Metabolic changes following eccentric exercise in trained and untrained men

The effects of one 45-min bout of high-intensity eccentric exercise (250 W) were studied in four male runners and five untrained men. Plasma creatine kinase (CK) activity in these runners was higher (P less than 0.001) than in the untrained men before exercise and peaked at 207 IU/ml 1 day after exercise, whereas in untrained men the maximum was 2,143 IU/ml 5 days after exercise. Plasma interleukin-1 (IL-1) in the trained men was also higher (P less than 0.001) than in the untrained men before exercise but did not significantly increase after exercise. In the untrained men, IL-1 was significantly elevated 3 h after exercise (P less than 0.001). In the untrained group only, 24-h urines were collected before and after exercise while the men consumed a meat-free diet. Urinary 3-methylhistidine/creatinine in the untrained group rose significantly from 127 mumol/g before exercise to 180 mumol/g 10 days after exercise. The results suggest that in untrained men eccentric exercise leads to a metabolic response indicative of delayed muscle damage. Regularly performed long distance running was associated with chronically elevated plasma IL-1 levels and serum CK activities without acute increases after an eccentric exercise bout.     

Transfer effects in endurance exercise. Adaptations in trained and untrained muscles

The effects of 8 weeks of bicycle endurance training (5 X /week for 30 min) on maximal oxygen uptake capacity (VO2max) during arm and leg ergometry, and on the ultrastructure of an untrained arm muscle (m. deltoideus), and a trained leg muscle (m. vastus lateralis) were studied. With the training, leg-VO2max for bicycling increased by +13%, while the capillary per fiber ratio and the volume density of mitochondria in m. vastus lateralis increased by +15% and +40%, respectively. In contrast, the untrained m. deltoideus showed an unchanged capillary per fiber ratio and a decreased mitochondrial volume density (-17%). Despite this decrease of mitochondrial volume arm-VO2max increased by +9%. It seems unlikely that the observed discrepancy can be explained by cardiovascular adaptations, since arm cranking did not fully tax the cardiovascular system (arm-VO2max/leg-VO2max: 0.74 and 0.71 before and after training, respectively). Thus neither cardiovascular adaptations nor local structural changes in the untrained muscles could explain the increased arm-VO2max. However, the enhanced capacity for lactate clearance after endurance training could be sufficient to account for the larger VO2max during arm cranking. We propose that an increased net oxidation of lactate might be responsible for the increased arm-VO2max found after bicycle endurance training.     

Potassium and ventilation during incremental exercise in trained and untrained men.

The present investigation was undertaken to examine the relationship between plasma potassium (K+) and ventilation (VE) during incremental exercise. Blood lactate (La-) was also measured, and its relationship with VE was similarly examined. Eight endurance-trained triathletes (ET) and eight active but untrained men (UT) performed an incremental cycling test to volitional fatigue. Maximal oxygen uptake (VO2max) and oxygen uptake (VO2) at lactate threshold (LT) were higher (P < 0.05) in ET (VO2max 4.60 +/- 0.10 l/min, LT 2.77 +/- 0.85 l/min) than in UT (VO2max 3.79 +/- 0.11 l/min, LT 1.94 +/- 0.60 l/min). There were significant (P < 0.05) correlations between VE and K+ (UT 0.87, ET 0.77) and between VE and La- (UT 0.88, ET 0.85). In ET compared with UT, VE was lower (P < 0.05) at 330 W, K+ was lower at 300 and 330 W, and La- was lower at all work loads > 90 W. These results suggest that K+ may make an important contribution to the regulation of ventilation during incremental exercise and that endurance training attenuates the K+ response to that exercise.     

Hormonal responses to resistance exercise in long-term trained and untrained middle-aged men

This cross-sectional study compared hormonal responses to resistance exercise between trained and untrained men to investigate the adaptations of the endocrine system to long-term strength training in middle-aged men. Twenty-one middle-aged men were recruited for this study and matched into a strength-trained group (SG) (n = 10) and an untrained group (UG) (n = 11). In the SG, the individuals had practiced strength training for hypertrophy for at least 3 years. Upper- and lower-body muscle strength was measured with a 1 repetition maximum (1RM) test. Blood samples were collected at rest and after multiple sets of a superset strength training protocol (SSTP), with an intensity of 75% of 1RM values. With these blood samples, the levels of total testosterone (TT), free testosterone (FT), dehydroepiandrosterone (DHEA), cortisol, and sex hormone-binding globulin (SHBG) were determined. In addition, the TT-to-cortisol ratio and TT-to-SHBG ratio were calculated. There was no difference at rest between groups in hormonal values for TT, FT, DHEA, cortisol, the TT-to-SHBG ratio, and the TT-to-cortisol ratio. There were increases after SSTP in the levels of TT, FT, DHEA, and cortisol and the TT-to-SHBG ratio in the UG, but only FT increased in the SG. The SG demonstrated lower values in the TT-to-SHBG ratio after the training session. These results suggest the presence of alterations in anabolic and catabolic hormonal responses to resistance exercise in long-term trained middle-aged men, with the trained subjects demonstrating lower responsiveness in the hormone values. Long-term trained men seem to require a higher volume of training, at least similar to their daily workout, to stimulate greater hormone responses.     

Beta-blockade reduces tidal volume during heavy exercise in trained and untrained men

The effects of beta-blockade on tidal volume (VT), breath cycle timing, and respiratory drive were evaluated in 14 endurance-trained [maximum O2 uptake (VO2max) approximately 65 ml X kg-1 X min-1] and 14 untrained (VO2max approximately 50 ml X kg-1 X min-1) male subjects at 45, 60, and 75% of unblocked VO2max and at VO2max. Propranolol (PROP, 80 mg twice daily), atenolol (ATEN, 100 mg once a day) and placebo (PLAC) were administered in a randomized double-blind design. In both subject groups both drugs attenuated the increases in VT associated with increasing work rate. CO2 production (VCO2) was not changed by either drug during submaximal exercise but was reduced in both subject groups by both drugs during maximal exercise. The relationship between minute ventilation (VE) and VCO2 was unaltered by either drug in both subject groups due to increases in breathing frequency. In trained subjects VT was reduced during maximal exercise from 2.58 l/breath on PLAC to 2.21 l/breath on PROP and to 2.44 l/breath on ATEN. In untrained subjects VT at maximal exercise was reduced from 2.30 l/breath on PLAC to 1.99 on PROP and 2.12 on ATEN. These observations indicate that 1) since VE vs. VCO2 was not altered by beta-adrenergic blockade, the changes in VT and f did not result from a general blunting of the ventilatory response to exercise during beta-adrenergic blockade; and 2) blockade of beta 1- and beta 2-receptors with PROP caused larger reductions in VT compared with blockade of beta 1-receptors only (ATEN), suggesting that beta 2-mediated bronchodilation plays a role in the VT response to heavy exercise.     

The effect of resistance exercise on p53, caspase-9, and caspase-3 in trained and untrained men

Apoptosis is a programmed cell death that has been demonstrated in human and animal studies and plays an essential role to remove injured cells after acute strenuous exercise. Protein p53 plays important roles in regulating apoptosis via mitochondrial pathway. Therefore, the aims of this study were to determine the effects of acute resistance exercise (RE) on serum p53, caspase-9, and caspase-3, markers of apoptosis, and whether resistance training status influences the magnitude of the RE-induced apoptosis. Nine resistance-trained (RT) (age, 22.37 ± 1.99 years; height, 174 ± 5.04 cm; body weight, 71.32 ± 5.57 kg; and body mass index [BMI] 23.58 ± 2.05 kg·m(-2)) and 9 untrained (UT) college-age men (age, 22.25 ± 2.13 years; height, 171 ± 3.4 cm; body weight, 68.45 ± 3.23 kg; and BMI, 23.41 ± 1.08 kg·m(-2)) volunteered to participate in this study. Resistance-trained and UT men completed an RE bout consisting of 4 sets of 6 exercise at 80% of 1 repetition maximum until failure. Serum levels of p53, caspase-9, and caspase-3 were examined at preexercise (pre), immediately post (IP), 3 hours post (3 hours post), and 24 hours post RE (24 hours post). In UT, serum levels of p53, caspase-9, and caspase-3 were significantly increased at IP compared with RT. However, plasma insulin-like growth factor 1 level was higher for RT compared with UT at IP. Collectively, our data suggest the role of p53 in regulating apoptosis through mitochondrial pathway as measured by caspase-9 and caspase-3 after acute RE in UT. Our results also revealed that regular RT alters apoptosis biomarkers, especially the intrinsic pathway of apoptosis.     

Effect of acute exercise on citrate synthase activity in untrained and trained human skeletal muscle

Maximal citrate synthase activity (CS) is routinely used as a marker of aerobic capacity and mitochondrial density in skeletal muscle. However, reported CS has been notoriously variable, even with similar experimental protocols and sampling from the same muscles. Exercise training has resulted in increases in CS ranging from 0 to 100%. Previously, it has been reported that acute exercise may significantly affect CS. To investigate the hypothesis that the large variation in CS that occurs with training is influenced by alterations during the exercise itself, we studied CS in human vastus lateralis both in the rested and acutely exercised state while trained and untrained (n = 6). Tissues obtained from four biopsies (untrained rested, untrained acutely exercised, trained rested, and trained acutely exercised) were analyzed spectrophotometrically for maximal CS. Exercise training measured in a rested state resulted in an 18.2% increase in CS (12.3 +/- 0.3 to 14.5 +/- 0.3 micromol x min(-1) x g tissue(-1), P < or = 0.05). However, even greater increases were recorded 1 h after acute exercise: 49.4% in the untrained state (12.3 +/- 0.3 to 18.3 +/- 0.5 micromol x min(-1) x g tissue(-1), P < or = 0.05) and 50.8% in the trained state (14.5 +/- 0.3 to 21.8 +/- 0.4 micromol x min(-1) x g tissue(-1), P < or = 0.05). Ultrastructural analysis, by electron microscopy, supported an effect of acute exercise with the finding of numerous swollen mitochondria 1 h after exercise that may result in greater access to the CS itself in the CS assay. In conclusion, although unexplained, the increased CS with acute exercise can clearly confound training responses and artificially elevate CS values. Therefore, the timing of muscle sampling relative to the last exercise session is critical when measuring CS and offers an explanation for the large variation in CS previously reported.     

Control of the rate of phosphocreatine resynthesis after exercise in trained and untrained human quadriceps muscles

We examined the effect of differences in exercise intensity on the time constant (t _c) of phosphocreatine (PCr) resynthesis after exercise and the relationships betweent _c and maximal oxygen uptake (VO_2max) in endurance-trained runners (n = 5) and untrained controls (n = 7) (average VO_2max = 66.2 and 52.0 ml · min^–1 · kg^–1, respectively). To measure the metabolism of the quadriceps muscle using phosphorus nuclear magnetic resonance spectroscopy, we developed a device which allowed knee extension exercise inside a magnet. All the subjects performed four types of exercise: light, moderate, severe and exhausting. The end-exercise PCr: [PCr + inorganic phosphate (P_i)] ratio decreased significantly with the increase in the exercise intensity (P < 0.01). Although there was little difference in the end-exercise pH, adenosine diphosphate concentration ([ADP]) and the lowest intracellular pH during recovery between light and moderate exercise, significant changes were found at the two higher intensities (P < 0.01). These changes for runners were smaller than those for the controls (P < 0.05). The _c remained constant after light and moderate exercise and then lengthened in proportion to the increase in intensity (P < 0.05). The runners had a lowert _c at the same PCr and pH than the controls, particularly at the higher intensity (P < 0.05). There was a significant correlation betweent _c and [ADP] in light exercise and betweent _c and both end-exercise PCr and pH in severe and exhausting exercise (P < 0.05). The threshold of changes in pH andt _c was a PCr: (PCr + P_i) ratio of 0.5. There was a significant negative correlation between the VO_2max andt _c after all levels of exercise (P<0.05).However, in the controls a significant correlation was found in only light and moderate exercise (P < 0.05). These findings suggest the validity of the use oft _c at an end-exercise PCr:(PCr + P_i) ratio of more than 0.5 as a stable index of muscle oxidative capacity and the correlation between local and general aerobic capacity. Moreover, endurance-trained runners are characterized by the faster PCr resynthesis at the same PCr and intracellular pH.     

Respiratory gas-exchange ratios during graded exercise in fed and fasted trained and untrained men

We evaluated the hypotheses that endurance training increasesrelative lipid oxidation over a wide range of relative exercise intensities in fed and fasted states and that carbohydrate nutrition causes carbohydrate-derived fuels to predominate as energy sources during exercise. Pulmonary respiratory gas-exchange ratios [(RER) = CO₂production/O₂ consumption(O₂)] were determinedduring four relative, graded exercise intensities in both fed andfasted states. Seven untrained (UT) men and seven category 2 and 3 US Cycling Federation cyclists (T) exercised in the morning in random order, with target power outputs of 20 and 40% peakO₂(O_{2 peak}) for 2 h,60% O_{2 peak} for 1.5 h, and 80%O_{2 peak} fora minimum of 30 min after either a 12-h overnight fast or 3 h after astandardized breakfast. Actual metabolic responses were 22 ± 0.33, 40 ± 0.31, 59 ± 0.32, and 75 ± 0.39%O_{2 peak}. T subjectsshowed significantly (P < 0.05)decreased RER compared with UT subjects at absolute workloads when fedand fasted. Fasting significantly decreased RER values compared withthe fed state at 22, 40, and 59%O_{2 peak} inT and at 40 and 59%O_{2 peak} in UTsubjects. Training decreased (P < 0.05) mean RER values compared with UT subjects at 22%O_{2 peak} when theyfasted, and at 40%O_{2 peak} when fed orfasted, but not at higher relative exercise intensities in eithernutritional state. Our results support the hypothesis that endurancetraining enhances lipid oxidation in men after a 12-h overnight fast at low relative exercise intensities (22 and 40%O_{2 peak}). However, atraining effect on RER was not apparent at high relative exercise intensities (59 and 75%O_{2 peak}). Becausemost athletes train and compete at exercise intensities >40% maximalO₂, they will not oxidize agreater proportion of lipids compared with untrained subjects,regardless of nutritional state.     

Effects of beta-blockade on exercise capacity of trained and untrained men: a hemodynamic comparison

To study the effects of cardiovascular fitness on hemodynamic responses to exercise during beta-adrenergic blockade (BAB), submaximal [60% of maximum O2 uptake (VO2max)] and maximal treadmill exercise data were collected in 11 trained (T, VO2max 63.3 ml X kg-1 X min-1, 26.8 yr) and 11 untrained (UT, VO2max 44.5 ml X kg-1 X min-1, 25.0 yr) male subjects. Subjects completed two maximal control tests followed by a randomized, double-blind series of maximal tests after 1-wk treatments with placebo (PLAC), propranolol (PROP, 160 mg/day, beta 1- and beta 2-blockade), and atenolol (ATEN, 100 mg/day, beta 1-blockade). Treatments were separated by 1-wk washout periods. At 60% of control VO2max T and UT subjects experienced no reductions in O2 uptake (VO2) with either drug. Submaximal heart rate (HR, beats/min) was 134.8 PLAC, 107.0 PROP, 107.9 ATEN (P less than 0.05 both drugs vs. PLAC) in T subjects and 141.1 PLAC, 106.1 PROP, and 105.0 ATEN (P less than 0.05 both drugs vs. PLAC) in UT subjects. Cardiac output (1/min) for T was 17.3 PLAC, 16.9 PROP, 16.5 ATEN (P less than 0.05 ATEN vs. PLAC in T only) and for UT it was 12.2 (PLAC), 11.7 (PROP), 11.5 (ATEN) (P less than 0.05 both drugs vs. PLAC in UT). Stroke volume increased from 129.8 ml (PLAC) to 158.6 (PROP) and 156.2 (ATEN) in T (P less than 0.05 both drugs vs. PLAC) and from 86.8 (PLAC) to 110.0 (PROP) and 109.8 (ATEN) (P less than 0.05 both drugs vs. PLAC) in UT. The increases in stroke volume (SV) were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Maximal vascular leg conductance in trained and untrained men

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.     

The effect of acute resistance exercise on serum malondialdehyde in resistance-trained and untrained collegiate men

The purposes of this study were to determine whether acute resistance exercise increases serum malondialdehyde (MDA) levels postexercise, and if so, whether resistance exercise training status influences the magnitude of the exercise-induced lipid peroxidation response. Twelve recreationally resistance-trained (RT) and 12 untrained (UT) men who did not have resistance exercise experience in the past year participated in this study. All subjects completed an 8-exercise circuit resistance exercise protocol consisting of 3 sets of 10 repetitions at 10 repetitions maximum for each exercise. Blood samples were obtained pre-exercise, at 5 minutes postexercise, and at 6, 24, and 48 hours postexercise. At pre-exercise, MDA (nmol.ml(-1)) averaged 3.41 +/- 0.25 (RT) and 3.20 +/- 0.25 (UT) and did not differ (p > 0.05) either between groups or over time. Creatine kinase (IU.L(-1)) was significantly (p < 0.05) elevated 5 minutes postexercise (170.6 +/- 25.8), 6 hours postexercise (290.3 +/- 34.4), 24 hours postexercise (365.5 +/- 49.9), and 48 hours postexercise (247.5 +/- 38.5) as compared with pre-exercise (126.4 +/- 20.2) for both groups. There was no difference (p > 0.05) in CK activity between groups. This study indicated that moderate-intensity whole-body resistance exercise had no effect on serum MDA concentration in RT and UT subjects.     

Naloxone effect on ANP in trained and untrained rats

1. The effect of a dose of naloxone (1 mg·kg⁻¹ b.w.) on peripheral (plasma, atria) and central (hypothalamus, hypophysis) levels of atrial natriuretic peptide (ANP) was investigated in the rat.2. In control rats, an acute subcutaneous dose of naloxone produced no significant change in plasma ANP, but a decrease (NS) in atrial ANP concentration.3. In physically conditioned animals, naloxone produced a significant decrease in atrial ANP levels. Receptor sensitivity may thus be involved in this differential response.4. In hypothalamus and hypophysis, no effect on ANP concentrations was seen after a high dose of naloxone whether in control or in physically conditioned animals, suggesting peripheral and central ANP might be differently regulated, at least after chronic endurance physical training.     

The effect of exercise on the production and clearance of testosterone in well trained young men

Tritium-labelled testosterone was infused into four well-trained subjects at rest and during one hour of exercise at about 60% of their maximum aerobic power. This exercise regime led to a mean increase of 27% (range 10-51%) in plasma testosterone concentration. At the same time there were significant decreases in the estimated hepatic plasma flow (EHPF) (45%; range 28-67%), metabolic clearance rate of testosterone (MCRT) (29%; range 18-37%) and plasma volume (8.2%; range 3-10%). The production rate of testosterone decreased by 10% (range 9-22%) but this was not statistically significant. The ratio MCRT:EHPF increased in 3 out of 4 subjects in response to exercise but there was considerable inter-subject variation both at rest and during exercise. These findings suggest that the exercise-induced elevation of testosterone level is due solely to the reduction in the rate at which testosterone is cleared from the plasma. The principal cause of the reduction in MCRT is probably the reduction in EHPF but the variation in the ratio MCRT:EHPF suggests that changes in the extrahepatic clearance of testosterone may also be involved.     

Cardiovascular response to static handgrip in trained and untrained men

The influence of aerobic capacity on the cardiovascular response to handgrip exercise, in relation to the muscle mass involved in the effort, was tested in 8 trained men (T) and 17 untrained men (U). The subjects performed handgrip exercises with the right-hand (RH), left-hand (LH) and both hands simultaneously (RLH) at an intensity of 25% of maximal voluntary contraction force. Maximal aerobic capacity was 4.3 l.min-1 in T and 3.21 l.min-1 in U (P less than 0.01). The endurance time for handgrip was longer in T than in U by 29% (P less than 0.05) for RH, 38% (P less than 0.001) for LH and 24% (P less than 0.001) for RLH. Heart rate (fc) was significantly lower in T than in U before handgrip exercise, and showed smaller increases (P less than 0.01) at the point of exhaustion: 89 vs 106 beats.min-1 for RH, 93 vs 100 beats.min-1 for LH and 92 vs 108 beats.min-1 for RLH. Stroke volume (SV) at rest was greater in T than in U and decreased significantly (P less than 0.05) during handgrip exercise in both groups of subjects. At the point of exhaustion SV was still greater in T than in U: 75 vs 57 ml for RH, 76 vs 54 ml for LH and 76 vs 56 ml for RLH. During the last seconds of handgrip exercise, the left ventricular ejection time was longer in T than in U. Increases in cardiac output (Qc) and systolic blood pressure did not differ substantially between T and U, nor between the handgrip exercise tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of food intake on exercise fatigue in trained and untrained subjects

The effects of carbohydrate and fat intake on exercise-induced fatigue was investigated in 30 untrained--(VO2max of 40.6 +/- 2.7 ml X kg-1 X min-1) and 24 trained-subjects (VO2max of 52.3 +/- 2.7 ml X kg-1 X min-1) performing a 34 km march with a 25 kg backpack. Marching time was 8 1/2 h and 6 1/3 h in the untrained and trained-subjects respectively. The subjects were divided into 3 dietary groups. One group had free access to sugar cubes, the second group was offered almonds and the third one served as a control. Triglyceride levels decreased by 65 mg X dl-1 in untrained, and by 115 mg X dl-1 in trained subjects, while blood glucose remained at normal levels. In the untrained subjects, ingestion of almonds delayed the subjective sensation of exhaustion, while 50% of the controls and the sugar consuming subjects complained of exhaustion. The data suggest that ingestion of food containing fat delays exercise induced exhaustion or fatigue to a greater extent than does carbohydrate ingestion.     

Effect of exercise on epinephrine turnover in trained and untrained male subjects

The kinetics underlying plasma epinephrine concentrations were studied. Six athletes (T) and six sedentary males (C) were given intravenous infusions of 3H-labeled epinephrine, after which arterial blood was drawn. They rested sitting and bicycled continuously to exhaustion (60 min at 125 W, 60 min at 160 W, 40 min at 200 W, and 240 W to the end). Work time was 154 +/- 13 (SE) (T) and 75 +/- 6 (C) min. At rest, epinephrine clearance was identical [28.4 +/- 1.3 (T) vs. 29.2 +/- 1.8 (C) ml . kg-1 . min-1], but plasma concentration [1.42 +/- 0.27 (T) vs. 0.71 +/- 0.16 (C) nmol . l-1] and, accordingly, secretion [2.9 +/- 0.7 vs. 1.5 +/- 0.4 nmol . min-1] were higher (P less than 0.05) in T than C subjects. Epinephrine clearance was closely related to relative work load, decreasing from 15% above the basal level at 30% of maximal O2 uptake (VO2 max) to 22% below at 76% of VO2 max. Epinephrine concentrations increased much more with work intensity than could be accounted for by changes in clearance and were, at exhaustion, higher (P less than 0.05) in T (7.2 +/- 1.6) than in C (2.5 +/- 0.7 nmol . l-1) subjects despite similar glucose, heart rate, and hematocrit values. At a given load, epinephrine clearance rapidly became constant, whereas concentration increased continuously. Forearm extraction of epinephrine invalidated use of blood from a cubital vein or a hand vein arterialized by hot water in turnover measurements. During exercise, changes in epinephrine concentrations reflect changes in secretion rather than in clearance. Training may increase adrenal medullary secretory capacity.