To investigate 1) the blood rheological responses to high training volume and 2) the potential effect of these responses on arterial hypoxemia induced during submaximal running and cycling, 10 triathletes performed an incremental cycle test, 20 minutes of running (R), and 20 minutes of cycling (C). All trials were performed at nearly 75 % of VO2max. Hematocrit (H), blood viscosity (etab), plasma viscosity (etapl), index of erythrocyte rigidity (Tk), changes in plasma volume (DeltaPV), pulmonary diffusing capacity (DLco), and arteriolized blood gas (PaO2) were measured before and after each trial. Pulse oxymetry (SpO2) and cardioventilatory data were collected continuously. A significant increase in etab, etapl, and H was noted after R and C with respect to pre-exercise, whereas DeltaPV decreased, with a greater decrease after C. Tk was significantly higher after R than after C. A significantly greater drop in DLco was noted after C compared with R. SpO2 decreased significantly more during R, as did PaO2. We conclude that blood rheological responses are specific to running and cycling. Cycling induced a sharp decrease in plasma volume, which could partially explain the greater DLco alteration. Running was characterized by an increase in Tk, which could be implicated in the severity of the drop in arterial oxygenation observed.

To study the pathophysiological mechanisms involved in the decrease of post-triathlon diffusing capacity (DLco), blood rheologic properties (blood viscosity: eta(b); changes in plasma volume: deltaPV) and atrial natriuretic factor (ANF) were assessed in ten triathletes during cycle-run (CR) and run-cycle (RC) trials at a metabolic intensity of 75% of maximal oxygen consumption ( VO(2max)). The DLco was measured before and 10 min after trials. ANF and deltaPV were measured at rest, after the cycle and run of CR and RC trials, and at the end of and 10 min after exercise. RC led to a greater deltaDLco decrease, a lower ANF concentration and a lower deltaPV than did CR, whereas for both CR and RC eta(b) was increased throughout exercise and 10 min after. In addition, after CR the deltaDLco decrease was inversely correlated ( r=-0.764; P<0.01) with deltaPV. The association of decreased plasma volume, increased eta(b), and lower ANF concentrations after RC suggested that lower blood pulmonary volume may have caused the greater decrease in Dlco as compared with CR. The inverse correlation between deltaPV and deltaDLco reinforces the hypothesis that fluid shifts limit the post-exercise DLco decrease after the CR succession in triathletes. Lastly, cycling in the crouched position might increase intra-thoracic pressure, decrease thorax volume due to the forearm position on the handlebars, and weaken peripheral muscular pump efficacy, all of which would limit venous return to the heart, and thus result in low pulmonary blood volume. Compared with cycling, running appeared to induce the opposite effects.

Design: Growth hormone (GH) has demonstrated water-retaining effects in subjects at rest, whereas other research has indicated that GH may stimulate sweating. Thus, the aim of this study was to investigate the effect of¯uid intake on the exercise-induced GH response. Methods: Seven healthy male volunteers (age: 27X4^1X3 years, weight: 74X5^1X1 kgY height: 179X32X3 cm performed a 40-min submaximal rectangular cycling exercise in two different sessions. The ®rst session (Session 1) was performed without water intake, and the second (Session 2) involved the ingestion of spring water (four intakes) corresponding to the volume of water lost during the ®rst session. Results: In session 1, the water loss was 568^32 mlX In Session 2, the volume of water loss was not signi®cantly different from the volume of¯uid intake 524^16 versus 568^32 ml respectively). The decrease in plasma volume was signi®cantly reduced in Session 2 26X69^1X59% versus 211X31 X89%; P , 0X05X In Session 1, the GH concentration was signi®cantly lower than that during Session 2 after 25 min 3X04^1X05 versus 5X26^1X81; P , 0X05 and after 40 min 13X7^3X55 versus 17X60^4X14 ngaml; P , 0X05 of exercise. The total GH response was signi®cantly lower in Session 1 than in Session 2 136X6^39X2 versus 202X4^58X9 ngamlXmin; P , 0X05X Conclusions: We conclude that the exercise-induced GH response decreases when exercise is performed without¯uid intake.

Previous studies have shown that undernutrition induces an impairment of the respiratory muscle function in patients with chronic lung disease. To explain this, we hypothesized that undernutrition could decrease oxidative metabolism in the diaphragm. We therefore examined the effect of prolonged undernutrition on diaphragm mitochondrial oxygen uptake with pyruvate and palmitate as substrates in adult rats. Ten rats served as controls (CTL). Ten nutritionally deprived rats (ND) received 40% of their estimated daily nutrition. Five weeks of undernutrition induced a 33% decrease in state 3 respiration with pyruvate plus malate as substrate (993 +/- 171 versus 1488 +/- 167 nmol atomic O/mg/min, P < 0.01) and a 39% decrease with palmitate plus malate (516 +/- 89 versus 850 +/- 165 nmol atomic O/mg/min, P < 0.05). With succinate plus rotenone, there was no significant difference in the respiratory rate between groups. In the ND group, we found a significant decrease in citrate synthase activity (P < 0.01), and also in reduced nicotinamine adenine dinucleotide (NADH) dehydrogenase activity (P < 0.05), which cannot alone induce such a state 3 respiratory decrease. This showed that undernutrition in rat diaphragm does not induce an alteration in protein complexes I, II, III, and IV, or the F complex containing the mitochondrial ATPase of the electron transport chain. In conclusion, the main result of this study was that prolonged undernutrition induced a decrease in mitochondrial respiration secondary to a significant reduction in NADH generation by the Krebs cycle, which may affect respiratory muscle function with implications for patient care.

Objective: Growth hormone (GH) has been shown to stimulate lipolysis and enhance lipid oxidation. We investigated whether GH could improve mitochondrial oxidative capacity. Method: Fourteen male Wistar rats received 14-day treatment with biosynthetic human GH (10 IU/kg/24 h) or placebo. Mitochondria were isolated from the total muscle of one hind limb of the rat. Mitochondrial oxygen consumption was measured in vitro using a Clark-type electrode with three substrates: palmitoyl-L-carnitine, pyruvate and succinate (+ rotenone). Results: Muscle mitochondrial yield was not significantly different in the GH-treated group from that in controls. Neither the basal nor ADP-stimulated respiratory state reached a significant difference between the 2 groups with palmitoyl-L-carnitine, pyruvate, and succinate. Conclusion: GH treatment did not improve the oxidative capacity of skeletal muscle mitochondria.