Age is no barrier to muscle structural, biochemical and angiogenic adaptations to training up to 24 months in female rats.

Ageing is associated with reduced transport and utilization of O(2), diminishing exercise tolerance. Reductions may occur in cardiac output (delivery), and skeletal muscle oxidative capacity (utilization). To determine the reversibility of the declines in the muscular determinants of these limitations, skeletal muscle morphological, angiogenic and biochemical responses to acute exercise and endurance training were investigated in female Fischer 344 rats (n = 42; seven groups of six rats) aged 6 (Y) and 24 (O) months compared with resting untrained controls (Y(C), O(C)). Treadmill training lasted 8 weeks (10 deg incline, 1 h per day, 5 days per week). Two groups ran at maximum tolerated speeds (Y(TR), O(TR)), while an additional Y group (Y(TM)) trained at O(TR) speed. There was no effect of age on vascular endothelial growth factor gene expression in gastrocnemius muscles after acute exercise. Similarly, age did not impair the effects of training, with increases (P < 0.05; +/-s.e.m.) occurring in all of the following: 1 h exercise running speed (Y(TR) 92 +/- 4% versus O(TR) 140 +/- 25%); citrate synthase (Y(TR) 37 +/- 8% versus O(TR) 97 +/- 33%) and beta-hydroxyacyl-CoA-dehydrogenase (Y(TR) 31 +/- 7%, versus O(TR) 72 +/- 24%) activities; and capillary-to-fibre ratio (Y(TR) 5.2 +/- 0.2% versus O(TR) 8.1 +/- 0.2%). However, Y(TM) muscle was unchanged in each measure compared with Y(C). In conclusion, these muscular responses to training were (1) not reduced by ageing, but (2) dependent on relative and not absolute work rate, since, at the same speed, O(TR) rats showed greater changes than Y(TM). Therefore, increases in exercise tolerance and muscle adaptations are not impaired in female rats up to 24 months of age, and require a smaller absolute exercise stimulus (than young) to be manifest.

Effect of locomotor respiratory coupling on respiratory evaporative heat loss in the sheep.

During galloping, many animals display 1:1 coupling of breaths and strides. Locomotor respiratory coupling (LRC) may limit respiratory evaporative heat loss (REHL) by constraining respiratory frequency (f). Five sheep were exercised twice each, according to a five-step protocol: 5 min at the walk, 5 min at the trot (trot1), 10 min at the gallop, 5 min at the trot (trot2), and 5 min at the walk. Rectal temperature (T(re)), stride frequency, f, REHL, and arterial CO(2) tension and pH were measured at each step. Tidal volume (VT) was calculated. LRC was observed only during galloping. The coupling ratio remained at 1:1 while VT increased continuously during galloping, causing REHL to increase from 2.9 +/- 0.2 (SE) W/kg at the end of trot1 to a peak of 5.3 +/- 0.3 W/kg. T(re) rose from 39.0 +/- 0.1 degrees C preexercise to 40.2 +/- 0.2 degrees C at the end of galloping. At the gallop-trot2 transition, VT fell and f rose, despite a continued rise in T(re). Arterial CO(2) tension fell from 36.5 +/- 1.1 Torr preexercise to 31.8 +/- 1.4 Torr by the end of trot1 and then further to 21.5 +/- 1.2 Torr by the end of galloping, resulting in alkalosis. In conclusion, LRC did not prevent increases in REHL in sheep because VT increased. The increased VT caused hypocapnia and presumably elevated the cost of breathing.

Arterial blood gas tensions during exercise in neonatal lambs.

At the onset of exercise, adult animals increase ventilation to match or exceed the metabolic requirement. This error-free regulation of arterial blood gas tensions may be attributable to 'adaptive feed-forward control'--respiratory control based on experience gained in infancy. This hypothesis predicts that neonates exhibit hypercapnia at the onset of exercise. To test this prediction, seven lambs were exercised on a treadmill at 0.8 m/sec at the ages of 2-5 days, and again at 9-12 days. Arterial blood samples were drawn pre-exercise and at 0.5, 1, 2, 5, 7 and 10 min of exercise. Seven adult sheep were similarly tested for comparison. The lambs had significantly higher arterial CO2 tensions (PaCO2) and lower arterial O2 tensions (PaO2) than adult sheep both at rest and during exercise. Nonetheless, the lambs maintained PaCO2 at or below the resting level throughout exercise. PaO2 rose significantly during exercise in the sheep and lambs. The results do not support the hypothesis since hypercapnia was not observed in the exercising neonatal lambs.

Measurement of cardiac output during exercise by open-circuit acetylene uptake.

Noninvasive measurement of cardiac output (QT) is problematic during heavy exercise. We report a new approach that avoids unpleasant rebreathing and resultant changes in alveolar PO(2) or PCO(2) by measuring short-term acetylene (C(2)H(2)) uptake by an open-circuit technique, with application of mass balance for the calculation of QT. The method assumes that alveolar and arterial C(2)H(2) pressures are the same, and we account for C(2)H(2) recirculation by extrapolating end-tidal C(2)H(2) back to breath 1 of the maneuver. We correct for incomplete gas mixing by using He in the inspired mixture. The maneuver involves switching the subject to air containing trace amounts of C(2)H(2) and He; ventilation and pressures of He, C(2)H(2), and CO(2) are measured continuously (the latter by mass spectrometer) for 20-25 breaths. Data from three subjects for whom multiple Fick O(2) measurements of QT were available showed that measurement of QT by the Fick method and by the C(2)H(2) technique was statistically similar from rest to 90% of maximal O(2) consumption (VO(2 max)). Data from 12 active women and 12 elite male athletes at rest and 90% of VO(2 max) fell on a single linear relationship, with O(2) consumption (VO(2)) predicting QT values of 9.13, 15.9, 22.6, and 29.4 l/min at VO(2) of 1, 2, 3, and 4 l/min. Mixed venous PO(2) predicted from C(2)H(2)-determined QT, measured VO(2), and arterial O(2) concentration was approximately 20-25 Torr at 90% of VO(2 max) during air breathing and 10-15 Torr during 13% O(2) breathing. This modification of previous gas uptake methods, to avoid rebreathing, produces reasonable data from rest to heavy exercise in normal subjects.

Thermal drive contributes to hyperventilation during exercise in sheep.

The etiology of exercise hypocapnia is unknown. The contributions of exercise intensity (ExInt), lactic acid, environmental temperature, rectal temperature (Tre), and physical conditioning to the variance in arterial CO2 tension (PaCO2) in the exercising sheep were quantified. We hypothesized that thermal drive contributes to hyperventilation. Four unshorn sheep were exercised at approximately 30, 50, and 70% of maximal O2 consumption for 30 min, or until exhaustion, both before and after 5 wk of physical conditioning. In addition, two of the sheep were shorn and exercised at each intensity in a cold (<15 degrees C) environment. Tre and O2 consumption were measured continuously. Lactic acid and PaCO2 were measured at 5- to 10-min intervals. Data were analyzed by multiple regression on PaCO2. During exercise, Tre rose and PaCO2 fell, except at the lowest ExInt in the cold environment. Tre explained 77% of the variance in PaCO2, and ExInt explained 5%. All other variables were insignificant. We conclude that, in sheep, thermal drive contributes to hyperventilation during exercise.