Norepinephrine response to exercise at the same relative intensity before and after endurance exercise training

It is well documented that endurance exercise training results in a blunted norepinephrine (NE) response to exercise of a given absolute exercise intensity. However, it is not clear what effect training has on the catecholamine response to exercise of the same relative intensity because previous studies have provided conflicting results. The purpose of the present study was, therefore, to determine the catecholamine response to exercise of the same relative exercise intensity before and after endurance exercise training. Six women and three men [age 28 +/- 8 (SD) yr] performed 10 wk of training. Maximal O2 uptake (VO2 max) was determined during treadmill exercise. Fifteen-minute treadmill exercise bouts were performed at 60, 65, 70, 75, 80, and 85% of VO2 max before and after training. VO2 max was increased by 20% (from 39.2 +/- 7.7 to 46.9 +/- 8.1 ml. kg-1. min-1; P < 0.05) in response to training. Plasma NE concentrations were higher (P < 0.05) during exercise at the same relative intensity after, compared with before, training at 65-85% of VO2 max. Differences between heart rates and plasma epinephrine concentrations after, compared with before, training were not statistically significant. These results provide evidence that the NE response to exercise is dependent on the absolute as well as the relative intensity of the exercise.     

Progressive effect of endurance training on VO2 kinetics at the onset of submaximal exercise

The rates of increase in O2 uptake (VO2) after step changes in work rate from 25 W to 60% of pretraining peak VO2 (VO2 peak) were measured at various times during an endurance training program (2 h/day at 60% pretraining VO2 peak). Seven untrained males [23 +/- 1 (SE) yr] performed a series of repeated step changes in work rate before training (PRE) and after 4 days (4D), 9 days (9D), and 30 days (30D) of training. VO2 kinetic responses were determined from breath-by-breath data averaged across four repetitions and analyzed using a two-component exponential model. Mean response time (time taken to reach 63% of steady-state VO2) was faster (P < 0.01) than PRE (38.1 +/- 2.6 s) at both 4D (34.9 +/- 2.4 s) and 9D (32.5 +/- 1.8 s) and was faster (P < 0.01) at 30D than at all other times (28.3 +/- 1.0 s). Blood lactate concentrations (after 6 min of cycling) were also lower at 4D and 9D than PRE (P < 0.01) and were lower at 30D than at all other times (P < 0.01). VO2 peak was unchanged from PRE (3.52 +/- 0.20 l/min) at 8D (3.55 +/- 0.20 l/min) but was increased (P < 0.01) at 30D (3.89 +/- 0.18 l/min). Muscle oxidative capacity (maximal citrate synthase activity) was not significantly increased until 30D (P < 0.01). It is concluded that at least part of the acceleration of whole body VO2 kinetics with endurance training is a rapid phenomenon, occurring before changes in VO2 peak and/or muscle oxidative potential.     

Impaired pituitary hormonal response to exhaustive exercise in overtrained endurance athletes

The effects of 3,5-diiodo-L-thyronine (3,5-T2, 2.5-10 microg/100 g BW) on cold tolerance, energy expenditure and oxidative capacity of four metabolically very active tissues (brown adipose tissue, skeletal muscle, liver and heart) were determined in hypothyroid, cold-exposed rats. Hypothyroid rats survived cold for only 3-4 days. 3,5-T2 improved survival dose dependently; with 10 microg/100 g BW the rats survived 3 weeks (limit of observation). This effect was paralleled by an increased energy expenditure of the whole animal for the entire 3 weeks. Similar effects were observed in hypothyroid rats treated with 3,3',5-triiodo-L-thyronine (T3). 3,5-T2 stimulated the specific oxidative capacity (expressed as cytochrome oxidase activity per milligram protein) of all four tissues dose dependently. When the oxidative capacity was expressed as total activity (cytochrome oxidase activity times organ weight), the percentage increases were of the same order. T3 exerted similar effects, but the changes in total activity were much greater than in specific activity, indicating an effect on the tissue trophism. The effect of 3,5-T2 on cold tolerance thus mimics the effect of T3, but via different cellular mechanisms. T3 seems to act primarily on the trophism of the tissues, while 3,5-T2 may act directly on mitochondria without an effect on tissue trophism.     

Kinetics of oxygen uptake at the onset of exercise in boys and men

The objective of this study was to compare the O2 uptake (VO2) kinetics at the onset of heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cycling task to determine peak VO2 (VO2 peak). On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice by cycling at 50% VO2 peak for 3.5 min, once by cycling at 100% VO2 peak for 2 min, and once by cycling at 130% VO2 peak for 75 s. O2 deficit was not significantly different between boys and men (respectively, 50% VO2 peak task: 6.6 +/- 11.1 vs. 5.5 +/- 7.3 ml . min-1 . kg-1; 100% VO2 peak task: 28.5 +/- 8.1 vs. 31.8 +/- 6.3 ml . min-1 . kg-1; and 130% VO2 peak task: 30.1 +/- 5.7 vs. 35.8 +/- 5.3 ml . min-1 . kg-1). To assess the kinetics, phase I was excluded from analysis. Phase II VO2 kinetics could be described in all cases by a monoexponential function. ANOVA revealed no differences in time constants between boys and men (respectively, 50% VO2 peak task: 22. 8 +/- 5.1 vs. 26.4 +/- 4.1 s; 100% VO2 peak task: 28.0 +/- 6.0 vs. 28.1 +/- 4.4 s; and 130% VO2 peak task: 19.8 +/- 4.1 vs. 20.7 +/- 5. 7 s). In conclusion, O2 deficit and fast-component VO2 on-transients are similar in boys and men, even at high exercise intensities, which is in contrast to the findings of other studies employing simpler methods of analysis. The previous interpretation that children rely less on nonoxidative energy pathways at the onset of heavy exercise is not supported by our findings.     

Cardiovascular responses at the onset of static exercise in patients with dual-chamber pacemakers

Cardiac output (CO) responses to exercise can be altered by ventricular pacing in pacemaker-dependent patients. The relative contributions of CO and peripheral vascular resistance (PVR) toward the initial increase in blood pressure with the initiation of static exercise were investigated in eight otherwise healthy pacemaker-dependent subjects [age 24 +/- 2 yr (range 17-37 yr)]. Beat-by-beat measures of heart rate (HR; electrocardiography), mean arterial pressure (MAP), and CO derived from stroke volume (SV) (CO = HR.SV; 2-D echocardiography) were determined during the first 20 s of a one-legged static knee extension performed at 20% maximal voluntary effort by using three pacing modalities: dual pacing and sensing mode (DDD, i.e., normal physiological HR response), fixed at resting HR (DOO-R), and fixed at peak exercise HR (DOO-E), as previously achieved during 5 min of sustained contraction in the DDD mode. There were no differences in MAP, CO, or PVR (PVR = MAP/CO) between modes at rest (P > 0.05). With DOO-E pacing, SV was lower at rest compared with the other modes and increased with exercise (P < 0.05). Although there were no significant increase in MAP or CO during DOO-R pacing, both variables were elevated by leg contraction during DDD and DOO-E pacing (P < 0.05), with no significant change in PVR. Additionally, the CO and MAP increases were significantly greater with DOO-E pacing (P < 0.05). Thus the magnitude of the initial increase in arterial pressure at the onset of mild one-legged static exercise was dictated by the changes in CO as PVR remained unchanged.     

Velocity of oxygen uptake response at the onset of exercise: A comparison between children after cardiac surgery and healthy boys

A comparison was carried out concerning maximal oxygen uptake, oxygen uptake adjustment at the onset of high-intensity exercise, and maximal blood lactate between 10 healthy prepubertal boys and 35 children after repair of cardiac malformations or after Fontan operation. Mean maximal oxygen uptake (VO2) was moderately reduced in children after repair of tetralogy of Fallot or after Mustard or Senning operations and severely reduced after Fontan operations. Conversely, mean half-time of VO2 response was moderately prolonged in children after repair of tetralogy of Fallot or after Senning and Mustard operations and considerably prolonged after Fontan operations. According to our results unfavorable kinetics of VO2 response to physical exercise are present in addition to reduced aerobic power in many of the operated children. Besides being less qualified for endurance performance, these children are also less prepared for short, high-intensity exercise.     

Comparison of femoral blood gases and muscle near-infrared spectroscopy at exercise onset in humans

We hypothesized that near-infrared spectroscopy (NIRS) measures of hemoglobin and/or myoglobin O2 saturation (IR-SO2) in the vascular bed of exercising muscle would parallel changes in femoral venous O2 saturation (SfvO2) at the onset of leg-kicking exercise in humans. Six healthy subjects performed transitions from rest to 48 +/- 3 (SE)-W two-legged kicking exercise while breathing 14, 21, or 70% inspired O2. IR-SO2 was measured over the vastus lateralis muscle continuously during all tests, and femoral venous and radial artery blood samples were drawn simultaneously during rest and during 5 min of exercise. In all gas-breathing conditions, there was a rapid decrease in both IR-SO2 and SfvO2 at the onset of moderate-intensity leg-kicking exercise. Although SfvO2 remained at low levels throughout exercise, IR-SO2 increased significantly after the first minute of exercise in both normoxia and hyperoxia. Contrary to the hypothesis, these data show that NIRS does not provide a reliable estimate of hemoglobin and/or O2 saturation as reflected by direct femoral vein sampling.     

Effect of endurance exercise training on heart rate variability at rest in healthy young and older men

Heart rate variability (HRV) (SD of the RR interval), an index of parasympathetic tone, was measured at rest and during exercise in 13 healthy older men (age 60 to 82 years) and 11 healthy young men (age 24 to 32 years) before and after 6 months of aerobic exercise training. Before exercise training, the older subjects had a 47% lower HRV at rest compared with the young subjects (31 +/- 5 ms vs 58 +/- 4 ms, p = 0.0002). During peak exercise, the older subjects had less parasympathetic withdrawal than the young subjects (-45% vs -84%, p = 0.0001). Six months of intensive aerobic exercise training increased maximum oxygen consumption by 21% in the older group and 17% in the young group (analysis of variance: overall training effect, p = 0.0001; training effect in young vs old, p = NS). Training decreased the heart rate at rest in both the older (-9 beats/min) and the young groups (-5 beats/min, before vs after, p = 0.0001). Exercise training increased HRV at rest (p = 0.009) by 68% in the older subjects (31 +/- 5 ms to 52 +/- 8 ms) and by 17% in the young subjects (58 +/- 4 ms to 68 +/- 6 ms). Exercise training increases parasympathetic tone at rest in both the healthy older and young men, which may contribute to the reduction in mortality associated with regular exercise.     

Ventilatory pattern at rest and response to hypercapnic stimulation in patients with obstructive sleep apnea syndrome

The first radiographic appearance of adductor sesamoid bone of thumb is considered reliable and is the most commonly used indicator of puberty growth spurt. The purpose of this study was to find out whether the tooth mineralization stage/stages were as reliable an indicator of puberty growth spurt as the adductor sesamoid bone. Puberty assessment has its necessary application in diagnosis, treatment planning of various malocclusions and in medico legal cases. The results indicated that a close relationship existed between tooth mineralization Stage G and appearance of the sesamoid bone. Hence it can be used in dentistry as an indicator for onset of puberty growth spurt via periapical or panoramic radiographs. The result of this study were not applicable to boys as the apical closure of these teeth had already occurred at the time of early radiographic appearance of the adductor sesamoid bone.     

Ventilatory and arterial blood gas tension adjustments to strenuous exercise in standardbreds

Five healthy, fit Standardbreds (mean +/- SEM, 490.4 +/- 15.0 kg, 4.0 +/- 0.5 years) were studied during a standardized test carried out on a treadmill. The test consisted of an 8-minute warm-up and a 9-minute exercise period (1 minute at 1.7, 4, 7, 8, 9, and 10 m/s; 2 minutes at 4 m/s; and a 1-minute walk at a 6% slope). Respiratory airflow, tidal volume (V(T)), and respiratory frequency (f) were continuously recorded, using 2 ultrasonic pneumotachographs connected to a face mask and mass spectrometer. Oxygen uptake, carbon dioxide output, and expired minute volume (V(E)) were obtained on a breath by breath basis. Arterial blood was tested at the end of each step for O2 and CO2 partial pressures. Heart rate was continuously recorded, using a heart rate recording system. Stride frequency was measured at each step, and the stride frequency-to-f ratio was calculated. Venous blood was tested for plasma lactate concentration be fore and 2 minutes after completion of the test. Some horses had a locomotion-respiration coupling (LRC), but this coupling was occasional and intermittent. The f was lower and V(T) was higher than values reported for thoroughbreds working under similar experimental conditions. Nevertheless, maximal V(E) did not overshoot maximal V(E) reported in Thoroughbreds. All horses were hypoxemic and hypercapnic, but there was wide variability between subjects. The horses with the highest oxygen uptake and the lowest plasma lactate concentration were more hypoxemic and hypercapnic. The Standardbreds, studied under our laboratory conditions, did not have constant LRC and had lower f with higher V(T) than did Thoroughbreds under similar experimental conditions. Despite these differences in breathing strategy, the Standardbreds did not have higher V(E) than did Thoroughbreds, and they were hypoxemic and hypercapnic. The fact that these Standardbreds, which obviously freely selected their breathing strategy, were unable or unwilling to adopt compensatory hyperventilation reinforces the hypothesis that, in strenuous exercising horses, there could be a physiologic limit to ventilation, most probably related to mechanical factors, but independent of any LRC.     

Unaltered oxygen uptake kinetics at exercise onset with lower-body positive pressure in humans

The purpose of this study was to determine the influence of a reduced skeletal muscle blood flow on oxygen uptake (VO2) kinetics at the onset of cycle ergometer exercise. Seven healthy subjects performed rest-to-exercise transitions with a lower-body positive pressure (LBPP) of 45 Torr. Two work rates were selected for each subject: a moderate intensity (VO2, approximately 1.9 l min-1; delta[lactate], approximately 1 mequiv l-1) below the estimated lactate threshold and a heavy intensity (VO2, approximately 2.6 l min-1; delta[lactate], approximately 3 mequiv l-1) above this threshold. Pulmonary gas exchange variables and ventilatory (VE) responses were computed breath-by-breath from mass spectrometer and turbine volume meter signals, respectively, and mean response times (MRT) calculated. Samples of 'arterialized' venous blood were used for the determination of [lactate], pH and [K+]. While the application of 45 Torr LBPP had no effects on VO2 kinetics during moderate exercise (MRT: 33.5 +/- 1.2 s at 45 Torr vs. 32.8 +/- 1.3 s at 0 Torr; P > 0.05) or on [lactate], pH or [K+], breathing frequency (f) was increased (P < 0.05) and tidal volume (VT) reduced (P < 0.05). The addition of LBPP during heavy exercise did not alter VO2 kinetics (MRT: 35.2 +/- 1.5 s at 45 Torr vs. 34.8 +/- 1.5 s at 0 Torr; P > 0.05), or [lactate], pH or [K+]. Although both the VE (via an increased f) and CO2 output (VCO2) were significantly greater with LBPP by approximately 30 l min-1 and approximately 500 ml min-1, respectively, end-tidal CO2 partial pressure was decreasing, suggesting an additional ventilatory stimulus. These data can be interpreted to suggest that oxygen delivery is not critically dependent upon blood flow to the working muscle at exercise onset, while LBPP-induced increases in VE during suprathreshold exercise may be related to an accumulation of metabolites at the working muscle or the effects of pressure per se.     

Metabolic and exercise endurance effects of coffee and caffeine ingestion

Caffeine (Caf) ingestion increases plasma epinephrine (Epi) and exercise endurance; these results are frequently transferred to coffee (Cof) consumption. We examined the impact of ingestion of the same dose of Caf in Cof or in water. Nine healthy, fit, young adults performed five trials after ingesting (double blind) either a capsule (Caf or placebo) with water or Cof (decaffeinated Cof, decaffeinated with Caf added, or regular Cof). In all three Caf trials, the Caf dose was 4.45 mg/kg body wt and the volume of liquid was 7.15 ml/kg. After 1 h of rest, the subject ran at 85% of maximal O2 consumption until voluntary exhaustion (approximately 32 min in the placebo and decaffeinated Cof tests). In the three Caf trials, the plasma Caf and paraxanthine concentrations were very similar. After 1 h of rest, the plasma Epi was increased (P < 0.05) by Caf ingestion, but the increase was greater (P < 0.05) with Caf capsules than with Cof. During the exercise there were no differences in Epi among the three Caf trials, and the Epi values were all greater (P < 0.05) than in the other tests. Endurance was only increased (P < 0. 05) in the Caf capsule trial; there were no differences among the other four tests. One cannot extrapolate the effects of Caf to Cof; there must be a component(s) of Cof that moderates the actions of Caf.     

Muscle glycogen accumulation after endurance exercise in trained and untrained individuals

Muscle glycogen accumulation was determined in six trained cyclists (Trn) and six untrained subjects (UT) at 6 and either 48 or 72 h after 2 h of cycling exercise at approximately 75% peak O2 uptake (VO2 peak), which terminated with five 1-min sprints. Subjects ate 10 g carbohydrate . kg-1 . day-1 for 48-72 h postexercise. Muscle glycogen accumulation averaged 71 +/- 9 (SE) mmol/kg (Trn) and 31 +/- 9 mmol/kg (UT) during the first 6 h postexercise (P < 0.01) and 79 +/- 22 mmol/kg (Trn) and 60 +/- 9 mmol/kg (UT) between 6 and 48 or 72 h postexercise (not significant). Muscle glycogen concentration was 164 +/- 21 mmol/kg (Trn) and 99 +/- 16 mmol/kg (UT) 48-72 h postexercise (P < 0.05). Muscle GLUT-4 content immediately postexercise was threefold higher in Trn than in UT (P < 0.05) and correlated with glycogen accumulation rates (r = 0.66, P < 0.05). Glycogen synthase in the active I form was 2.5 +/- 0.5, 3.3 +/- 0.5, and 1.0 +/- 0.3 micromol . g-1 . min-1 in Trn at 0, 6, and 48 or 72 h postexercise, respectively; corresponding values were 1.2 +/- 0.3, 2.7 +/- 0.5, and 1.6 +/- 0.3 micromol . g-1 . min-1 in UT (P < 0.05 at 0 h). Plasma insulin and plasma C-peptide area under the curve were lower in Trn than in UT over the first 6 h postexercise (P < 0.05). Plasma creatine kinase concentrations were 125 +/- 25 IU/l (Trn) and 91 +/- 9 IU/l (UT) preexercise and 112 +/- 14 IU/l (Trn) and 144 +/- 22 IU/l (UT; P < 0.05 vs. preexercise) at 48-72 h postexercise (normal: 30-200 IU/l). We conclude that endurance exercise training results in an increased ability to accumulate muscle glycogen after exercise.     

Generalisability of sensory gating during passive movement of the legs

Movement-related gating of somatosensory evoked potentials in the upper limb is restricted mainly to nerve stimulation supplying the moved limb segment. In the lower limb, this principle may not be followed. Tibial nerve (stimulation at the knee) somatosensory evoked potentials (SEPs) and soleus H reflexes exhibit quite similar patterns of modulation during movement. We hypothesised that movement-related gating of initial SEPs in the leg would be generalised from ipsilateral to contralateral leg movement and that such sensory gating would not be generalised to modalities with no functional relevance to the movement. Somatosensory, visual, and auditory evoked potentials (SEPs, VEPs, and AEPs) were recorded from scalp electrodes during unilateral passive movement. Short-latency tibial nerve SEPs, representing the first cortical components, and soleus H reflexes in both the moved leg and the stationary leg were attenuated compared to non-movement controls (p<0.05). Neither VEPs nor middle latency AEPs were modulated (p>0.05). We conclude that sensory gating occurs during contralateral movement. This gating is absent in other sensory modalities with no apparent functional relationship to the imposed movement.     

Immune response to changes in training intensity and volume in runners

We examined the acute and chronic effects of changes in training volume and intensity on the blood lymphocyte percentages and immunoglobulin levels in runners. Twelve runners participated in four 10-d phases of low volume/low intensity (LV/LI), high volume/low intensity (HV/LI), or high volume/high intensity (HV/HI) running. Subjects were assigned to one of two different training group orders: 1) LV/LI, HV/LI, LV/LI, HV/HI; or 2) LV/LI, HV/HI, LV/LI, HV/LI. Venous blood was drawn at rest on days 1, 4, and 7; and 5 min post-exercise on days 1 and 7 of each 10-d phase. Lymphocyte subsets were determined by flow cytometry for CD3+, CD4+, CD8+, and HLA-DR+. IgG, and IgM levels were obtained by ELISA analysis. Immunoglobulin, CD8+ and HLA-DR+ levels, and pre-exercise plasma cortisol concentrations were not significantly affected by alterations in volume or intensity. A transient decrease (P < 0.05) was observed in CD4+ and the CD4/CD8 ratio 5 min post-exercise during the HV/LI and HV/HI phases. Results indicate that the exercise-induced lymphocyte subset reduction is transient and suggest that it is more dependent upon training intensity than volume, and the training order of exposure to the high-intensity stimulus may determine the magnitude of subsequent responses.     

Effects of voluntary exercise on nonspecific immunological mechanisms in mice

We studied the effects of voluntary exercise on nonspecific immunological mechanisms in mice. In this study, 7 week old male ICR mice were divided into two groups: a non-exercise group (control) and a group given voluntary exercise (Vex group). Each mouse of the Vex group was kept in an individual cage equipped with a voluntarily revolving wheel that the mouse had free access to. The duration of voluntary exercise was 3 days per week for 8 weeks. The following results were obtained: 1) After 8 weeks of voluntary exercise, food consumption, the weight of the anterior tibialis muscle and succinate dehydrogenase activity in the anterior tibialis muscle increased significantly in the Vex group compared to the control group. 2) By means of the carbon clearance method, phagocytosis of the reticuloendothelial system was increased in the Vex group. 3) Glucose consumption capacity and O-2 production capacity of peritoneal macrophages (M phi) were significantly increased in the Vex group compared to the control group. 4) The acid phosphatase (APH), beta-glucuronidase (GLU) and lactate dehydrogenase (LDH) activities of peritoneal M phi increased significantly in the Vex group. 5) Concanavalin A (Con A)-induced cell proliferation in the spleen was high in the Vex group. Based on the above findings, it may be surmised that voluntary exercise enhances nonspecific immunological mechanisms and thereby improves the host defense mechanisms in mice.