Exercise training induces similar elevations in the activity of oxoglutarate dehydrogenase and peak oxygen uptake in the human quadriceps muscle

During exercise involving a small muscle mass, peak oxygen uptake is thought to be limited by peripheral factors, such as the degree of oxygen extraction from the blood and/or mitochondrial oxidative capacity. Previously, the maximal activity of the Krebs cycle enzyme oxoglutarate dehydrogenase has been shown to provide a quantitative measure of maximal oxidative metabolism, but it is not known whether the increase in this activity after a period of training reflects the elevation in peak oxygen consumption. Fourteen subjects performed one-legged knee extension exercise for 5–7 weeks, while the other leg remained untrained. Thereafter, the peak oxygen uptake by the quadriceps muscle was determined for both legs, and muscle biopsies were taken for assays of maximal enzyme activities (at 25°C). The peak oxygen uptake was 26% higher in the trained than in the untrained muscle (395 vs. 315 ml min⁻¹ kg⁻¹, respectively; P < 0.01). The maximal activities of the Krebs cycle enzymes in the trained and untrained muscle were as follows: citrate synthase, 22.4 vs. 18.2 μmol min⁻¹ g⁻¹ (23%, P < 0.05); oxoglutarate dehydrogenase, 1.88 vs. 1.54 μmol min⁻¹ g⁻¹ (22%, P < 0.05); and succinate dehydrogenase, 3.88 vs. 3.28 μmol min⁻¹ g⁻¹ (18%, P < 0.05). The difference between the trained and untrained muscles with respect to peak oxygen uptake (80 ml min⁻¹ kg⁻¹) corresponded to a flux through the Krebs cycle of 1.05 μmol min⁻¹ g⁻¹, and the corresponding difference in oxoglutarate dehydrogenase activity (at 38°C) was 0.83 μmol min⁻¹ g⁻¹. These parallel increases suggest that there is no excess mitochondrial capacity during maximal exercise with a small muscle mass.     

Skin microvascular reactivity in trained adolescents

Whilst endothelial dysfunction is associated with a sedentary lifestyle, enhanced endothelial function has been documented in the skin of trained individuals. The purpose of this study was to investigate whether highly trained adolescent males possess enhanced skin microvascular endothelial function compared to their untrained peers. Seventeen highly and predominantly soccer trained boys ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 55 ± 6 mL kg⁻¹ min⁻¹) and nine age- and maturation-matched untrained controls ( [(V)\dot]\textO_2 \textpeak \dot{V}{\text{O}}_{{2\,{\text{peak}}}} : 43 ± 5 mL kg⁻¹ min⁻¹) aged 13–15 years had skin microvascular endothelial function assessed using laser Doppler flowmetry. Baseline and maximal thermally stimulated skin blood flow (SkBF) responses were higher in forearms of trained subjects compared to untrained participants [baseline SkBF: 11 ± 4 vs. 9 ± 3 perfusion units (PU), p < 0.05; SkBF_max: 282 ± 120 vs. 204 ± 68 PU, p < 0.05]. Similarly, cutaneous vascular conductance (CVC) during local heating was superior in the forearm skin of trained versus untrained individuals (CVC_max: 3 ± 1 vs. 2 ± 1 PU mmHg⁻¹, p < 0.05). Peak hyperaemia following arterial occlusion and area under the reactive hyperaemia curve were also greater in forearm skin of the trained group (peak hyperaemia: 51 ± 21 vs. 35 ± 15 PU, p < 0.05; area under curve: 1596 ± 739 vs. 962 ± 796 PUs, p < 0.05). These results suggest that chronic exercise training in adolescents is associated with enhanced microvascular endothelial vasodilation in non-glabrous skin.     

Pulmonary oxygen uptake and muscle deoxygenation kinetics during recovery in trained and untrained male adolescents

Previous studies have demonstrated faster pulmonary oxygen uptake ( [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} ) kinetics in the trained state during the transition to and from moderate-intensity exercise in adults. Whilst a similar effect of training status has previously been observed during the on-transition in adolescents, whether this is also observed during recovery from exercise is presently unknown. The aim of the present study was therefore to examine [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics in trained and untrained male adolescents during recovery from moderate-intensity exercise. 15 trained (15 ± 0.8 years, [(V)\dot]\textO_2max \dot{V}{\text{O}}_{2\max} 54.9 ± 6.4 mL kg⁻¹ min⁻¹) and 8 untrained (15 ± 0.5 years, [(V)\dot]\textO_2max \dot{V}{\text{O}}_{2\max } 44.0 ± 4.6 mL kg⁻¹ min⁻¹) male adolescents performed two 6-min exercise off-transitions to 10 W from a preceding “baseline” of exercise at a workload equivalent to 80% lactate threshold; [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} (breath-by-breath) and muscle deoxyhaemoglobin (near-infrared spectroscopy) were measured continuously. The time constant of the fundamental phase of [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} off-kinetics was not different between trained and untrained (trained 27.8 ± 5.9 s vs. untrained 28.9 ± 7.6 s, P = 0.71). However, the time constant (trained 17.0 ± 7.5 s vs. untrained 32 ± 11 s, P < 0.01) and mean response time (trained 24.2 ± 9.2 s vs. untrained 34 ± 13 s, P = 0.05) of muscle deoxyhaemoglobin off-kinetics was faster in the trained subjects compared to the untrained subjects. [(V)\dot]\textO₂ \dot{V}{\text{O}}_{2} kinetics was unaffected by training status; the faster muscle deoxyhaemoglobin kinetics in the trained subjects thus indicates slower blood flow kinetics during recovery from exercise compared to the untrained subjects.     

Acute EPOC response in women to circuit training and treadmill exercise of matched oxygen consumption

The purpose of the study was to evaluate the effects of circuit training (CT) and treadmill exercise performed at matched rates of oxygen consumption and exercise duration on elevated post-exercise oxygen consumption (EPOC) in untrained women, while controlling for the menstrual cycle. Eight, untrained females (31.3±9.1 years; 2.04±0.26 l min^–1 estimated VO_2max; BMI=24.6±3.9 kg/m²) volunteered to participate in the study. Testing was performed during the early follicular phase for each subject to minimize hormonal variability between tests. Subjects performed two exercise sessions approximately 28 days apart. Resting, supine energy expenditure was measured for 30 min preceding exercise and for 1 h after completion of exercise. Respiratory gas exchange data were collected continuously during rest and exercise periods via indirect calorimetry. CT consisted of three sets of eight common resistance exercises. Pre-exercise and exercise oxygen consumption was not different between testing days (P>0.05). Thus, exercise conditions were appropriately matched. Analysis of EPOC data revealed that CT resulted in a significantly higher (p<0.05) oxygen uptake during the first 30 min of recovery (0.27±0.01 l min^–1 vs 0.23±0.01 l min^–1); though, at 60 min, treatment differences were not present. Mean VO₂ remained significantly higher (0.231±0.01 l min^–1) than pre-exercise measures (0.193±0.01 l min^–1) throughout the 60-min EPOC period (p<0.05). Heart rate, RPE, V_E and RER were all significantly greater during CT (p<0.05). When exercise VO₂ and exercise duration were matched, CT was associated with a greater metabolic disturbance and cost during the early phases of EPOC.     

Do gender differences exist in the ventilatory response to progressive exercise in males and females of average fitness?

Gender differences in lung volumes and flow rates, and in respiratory control have been documented previously. How these gender differences affect exercise responses in normal subjects is less clear, particularly as many studies involved highly fit subjects. This study aimed to investigate potential gender differences occurring during progressive exercise in healthy males and females of average fitness. Fourteen males and ten females of mean (SD) age 23 (0.35) years completed a progressive exercise test to exhaustion on a cycle ergometer, with a ramp increase of 15 W min⁻¹ (female) or 20 W min⁻¹ (male). All females were studied during the follicular phase of their menstrual cycle. Cardiorespiratory variables were measured, breath by breath, and values were compared at rest, at 40 W, at physiologically equivalent workloads below, at and above the gas exchange threshold and at peak oxygen uptake (V̇O_2peak). Mean V̇O_2peak (SEM) was 32.4 (2.01) ml kg⁻¹ min⁻¹ for the females and 41.9 (1.80) ml kg⁻¹ min⁻¹ for the males. Females had a significantly lower end-tidal partial CO₂ pressure at rest and throughout exercise. Increases in exercise minute ventilation were achieved by a significantly greater tidal volume in males, whereas females adopted a significantly greater breathing frequency. Ratings of respiratory discomfort were significantly greater in the male group at physiologically equivalent workloads compared to the female group. This study shows gender differences exist in the ventilatory and sensory response to progressive exercise in untrained subjects. Further work is required to ascertain if these effects are altered during the luteal phase of the menstrual cycle.     

Pituitary–adrenal responses to arm versus leg exercise in untrained man

The purpose of this study was to examine pituitary–adrenal (PA) hormone responses [beta-endorphin (β-END), adrenocorticotropic hormone (ACTH) and cortisol] to arm exercise (AE) and leg exercise (LE) at 60 and 80% of the muscle-group specific VO₂ peak. Eight healthy untrained men (AE VO₂ peak=32.4±3.0 ml kg⁻¹ min⁻¹, LE VO₂ peak=46.9±5.3 ml kg⁻¹ min⁻¹) performed two sub-maximal AE and LE tests in random order. Plasma β-END, ACTH and cortisol were not different (P>0.05) between AE and LE at either exercise intensity; the 60% testing elicited no changes from pre-exercise (PRE) values. For 80% testing, plasma β-END, ACTH and cortisol were consistently, but not significantly, greater during LE than AE. In general, plasma β-END and ACTH were higher (P<0.05) during 80% exercise, than PRE, for both AE and LE. Plasma cortisol was elevated (P<0.05) above PRE during 80% LE, and following 80% for both AE and LE. Plasma ACTH was higher (P<0.05) during 80% LE and AE versus 60% LE and AE, respectively. Plasma β-END and cortisol were significantly higher during and immediately after 80% LE than 60% LE. Thus, plasma β-END, ACTH and cortisol responses were similar for AE and LE at the two relative exercise intensities, with the intensity threshold occurring somewhere between 60 and 80% of VO₂ peak. It appears that the smaller muscle mass associated with AE was sufficient to stimulate these PA axis hormones in a manner similar to LE, despite the higher metabolic stress (i.e., plasma La^-) associated with LE.     

The effect of prolonged submaximal exercise on gas exchange kinetics and ventilation during heavy exercise in humans

This study compared ventilation, gas exchange (oxygen uptake, V̇O₂) and the surface electromyogram (EMG) activity of four major lower limb muscles during heavy exercise before (Pre-Ex) and after (Post-Ex) a sustained 90-min cycling exercise at 60% V̇O_2peak. The 90-min exercise was incorporated under the hypothesis that sustained exercise would alter substrate availability in the second exercise bout causing differences in fibre recruitment patterns, gas exchange and ventilation. Nine trained male subjects [V̇O_2peak=60.2 (1.7) ml·kg⁻¹·min⁻¹] completed two identical 6-min bouts of cycling performed at high intensity [~90% V̇O_2peak; 307 (6) W, mean (SE)]. Ventilation and gas exchange were measured breath-by-breath and the EMG was recorded during the last 12 s of each minute of the two 6-min bouts. EMG signals were analysed to determine integrated EMG (iEMG) and mean power frequency (MPF). V̇O₂ at min 3 and min 6 in Post-Ex were significantly higher (i.e., +201 and 141 ml·min⁻¹, respectively, P<0.05) than in Pre-Ex but there was a ~25% decrease of the slow component, taken as the difference between min 6 and min 3 [187 (27) vs 249 (35) ml·min⁻¹, respectively, P<0.05]. The greater whole-body V̇O₂ after 3 min of exercise in Post-Ex was not accompanied by clear alterations in the iEMG and MPF of the examined leg muscles. Ventilation and heart rate were elevated (~12–16 l·min⁻¹ and ~10 beats·min⁻¹, respectively, P<0.05) as were the ratios V̇ _E/O₂ and V̇ _E/V̇CO₂ in the Post-Ex tests. It was concluded that the V̇O₂ and ventilation responses to high-intensity exercise can be altered following prolonged moderate intensity exercise in terms of increased amplitude without associated major changes in either iEMG or MPF values among conditions.     

Is the balance between skeletal muscular metabolic capacity and oxygen supply capacity the same in endurance trained and untrained subjects?

We attempted to test whether the balance between muscular metabolic capacity and oxygen supply capacity in endurance-trained athletes (ET) differs from that in a control group of normal physically active subjects by using exercises with different muscle masses. We compared maximal exercise in nine ET subjects [Maximal oxygen uptake (VO₂max) 64 ml kg⁻¹ min⁻¹ ± SD 4] and eight controls (VO₂max 46 ± 4 ml kg⁻¹ min⁻¹) during one-legged knee extensions (1-KE), two-legged knee extensions (2-KE) and bicycling. Maximal values for power output (P), VO₂max, concentration of blood lactate ([La⁻]), ventilation (VE), heart rate (HR), and arterial oxygen saturation of haemoglobin (SpO₂) were registered. P was 43 (2), 89 (3) and 298 (7) W (mean ± SE); and VO₂max: 1,387 (80), 2,234 (113) and 4,115 (150) ml min⁻¹) for controls in 1-KE, 2-KE and bicycling, respectively. The ET subjects achieved 126, 121 and 126% of the P of controls (p < 0.05) and 127, 124, and 117% of their VO₂max (p < 0.05). HR and [La⁻] were similar for both groups during all modes of exercise, while VE in ET was 147 and 114% of controls during 1-KE and bicycling, respectively. For mass-specific VO₂max (VO₂max divided by the calculated active muscle mass) during the different exercises, ET achieved 148, 141, and 150% of the controls’ values, respectively (p < 0.05). During bicycling, both groups achieved 37% of their mass-specific VO₂ during 1-KE. Finally we conclude that ET subjects have the same utilization of the muscular metabolic capacity during whole body exercise as active control subjects.     

The effect of training in male prepubertal and pubertal monozygotic twins

Nine male pairs of monozygotic twins aged 11–14 years, height 147 (7.6) cm and body mass 39.7 (9.6) kg, participated in this study. Twin zygocity was tested using morphological, dermatoglyphic and hematologic methods, and Tanner's five stages were used for the evaluation of biological maturation. One twin from each pair undertook training for 6 months, three times a week, with running at 85–120% of the lactate anaerobic threshold (LT). Anthropometrics, determination of maximum O₂ uptake (V˙O_2max), LT and maximal blood lactate concentration ([La]_max) was carried out before, during and after training. No significant difference existed between the trained twins and their untrained brothers before training. After training, the trained twins increased their V˙O_2max (per kg body mass) by 10.6% and their LT by 18.2% (P<0.01), reaching values that differed significantly from those of their untrained brothers [57.5 (3.6) ml·kg⁻¹·min⁻¹ vs 55.4 (3.3) ml·kg⁻¹·min⁻¹ and 13.4 (1.1) km·h⁻¹ vs 12.7 (1.1) km·h⁻¹, respectively]. In addition, in the trained twins relative body fat was reduced (P<0.05) from 17.8 to 16.2% and their somatotype altered significantly (decrease of endomorphy and mesomorphy and increase of ectomorphy), while in the untrained twins there was no change in these parameters. Both groups of twins significantly increased their absolute V˙O_2max after the 6 months of training, the trained by 14,9% [from 2.08 (0.43) to 2.37 (0.45) l·min⁻¹] and the untrained by 10.5% [from 2.10 (0.41) to 2.32 (0.47) l·min⁻¹], but no difference was registered between them. A comparison of the intrapair changes in V˙O_2max of prepubertal and pubertal twins showed an influence of training in the prepubertal (19.3% vs 5.2%) but not in the pubertal twins (12.7% vs 13.1%). Using analysis of variance, the relative importance of training, heredity and their interaction was evaluated to be 20%, 70% and 10%, respectively, for the change in body fat, 35%, 45% and 20%, respectively, for the change in relative V˙O_2max and 25–30%, 50–60% and 15–20%, respectively, for the change in LT. In conclusion, training during pubertal growth can favour aerobic power (depending on body composition) as well as aerobic capacity, but it has no effect on absolute V˙O_2max. Genetic control seems to have a strong effect on the extent of adaptations, and the genotype—training interaction explains a small, but prominent part of them. Electronic Publication     

Effects of exercise on the serum concentrations of FSH,LH, progesterone,and estradiol

Summary The effects of 30 min of exercise (74.1±3.0% (VO₂), on the responses of progesterone (P), estradiol (E₂), follicle stimulating hormone (FSH), and luteinizing hormone (LH) were investigated in 10 women. With such exercise significant increments occurred in P (37.6±9.5%) and E₂ (13.5±7.5%) (p<0.05), whereas no changes were observed in FSH and LH (p>0.05). Exercise in the luteal phase and during menses provoked similar changes in P, but E₂ concentrations remained unchanged when exercise occurred during menses (p>0.05). With 8–11 weeks of training the menstrual cycles were quite irregular and retesting of subjects in the same phase of the cycle was not possible. Yet, when subjects were retested after training, no changes occurred in P, E₂ or LH (p>0.05) but a decrement did occur in FSH (p<0.10). Thus, heavy exercise in untrained subjects provokes significant increments in ovarian hormones, whereas no such increments are observed in trained subjects exercising at the same absolute workload.     

Ultra short-term heart rate recovery after maximal exercise in continuous versus intermittent endurance athletes

This study tested the hypothesis that athletes participating in intermittent sports would exhibit a faster heart rate recovery (HRR) during the initial phase (<30 s) following maximal exercise than athletes participating in continuous endurance sports. Forty-six male athletes were allocated into continuous (CNT, n = 24) or intermittent groups (INT, n = 22), matched for age and aerobic fitness. Athletes performed maximal exercise on a treadmill using the ramp protocol. Immediately upon exercise cessation, subjects were placed supine with continuous measurement of HR during the first minute of recovery. Data were analyzed in 10-s intervals and compared between the groups. Repeated measures ANOVA showed a group × time interaction effects (p ≤ 0.01) for HRR expressed in both beats min⁻¹ and in percentage of peak post-exercise HR (% HR_peak). The INT group had lower HR than CNT group at 10 s (189 vs. 192 beats min⁻¹, p = 0.04; and 96.3 vs. 97.9% HR_peak, p = 0.009) and 20 s (184 vs. 188 beats min⁻¹, p = 0.049; and 93.6 vs. 95.7% HR_peak, p = 0.021) intervals of recovery. The results suggest that athletes engaged in intermittent sports are likely to have faster HRR during the first 20 s after maximal exercise than their counterparts trained for continuous performance.     

Substrate utilization in boys during exercise with [13C]-glucose ingestion

The influence of glucose ingestion on substrate utilization during prolonged exercise in children and adolescents is currently unknown. In the present study we determined the effect of intermittent exogenous glucose (GLU_exo) ingestion on substrate utilization during prolonged exercise, in adolescent boys ages 13–17 years. Healthy untrained volunteers performed four 30-min exercise bouts on a cycle ergometer, separated by 5-min rest periods (≅60% maximum O₂ consumption), on two occasions spaced 1–4 weeks apart. Two trials were performed, a control trial (CT), in which subjects ingested water intermittently during the exercise, and a glucose trial (GT), in which subjects ingested a ¹³C-enriched GLU_exo drink (≅3 g glucose · kg body mass⁻¹), also intermittently during the exercise. Total free fatty acids (FAT_total), glucose (GLU_total) and carbohydrate (CHO_total) oxidation was determined from indirect calorimetry, while GLU_exo oxidation was calculated from the ¹³C/¹²C ratio in expired air after 5–10 min and 25–30 min of exercise in each bout. Heart rate and rating of perceived exertion (RPE) were determined at the same time intervals. The oxidation of CHO_total was 169.1 (12.9) g · 120 min⁻¹ and 203.1 (15.9) g · 120 min⁻¹ (P < 0.01) and that of FAT_total was 31.0 (4.2) g · 120 min⁻¹ and 17.1 (2.5) g · 120 min⁻¹ (P < 0.01) in CT and GT, respectively. GLU_exo oxidation in GT was 57.8 (4.3) g · 120 min⁻¹, or 34.2 (2.2)% of that ingested. Endogenous glucose oxidation was 169.1 (12.9) g · 120 min⁻¹ and 145.3 (11.9) g · 120 min⁻¹ (P < 0.01) in CT and GT, respectively. Insulin and glucose concentrations were higher in GT than in CT by 226% and 37%, respectively (both P < 0.05). Free fatty acids and glycerol concentrations were lower in GT than in CT, by 27% and 79%, respectively (both P < 0.05). Heart rate was similar between trials, but RPE was lower in GT vs CT at both 115 and 135 min. Thus, under these experimental conditions, GLU_exo intake spares endogenous carbohydrate and fat by 16% and 45%, respectively, contributes to approximately 25% of the total energy demand of exercise, and lowers the RPE. Accepted: 21 May 2000     

Substrate utilisation during exercise and shivering

It is generally assumed that exercise and shivering are analogous processes with regard to substrate utilisation and that, as a consequence, exercise can be used as a model for shivering. In the present study, substrate utilisation during exercise and shivering at the same oxygen consumption (V˙O₂) were compared. Following an overnight fast, eight male subjects undertook a 2-h immersion in cold water, designed to evoke three different intensities of shivering. At least 1 week later they undertook a 2-h period of bicycle ergometry during which the exercise intensity was varied to match the V˙O₂ recorded during shivering. During both activities hepatic glucose output (HGO), the rate of glucose utilisation (Rd), blood glucose, plasma insulin, free fatty acid (FFA) and beta-hydroxybutyrate (B-HBA) concentrations were measured. The V˙O₂ measured during the different levels of shivering averaged 0.49 l · min⁻¹ (level 1: low), 0.6 l · min⁻¹ (level 2: low-moderate), and 0.9 l · min⁻¹ (level 3: moderate), and corresponded closely to the levels measured during exercise. HGO and Rd were greater (P < 0.05) during exercise than during shivering at the same V˙O₂ (9.5% and 14.7%, respectively). The average (SD) HGO during level 3 exercise was 3.0 (0.91) mg · kg⁻¹ . min⁻¹ compared to 2.76 (1.0) mg · kg⁻¹ . min⁻¹ during shivering. The values for Rd were 3.06 (0.98) mg · kg⁻¹ · min⁻¹ during level 3 exercise and 2.68 (0.82) mg · kg⁻¹ · min⁻¹ during shivering. Blood glucose levels did not differ between conditions, averaging 5.4 (0.3) mmol . l⁻¹ over all levels of shivering and 5.2 (0.3) mmol · l⁻¹ during exercise. Plasma FFA and B-HBA were higher (P < 0.01) during shivering than during corresponding exercise (12.3% and 33.3%, respectively). FFA averaged 0.61 (0.2) mmol · l⁻¹ over all levels of shivering and 0.47 (0.16) mmol · l⁻¹ during exercise. The figures for B-HBA were 0.44 (0.13) mmol · l⁻¹ during all levels of shivering and 0.32 (0.1) mmol · l⁻¹ during exercise. Plasma insulin was higher (P < 0.05) during level 2 and 3 shivering compared to corresponding exercise; at these levels the average value for plasma insulin was 95.9 (21.9) pmol · l⁻¹ during shivering and 80.6 (16.1) pmol · l⁻¹ during exercise. On the basis of the present findings it is concluded that, with regard to substrate utilisation, shivering and exercise of up to 2 h duration should not be regarded as analogous processes. Accepted: 12 February 1997     

Contraction-induced changes in skeletal muscle Na+,K+ pump mRNA expression – importance of exercise intensity and Ca2+-mediated signalling

Aim: To investigate if exercise intensity and Ca²⁺ signalling regulate Na⁺,K⁺ pump mRNA expression in skeletal muscle. Methods: The importance of exercise intensity was evaluated by having trained and untrained humans perform intense intermittent and prolonged exercise. The importance of Ca²⁺ signalling was investigated by electrical stimulation of rat soleus and extensor digitorum longus (EDL) muscles in combination with studies of cell cultures. Results: Intermittent cycling exercise at ∼85% of VO_2peak increased (P < 0.05) α1 and β1 mRNA expression ∼2-fold in untrained and trained subjects. In trained subjects, intermittent exercise at ∼70% of VO_2peak resulted in a less (P < 0.05) pronounced increase (∼1.4-fold; P < 0.05) for α1 and no change in β1 mRNA. Prolonged low intensity exercise increased (P < 0.05) mRNA expression of α1 ∼3.0-fold and α2 ∼1.8-fold in untrained but not in trained subjects. Electrical stimulation of rat soleus, but not EDL, muscle increased (P < 0.05) α1 mRNA expression, but not when combined with KN62 and cyclosporin A incubation. Ionomycin incubation of cultured primary rat skeletal muscle cells increased (P < 0.05) α1 and reduced (P < 0.001) α2 mRNA expression and these responses were abolished (P < 0.05) by co-incubation with cyclosporin A or KN62. Conclusion: (1) Exercise-induced increases in Na⁺,K⁺ pump α1 and β1 mRNA expression in trained subjects are more pronounced after high- than after moderate- and low-intensity exercise. (2) Both prolonged low and short-duration high-intensity exercise increase α1 mRNA expression in untrained subjects. (3) Ca²⁺_i regulates α1 mRNA expression in oxidative muscles via Ca²⁺/calmodulin-dependent protein kinase (CaMK) and calcineurin signalling pathways.     

The effect of acute aerobic exercise on pulse wave velocity and oxidative stress following postprandial hypertriglyceridemia in healthy men

Oxidative stress is postulated to be responsible for the postprandial impairments in vascular function. The purpose of this study was to measure pulse wave velocity (PWV) and markers of postprandial oxidative stress before and after an acute bout of moderate exercise. Ten trained male subjects (age 21.5 ± 2.5 years, VO₂ max 58.5 ± 7.1 ml kg⁻¹ min⁻¹) participated in a randomised crossover design: (1) high-fat meal alone (2) high-fat meal followed 2 h later by a bout of 1 h moderate (60% max HR) exercise. PWV was examined at baseline, 1, 2, 3, and 4 h postprandially. Blood Lipid hydroperoxides (LOOHs), Superoxide dismutase (SOD) and other biochemical markers were measured. PWV increased at 1 h (6.49 ± 2.1 m s⁻¹), 2 h (6.94 ± 2.4 m s⁻¹), 3 h (7.25 ± 2.1 m s⁻¹) and 4 h (7.41 ± 2.5 m s⁻¹) respectively, in the control trial (P < 0.05). There was no change in PWV at 3 h (5.36 ± 1.1 m s⁻¹) or 4 h (5.95 ± 2.3 m s⁻¹) post ingestion in the exercise trial (P > 0.05). LOOH levels decreased at 3 h post ingestion in the exercise trial compared to levels at 3 h (P < 0.05) in the control trial. SOD levels were lower at 3 h post ingestion in the control trial compared to 3 h in the exercise trial (0.52 ± 0.05 vs. 0.41 ± 0.1 units μl⁻¹; P < 0.05). These findings suggest that a single session of aerobic exercise can ameliorate the postprandial impairments in arterial function by possibly reducing oxidative stress levels.     

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

Summary The effects of carbohydrate and fat intake on exercise-induced fatigue was investigated in 30 untrained — ( of 40.6±2.7 ml · kg⁻¹ · min⁻¹) and 24 trained-subjects ( of 52.3±2.7 ml · kg⁻¹ · 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 · dl⁻¹ in untrained, and by 115 mg · 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.     

Sweat sodium concentration during exercise in the heat in aerobically trained and untrained humans

The purpose of this study was to determine whether sweat sodium concentration ([Na⁺]_sweat) during exercise in the heat differs between aerobically trained and untrained individuals. On three occasions, ten endurance-trained (Tr) and ten untrained (UTr) subjects ( [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{{2{\text{peak}}}}  = 4.0 ± 0.8 vs. 3.4 ± 0.7 L min⁻¹, respectively; P < 0.05) cycled in a hot-ventilated environment (36 ± 1°C; 25 ± 2% humidity, airflow 2.5 m s⁻¹) at three workloads (i.e., 40, 60, and 80% [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{{2{\text{peak}}}} ). Whole-body (SR_WB) and back sweat rates (SR_BACK) were measured. At the conclusion of the study, Na⁺ in sweat and blood samples was analyzed to calculate Na⁺ secretion and reabsorption rates. SR_WB and SR_BACK were highly correlated in Tr and UTr (r = 0.74 and 0.79, respectively; P < 0.0001). In both groups, SR_BACK increased with the increases in exercise intensity (P < 0.05). Likewise, [Na⁺]_sweat increased with the exercise intensity in both groups (P < 0.05) and it tended to be higher in Tr than in UTr at 60 and 80% [(V)\dot]\textO_2\textpeak \dot{V}{\text{O}}_{{2{\text{peak}}}} (~22 mmol L⁻¹ higher; P = 0.06). However, when normalized for SR_BACK, [Na⁺]_sweat was not different between groups. In both groups, Na⁺ secretion and reabsorption rates increased with the increases in SR_BACK (P < 0.05). However, Na⁺ reabsorption rate was lower in the Tr than in the UTr (mean slope = 48 vs. 82 ηmol cm⁻² min⁻¹; P = 0.03). In conclusion, using a cross-sectional study design, our data suggest that aerobic fitness level does not reduce sweat Na⁺ secretion or enhance Na⁺ reabsorption during prolonged exercise in the heat that induced high sweat rates.     

Oxygen uptake kinetics during severe intensity running and cycling

The purpose of this study was to investigate the effect of exercise mode on the characteristics of the oxygen uptake ( V̇O₂) response to exercise within the severe intensity domain. Twelve participants each performed a treadmill running test and a cycle ergometer test to fatigue at intensities selected to elicit a mode-specific V̇O₂max and to cause fatigue in ~5 min. The tests were at 234 (30) m·min⁻¹ and 251 (59) W, and times to fatigue were 297 (15) s and 298 (14) s, respectively. The overall rapidity of the V̇O₂response was influenced by exercise mode [ V̇O₂max was achieved after 115 (20) s in running versus 207 (36) s in cycling; p<0.01]. V̇O₂ responses were fit to a three-phase exponential model. The time constant of the primary phase was faster in treadmill tests than in cycle ergometer tests [14 (6) s versus 25 (4) s; p<0.01], and the amplitude of the primary phase was greater in running than in cycling when it was expressed in absolute terms [2327 (393) ml·min⁻¹ versus 2036 (301) ml·min⁻¹; p=0.02] but not when it was expressed as a percentage of the total increase in V̇O₂ [86 (6)% versus 82 (6)%; p=0.09]. When quantified as the difference between the end-exercise V̇O₂ and the V̇O₂ at 2 min, the amplitude of the slow component was ~40% smaller in running [177 (92) ml·min⁻¹ versus 299 (153) ml min⁻¹; p=0.03]. It is concluded that exercise modality affects the characteristics of the V̇O₂ response at equivalent intensities in the severe domain.     

Limb vasodilatory capacity and venous capacitance of trained runners and untrained males

Aerobically trained athletes possess enhanced vasodilatory capacity and venous capacitance in their exercising muscles. However, whether they also possess these characteristics in their non-specific exercising muscles is undetermined. This study examined vasodilatory capacity and venous capacitance of specific (legs) and non-specific exercising muscles (arms) of ten trained runners and ten active but untrained males aged 18–35 years. Venous occlusion plethysmography determined baseline and peak blood flow after 5 min of reactive hyperaemia. Forearm and leg venous capacitance were determined as the difference between baseline and 2 min of venous occlusion at 50 mmHg. During reactive hyperaemia, trained runners had higher leg (48.4±5.3 ml·100 ml tissue^–1·min^–1) and arm (40.8±2.1 ml·100 ml tissue^–1·min^–1) vasodilatory capacity compared to the untrained (leg: 37.3±2.5 ml·100 ml tissue^–1·min^–1; arm: 34.2±2.2 ml·100 ml tissue^–1·min^–1; P<0.05), and higher calf vascular conductance (0.51±0.06 ml·100 ml tissue^–1·min^–1·mmHg^–1 versus 0.35±0.03 ml·100 ml tissue^–1·min^–1·mmHg^–1; P<0.05). The trained also had higher venous capacitance in both arms (3.5±0.2 ml 100·ml^–1) and legs (4.8±0.1 ml·100 ml^–1) compared to the untrained (3.0±0.2 ml 100·ml^–1; 4.2±0.2 ml·100 ml^–1; P<0.05). These findings show that vasculature adaptations to running occur in both specific and non-specific exercising muscles.