Corinne Caillaud

Exercise-Induced Arterial Hypoxaemia in Athletes

AbstractDuring exercise, healthy individuals are able to maintain arterial oxygenation, whereas highly-trained endurance athletes may exhibit an exercise-induced arterial hypoxaemia (EIAH) that seems to reflect a gas exchange abnormality. The effects of EIAH are currently debated, and different hypotheses have been proposed to explain its pathophysiology. For moderate exercise, it appears that a relative hypoventilation induced by endurance training is involved. For high-intensity exercise, ventilation/perfusion (V̇A/Q̇) mismatching and/or diffusion limitation are thought to occur. The causes of this diffusion limitation are still under debate, with hypotheses being capillary blood volume changes and interstitial pulmonary oedema. Moreover, histamine is released during exercise in individuals exhibiting EIAH, and questions persist as to its relationship with EIAH and its contribution to interstitial pulmonary oedema. Further investigations are needed to better understand the mechanisms involved and to determine the long term consequences of repetitive hypoxaemia in highly trained endurance athletes.

Cardiovascular strain impairs prolonged self-paced exercise in the heat.

It has been proposed that self‐paced exercise in the heat is regulated by an anticipatory reduction in work rate based on the rate of heat storage. However, performance may be impaired by the development of hyperthermia and concomitant rise in cardiovascular strain increasing relative exercise intensity. This study evaluated the influence of thermal strain on cardiovascular function and power output during self‐paced exercise in the heat. Eight endurance‐trained cyclists performed a 40 km simulated time trial in hot (35°C) and thermoneutral conditions (20°C), while power output, mean arterial pressure, heart rate, oxygen uptake and cardiac output were measured. Time trial duration was 64.3 ± 2.8 min (242.1 W) in the hot condition and 59.8 ± 2.6 min (279.4 W) in the thermoneutral condition (P < 0.01). Power output in the heat was depressed from 20 min onwards compared with exercise in the thermoneutral condition (P < 0.05). Rectal temperature reached 39.8 ± 0.3 (hot) and 38.9 ± 0.2°C (thermoneutral; P < 0.01). From 10 min onwards, mean skin temperature was ∼7.5°C higher in the heat, and skin blood flow was significantly elevated (P < 0.01). Heart rate was ∼8 beats min−1 higher throughout hot exercise, while stroke volume, cardiac output and mean arterial pressure were significantly depressed compared with the thermoneutral condition (P < 0.05). Peak oxygen uptake measured during the final kilometre of exercise at maximal effort reached 77 (hot) and 95% (thermoneutral) of pre‐experimental control values (P < 0.01). We conclude that a thermoregulatory‐mediated rise in cardiovascular strain is associated with reductions in sustainable power output, peak oxygen uptake and maximal power output during prolonged, intense self‐paced exercise in the heat.

Exercise training reduces myocardial lipid peroxidation following short-term ischemia-reperfusion

PURPOSE The purpose of these experiments was to test the hypothesis that endurance exercise training will reduce myocardial lipid peroxidation following short-term ischemia and reperfusion (I-R). METHODS Female Sprague-Dawley rats (4 months old) were randomly assigned to either a sedentary control group (N = 13) or to an exercise training group (N = 13). The exercise trained animals ran 4 d.wk-1 (90 min.d-1) at approximately 75% V02max. Following a 10-wk training program, animals were anesthetized, mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was achieved by a ligature around the left coronary artery; occlusion was maintained for 5 min followed by a 10-min period of reperfusion. RESULTS Although training did not alter (P > 0.05) myocardial activities of antioxidant enzymes (superoxide dismutase and glutathione peroxidase), training was associated with significant increase (P > 0.05) in heat shock protein (HSP72) in the left ventricle. Compared with controls, trained animals exhibited significantly lower levels (P < 0.05) of myocardial lipid peroxidation following I-R. CONCLUSION These data support the hypothesis that exercise training provides protection against myocardial lipid peroxidation induced by short-term I-R in vivo.

β2-agonists and exercise-induced asthma

Abstractβ2-Agonists taken immediately before exercise provide significant protection against exercise-induced asthma (EIA) in most patients. However, when they are taken daily, there are some negative aspects regarding severity, control, and recovery from EIA. First, there is a significant minority (15–20%) of asthmatics whose EIA is not prevented by β2-agonists, even when inhaled corticosteroids are used concomitantly. Second, with daily use, there is a decline in duration of the protective effect of long-acting β2-agonists. Third, if breakthrough EIA occurs, recovery of lung function is slower in response to a β2-agonist, and additional doses are often required to achieve pre-exercise values. If a person who takes a β2-agonist daily experiences problems with exercise, then the physician should consider changing the treatment regimen to achieve better control of EIA. These problems likely result from desensitization of the β2-receptor on the mast cell, which enhances mediator release, and on the bronchial smooth muscle, which enhances the bronchoconstrictor response and delays recovery from EIA. These effects are reversed within 72 h after cessation of a β2-agonists. The important clinical question is: Are we acutally compromising the beneficial effects of β2-agonists on the prevention and recovery from EIA by prescribing them daily? Patients with EIA need to ensure that their doses of inhaled corticosteroid or other anti-inflammatory therapy are optimized so that, if necessary, a β2-agonist can be used intermittently as prophylactic medication with greater confidence in the outcome.

Inhibition of histamine release by nedocromil sodium reduces exercise-induced hypoxemia in master athletes.

During exercise in highly-trained older master athletes (MA), the impairment of pulmonary gas exchanges has been shown to be associated with a concomitant increase in histamine release (2). To determine the role of the histamine released (% H) during exercise-induced hypoxemia, seven MA (age 63.2 yr +/- 1.9), all of whom were known to develop exercise-induced hypoxemia, performed two maximal incremental exercise tests at a one-month interval after administration of nedocromil sodium (which inhibits histamine and other mediator release) or placebo in random double-blind order. During exercise testing, blood samples for arterial blood gas analysis and histamine assay were drawn at rest, exercise and recovery. Nedocromil sodium induced an inhibition in % H (0.57 +/- 0.03 at maximal load (Pmax) with placebo vs 0.24 +/- 0.02 with nedocromil sodium) linked with an improvement of pulmonary gas exchange (PaO2: 71.1 +/- 1.4 at Pmax with placebo vs 83.4 +/- 3 with nedocromil sodium; D(Ai-a)O2: 37.5 +/- 1.4 at Pmax vs 19.1 +/- 3.1, respectively). These results confirm the link established between the increase in histamine and exercise-induced hypoxemia in master athletes.

Response of bone metabolism related hormones to a single session of strenuous exercise in active elderly subjects

Objective: To evaluate the effect of strenuous exercise on bone metabolism and related hormones in elderly subjects. Methods: Twenty one active elderly subjects (11 men and 10 women; mean age 73.3 years) showing a mean theoretical Vo2max of 151.4% participated. Concentrations of plasma ionised calcium (iCa), serum intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25(OH)D), and 1.25-dihydroxy-vitamin D3 (1.25(OH)2D3), as well as the bone biochemical markers type I collagen C-telopeptide for bone resorption and osteocalcin and bone alkaline phosphatase for bone formation, were analysed before and after a maximal incremental exercise test. Results: At basal level, iPTH was positively correlated with age (r = 0.56, p<0.01) and negatively correlated with 25(OH)D (r = −0.50; p<0.01) and 1.25(OH)2D3 (r = −0.47; p<0.05). Moreover, 25(OH)D and 1.25(OH)2D3 levels were negatively correlated with age (r = −0.50, p<0.01 and r = −0.53, p<0.01, respectively). After exercise, iCa and 25(OH)D decreased (p<0.001 and p = 0.01, respectively) while iPTH increased (p<0.001). The levels of 1.25(OH)2D3, bone biochemical markers, haematocrit, and haemoglobin were unchanged. The variations in iCa and 25(OH)D were not related to age and/or sex. The iPTH variation was directly related to basal iPTH levels (p<0.01) and indirectly related to age. Conclusions: In active elderly subjects, strenuous exercise disturbed calcium homeostasis and bone related hormones without immediate measurable effect on bone turnover. Although an increase in iPTH could have an anabolic action on bone tissue, our findings from our short term study did not allow us to conclude that such action occurred.

Central and peripheral fatigue during passive and exercise-induced hyperthermia.

PURPOSE Hyperthermia was induced during prolonged exercise (ExH) and passive heating (PaH) to isolate the influence of exercise on neuromuscular function during a maximal voluntary isometric contraction (MVC) of the quadriceps under heat stress. The influence of cardiovascular strain in limiting endurance performance in the heat was also examined. METHODS On separate days, eight males cycled to exhaustion at 60% maximal oxygen uptake or were immersed in a water bath (∼41°C) until rectal temperature (Tre) increased to 39.5°C. The ExH and PaH interventions were performed in ambient conditions of 38°C and 60% relative humidity with Tre reaching 39.8°C during exercise. Before (control) and after each intervention, voluntary activation and force production capacity were evaluated by superimposing an electrically stimulated tetanus during a 45-s MVC. RESULTS Force production decreased immediately after PaH and ExH compared with control, with the magnitude of decline being more pronounced after ExH (P < 0.01). Mean voluntary activation was also significantly depressed after both interventions (P < 0.01 vs control). However, the extent of decline in voluntary activation was maintained at ∼90% during both PaH and ExH MVC. This decline accounted for 41.5% (PaH) and 33.1% (ExH) of the decrease in force production. In addition, exhaustion coincided with a marked increase in HR (∼96% of maximum) and a decline in stroke volume (25%) and mean arterial pressure (10%) (P < 0.05). CONCLUSIONS The loss of force production capacity during hyperthermia originated from central and peripheral fatigue factors, with the combination of heat stress and previous contractile activity exacerbating the rate of decline. Thus, the observed significant rise in thermal strain in ExH and PaH impaired neuromuscular function and was associated with an exercise performance limiting increase in cardiovascular strain.

Antioxidants and mitochondrial respiration in lung, diaphragm, and locomotor muscles : effect of exercise

Previous studies have shown that exhaustive exercise may increase reactive oxygen species (ROS) generation in oxidative muscles that may in turn impair mitochondrial respiration. Locomotor muscles have been extensively examined, but there is few report about diaphragm or lung. The later is a privileged site for oxygen transit. To compare the antioxidant defense system and mitochondrial function in lung, diaphragm and locomotor muscles after exercise, 24 young adult male rats were randomly assigned to a control (C) or exercise (E) group. E group rats performed an exhaustive running test on a motorized treadmill at 80-85% VO2max Mean exercise duration was 66+/-2.7 min. Lung, costal diaphragm, mixed gastrocnemius, and oxidative muscles (red gastrocnemius and soleus: RG/SOL homogenate) were sampled. Mitochondrial respiration was assessed in tissue homogenates by respiratory control index (RCI: rate of uncoupled respiration/rate of basal respiration) measurement. Lipid peroxidation was evaluated by malondialdehyde concentration (MDA) and we determined the activity of two antioxidant enzymes: superoxide dismutase (SOD) and glutathione peroxidase (GPX). We found elevated basal (C group data) SOD and GPX activities in both lung and diaphragm compared to locomotor muscles (p<.001). Exercise led to a rise in GPX activity in red locomotor muscles homogenate (GR/SOL; C = 10.3+/-0.29 and E = 14.4+/-1.51 micromol x min(-1) x gww(-1); p<.05), whereas there was no significant change in lung and diaphragm. MDA concentration and mitochondrial RCI values were not significantly changed after exercise. We conclude that lung and diaphragm had higher antioxidant protection than locomotor muscles. The exercise test did not lead to significant oxidative stress or alteration in mitochondrial respiration, suggesting that antioxidant function was adequate in both lung and diaphragm in the experimental condition.

Effect of an overground walking training on gait performance in healthy 65- to 80-year-olds.

The aim of this study was to examine the effect of an individualized overground walking interval training on gait performance [i.e., speed and energy cost (C(w))] in healthy elderly individuals. Twenty-two older adults were assigned to either a training group (TG; n=12, 73.4+/-3.9yr) or a non-training control group (CG; n=10, 70.9+/-9.6yr). TG participated in a 7-week individualized walking interval training at intensities progressing from 50 to 100% of ventilatory threshold (T (VE)). Aerobic fitness [maximal oxygen uptake (V O(2max)) and T (VE)], preferred walking speed (PWS), gross and net C(w) (GC(w) and NC(w), respectively) and relative effort (%V O(2max)) at PWS measured before training (PWS(1)) were assessed prior and following the intervention. All outcomes were measured on a treadmill. Significant improvements in GC(w) (-8%; P=0.007), NC(w) (-12%; P=0.003), relative effort (%V O(2max): -12%; P<0.001) and PWS (+12%; P<0.001) were observed in TG but not in CG (P>0.71). V O(2max) and T (VE) remained unchanged in both groups (P>0.57). Changes in GC(w) at PWS(1) (difference between GC(w) at PWS(1) measured pre and post intervention) were inversely correlated with changes in PWS (difference between pre and post PWS; r=-0.67; P=0.02). The decreased C(w) at PWS(1), with no concomitant improvement in aerobic fitness, represents the main contributing factor for the reduction of the relative effort at this speed. This also allows elderly people to increase their PWS post training. Therefore, the present walking training may be an effective way to improve walking performance and delay mobility impairment in older adults.

Effects of two successive maximal exercise tests on pulmonary gas exchange in athletes

Pulmonary extravascular water accumulation may be involved in exercise-induced hypoxaemia in highly aerobically trained athletes. We hypothesized that if such an alteration were present in elite athletes performing a maximal exercise test, the impairment of gas exchange would be worse during a second exercise test following the first one. Eight male athletes performed two incremental exercise tests separated by a 30-min recovery period. Pulmonary gas exchange and ventilatory data were measured during exercise tests performed in normoxia. Arterial blood samples were drawn each minute during rest, exercise, and recovery. Pulmonary diffusing capacity for CO (DLCO) was measured at rest, after the first (T1) and the second (T2) test. All the subjects underwent a spirometric test at rest and after T2. Maximal and recovery data for 02 uptake and minute ventilation were not statistically different between T1 and T2. Partial pressure of arterial 02 (PaO2) decreased during both tests but was lower during T2 for rest, 60 W, and 120 W (P < 0.02). Alveolar-arterial difference in partial pressure of 02 (PA-a02) increased during both the tests but was significantly larger during T2 for rest, 60 W, and 120 W (P < 0.01). The PaO2 and PA-aO2 data at maximal exercise were not significantly different between T1 and T2. Compared to rest, PA-aO2 remained significantly larger during recovery for both T1 and T2 (P < 0.0001). The PA-aO2 during T2 recovery was larger than T1 recovery (P < 0.008). Spirometric data did not change. The DLCO measurements after T1 and T2 were not significantly different from rest. These results showed an alteration of PaO2 and PA-aO2 during T1, which tended to be worse during and after T2; however, these data do not allow us to make a definitive statement as to the cause of the hypoxaemia. Our study confirmed that exhausting exercise caused hypoxaemia. It also demonstrated that the disturbance in pulmonary gas exchange persisted for at least 30 min following the end of the exercise period and became worse during submaximal intensities of the following incremental exercise test.