect.

Adult↗

Dietary fat saturation and endurance exercise alter lipolytic sensitivity of adipocytes isolated from Yucatan miniature swine.

This study examined the effects of dietary fat saturation and endurance exercise on lipolytic sensitivity of adipocytes isolated from Yucatan miniature swine. Twenty-four female swine had free access to a high fat diet with a polyunsaturated to saturated fat ratio (P:S) of 0.3 or 1.0, and were treadmill-exercised or remained sedentary. After 3 months, biopsies were taken, adipocytes were isolated and lipolytic activity was determined. Adipocytes were incubated with adenosine deaminase followed by epinephrine, isoproterenol, or epinephrine plus phenylisopropyladenosine, and glycerol release was measured. Backfat thickness was measured by ultrasonography. Our findings revealed that 1) adipocytes from 1.0 P:S diet-fed swine released 30% more glycerol than adipocytes from 0.3 P:S diet-fed swine when stimulated by 1 micromol/L isoproterenol; 2) adipocytes from exercised swine released 45% more glycerol than adipocytes from sedentary swine when stimulated by 1 micromol/L epinephrine; 3) body weight of exercised swine was significantly lower than sedentary swine; and 4) backfat thickness was less in exercised swine than in sedentary swine (2.39 vs. 2.95 cm, P = 0.002). We conclude that ad libitum consumption of diet with a P:S of 1.0, combined with endurance exercise, increases lipolytic sensitivity, lowers body weight gain, and reduces fat accumulation in female Yucatan miniature swine.

Adipocytes↗

Homocysteine increases during endurance exercise.

Hyperhomocysteinemia is a risk factor for cardiovascular and other diseases. Recently many endogenous and exogenous modulators of homocysteine (Hcy) have become known, e.g., B-vitamins. However, little is known about the effect of exercise on Hcy. The purpose of this study was to investigate the effect of three different types of acute endurance exercise on serum Hcy. We measured Hcy in 100 recreational athletes (87 males, 13 females) who participated in a marathon race (n = 46), a 100 km run (100 km; n = 12) or a 120 km mountain bike race (n = 42). Blood samples were taken before, 15 min and 3 h after the race. In athletes with pre-race Hcy > 12 micromol/l we also determined folate and vitamin B12. Marathon running induced a Hcy increase of 64%, while mountain biking and 100 km running had no significant effect on Hcy. Pre-race Hcy (25th-75th percentile) overall; marathon race; 100 km; mountain bike race was 9.7 (7.1-11.5) micromol/l; 9.8 (7.4-11.1) micromol/l; 10.2 (6.6-13.2) micromol/l; 9.1 (6.9-13.5) micromol/l, respectively. At 15 min and 3 h post-race, Hcy was 11.9 (8.4-16.4) micromol/l; 16.1 (12.7-20.4) micromol/l; 9.5 (7.8-15.9) micromol/l; 8.8 (7.1-11.2) micromol/l, respectively, and 11.5 (8.9-15.7) micromol/l; 14.9 (11.5-20.0) micromol/l; 10.0 (8.1-11.8) micromol/l; 9.4 (7.4-12.1) micromol/l, respectively. The change in Hcy correlated negatively with the running time. Twenty-three athletes had pre-race Hcy levels > 12 micromol/l, which were associated with relatively low folate (14.3 (11.6-18.9) nmol/l) and vitamin B12 levels (231 (183-261) pmol/l). Endurance exercise may induce a considerable Hcy increase, which varies between different disciplines and is most probably determined by the duration and intensity of exercise. Furthermore, about 25% of recreational endurance athletes exhibited hyperhomocysteinemia in association with low vitamin B12 and folate levels.

Adult↗

Role of AMP-activated protein kinase in the molecular adaptation to endurance exercise.

What are the molecular signals induced by muscle contraction that result in an increase in GLUT4, hexokinase 2, mitochondrial oxidative enzymes, and other adaptations to endurance exercise training? Could repetitive activation of AMP-activated protein kinase (AMPK) be responsible in part? There is substantial evidence for a role of AMPK in inducing adaptations to endurance training: 1) AMPK is activated in response to muscle contraction; 2) chronic chemical activation of AMPK results in increases in GLUT4, hexokinase 2, UCP-3, and citric acid cycle enzymes; 3) muscle contraction and chemical activation of AMPK both result in increases in PGC-1alpha, a transcriptional coactivator involved in stimulation of mitochondrial biogenesis; and 4) increases in muscle PGC-1 alpha, delta-aminolevulinic acid synthetase, and mitochondrial DNA induced by chronic creatine phosphate depletion in wild-type mice are not observed in dominant-negative AMPK mice. These observations lend credence to the hypothesis that AMPK activation induced by muscle contraction is responsible in part for adaptations to endurance exercise training.

AMP-Activated Protein Kinase Kinases↗

[Effects of acute endurance exercise and 8 week training on the production of reactive oxygen species from neutrophils in untrained men].

We investigated the effects of acute endurance exercise and habitual physical activity for health maintenance on human neutrophil function in 12 untrained men. The acute exercise condition was a continuous exercise for 90 minutes at the intensity of 50% and 55% of maximal oxygen uptake (VO2max) on an ergometer. The training program was 3 km jogging three times per week for 8 weeks. The capacity of neutrophils to produce reactive oxygen species (ROS) was detected with lucigenin-dependent chemiluminescence (LgCL) and luminol-dependent chemiluminescence (LmCL) on stimulation with opsonized zymosan (OZ) and phorbol myristate acetate (PMA). As for the acute exercise effects, both LgCL and LmCL responses of neutrophils, stimulated using PMA consistently increased after exercise at 50%VO2max, whereas those stimulated with OZ remained unchanged. At 55%VO2max, LgCL responses to both stimulants increase maximally 1 h after exercise, and then decreased 3 h after exercise, whereas LmCL responses to both stimulants increased continuously after exercise at 55%VO2max. These phenomena observed at 55%VO2max compared to 50%VO2max suggests the improved capacity of producing ROS neutrophils after exercise. The number of neutrophils also increased maximally 1 h after exercise, due to the mobilization of band neutrophils (shift to the left), suggesting that functional changes was associated with cell mobilization. The increase in the capacity of neutrophils to produce ROS and marked neutrophilia following the acute endurance exercise suggests that a large quantity of ROS may be produced in vivo. As for the training effects, the LgCL and LmCL responses were maintained in the exercise group as compared to the decreased ones in the control group. The difference between the exercise group and the control group was observed only in LgCL response to OZ. Humoral immune factors (IgG, IgA, IgM, C3, C4) and serum opsonic activity were also unaltered. These phenomena suggest that homeostasis might be kept constant in terms of immunity through regular physical activity.

Adult↗

The influence of endurance exercise on delayed onset muscle soreness.

BACKGROUND: Despite several review articles supporting the existence of exercise induced analgesia, it is unclear whether exercise reduces delayed onset muscle soreness (DOMS). The purpose of this investigation was to examine the influence of an acute bout of endurance exercise on delayed onset muscle pain. METHODS: DOMS was induced in the elbow flexors of the non-dominant arm using eccentric isotonic exercise with the intensity of the eccentric contractions based upon concentric strength. Forty-eight hours after the eccentric contractions participants were randomly assigned to a group that completed 20 min of endurance exercise at 80% of estimated maximum cardiorespiratory endurance (n=23) or a group that watched a 20 min emotionally neutral video (n=27). The dependent variables were pressure pain threshold, pain intensity during arm movement through active range of motion, a standardized pain rating that was determined from a magnitude matching procedure, and state anxiety. RESULTS: A significant decrease in pressure pain threshold and an increase in the standardized pain ratings after the DOMS procedure (p<0.05) indicated that muscle pain was successfully induced. These changes were components of significant quadratic trends for pressure threshold (p<0.05) and the standardized pain ratings (p<0.01). During the 2nd session a decrease in pain intensity approached significance (p=0.05) regardless of group assignment. However, no significant group by time interactions were detected for any of the pain measures or state anxiety. CONCLUSIONS: Cycle ergometer exercise was not found to alter delayed onset muscle pain.

Adult↗

Variability in exercise capacity and metabolic response during endurance exercise after a low carbohydrate diet.

The impact of altered blood glucose concentrations on exercise metabolism and performance after a low carbohydrate (CHO) diet was investigated. In random order, 1 wk apart, 9 trained men underwent euglycemic (CI) or placebo (PI) clamps, while performing up to 150 min of cycling at 70% VO2(max), after 48 h on a low CHO diet. The range in improvement in endurance capacity with glucose infusion was large (28 +/- 26%, P < 0.05). Fifty-six percent of subjects in CI failed to complete 150 min of exercise despite maintenance of euglycemia, while only 2 subjects in PI completed 150 min of exercise, despite being hypoglycemic. Total CHO oxidation remained similar between trials. Despite longer exercise times in CI, similar amounts of muscle glycogen were used to PI. Maintenance of euglycemia in the CHO-depleted state might have an ergogenic effect, however, the effect is highly variable between individuals and independent of changes in CHO oxidation.

Adult↗