Biometric approximation of diaphragmatic contractility during sustained hyperpnea

Imposing load on respiratory muscles results in a loss of diaphragmatic contractility that develops early, is independent of task failure, and levels off following the initial decrease. This study assessed the progression of diaphragmatic contractility during sustained normocapnic hyperpnea and applied a biometric approximation (hypothesis: non-linear decay). Ten healthy subjects performed three consecutive hyperpnea bouts (I:6 min warm up/II:9 min/III:task failure 28.6 ± 11.5 min; mean ± SD) at maximal voluntary ventilation fractions (I:30-60%/II:70%/III:70%), followed by recovery periods (I:18 min/II:6 min/III:30 min). Twitch transdiaphragmatic pressure (TwPdi) was assessed throughout the protocol. Bouts II and III induced diaphragmatic fatigue (TwPdi baseline vs. Recovery -19 ± 17% and -30 ± 16%, both p < 0.05 RM-ANOVA) while bout I did not. During sustained hyperpnea (II/III), TwPdi followed an exponential decay (r(2) = 0.91). The reduction in diaphragmatic contractility closely follows a non-linear function with an early loss in diaphragmatic contractility during sustained hyperpnea, levels off thereafter, and is independent of task failure. Thus, reasons other than diaphragmatic fatigue are likely to be responsible for task failure during sustained hyperpnea.     

New physiological insights into exercise-induced diaphragmatic fatigue

Data on the dynamic process and time-point of manifestation of exercise-induced diaphragmatic fatigue (DF) are lacking. Therefore, this study was aimed assessing dynamic changes of diaphragmatic strength during exercise and determining the time-point of DF manifestation. Fourteen trained subjects (maximal oxygen uptake (VO2(max)) 59.3+/-5.5 ml/min/kg) performed standardized exercise protocols (maximal workload: 85% VO2(max)) followed by recovery (6 min). Ergospirometric data and twitch transdiaphragmatic pressure (TwPdi) were consecutively assessed. DF was induced (TwPdi-rest: 2.34+/-0.26 versus TwPdi-end-recovery 2.01+/-0.21 kPa, p<0.01). TwPdi progressively increased during exercise (TwPdi-rest: 2.34+/-0.26 versus TwPdi-maximal-workload: 3.28+/-0.38 kPa, p<0.001). DF was detectable immediately after exercise-termination (TwPdi-maximal-workload: 3.28+/-0.38 versus TwPdi-early-recovery 2.55+/-0.34 kPa, p<0.001). TwPdi during exercise was highly correlated to workload, VO2(max) and dyspnea (r=0.96/r=0.92/r=0.97; all p<0.0001). In conclusion, diaphragmatic strength progressively increases with increasing workload, and DF manifests after - rather than during - exercise. In addition, TwPdi is highly correlated to key-measures of ergospirometry, approving the physiological thesis that muscle strength is progressively enhanced and escapes fatiguing failure during high-intensity exercise performance.     

Independence of exercise-induced diaphragmatic fatigue from ventilatory demands

Exercise-induced diaphragmatic fatigue (DF) manifests after - rather than during - exercise. This suggests that DF reflects post-exercise diaphragm-shielding. This study tested the physiological hypothesis that diaphragmatic force-generation undergoes similar regulations during either whole-body-exercise or controlled hyperventilation, but differs during recovery. Ten trained subjects (VO2(max) 60.3+/-6.4 ml/kg/min) performed: I, cycling exercise (maximal workload: 85% VO2(max)); II, controlled hyperventilation (exercise breathing pattern) followed by recovery. Ergospirometric data and twitch transdiaphragmatic pressure (TwPdi) were consecutively assessed. DF occurred following exercise, while hyperventilation enhanced diaphragmatic force-generation (TwPdi-rest 2.28+/-0.58 vs. 2.52+/-0.54, TwPdi-end-recovery: 1.94+/-0.32 kPa vs. 2.81+/-0.49 kPa, both p<0.05). TwPdi was comparable between the two protocols until recovery (p>0.05, RM-ANOVA) whereby it underwent a progressive increase. In conclusion, TwPdi progressively increases and is subject to similar regulations during exercise versus controlled hyperventilation, but differs markedly during recovery. Here, DF occurred after exercise while TwPdi increased subsequent to hyperventilation. Therefore, ventilatory demands regulate diaphragmatic force-generation during exercise, whereas DF must be attributed to non-ventilatory controlled feedback mechanisms.     

Post-exercise diaphragm shielding: a novel approach to exercise-induced diaphragmatic fatigue

Based on the "post-exercise diaphragm shielding" hypothesis this study tested whether both diaphragmatic force-generation (DFG) and diaphragmatic fatigue (DF) remain unchanged during consecutive exercise-trials. Twelve subjects ( [Formula: see text] 58.4+/-6.6mlkg(-1)min(-1)) performed three consecutive exercise-trials (T(alpha)/T(beta)/T(gamma); workload(max) 85% [Formula: see text] ) each followed by recovery (6min). Twitch transdiaphragmatic pressure during supramaximal magnetic phrenic nerve stimulation (TwPdi, every 30s), ratings of perceived exertion (RPE, every 90s) and ergospirometric data (continuously) were assessed throughout the entire protocol (46.5min). DFG and DF did not differ among all trials (TwPdi-baseline: 2.2+/-0.7kPa; TwPdi-peak: T(alpha)/T(beta)/T(gamma) 3.1+/-0.7kPa vs 3.0+/-0.8kPa vs 3.2+/-0.8kPa; TwPdi-bottom: T(alpha)/T(beta)/T(gamma) 1.9+/-0.6kPa vs 2.0+/-0.7kPa vs 1.8+/-0.5kPa, both p>0.4, RM-ANOVA). Furthermore, TwPdi revealed close relationships with RPE (r=0.91, p<0.0001) and oxygen uptake (r=0.94, p<0.0001) during exercise. In conclusion, both DFG (baseline-to-peak) and DF (baseline-to-bottom) achieve similar magnitudes during and after consecutive exercise-trials and are closely linked to RPE and oxygen uptake. This suggests that DF neither reflects impaired diaphragmatic function nor impairs exercise performance; rather it is likely to reflect post-exercise diaphragm shielding.     

Influence of diaphragm and rib cage muscle fatigue on breathing during endurance exercise

Inspiratory muscle fatigue (IMF) can develop during exhaustive exercise and cause tachypnea or rapid shallow breathing. We assessed the effects of rib cage muscle (RCM-F) and diaphragm fatigue (DIA-F) on breathing pattern and respiratory mechanics during high-intensity endurance exercise. Twelve healthy subjects performed a constant-load (85% maximal power) cycling test to exhaustion with prior IMF and a cycling test of similar intensity and duration without prior IMF (control). IMF was induced by resistive breathing and assessed by oesophageal and gastric twitch pressure measurements during cervical magnetic stimulation. Both RCM-F and DIA-F increased RCM and abdominal muscle force production during exercise compared to control. With RCM-F, tidal volume decreased while it increased with DIA-F. RCM-F was associated with a smaller increase in end-expiratory oesophageal pressure (i.e. decrease in lung volume) than DIA-F. These results suggest that RCM-F and not DIA-F is associated with rapid shallow breathing and that lowering the operating lung volume with DIA-F may help to preserve diaphragmatic function.     

Mouth pressure twitches induced by cervical magnetic stimulation to assess inspiratory muscle fatigue

This study aimed at determining whether twitch mouth pressure (TwPmo) induced by cervical magnetic stimulation (CMS) was sensitive to inspiratory muscle fatigue produced by whole body exercise (WBE) in normal subjects. Twenty subjects performed one or two of the following protocols: (i). cycling at 85% V(O(2),max) until exhaustion; (ii). inspiratory resistive load (IRL) breathing at 62% of maximal inspiratory pressure until task failure. In eight subjects, oesophageal (TwPoes), gastric (TwPga) and transdiaphragmatic (TwPdi) pressures were recorded. The TwPmo was significantly reduced (P<0.05) 20 min after both WBE and IRL, from 17.5+/-4.4 to 15.9+/-3.9 cmH(2)O and from 19.4+/-4.9 to 17.7+/-4.5 cmH(2)O, respectively. Subsequently to IRL, the TwPdi decrease was associated with a reduction in TwPoes/TwPga ratio; not after WBE. Independently of the mode of ventilatory loading, inspiratory muscle fatigue was detected. Thus, inspiratory muscle fatigue after WBE can be assessed in normal subjects with a noninvasive technique.     

Effects of theophylline on diaphragmatic strength and fatigue in patients with chronic obstructive pulmonary disease

We studied the effects of theophylline on diaphragmatic strength and fatigue in 15 patients with severe chronic obstructive pulmonary disease. Diaphragmatic strength was assessed by measurement of the transdiaphragmatic pressure generated at functional residual capacity during a maximal inspiratory effort against closed airways. Diaphragmatic fatigue was induced by resistive loaded breathing. The electrical activity of the diaphragm was recorded with an esophageal electrode during the fatigue runs, and the high-low ratio of the electrical signal was analyzed to assess diaphragmatic fatigue. Studies were performed before and after 7 and 30 days of theophylline administration (mean plasma level, 13 +/- 2 mg per liter). A control group received a placebo instead of theophylline. Theophylline increased maximal transdiaphragmatic pressure by 16 per cent after 7 days of administration (P less than 0.01), and this increase persisted after 30 days. No significant change in maximal transdiaphragmatic pressure was observed in the group given the placebo. Theophylline also suppressed diaphragmatic fatigue in all patients who received it. We conclude that theophylline has a potent and long-lasting effect on diaphragmatic strength and fatigue in patients with fixed airway obstruction.     

Ocular circulatory responses to exhaustive exercise in humans

It is unclear whether exhaustive dynamic exercise increases ocular blood flow, although we have reported that submaximal exercise increases ocular blood flow. We hypothesized that ocular blood flow decreases at exhaustion, since exhaustion causes hyperventilation, which induces a reduction in PaCO(2). To test this hypothesis, ocular blood flow, blood pressure, and respiratory measurements were made in 12 healthy male subjects during cycle ergometer exercise at 75% of maximal heart rate, until exhaustion. Blood flows in the retinal and choroidal vasculature (RCV), the superior temporal retinal arteriole (STRA), and the superior nasal retinal arteriole (SNRA) were measured with the aid of laser-speckle flowgraphy every 3 min during the exercise. The conductance index (CI) in the ocular vasculature was calculated by dividing the blood flow by the mean arterial pressure (MAP). The mean arterial partial pressure of CO(2) (PaCO(2)) was estimated from tidal volume and end-tidal CO(2) partial pressure. MAP significantly increased from the resting baseline throughout the exercise, while PaCO(2) was significantly decreased at exhaustion and during the recovery period. By 6 min after the onset of exercise, blood flow velocity in the RCV significantly increased by 32 ± 6% (mean ± SD) from the resting baseline value. At exhaustion, blood flow velocity in the RCV did not differ significantly from the resting baseline value, and the STRA blood flow was significantly decreased by 13 ± 4%. The CIs in the RCV, STRA, and SNRA were significantly decreased compared to baseline at exhaustion. These findings suggest that ocular blood flow is increased by submaximal exercise, whereas it is suppressed by the hypocapnia associated with exhaustion.     

Rapid intravenous infusion of 20 mL/kg saline alters the distribution of perfusion in healthy supine humans

Rapid intravenous saline infusion, a model meant to replicate the initial changes leading to pulmonary interstitial edema, increases pulmonary arterial pressure in humans. We hypothesized that this would alter lung perfusion distribution. Six healthy subjects (29 ± 6 years) underwent magnetic resonance imaging to quantify perfusion using arterial spin labeling. Regional proton density was measured using a fast-gradient echo sequence, allowing blood delivered to the slice to be normalized for density and quantified in mL/min/g. Contributions from flow in large conduit vessels were minimized using a flow cutoff value (blood delivered > 35% maximum in mL/min/cm(3)) in order to obtain an estimate of blood delivered to the capillary bed (perfusion). Images were acquired supine at baseline, after infusion of 20 mL/kg saline, and after a short upright recovery period for a single sagittal slice in the right lung during breath-holds at functional residual capacity. Thoracic fluid content measured by impedance cardiography was elevated post-infusion by up to 13% (p<0.0001). Forced expiratory volume in 1s was reduced by 5.1% post-20 mL/kg (p=0.007). Infusion increased perfusion in nondependent lung by up to 16% (6.4 ± 1.6 mL/min/g baseline, 7.3 ± 1.8 post, 7.4 ± 1.7 recovery, p=0.03). Including conduit vessels, blood delivered in dependent lung was unchanged post-infusion; however, was increased at recovery (9.4 ± 2.7 mL/min/g baseline, 9.7 ± 2.0 post, 11.3 ± 2.2 recovery, p=0.01). After accounting for changes in conduit vessels, there were no significant changes in perfusion in dependent lung following infusion (7.8 ± 1.9 mL/min/g baseline, 7.9 ± 2.0 post, 8.5 ± 2.1 recovery, p=0.36). There were no significant changes in lung density. These data suggest that saline infusion increased perfusion to nondependent lung, consistent with an increase in intravascular pressures. Dependent lung may have been "protected" from increases in perfusion following infusion due to gravitational compression of the pulmonary vasculature.     

Effect of pentoxifylline on diaphragmatic contractility in septic rats

We investigated the effects of pentoxifylline (PTX) on endotoxin-induced diaphragmatic dysfunction in vitro. Seventy-two rats were divided into 3 groups: a group in which endotoxin (20 mg/kg) was injected intraperitoneally (endotoxin-group), a group in which PTX (100 mg/kg) was injected intraperitoneally 30 min before injection of endotoxin (endotoxin-PTX group), and a group in which only saline was given (sham group). Left hemidiaphragms were removed 4 h after injection of endotoxin. We evaluated the diaphragmatic contractility by twitch characteristics and force-frequency curves in vitro. We measured serum TNF-alpha concentrations, diaphragm malondialdehyde (MDA) levels (an index of oxygen-derived free radical-mediated lipid peroxidation), and diaphragm cAMP concentrations. Diaphragmatic force generation capacity was signifi cantly reduced after injection of endotoxin. Serum TNF-alpha concentrations and diaphragmatic MDA levels were significantly elevated after injection of endotoxin. PTX administration significantly improved diaphragmatic contractility and prevented the elevation in TNF-alpha concentrations and MDA levels after injection of endotoxin. There were no significant changes in the diaphragm cAMP concentrations among the 3 groups. These results demonstrated that PTX administration prevented endotoxin-induced diaphragmatic dysfunction without changing diaphragm muscle cAMP concentrations. The protective effects of PTX against endotoxininduced diaphragmatic contractile deterioration might be caused by attenuating TNF-alpha-mediated oxygen-derived free radical production.     

Effect of carbon dioxide on diaphragmatic function in human beings

We studied the effects of acute changes in the partial pressure of arterial carbon dioxide on diaphragmatic contractility and performance in four normal men. To study contractility we measured the ability of the diaphragm to generate pressure at a given level of excitation by determining the relation between the electrical activity of the diaphragm and transdiaphragmatic pressure during a voluntary quasi-isometric inspiratory effort carried out at different levels of end-tidal carbon dioxide. Our results show that contractility was reduced with hypercapnia (when end-tidal carbon dioxide was 7.5 per cent or higher), although hypocapnia (end-tidal carbon dioxide, 3 per cent) had no effect on diaphragmatic contractility. We also studied the development of diaphragmatic fatigue before and during carbon dioxide breathing. Subjects were studied at the same diaphragmatic tension-time index, a value analogous to the more familiar myocardial tension-time index, while the same inspiratory flow was maintained. Electromyographic signs of fatigue appeared at a lower tension-time index during hypercapnia than during normocapnia, indicating that endurance is diminished during hypercapnia. These findings show that acute respiratory acidosis equivalent to an arterial carbon dioxide tension of about 54 mm Hg decreases the contractility and endurance time of the diaphragm in human beings.     

Effects of long- and short-term fatiguing stretch-shortening cycle exercises on reflex EMG and force of the tendon-muscle complex

This study examined the fatigue effects of stretch-shortening cycle exercises of different intensity and duration on stretch reflex EMG and mechanical responses of the triceps surae muscle. Twelve subjects performed either a 10-km run (n=6) or short but exhaustive rebound exercise on a sledge apparatus (n=6). Passive reflex tests (mechanically induced ankle dorsiflexions) were examined before, after as well as 2 h, 2 and 7 days after exercise. Mechanical reflex responses were recorded from the ergometer torque signal. An acute contractile failure was observed as large reductions in twitch responses, especially in the sledge subgroup who showed high post-exercise peak blood lactate and an increased EMG/torque ratio. Independently of the exercise, the delayed fatigue analysis revealed strong relationships between the reflex-induced EMG and mechanical changes. In addition to muscle damage, these results may be explained by inhibitory effects via the sensitisation of small muscle afferents particularly during the exercise-induced delayed recovery process.     

Acute and delayed neuromuscular adjustments of the triceps surae muscle group to exhaustive stretch–shortening cycle fatigue

Stretch–shortening cycle (SSC)-type fatigue is associated with acute and delayed functional defects, and appears to be a useful model to reveal the flexibility of both central and reflex adjustments to the contractile failure. SSC fatigue was induced in an experimental (EXP) group (n=6) on a sledge ergometer with an exhaustive rebound exercise with submaximal effort. The acute (POST) and 2-day delayed (2D) neuromuscular changes with fatigue were examined in a short submaximal rebound task (REBOUND) and in a maximal isometric plantarflexion test (ISOM). The EXP group results were compared to those of a control group (n=6) who did not perform the exhaustive SSC exercise and did not present any change in the tests. In the EXP group, the ISOM test revealed mostly a large decrease in maximal plantarflexion force at 2D that was correlated with the reduced mean soleus muscle (SOL) activation. Indicating task-dependent fatigue effects on the neural changes, the REBOUND test revealed both acute and delayed increases in SOL activation. Supporting central neural changes, SOL preactivation increased in POST and 2D. The neural flexibility along time and across muscles was demonstrated by the shifted increase in SOL activation from the braking phase in POST to the push-off phase in 2D, and associated increased gastrocnemius medialis preactivation in 2D. In contrast, activation during the stretch–reflex period was constant in POST, and decreased in 2D. These results would support the influence of musculotendinous afferents on the flexible neural adjustments to the SSC-induced contractile failure.     

Task failure from inspiratory resistive loaded breathing: a role for inspiratory muscle fatigue?

The use of non-invasive resistive breathing to task failure to assess inspiratory muscle performance remains a matter of debate. CO₂ retention rather than diaphragmatic fatigue was suggested to limit endurance during inspiratory resistive breathing. Cervical magnetic stimulation (CMS) allows discrimination between diaphragmatic and rib cage muscle fatigue. We tested a new protocol with respect to the extent and the partitioning of inspiratory muscle fatigue at task failure. Nine healthy subjects performed two runs of inspiratory resistive breathing at 67 (12)% of their maximal inspiratory mouth pressure, respiratory rate ( f_R), paced at 18 min^–1, with a 15-min pause between runs. Diaphragm and rib cage muscle contractility were assessed from CMS-induced esophageal (P_es,tw), gastric (P_ga,tw), and transdiaphragmatic (P_di,tw) twitch pressures. Average endurance times of the first and second runs were similar [9.1 (6.7) and 8.4 (3.5) min]. P_di,tw significantly decreased from 33.1 to 25.9 cmH₂O in the first run, partially recovered (27.6 cmH₂O), and decreased further in the second run (23.4 cmH₂O). P_es,tw also decreased significantly (–5.1 and –2.4 cmH₂O), while P_ga,tw did not change significantly (–2.0 and –1.9 cmH₂O), indicating more pronounced rib cage rather than diaphragmatic fatigue. End-tidal partial pressure of CO₂ (P_ETCO₂) rose from 37.2 to 44.0 and 45.3 mmHg, and arterial oxygen saturation (S_aO₂) decreased in both runs from 98% to 94%. Thus, task failure in mouth-pressure-targeted, inspiratory resistive breathing is associated with both diaphragmatic and rib cage muscle fatigue. Similar endurance times despite different degrees of muscle fatigue at the start of the runs indicate that other factors, e.g. increases in P_ETCO₂, and/or decreases in S_aO₂, probably contributed to task-failure.     

小鼠病毒性心肌炎的心肌结构及左室功能变化的初步研究

目的:探讨病毒性心肌炎时的心肌结构与收缩力变化的关系。方法:建立病毒性心肌炎的动物模型,观测病毒损伤阶段和免疫损伤阶段心肌的超微结构和心肌收缩力改变。结果:病毒性心肌炎早期的心肌细胞的线粒体超微结构发生了变化,心肌细胞收缩力下降,左室压(LVP)为(14.2±0.8)kPa,dp/dt为(273.1±10.0)kPa/s,正常对照LVP为(17.1±0.7)kPa,dp/dt为(359.8±9.3)kPa/s,P＜0.01;后期心肌组织严重损害,不仅有线粒体溶解破坏,而且肌原纤维变细、减少等,并且心肌收缩力指标明显下降,LVP为(11.8±0.2)kPa,dp/dt为(209.5±6.9)kPa/s,与早期相比差异有显著,P＜0.01。结论:病毒性心肌炎早期,即病毒损伤期,造成心脏功能下降的原因主要是病毒引起心肌细胞的超微结构改变,特别是对线粒体的损伤,使心肌细胞供能障碍,心肌收缩力减小;病毒性心肌炎后期,免疫反应造成心肌组织损害较病毒直接损害更严重,造成心肌收缩力明显减小。     

Spinal opioid receptor-sensitive muscle afferents contribute to the fatigue-induced increase in intracortical inhibition in healthy humans

We investigated the influence of spinal opioid receptor-sensitive muscle afferents on cortical changes following fatiguing unilateral knee-extensor exercise. On separate days, seven subjects performed an identical five sets of intermittent isometric right-quadriceps contractions, each consisting of eight submaximal contractions [63 ± 7% maximal voluntary contraction (MVC)] and one MVC. The exercise was performed following either lumbar interspinous saline injection or lumbar intrathecal fentanyl injection blocking the central projection of spinal opioid receptor-sensitive lower limb muscle afferents. To quantify exercise-induced peripheral fatigue, quadriceps twitch force (Q(tw,pot)) was assessed via supramaximal magnetic femoral nerve stimulation before and after exercise. Motor evoked potentials and cortical silent periods (CSPs) were evaluated via transcranial magnetic stimulation of the motor cortex during a 3% MVC pre-activation period immediately following exercise. End-exercise quadriceps fatigue was significant and similar in both conditions (Q(tw,pot) -35 and -39% for placebo and fentanyl, respectively; P = 0.38). Immediately following exercise on both days, motor evoked potentials were similar to those obtained prior to exercise. Compared with pre-exercise baseline, CSP in the placebo trial was 21 ± 5% longer postexercise (P < 0.01). In contrast, CSP following the fentanyl trial was not significantly prolonged compared with the pre-exercise baseline (6 ± 4%). Our findings suggest that the central effects of spinal opioid receptor-sensitive muscle afferents might facilitate the fatigue-induced increase in CSP. Furthermore, since the CSP is thought to reflect inhibitory intracortical interneuron activity, which may contribute to central fatigue, our findings imply that spinal opioid receptor-sensitive muscle afferents might influence central fatigue by facilitating intracortical inhibition.     

Effects of induced fatigue on brain activity during sensorimotor control

The aim of this study was to study if accuracy in sensorimotor control and cortical activity was influenced after induced fatigue during a knee joint reproduction task. Twelve volunteers performed a sensorimotor task before, directly after and 60 min after a prolonged exhaustive exercise protocol. The task consisted of an active reproduction of a target knee angle. After three practice trials, visual feedback was taken and the task was performed for 10 repetitions at a suitable pace. Reproduction accuracy was analyzed and EEG raw data were obtained from the frontal, central, temporal, parietal and occipital scalp locations during the task. The average power spectra in theta and alpha frequencies were computed across conditions for each participant. Task accuracy decreases significantly related to fatigue and increases after recovery. This is accompanied by a significant decrease in frontal theta, alpha-1 and alpha-2 frequencies after inducing fatigue. The power values in all frequency bands recovered after 60 min. Sensorimotor control was influenced by induced fatigue, which could be demonstrated in behavior and brain activity. Characteristics of brain activity demonstrated an increase in theta and a decrease in alpha-1 and alpha-2 frequency band power. The changes were discussed related to attentional recourses, alertness and somatosensory information processing mechanisms.     

急性缺氧对膈肌疲劳的影响

本文观察急性缺氧对犬膈肌疲劳的影响，发现急性缺氧条件下，膈肌疲劳的耐受时间为１８．００±３．７０ｍｉｎ，较对照组４１．３３±５．３０ｍｉｎ明显缩短（Ｐ＜０．０５），而且疲劳膈肌恢复过程中产生跨膈压（ｔｒａｎｓｄｉａｐｈｒａｇｍａｔｉｃｐｒｅｓｓｕｒｅ，Ｐｄｉ）明显低于对照组（Ｐ＜０．０５），证实急性缺氧使膈肌疲劳的耐受性明显下降，且不利于疲劳膈肌肌力的恢复。     

The Influence of Aerobic Exercise on Physiological Stress Responsivity

The present study examined the relationship between aerobic exercise participation and physiological stress responsivity to psychosocial stressors. Male subjects (N = 107) who were either intense aerobic exercisers, moderate aerobic exercisers, or nonexereisers completed a telephone interview, a personality assessment battery, a life stress questionnaire, and a physical exercise and hobby questionnaire. Subjects then participated in a stressful laboratory procedure where they faced two stressors: an electric shock procedure, and a difficult “intelligence test.” Pulse rate, finger pulse volume, and skin resistance were assessed during the entire laboratory procedure. Although results demonstrated consistent significant cardiovascular (i.e., pulse rate and pulse volume) differences among the exercise groups during the entire laboratory procedure in that exercisers were less physiologically reactive to the stressors and the recovery periods, most of these results failed to reach significance when statistically controlling for the baseline/anticipation-of-stressors physiological measures. The implications of this study for further research are discussed.     

Mitochondrial function in human skeletal muscle is not impaired by high intensity exercise

 The hypothesis that high-intensity (HI) intermittent exercise impairs mitochondrial function was investigated with different microtechniques in human muscle samples. Ten male students performed three bouts of cycling at 130% of peak O₂ consumption (V ^·O_2,peak). Muscle biopsies were taken from the vastus lateralis muscle at rest, at fatigue and after 110 min recovery. Mitochondrial function was measured both in isolated mitochondria and in muscle fibre bundles made permeable with saponin (skinned fibres). In isolated mitochondria there was no change in maximal respiration, rate of adenosine 5’-triphosphate (ATP) production (measured with bioluminescence) and respiratory control index after exercise or after recovery. The ATP production per consumed oxygen (P/O ratio) also remained unchanged at fatigue but decreased by 4% (P<0.05) after recovery. In skinned fibres, maximal adenosine 5’-diphosphate (ADP)-stimulated respiration increased by 23% from rest to exhaustion (P<0.05) and remained elevated after recovery, whereas the respiratory rates in the absence of ADP and at 0.1 mM ADP (submaximal respiration) were unchanged. The ratio between respiration at 0.1 and 1 mM ADP (ADP sensitivity index) decreased at fatigue (P<0.05) but after the recovery period was not significantly different from that at rest. It is concluded that mitochondrial oxidative potential is maintained or improved during exhaustive HI exercise. The finding that the sensitivity of mitochondrial respiration to ADP is reversibly decreased after strenuous exercise may indicate that the control of mitochondrial respiration is altered. Received: 17 June 1998 / Received after revision: 11 November 1998 / Accepted: 26 November 1998