Mitochondrial IV complex and brain neurothrophic derived factor responses of mice brain cortex after downhill training

Twenty-four adult male CF1 mice were assigned to three groups: non-runners control, level running exercise (0 degrees incline) and downhill running exercise (16 degrees decline). Exercise groups were given running treadmill training for 5 days/week over 8 weeks. Blood lactate analysis was performed in the first and last exercise session. Mice were sacrificed 48 h after the last exercise session and their solei (citrate synthase activity) and brain cortices (BDNF levels and cytochrome c oxidase activity) were surgically removed and immediately stored at -80 degrees C for later analyses. Training significantly increased (P<0.05) citrate synthase activity when compared to untrained control. Blood lactate levels classified the exercise intensity as moderate to high. The downhill exercise training significantly reduced (P<0.05) brain cortex cytochrome c oxidase activity when compared to untrained control and level running exercise groups. BDNF levels significantly decreased (P<0.05) in both exercise groups.     

Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (V˙O₂) during exercise and their relationship to performance, 20?healthy, active subjects underwent 30?min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1?(SD 4.0)?min (P?P?V˙O₂ did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8?(SD 1.9)?mmol?·?l^?1, P??1, P?相似文献   

Cardiovascular response to exercise in humans following acclimatization to extreme altitude

The purpose of this study was to assess the effects of acclimatization to extreme altitude on the cardiovascular system, using vagal and adrenergic blockade and acute restoration of normoxia during exercise to maximum with one and two legs. Fourteen climbers on an expedition to the Himalayas were studied at a lower base camp (5250 m) following 56–81 days at altitudes between 5250 and 8700 m. After acclimatization, peak heart rate (HR_peak), oxygen uptake (o_2k) and noradrenaline (NA) were similar during maximal one- and two-legged cycling, whereas peak plasma lactate was higher during the one-legged protocol. HR_peak (range 113–168 beats min“¹) was lowest when subjects returned from the higher camps. The degree of partial restoration of HR_peak to more normal values within seconds of 60% 0₂ inhalation (range 5–35 beats min?^l HR_peak increase) was greatest in subjects with low HR_peak. HR responses to /?-l blockade increased as a function of HR_peak and the HR responses to atropine were the least in subjects with high HRpeak- These findings suggest that (a) the reduction in HR_peak is linked to the duration and severity of the hypoxaemia, (b) the degree of restoration of HR_peak with acute normoxia is dependent on the level of attenuation or down-regulation of cardiac sympathetic activation (SNA), (c) cardiac vagal drive is masked to a lesser extent in chronic hypoxia because of attenuated SNA and lower HR_peak values, and (d) the lower blood lactate levels at altitude is a function of muscle mass involvement rather than adrenergic activation, as normal peak values were reached during exercise with a small muscle mass.     

Cardiovascular and respiratory responses to submaximal exercise training in the thoroughbred horse

Cardiovascular and respiratory responses to submaximal exercise training were investigated in 6 thoroughbred racehorses. Oxygen uptake, heart rate (HR) and arteriovenous oxygen content difference were measured during incremental treadmill exercise tests, before and after 7 weeks of treadmill training. Cardiac output during exercise was calculated by the direct Fick technique. Maximal oxygen uptake ( ) was increased by 23% after training, from 129.7 ml/kg/min to 160.0 ml/kg/min. The treadmill speed at which was attained increased by 19%. The increased aerobic power after training was associated with an increase in maximal cardiac output and stroke volume, a decrease in arteriovenous oxygen difference and no change in HR. There was no change in pulmonary ventilation during exercise at . Mean mixed venous oxygen content ( ) at before training was 2.8±1.0 ml/100 ml blood (mean ±SE). After training the value was 8.6±1.4 ml/100 ml blood. It is concluded that the increase in after training in the horse is dependant on augmented blood flow, and is not dependent on either increased arterial oxygen content or arteriovenous oxygen content difference. Cardiac capacity to pump blood is therefore of primary importance as a determinant of increases in due to training in the horse.     

Heavy and moderate interval exercise training alters low-flow-mediated constriction but does not increase circulating progenitor cells in healthy humans

Moderate-intensity endurance exercise training improves vascular endothelial vasomotor function; however, the impact of high-intensity exercise training has been equivocal. Thus, the effect of the physiological stress of the exercise remains poorly understood. Furthermore, enhanced vascular repair mediated by circulating progenitor cells may also be improved. To address whether the physiological stress of exercise training is an important factor contributing to these adaptations, 20 healthy participants trained for 6 weeks. Training involved either moderate (MSIT; n = 9) or heavy metabolic stress (HSIT; n = 11) interval exercise training programmes matched for total work and duration of exercise. Before and after training, flow-mediated dilatation, low-flow-mediated constriction and total vessel reactivity were measured at the brachial artery using Doppler ultrasound. Circulating progenitor cells (CD34(+), CD133(+) and CD309/KDR(+)) were measured by flow cytometry (means ± SD). Relative (MSIT pre- 5.5 ± 3.4 versus post-training 6.6 ± 2.5%; HSIT pre- 6.6 ± 4.1 versus post-training 7.0 ± 3.4%, P = 0.33) and normalized (P = 0.16) flow-mediated dilatation did not increase with either training programme. However, low-flow-mediated constriction was greater after training in both groups (MSIT pre- -0.5 ± 3.2 versus post-training -1.9 ± 3.1%; HSIT pre- -1.0 ± 1.7 versus post-training -2.9 ± 3.0%, P = 0.04) and contributed to greater total vessel reactivity (MSIT pre- 7.4 ± 3.3 versus post-training 10.1 ± 3.7%; HSIT pre- 10.9 ± 5.9 versus post-training 12.7 ± 6.2%, P = 0.01). Peak reactive hyperaemia and the area under the shear rate curve were not different between groups, either before or after training. Although circulating progenitor cell numbers increased following heavy-intensity interval exercise training, variability was great amongst participants [MSIT pre- 16 ± 18 versus post-training 14 ± 12 cells (ml whole blood)(-1); HSIT pre- 8 ± 6 versus post-training 19 ± 23 cells (ml whole blood)(-1), P = 0.50]. Overall, vasoconstrictor function may be augmented by moderate- and heavy-intensity interval exercise training in young adults. However, circulating progenitor cell numbers were not increased, suggesting that these cells are not likely to be upregulated as a result of training.     

Leptin response to acute prolonged exercise after training in rowers

The aim of this study was to determine if there is a training effect on leptin levels at rest or after prolonged exercise during an 8-month training season of rowers. Eleven trained rowers were evaluated at three sessions (control, early and late) during the season. At the early and late sessions, leptin and insulin concentrations were measured before and after 90 min of rowing exercise (70–75% maximal oxygen consumption, O₂max), 120 min and 24 h afterwards. Anthropometrics data were collected at each session. Energy balance was determined on the days of exercise sessions. Resting leptin levels were not modified over the season and were in correlation with weight and body fat (P<0.05). At exercise sessions, a delayed reducing effect of acute exercise on leptin levels appeared (P<0.01 compared to pre-exercise). After 24 h of recovery, leptin levels remained lower at early (P<0.001) but not at late sessions, and a training effect appeared between early and late sessions (P<0.001). Leptin levels were correlated with energy balance at early and late sessions (P<0.05). At the two training sessions, insulin levels were decreased immediately post-exercise and at 120 min of recovery compared to pre-exercise (P<0.01 and P<0.001 respectively for the two sessions). A training effect on insulin levels appeared at 24 h of recovery (P<0.05 between early and late sessions). We concluded that rowing training over a season did not alter resting leptin levels but it attenuated the exercise-induced reduction in leptin. This could be attributed to an alteration in energy balance, although an influence of training on insulin may also be involved in the leptin response to acute exercise.An erratum to this article can be found at     

Effects of exercise training on the matrix metalloprotease response to acute exercise

Matrix metalloproteases (MMPs) in the circulation are thought to modulate the activation of growth factors, cytokines, and angiogenesis, facilitating physiological adaptations to exercise training. The purpose of this work was to characterize serum MMP-1, MMP-2, MMP-3, and MMP-9 concentrations pre- and post-eight weeks of exercise training. We tested the hypothesis that exercise training would influence serum MMP concentrations in response to an acute resistance exercise test (ARET). Participants were randomized into an 8-week training program (5 days per week) that emphasized callisthenic (CT, N = 8) or resistance (RT, N = 8) exercise. Serum MMP concentrations (MMP-1, -2, -3, -9) were assessed in men (N = 16) in response to an acute bout of high-intensity resistance exercise (six sets of 10-RM squats with 2-min inter-set rest periods) both before and after 8 weeks of training. Training resulted in a temporal shift in the peak MMP-1 concentration from post-ARET to mid-ARET in both groups. Post-training, MMP-9 concentrations were increased immediately after the ARET in the CT group as compared to pre-training ARET concentrations. RT did not alter MMP-3 and -9 concentrations. These data suggest that the mode of exercise training influences the MMP response to an acute bout of exercise, revealing a possible role of MMPs in initiating training-specific adaptations. The opinions or assertions contained herein are the private views of the author(s) and are not to be construed as official or as reflecting the views of the Army or the Department of Defense. Citations of commercial organizations and trade names in this report do not constitute an official Department of the Army endorsement or approval of the products or services of these organizations.     

VE response to VCO2 during exercise is unaffected by exercise training and different exercise limbs

We designed two experiments to investigate the relationship between ventilation (VE) and CO2 output (VCO2) during exercise under the conditions of exercising different limbs, the arms as opposed to the legs (experiment 1), and of different physical training states after undergoing standard exercise training for 90 d (experiment 2). Six healthy young subjects underwent submaximal ramp exercise at an incremental work rate of 15 W/min for the arm and leg, and 11 healthy middle-aged subjects underwent an incremental exercise test at the rate of 30 W/3 min before and after exercise training. We measured pulmonary breath-by-breath VE, VCO2, oxygen uptake (VO2), tidal volume (VT), breathing frequency (bf), and end-tidal O2 and CO2 pressures (PETO2, PETCO2) via a computerized metabolic cart. In experiment 1, arm exercise produced significantly greater VE than did leg exercise at the same work rates, as well as significantly higher VO2, VCO2, and bf. The slopes of the regression lines in the VE-VCO2 relationship were not significantly different: the values were 27.8 +/- 2.1 (SD) during the arm exercise, and 25.3 +/- 3.9 during the leg exercise, with no differences in their intercepts. In experiment 2, the VO2, VCO2, and VE responses at the same work rates were similar in both before and after the 90-d exercise training, whereas the heart rate (HR) and mean blood pressure (MBP) were significantly reduced after training. Exercise training did not alter the VE-VCO2 relationship, the slope of which was 31.9 +/- 4.9 before exercise training and 34.2 +/- 4.4 after exercise training. We concluded that the VE-VCO2 relationship during exercise is unaltered, independent of not only working muscle regions but also exercise training states.     

Resistance exercise training and the orthostatic response

Resistance exercise has been suggested to increase blood volume, increase the sensitivity of the carotid baroreceptor cardiac reflex response (BARO), and decrease leg compliance, all factors that are expected to improve orthostatic tolerance. To further test these hypotheses, cardiovascular responses to standing and to pre-syncopal limited lower body negative pressure (LBNP) were measured in two groups of sedentary men before and after a 12-week period of either exercise (n = 10) or no exercise (control, n = 9). Resistance exercise training consisted of nine isotonic exercises, four sets of each, 3 days per week, stressing all major muscle groups. After exercise training, leg muscle volumes increased (P?P = 0.00) by 2.0 (0.5)?kg, leg compliance and BARO were not significantly altered, and the maximal LBNP tolerated without pre-syncope was not significantly different. Supine resting heart rate was reduced (P = 0.03) without attenuating the heart rate or blood pressure responses during the stand test or LBNP. Also, blood volume (¹²⁵I and ⁵¹Cr) and red cell mass were increased (P?相似文献   

Central command and the cutaneous vascular response to isometric exercise in heated humans

Cutaneous vascular conductance (CVC) decreases during isometric handgrip exercise in heat stressed individuals, and we hypothesized that central command is involved in this response. Seven subjects performed 2 min of isometric handgrip exercise (35% of maximal voluntary contraction) followed by postexercise ischaemia in normothermia and during heat stress (increase in internal temperature ∼1°C). To augment the contribution of central command independent of force generation, on a separate day the protocol was repeated following partial neuromuscular blockade (PNB; i.v. cisatracurium). Forearm skin blood flow was measured by laser-Doppler flowmetry, and CVC was the ratio of skin blood flow to mean arterial pressure. The PNB attenuated force production despite encouragement to attain the same workload. During the heat stress trials, isometric exercise decreased CVC by ∼12% for both conditions, but did not change CVC in either of the normothermic trials. During isometric exercise in the heat, the increase in mean arterial pressure (MAP) was greater during the control trial relative to the PNB trial (31.0 ± 9.8 versus 18.6 ± 6.4 mmHg, P < 0.01), while the elevation of heart rate tended to be lower (19.4 ± 10.4 versus 27.4 ± 8.1 b.p.m., P = 0.15). During postexercise ischaemia, CVC and MAP returned to pre-exercise levels in the PNB trial but remained reduced in the control trial. These findings suggest that central command, as well as muscle metabo-sensitive afferent stimulation, contributes to forearm cutaneous vascular responses in heat stressed humans.