Effects of different strength training regimes on moment and power generation during dynamic knee extensions

This study examined the effect of different training regimes on moment and power generation during maximal knee extensions at low to very high extension velocities (0–1000°·s^–1 individual range). A group of 24 soccer players performed 12 weeks of progressively adjusted strength training of the knee extensors at either high resistance (HR,n=7), low resistance (LR,n=6), loaded kicking movements (FU,n=6), while one group served as controls (n=5). Moment and power generation of the knee extensors were determined before and after the training period with a nonisokinetic measuring method recently described. Following HR training, knee extension moment increased 9%–10% at knee angular velocities 0 (isometric) and 30° · s^–1 (P<0.05), peak moment increased 20% at 240–300°·s^–1 (P<0.05), while power generation increased 5%–29% at 240–480° · s^–1 (P<0.01). In addition, in the HR group maximal recorded power increased 45% (P<0.01). After FU training a 7%–13% increase in moment and power was observed at 30–180° · s^–1 (P<0.05). Following LR training, peak moment increased 9% at 120° · s^–1 (P<0.05). Improvements in knee extension moment and power were generally related to the angular velocities employed during training. However, as evaluated using the present measuring method, moment and power increased not only at very low but also at high knee angular velocities following the high-resistance strength training.     

The effects of altered exercise distribution on lymphocyte subpopulations

The effects of exercise distribution on lymphocyte count, lymphocyte subpopulations and plasma cortisol concentration in peripheral blood were assessed in 19 healthy subjects. The subjects were randomly divided into group A (n = 10) or group B (n = 9) according to exercise distribution. Both groups underwent a 10-week programme involving 5 × 2-week blocks: baseline (B), training period 1 (TP1), stabilisation 1 (S1), training period 2 (TP2), and stabilisation 2 (S2). During B, S1 and S2 normal training was undertaken. During TP1 and TP2 the subjects increased the amount of training by 50% in week 1 and by 100% in week 2. During TP1 subjects in group A exercised 6 days·week^–1, while during TP2 these subjects exercised on 3 alternate days·week^–1, but doubled the duration of each training session. The subjects in group B reversed this training order. Blood was collected 36–42 h following exercise period B, and at the end of periods TP1, S1, TP2 and S2, and also 12–18 h following completion of exercise at the end of TP1 and TP2. There were no significant differences (P > 0.05) between the 6 day·week^–1 programme and the 3 alternate day·week^–1 programme in total lymphocyte count, CD3⁺, CD4⁺, CD8+, CD16⁺, or CD19⁺ cells, the CD4:CD8 ratio, HLA-DR⁺ (activated) T cells or plasma cortisol concentrations. Following both TP1 and TP2 there was a nonsignificant decrease in lymphocyte subpopulations. However following both S1 and S2 (baseline training) there was a significant increase in total lymphocyte count, CD3⁺, CD4⁺ and CD8⁺ lymphocytes. The S2 variables statistically significant from B were: total lymphocyte count (P < 0.01), CD3⁺ T-cells and percentage of circulating lymphocytes (^P < 0.01), CD4⁺ cells (P < 0.0001), CD8⁺ cells (P < 0.05), and HLA-DR⁺ (activated) T-cells (P < 0.05). The results indicated that provided the amount of exercise is constant for a given period, then exercise distribution is not a critical variable in the alteration of lymphocyte subpopulations that may occur in response to overload training. However 2 weeks of overload training followed by 2 weeks of active recovery (baseline) training may induce an increase in the lymphocyte count.     

The effects of a reduced exercise duration taper programme on performance and muscle enzymes of endurance cyclists

Summary The influence of tapering on the metabolic and performance parameters in endurance cyclists was investigated. Cyclists (n = 25) trained 5 days · week^–1, 60 min·day^–1, at 75–85% maximal oxygen consumption (VO_2max) for 8 weeks and were then randomly assigned to a taper group: 4D (4 days;n = 7), 8D (8 days;n = 6), CON (control, 4 days rest;n = 6), NOTAPER (non-taper, continued training;n = 6). Muscle biopsy specimens taken before and after training and tapering were analysed for carnitine palmityltransferase (CPT), citrate synthase, ß-hydroxyacyl CoA dehydrogenase (HOAD), cytochrome oxidase (CYTOX), lactate dehydrogenase, glycogen and protein. Significant increases inVO_2max (6%), a 60-min endurance cycle test (34.5%), oxidative enzymes (77–178%), glycogen (35%) and protein (34%) occurred following training. After the taper, HOAD and CPT decreased 25 % (P<0.05) and 26% respectively, in the CON. Post-taper CYTOX values were different (P<0.05) for 4D and 8D compared with CON. Muscle glycogen levels were increased (P<0.05) after tapering in the 4D, 8D and CON, but decreased in NOTAPER. Similarly, power output at ventilation threshold was significantly increased in the 4D (27.4 W) and 8D (27 W) groups, but decreased (22 W) in the NOTAPER. These findings suggest that tapering elicited a physiological adaptation by altering oxidative enzymes and muscle glycogen levels. Such an adaptation may influence endurance cycling during a laboratory performance test.     

Finger and forearm vasodilatatory changes after local cold acclimation

Summary To determine the vascular changes induced by local cold acclimation, post-ischaemia and exercise vasodilatation were studied in the finger and the forearm of five subjects cold-acclimated locally and five non-acclimated subjects. Peak blood flow was measured by venous occlusion plethysmography after 5 min of arterial occlusion (PBF_isc), after 5 min of sustained handgrip at 10% maximal voluntary contraction (PBF_exe), and after 5 min of both treatments simultaneously (PBF_isc+exe). Each test was performed at room temperature (25° C, SE 1 C) (non-cooled condition) and after 5 min of 5'C cold water immersion (cooled condition). After the cold acclimation period, the decrease in skin temperature was more limited in the cold-acclimated compared to the non-acclimated (P<0.01). The PBF_isc was significantly reduced in the cooled condition only in the cold-acclimated subjects (finger: 8.4 ml · 100 ml^–1 · min^–1, SE 1.1,P<0.01; forearm: 5.8 ml · 100 ml^–1 · min^–1, SE 1.5,P<0.01) compared to the non-cooled condition. Forearm PBF_exe was significantly decreased in the cooled condition only in the cold-acclimated subjects (non-cooled: 7.4 ml · 100 ml^–1 · min^–1, SE 1.2; cooled: 3.9 ml · 100 ml^–1 ·min^–1, SE 2.6,P<0.05) indicating that muscle blood flow was also reduced. The application of PBF_isc+exe elicited an increase in peak blood flow only in the forearm of the non-acclimated subjects (non-cooled: 10.4 ml· 100 ml^–1 · min^–1, SE 2.0; cooled: 14.3 ml · 100 ml^–1 · min^–1, SE 2.6,P<0.05) and conversely only in the finger of the cold-acclimated (non-cooled finger: 25.7 ml · 100 ml^–1 · min^–1, SE 4.4; cooled finger: 19.2 ml · 100 ml^–1 · min^–1, SE 3.3,P<0.01). Therefore, subjects cold-acclimated locally showed decreased vasodilatatory responses only when exposed to cold.     

Naloxone-provoked vaso-vagal response to head-up tilt in men

A double-blind paired protocol was used to evaluate, in eight male volunteers, the effects of the endogenous opiate antagonist naloxone (NAL; 0.05 mg· kg^–1) on cardiovascular responses to 50° head-up tilt-induced central hypovolaemia. Progressive central hypovolaemia was characterized by a phase of normotensive-tachycardia followed by an episode of hypotensive-bradycardia. The NAL shortened the former from 20 (8–40) to 5 (3–10) min (median and range; (P < 0.02). Control head-up tilt increased the means of thoracic electrical impedance [from 35.8 (SEM 2.1) to 40.0 (SEM 1.8) ; P < 0.01 of heart rate [HR; from 67 (SEM 5) to 96 (SEM 8) beats · min^–1, P < 0.02], of total peripheral resistance [TPR; from 25.5 (SEM 3.2) to 50.4 (SEM 10.5)mmHg min 1^–1,P < 0.05] and of mean arterial pressure [MAP; from 96 (SEM 2) to 101 (SEM 2)mmHg, P < 0.02]. Decreases were observed in stroke volume [from 65 (SEM 12) to 38 (SEM 9) ml, P < 0.01], in cardiac output [from 3.7 (SEM 0.7) to 2.5 (SEM 0.5) 1 · mint, P < 0.01], in pulse pressure [from 55 (SEM 4) to 37 (SEM 3)mmHg, P < 0.01] and in central venous oxygen saturation [from 73 (SEM 2) to 59 (SEM 4)%, P < 0.01]. During NAL, mean HR increased from 70 (SEM 3); n.s. compared to control) to only 86 (SEM 9) beats · min^–1 (P < 0.02 compared to control) and MAP remained stable. The episode of hypotensive-bradycardia appeared as mean control HR decreased to 77 (SEM 7)beats · min^–1, TPR to 31.4(SEM 7.7)mmHg · min · 1^–1 and MAP to 60 (SEM 5)mmHg (P < 0.01), and the volunteers were tilted supine. Cardiovascular effects of naloxone on central hypovolaemia included a reduced elevation of HR and blood pressures and provocation of the episode of hypotensive-bradycardia.     

The interaction between short-term exercise training and a diuretic-induced hypovolemic stimulus

Nine healthy untrained males [mean (SEM) age, 20.2 (1) years; peak oxygen uptake (VO_2max, 48.2 (2) ml · kg^–1 · min^–1] took part in a study to examine whether short-term exercise training (cycle exercise 2 h · day^–1 for 3 days at 60% ), which normally results in an expansion of plasma volume (PV), can counteract a diuretic-induced hypovolemic stimulus (100 mg triamterene + 50 mg hydrochlorothiazide day^–1 for 5 days concurrent with exercise training) and restore PV to control levels. Resting and exercise responses (90 min, 60% ) in the diuretic plus exercise training condition (D + E) were compared to a control (C) and a diuretic (D) condition in which no exercise was performed. Following the short-term training, PV was still decreased (P < 0.05) below C by –8.3 (3)% in D + E and was similar (P > 0.05) to the reduction in D [–12.4 (2)%]. The reduced PV in response to the diuretic was associated with similar (P > 0.05) elevations in resting aldosterone (ALDO) and norepinephrine (NOREPI) levels (ng · 100 ml^–1) in D [101 (12), 61 (4)] and D + E [85 (16), 60 (10)] above (P < 0.05) C [22 (5), 37 (4)]. During exercise, ALDO levels were increased (P < 0.05) by 66 (5) and 70 (10) ng · 100 ml^–1 in D and D + E, respectively, and the increase was greater (P < 0.05) than C [44 (8) ng · 100 ml^–1]. The rise in NOREPI during exercise was lower (P < 0.05) in D + E [164 (44) ng · 100 ml^–1] than in D [244 (24) ng · 100 ml^–1] with levels similar to C [176 (25) ng · 100 ml^–1]. Thus, the ALDO response to the diuretic was heightened at rest and during exercise but was not additionally affected by the short-term training session. Results suggest that 3 days of exercise training are unable to counteract the hypovolemic effects of a diuretic and restore PV to control levels despite chronic elevations in NOREPI and ALDO.     

Neuromuscular characteristics and fatigue in endurance and sprint athletes during a new anaerobic power test

The purpose of this study was to investigate neuromuscular and energy performance characteristics of anaerobic power and capacity and the development of fatigue. Ten endurance and ten sprint athletes performed a new maximal anaerobic running power test (MARP), which consisted ofn x 20-s runs on a treadmill with 100-s recovery between the runs. Blood lactate concentration [la^–]_b was measured after each run to determine submaximal and maximal indices of anaerobic power (P _3mmol·1 ^–1,P_5mmol·1 ^–1,P_10mmol·1 ^–1andP _max) which was expressed as the oxygen demand of the runs according to the American College of Sports Medicine equation: the oxygen uptake (ml·kg^–1·min^–1)=0.2·velocity (m·min^–1) +0.9·slope of treadmill (frac)·velocity (m·min^–1)+3.5. The height of rise of the centre of gravity of the counter movement jumps before (CMJ_rest) and during (CMJ) the MARP test, as well as the time of force production (t _F) and electromyographic (EMG) activity of the leg muscles of CMJ performed after each run were used to describe the neuromuscular performance characteristics. The maximal oxygen uptake ( _max), anaerobic and aerobic thresholds were determined in the _max test, which consisted ofn x 3-min runs on the treadmill. In the MARP-testP _max did not differ significantly between the endurance [116 (SD 6) ml·kg^–1·min^–1] and sprint [120 (SD 4) ml·kg^–1·min^–1] groups, even though CMJ_rest and peak [la^–]_b were significantly higher and _max was significantly lower in the sprint group than in the endurance group and CMJ_rest height correlated withP _max (r=0.50,P<0.05). The endurance athletes had significantly higher mean values ofP _3mmol·1 ^–1andP _5mmol·1 ^–1[89 (SD 7) vs 76 (SD 8) ml·kg^–1·min^–,P<0.001 and 101 (SD 5) vs 90 (SD 8) ml·kg^–1·min^–1,P<0.01. Significant positive correlations were observed between theP _3mmol·l ^–1and _max, anaerobic and aerobic thresholds. In the sprint group CMJ and the averaged integrated iEMG decreased andt _F increased significantly during the MARP test, while no significant changes occurred in the endurance group. The present findings would suggest thatP _max reflected in the main the lactacid power and capacity and to a smaller extent alactacid power and capacity. The duration of the MARP test and the large number of CMJ may have induced considerable energy and neuromuscular fatigue in the sprint athletes preventing them from producing their highest alactacidP _max at the end of the MARP test. Due to lower submaximal [la^–]_b (anaerobic sprinting economy) the endurance athletes were able to reach almost the sameP _max as the sprint athletes.     

Effects of moderate endurance exercise and training on in vitro lymphocyte proliferation,interleukin-2 (IL-2) production,and IL-2 receptor expression

This study was designed to examine immunological responses to an acute bout of cycle ergometry exercise before and after moderate endurance training. Previously sedentary males were randomly assigned to matched training (n=9) or control (n=6) groups. Training comprised 12 weeks during which supervised cycle ergometer exercise took place [30 min at 65–70% of maximal oxygen intake , 4–5 days · week^–1]. An acute bout of exercise (60 min; 60% was performed initially and after the 12-week interval. Samples of peripheral venous blood were taken at rest, after 30 and 60 min of exercise, and at 30 and 120 min post-exercise. Training improved by an average of 20% (40.6 to 49.2 ml · kg^–1 · min^–1). Relative to baseline and control measures, the resting concentration of (CD3-CD16⁺/CD56⁺) natural killer (NK) cells increased by 22% (P<0.05). The resting count of total CD25⁺ [interleukin-2 receptor (IL-2R) chain] lymphocytes did not change following training, but dual staining analysis showed a 100% increase in the fraction of CD16⁺ CD25⁺ NK cells (P < 0.05). Likewise the resting CD122⁺ (IL-2R chain) lymphocyte count increased 35% after training, the greatest increases (44%) being in CD16⁺ CD122⁺ NK cells (P<0.05). Soluble IL-2R levels also increased 33% (P< 0.05) after training. Following acute exercise at the same relative intensity; trained individuals exhibited a larger increase in the NK cell count, reduced lymphocytopenia, and attenuation of exercise-induced suppression of lymphocyte proliferation and IL-2 production (P<0.05). In addition, smaller increases in CD4 and CD8 counts during exercise were noted, but with faster recovery post-exercise (P<0.05). Addition of recombinant IL-2 (rIL-2) to phytohemagglutinin-stimulated peripheral blood mononuclear cell cultures did not reverse exercise-induced suppression of cell proliferation, either before or after training. However, rIL-2 did augment the spontaneous blastogenesis of exercise and post-training samples relative to baseline (P < 0.05). We conclude that moderate endurance training is associated with sustained alterations in immune function, both at rest and when exercising. Further investigations are necessary to determine the impact on overall health and susceptibility to disease.     

Hormonal regulation of potassium shifts during graded exhausting exercise

Summary Serum potassium, aldosterone and insulin, and plasma adrenaline, noradrenaline and cyclic adenosine 3:5-monophosphate (cAMP) concentrations were measured during graded exhausting exercise and during the following 30 min recovery period in six untrained young men. During exercise there was an increase in concentration of serum potassium (4.74 mmol·1^–1, SEM 0.12 at the end of exercise vs 3.80 mmol·1^–1, SEM 0.05 basal,P<0.001), plasma adrenaline (2.14 nmol·1^–1, SEM 0.05 at the end of exercise vs 0.30 nmol·1^–1, SEM 0.02 basal,P<0.001), plasma noradrenaline (1.10 nmol·1^–1, SEM 0.64 at the end of exercise vs 1.50 nmol·1^–1, SEM 0.05 basal,P< 0.001), serum aldosterone (0.92 nmol·1^–1, SEM 0.14 at the end of exercise vs 0.36 nmol·1^–1, SEM 0.05 basal,P<0.01), and plasma cAMP (35.4 nmol·1^–1, SEM 2.3 at the end of exercise vs 21.4 nmol·1^–1, SEM 4.5 basal,P<0.05). While concentrations of serum potassium, plasma adrenaline and cAMP returned to their basal levels immediately after exercise, those of plasma noradrenaline and serum aldosterone remained elevated 30 min later (1.90 nmol·1^–1, SEM 0.01,P<0.01; and 0.85 nmol·1^–1, SEM 0.12,P<0.01, respectively). Serum insulin concentration did not change during exercise (6.47 mlU·1^–1, SEM 0.58 at the end of exercise vs 5.47 mlU·1^–1, SEM 0.41 basal, NS) but increased significantly (P<0.02) at the end of the recovery period (7.12 mlU·1^–1, SEM 0.65). Serum potassium increases with exhausting exercise appeared to be caused not only by its release from contracting muscles but also by an -adrenergic stimulation produced by adrenaline and noradrenaline. On the other hand, the increased levels of plasma noradrenaline maintained during the recovery period may have served to avoid excessive hypokalaemia through the stimulation of muscle -receptors. Thus, catecholamines may play an important role in the regulation of serum potassium concentrations during and after exercise. Any disturbance of these adrenergic effects may lead either to an excessive increase or to a decrease of kalaemia, with the consequent risk of arrhythmias linked to exercise.     

Influence of acute maximal exercise on lecithin: cholesterol acyltransferase activity in healthy adults of differing aerobic performance

Summary To document the possible influence of a single episode of maximal aerobic stress on the serum lecithin: cholesterol acyltransferase (LCAT) activity in subjects with differing histories of training, two groups of healthy male adults [controls (C),n = 18, 28.6 years, SD 5.2, 50.1 ml · kg^–1 · min^–1 maximal O₂ uptake (VO_2max), SD 5.3; endurance trained athletes (T),n = 18, 31.4 years, SD 8.8, 65.0 ml · kg^–1 · min^–1 VO_2max, SD 2.8] were examined in a maximal aerobic stress test. In addition to the routine assessment of lipid status, LCAT activity was measured immediately before and after exercise. At rest nearly identical LCAT activity values were found in both groups: C 64.4 nmol · ml^–1 · h^–1, SD 16.7 vs T 65.0 nmol · ml^–1 · h^–1, SD 20.9. The post-exercise LCAT values induced by the maximal stress test increased significantly to (C) 95.7 nmol · ml^–1 · h^–1, SD 23.5, +48.6%,P<0.001; (T) 83.5 nmol · ml^–1 · h^–1, SD 24.3, +29.1%,P<0.01. Neither the pre nor the post-exercise individual LCAT activity values showed any significant correlation to the corresponding data on physical performance.     

Effect of physical exhaustion and glucocorticoids (dexamethasone) on T-cells of trained rats

Summary Following a previous observation that moderate physical training (running) of rats did not impair T-cells, in this study moderately trained Wistar rats were run to exhaustion on 2 consecutive days: in one case (Tdex) this was preceded by an intraperitoneal injection of 0.5 mg·kg^–1 of dexamethasone (dex) and in the other case there was no prior injection (T). Similarly one group of sedentary control rats, was injected with dex (C-dex) and the other group was not (C). Rats were killed 24 h after the last treatment (dex, exercise). Compared with the C rats, the T rats exhibited a decreased number of thymocytes (75%), in particular CD4 + CD8 + thymocytes and splenocytes (55 %), notably CD4 + CD8 - splenocytes (P<0.01). Also noted in the T rats was a lower (45%) in vitro (+ mitogen) percentage of IL2r + CD4 - splenocytes (expressing the IL2 receptor), and reduced (40%,P<0.01) or unchanged in vitro production of T-cell growth factor (TCGF) by splenocytes or blood mononucleated cells (BMC), respectively. The dex decreased the number of thymocytes and splenocytes in the same way in T-dex rats (compared to T rats) and in C-dex rats (compared to C rats,P<0.01). In T-dex rats compared with C-dex rats, on the other hand, dex had little effect on in vitro TCGF production by BMC, and no effect on other in vitro parameters. These results would indicate that physical exhaustion was responsible for an alteration in T-cells in the moderately trained rat. This alteration was in part enhanced by dex.     

Ammonia and lactate in the blood after short-term sprint exercise

Summary Nine well-trained subjects performed 15-, 30-and 45-s bouts of sprint exercise using a cycle ergometer. There was a significant difference in the mean power between a 15-s sprint (706.0 W, SD 32.5) and a 30-s sprint (627.0 W, SD 27.8;P<0.01). The mean power of the 30-s sprint was higher than that of the 45-s sprint (554.7 W, SD 29.8;P<0.01). Blood ammonia and lactate were measured at rest, immediately after warming-up, and 2.5, 5, 7.5, 10, 12.5 min after each sprint. The peak blood ammonia content was 133.8 mol·1^–1, SD 33.5,- for the 15-s sprint, 130.2 ol·1^–1, SD 44.9, for the 30-s sprint, and 120.8 mol ·1^–1, SD 24.6, for the 45-s sprint. Peak blood lactates after the 15-, 30- and 45-s sprints were 8.1 mmol · 1^–1, SD 1.7, 11.2 mmol · 1^–1, SD 2.4, and 14.7 mmol ·1^–1, SD 2.1, respectively. There was a significant linear relationship between peak blood ammonia and lactate in the 15-s (r, 0.709;P< 0.05), 30-s (r, 0.797;P<0.05) and 45-s (r, 0.696;P<0.05) sprints. Though the peak blood lactate content increased significantly with increasing duration of the sprints (P<0.01), no significant difference was found in peak blood ammonia content among the 15-, 30- and 45-s sprints. These results suggest that the peak value of ammonia in the blood appears in sprints within 15-s and that the blood ammonia level is linked to the lactate in the blood.     

Atrial natriuretic peptide response to endurance physical training in the rat

Summary The effect of an endurance physical training programme on the plasma and atrial natriuretic peptides (ANP) and on renal glomerular ANP receptors was evaluated in male normotensive Wistar rats. Maximal O₂ uptake was significantly greater in the endurance trained (117.1 Ml O₂ · kg^–1 · min^–1, SEM 6.18 versus the control rats 84.2 ml O₂ · kg^–1 · min^–1, SEM 4.88, P<0.01. In addition, various muscle oxidative enzymes were also significantly higher in endurance trained animals. An increase in resting plasma [ANP] was observed after 11 weeks of physical training (40.02 pg · ml^–1, SEM 7.07 vs 22.8 pg.ml^–1, SEM 3.83, P<0.05). Glomerular ANP receptor density was lower in trained rats (272 fmol · mg^–1 protein, SEM 3.1 vs 380 fmol · mg^–1 protein, SEM 6.1, P < 0.05), whereas atrial tissue [ANP] was not significantly different between controls and trained animals. However, in trained rats, circulating [ANP] was closely correlated with left atrial [ANP] (r = –0.92, P<0.05). Resting systolic blood pressure had not changed at the end of this physical training programme. It is considered that under physiological conditions ANP may be involved in long-term extracellular fluid volume homeostasis through the regulation of renal glomerular ANP receptors, and that the left atrium might play a significant role in this long term fluid volume control.     

Effect of exercise training on aortic collagen content in spontaneously hypertensive rats (SHR)

Summary We investigated the effects of exercise training on the amount of aortic collagen and systolic blood pressure in spontaneously hypertensive rats (SHR). Ten-week old SHR were trained either by forced treadmill running (26.8 m·min^–1 h·day^–1, five times a week, 0% incline) or by voluntary running in revolving wheels (7,800 m·day^–1 at peak) for 8 weeks. Succinate dehydrogenase (SDH) activity measured as a marker of an endurance training effect was 13% higher (P<0.01) in the soleus of forced-exercised animals than in that of sedentary ones. (6.56±0.17 mol·g^–1·min^–1; mean ± SEM), whereas SDH activity in that of voluntarily-exercised group was found to be at the same level as in sedentary animals. The systolic blood pressure after training increased by 26.4 in sedentary, 21.1 in voluntarily-exercised, and 33.9 mm Hg in forced-exercised rats, when compared with the value of each group at the beginning of the training programm. A significant difference was observed in the increment of blood pressure only between the voluntarily- and forced-exercised groups (P<0.05). The amount of aortic collagen in voluntarily-trained rats (96.5±2.0 mg·g tissue^–1, 39.8±0.7 mg·100 mg protein^–1) was significantly less than that in forced-trained rats (P<0.05). These results suggest that voluntary, mild exercise training may be more effective in the reduction of collagen accumulation in the aorta associated with the suppression of blood pressure increase than forced, vigorous exercise training in SHR.     

The mechanical effects of contractions on blood flow to the muscle

To determine whether muscle contractions can increase muscle blood flow independently from metabolic factors, we isolated the vasculature of the left diaphragm or gastrocnemius muscle of anesthetized and mechanically ventilated dogs. Arterial blood flow was controlled with a constant pressure source and the arterial pressure (P _a) was decreased in steps to obtain pressure-flow relationships (P- ) . The local vasculatures were maximally dilated with nitroprusside [mean (SD)114.0 (32.0) g·min^–1], adenosine [1.43(0.41) mmol·l^–1·min^–1], and acetylcholine [l.43(0.41) mmol·l^–1·min^–1] and theP- with and without spontaneous contractions (n = 6) , stimulated twitches (n = 12, 2–4 Hz), or tetanic trains (n = 7, 25 Hz) in the diaphragm and stimulated twitches (n = 6, 2–4 Hz), or tetanic contractions (n = 6, 12–16 trains) in the gastrocnemius were compared. The pressure axis intercept decreased (P < 0.5) with spontaneous contractions in the diaphragm and the slope did not change. AtP _a of 13.3 kPa, flow increased from 36.2 (34.9) to 43.9 (38.2) ml·min^–1·100 g^–1 (P < 0.05). During twitch contractions, the slope and intercept of theP- were not significantly different from vasodilatation alone, but the flow at a pressure of 13.3 kPa increased slightly. In the gastrocnemius (n = 6), continuous and intermittent tetanic contractions did not affectP- or flow atP _a of 100 mmHg (n = 6). Furthermore, increasing venous pressure to 6.7 kPa did not affect flow in this muscle. We conclude that the muscle pump has only a small direct effect on muscle blood flow and its main effect is to reduce venous pressures.     

Effects of Growth hormone on rat skeletal muscle after hindlimb suspension

To examine the effects of growth hormone (GH) on the preferential atrophy of the soleus muscle (SOL) occurring after hindlimb suspension (HS), two groups of male rats received daily injections of 2 IU · kg ^–1 body mass of recombinant human growth hormone (rhGH). Rats were either suspended by the tail for 21 days (HS-GH, n = 5) or nonsuspended (CGH, n=5). The effects of rhGH treatment on SOL and extensor digitorum longus muscles (EDL) were compared in two groups of animals receiving daily injections of saline, either suspended by the tail (HS-SA, n = 5) or nonsuspended (C-SA, n = 5). The results showed that the SOL hypertrophy in response to rhGH administration was mostly observed in C rats (+33%, P<0.01). This increase in muscle mass was correlated with a concomitant increase in the size of type I fibres (+21%, P<0.05). Although SOL mass decreased during HS in rhGH treated animals (–44%, P<0.001), the mean normalized mass of this muscle did not significantly differ between C-SA and HS-GH groups. A statistically significant increase in the absolute mass of EDL occurred with rhGH treatment in CGH (+12%, P<0.05). The HS-induced decrease in the percentage distribution of type I fibres in SOL was unaffected by the rhGH treatment. In addition, a decrease in the citrate synthase activity in the whole SOL was observed in the two groups of tail-suspended rats (–31%, P<0.05; –21%, P<0.05 in SA and GH animals, respectively). The activity of 3-hydroxyacyl coenzyme A dehydrogenase was enhanced by the rhGH treatment (P<0.05) with similar magnitude in both C (+25%) and HS rats (+24%). Therefore, GH prevented only slightly the atrophy of SOL, occurring after 21 days of HS. The effects of rhGH treatment appeared most effective in C rats, suggesting that HS impaired the growth-promoting effects of this hormone on skeletal muscle.     

Effect of one- and two-leg training on arm and two-leg maximum aerobic power

Summary The purpose of this study was to examine the effect of one- and two-leg training on arm and two-leg maximum aerobic power. Seven subjects cycle-trained both legs simultaneously for 30 min·day^–1, 4 days·week^–1 for 4 weeks. Nine subjects cycle-trained each leg 15 min·day^–1, 4 days· week^–1 for 4 weeks. Both groups trained at a heart rate equal to that measured at 75% of their two-leg maximum aerobic power. Thus, during each training session the groups performed 30 min of work at the same heart rate intensity. Five subjects served as a non-training control group. Arm and leg maximum oxygen uptake tests were conducted before and after training. Only two-leg training induced significant gains in arm aerobic power (P<0.0003), whereas both modes of training resulted in signifcant increases in two-leg aerobic power (P<0.0008). The data demonstrate that improvements in arm aerobic power were dependent on the quantity of leg muscle mass involved in the training, whereas gains in two-leg aerobic power occurred regardless of whether the legs were trained separately or simultaneously.     

Energy expenditure and cardiorespiratory responses at the transition between walking and running

We investigated whether the spontaneous transition between walking and running during moving with increasing speed corresponds to the speed at which walking becomes less economical than running. Seven active male subjects [mean age, 23.7 (SEM 0.7) years, mean maximal oxygen uptake ( ), 57.5 (SEM 3.3) ml·kg ^–1·min ^–1, mean ventilatory threshold (VTh), 37.5 (SEM 3) ml·kg ^–1 ·min ^–1] participated in this study. Each subject performed four exercise tests separated by 1-week intervals: test 1, and VTh were determined; test 2, the speed at which the transition between walking and running spontaneously occurs (ST) during increasing speed (increases of 0.5 km·h ^–1 every 4 min from 5 km·h ^–1) was determined; test 3, the subjects were constrained to walk for 4 min at ST, at ST ± 0.5 km·h ^–1 and at ST ± 1 km·h ^–1; and test 4, the subjects were constrained to run for 4 min at ST, at ST±0.5 km·-h ^–1 and at ST±1 km·h ^–1. During exercise, oxygen uptake ( ), heart rate (HR), ventilation ( ), ventilatory equivalents for oxygen and carbon dioxide (% MathType!MTEF!2!1!+-% feaafiart1ev1aaatCvAUfeBSjuyZL2yd9gzLbvyNv2CaerbuLwBLn% hiov2DGi1BTfMBaeXatLxBI9gBaerbd9wDYLwzYbItLDharqqtubsr% 4rNCHbGeaGqiVu0Je9sqqrpepC0xbbL8F4rqqrFfpeea0xe9Lq-Jc9% vqaqpepm0xbba9pwe9Q8fs0-yqaqpepae9pg0FirpepeKkFr0xfr-x% fr-xb9adbaqaaeGaciGaaiaabeqaamaabaabaaGcbaGabmOvayaaca% WaaSbaaSqaaiaabweaaeqaaOGaai4laiqadAfagaGaamaaBaaaleaa% caqGYaaabeaakiaacYcacaqGGaGaaeiiaiqadAfagaGaamaaBaaale% aacaqGfbaabeaakiaac+caceWGwbGbaiaacaqGdbGaae4tamaaBaaa% leaacaaIYaaabeaaaaa!4240!\[\dot V_{\text{E}} /\dot V_{\text{2}} ,{\text{ }}\dot V_{\text{E}} /\dot V{\text{CO}}_2 \]), respiratory exchange ratio (R), stride length (SL), and stride frequency (SF) were measured. The results showed that: ST occurred at 2.16 (SEM 0.04) m·s ^–1; , HR and speed at ST were significantly lower than the values measured at VTh (P< 0.001, P< 0.001 and P< 0.05, respectively); changed significantly with speed (P< 0.001) but was greater during running than walking below ST (ST minus 1 km·h ^–1, P< 0.001; ST minus 0.5 km·h ^–1, P< 0.05) with the converse above ST (ST.plus 1 km·h ^–1, P<0.05), whereas at ST the values of were very close [23.9 (SEM 1.1) vs 23.7 (SEM 0.8) ml·kg ^–1 · min ^–1 not significant, respectively, for walking and running]; SL was significantly greater during walking than running (P<0.001) and SF lower (P<0.001); and HR and were significantly greater during running than walking below ST (ST minus 1 km·h ^–1, P<0.01; ST minus 0.5 km·h ^–1, P{<0.05) with the converse above ST (ST plus 1 km·h ^–1, P·< 0.05), whereas no difference appeared for and R between the two types of locomotion. We concluded from this study that ST corresponded to the speed at which the energy expenditure of running became lower than the energy expenditure of walking but that the mechanism of the link needed further investigation.     

Effects of exercise during normoxia and hypoxia on the growth hormone—insulin-like growth factor I axis

The response of plasma insulin-like growth factor I (IGF I) to exercise-induced increase of total human growth hormone concentration [hGH_tot] and of its molecular species [hGH_20kD] was investigated up to 48 h after an 1-h ergometer exercise at 60% of maximal capacity during normoxia (N) and hypoxia (H) (inspiratory partial pressure of oxygen = 92 mmHg (12.7 kPa);n = 8). Lactate and glucose concentrations were differently affected during both conditions showing higher levels under H. Despite similar maximal concentrations, the increase of human growth hormone (hGH) was faster during exercise during H than during N[hGH_tot after 30 min: 8.6 (SD 11.4) ng · ml^–1 (N); 16.2 (SD 11.6) ng · ml^–1 (H);P < 0.05]. The variations in plasma [hGH_20kD] were closely correlated to those of [hGH_tot], but its absolute concentration did not exceed 3% of the [hGH_tot]. Plasma IGF I concentration was significantly decreased 24 h after both experimental conditions [N from 319 (SD 71) ng · ml^-1 to 228 (SD 72) ng · ml^–1,P < 0.05; H from 253 (SD 47) to 200 (SD 47) ng · ml^–1,P < 0.01], and was still lower than basal levels 48 h after exercise during H [204 (SD 44) ng · ml^–1,P < 0.01]. Linear regression analysis yielded no significant correlation between increase in plasma [hGH_tot] or [hGH_20kD] during exercise and the plasma IGF I concentration after exercise. It was concluded that the exercise-associated elevated plasma [hGH] did not increase the hepatic IGF I production. From our study it would seem that the high energy demand during and after the long-lasting intensive exercise may have overridden an existing hGH stimulus on plasma IGH I, which was most obvious during hypoxia.     

Is exhaustive training adequate preparation for endurance performance?

Summary Our purpose was to test the significance of exhaustive training in aerobic or endurance capacity. The extent of adaptations to endurance training was evaluated by assessing the increase in physical performance capability and oxidative markers in the organs of rats trained by various exercise programs. Rats were trained by treadmill running 5 days · week^–1 at 30 m · min^–1 for 8 weeks by one of three protocols:T ₁ — 60 min · day^–1;T ₂ — 120 min · day^–1; andT ₃ — 120 min · day^–1 (3 days · week^–1) and to exhaustion (2 days · week^–1). GroupsT ₂ andT ₃ ran for longer thanT ₁ in an endurance exercise test (P<0.05), in which the animals ran at 30 m · min^–1 to exhaustion; no difference was observed between groupsT ₂ andT ₃. All 3 trained groups showed a similar increase (20–27%) in the fast-twitch oxidative-glycolytic (FOG) fibers with a concomitant decrease in the fast-twitch glycolytic (FG) fiber population in gastrocnemius (p<0.05). The capillary supply in gastrocnemius increased with the duration of exercise (p<0.05): no difference was found between groupsT ₂ andT ₃. Likewise, no distinction was seen between groupsT ₂ andT ₃ in the increase in succinate dehydrogenase activity in gastrocnemius and the heart. These results suggest that the maximal adaptive response to endurance training does not require daily exhaustive exercise.