Garry C. Scroop

Reduced performance of male and female athletes at 580 m altitude

Abstract This study examined the effect of mild hypobaria (MH) on the peak oxygen consumption (O2peak) and performance of ten trained male athletes [ (SEM); O2peak = 72.4 (2.2) ml · kg−1 · min−1] and ten trained female athletes [O2peak = 60.8 (2.1) ml · kg−1 · min−1]. Subjects performed 5-min maximal work tests on a cycle ergometer within a hypobaric chamber at both normobaria (N, 99.33 kPa) and at MH (92.66 kPa), using a counter-balanced design. MH was equivalent to 580 m altitude. O2peak at MH decreased significantly compared with N in both men [− 5.9 (0.9)%] and women [− 3.7 (1.0)%]. Performance (total kJ) at MH was also reduced significantly in men [− 3.6 (0.8)%] and women [− 3.8 (1.2)%]. Arterial oxyhaemoglobin saturation (SaO2) at O2peak was significantly lower at MH compared with N in both men [90.1 (0.6)% versus 92.0 (0.6)%] and women [89.7 (3.1)% versus 92.1 (3.0)%]. While SaO2 at O2peak was not different between men and women, it was concluded that relative, rather than absolute, O2peak may be a more appropriate predictor of exercise-induced hypoxaemia. For men and women, it was calculated that 67–76% of the decrease in O2peak could be accounted for by a decrease in O2 delivery, which indicates that reduced O2 tension at mild altitude (580 m) leads to impairment of exercise performance in a maximal work bout lasting ≈ 5 min.

Effect of muscle glycogen availability on maximal exercise performance

Abstract This investigation determined the influence of pre-exercise muscle glycogen availability on performance during high intensity exercise. Nine trained male cyclists were studied during 75 s of all-out exercise on an air-braked cycle ergometer following muscle glycogen-lowering exercise and consumption of diets (energy content approximately 14 MJ) that were either high (HCHO – 80% CHO) or low (LCHO – 25% CHO) in carbohydrate content. The exercise-diet regimen was successful in producing differences in pre-exercise muscle glycogen contents [HCHO: 578(SEM 55) mmol · kg−1 dry mass; LCHO: 364 (SEM 58) P < 0.05 mmol · kg−1 dry mass]. Despite this difference in muscle glycogen availability, there were no between trial differences for peak power [HCHO 1185 (SEM 50)W, LCHO 1179 (SEM 48)W], mean power [HCHO 547 (SEM 5)W, LCHO 554 (SEM  8)W] and maximal accumulated oxygen deficit [HCHO 54.4 (SEM 2.3) ml · kg−1, LCHO 54.6 (SEM 2.0) ml · kg−1]. Postexercise muscle lactate contents (HCHO 95.9 (SEM 4.6) mmol · kg−1 dry mass, LCHO 82.7 (SEM 12.3) mmol · kg−1 dry mass, n = 8] were no different between the two trials, nor were venous blood lactate concentrations immediately after and during recovery from exercise. These results would indicate that increased muscle glycogen availability has no direct effect on performance during all-out high intensity exercise.

Training-induced increases in sea level V˙O2 m a x and endurance are not enhanced by acute hypobaric exposure

Abstract The present study used untrained subjects to examine the effect of acute hypobaric exposure during endurance training on subsequent exercise performance at sea level. Two groups, each of nine subjects, completed 5 weeks of endurance training [cycle ergometer exercise for 45 min, three times per week at a heart rate corresponding to 70% of that achieved at the maximal O2 consumption (V˙O2max) either at sea level or at high altitude] in a hypobaric chamber, under either normobaric [sea level, SL; 750 mmHg (100 kPa) ≈90 m] or hypobaric [altitude, ALT; 554 mmHg (73.4 kPa) ≈ 2500 m] conditions and the changes in SL V˙O2max, SL endurance time and peak blood lactate during the endurance test compared. While each group showed increases in both SL V˙O2max (≈12%) and SL endurance time (≈71%), there were no significant differences between the groups [SL V˙O2max, mean (SE) – SL group: pre-training = 42.4 (3.5), post-training = 46.1 (3.5) ml · kg−1· min−1, P < 0.005; ALT group: pre-training = 40.8 (2.6), post-training = 47.2 (3.4) ml · kg−1· min−1, P < 0.01; SL endurance time – SL group: pre-training 7.1 (1.5), post-training 11.8 (2.9) min, P < 0.01; ALT group: pre-training = 7.5 (0.6), post-training = 13.3 (1.4) min, P < 0.001]. Peak blood lactate during the endurance test was not altered by either training regimen. It is concluded that acute exposure of untrained subjects to hypobaric hypoxia during endurance training has no synergistic effect on the degree of improvement in either SL V˙O2max or endurance time.

Plasma volume, osmolarity, total protein and electrolytes during treadmill running and cycle ergometer exercise

SummaryWhile haemoconcentration due to loss of plasma volume is well established during cycling, the existence of similar changes during running remains contentious. This study compared the changes in plasma volume and associated blood indices during 60 min of running and cycling at the same relative intensity (approximately 65%

Lactate disposal in resting trained and untrained forearm skeletal muscle during high intensity leg exercise

\dot VO_{2 max}

Exercise-induced hypoxemia: fact or fallacy?

), with all changes referenced to blood indices obtained after 30 min seated at rest on a cycle ergometer. Plasma osmolarity increased similarly with both forms of exercise but was less than predicted for water loss alone, such that there was a net loss of sodium during exercise and of potassium postexercise, with essentially no loss of protein. Plasma volume decreased similarly (approximately 6.5%) in both exercise trials, but while that with cycling was initiated by exercise itself and was essentially maximal within 5 min, the reduction in plasma volume in the running trial was induced by adopting the upright posture and was complete before exercise began. These data would indicate that different mechanisms are responsible for the changes in plasma volume induced by running and cycling, while the similarity of change would suggest that there is a lower limit to any reduction in plasma volume, regardless of mechanism. Furthermore, the observation that the changes in plasma volume were complete before or early in exercise, would imply that oral water ingestion during prolonged exercise, which is essential for thermoregulation, may be more concerned with homeostasis of extravascular water rather than plasma volume.

Rectal temperature correction overestimates the frequency of exercise-induced hypoxemia.

Vertebral and carotid artery infusions of bradykinin increased blood pressure and heart rate in anaesthetised greyhounds. Indomethacin pretreatment abolished the pressor response to vertebral infusion and reduced that to carotid infusion. Areas postrema ablation abolished the pressor response to bradykinin with both routes of administration. The tachycardia responses to cranial artery infusions and the entire cardiovascular response to intravenous infusion were unaffected by either treatment. It is concluded that intact areas postrema and normal prostaglandin synthesis are essential for the full expression of the central pressor action of bradykinin.

Vagal involvement in the pressor responses to cranial artery infusions of bradykinin in anaesthetised greyhounds

SummaryAt a given oxygen uptake (