Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25–75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore, higher pulmonary vascular pressures in such subjects.

The effect of a pattern of exercise and dietary modifications, which was designed to produce alterations in the muscle glycogen content, on the capacity to perform anaerobic exercise was investigated. Six young male subjects worked to exhaustion on a bicycle ergometer at a supramaximal work load equivalent to 104 +/- 5% of VO2max after a normal diet, after a carbohydrate (CHO)-free diet following prolonged exhausting exercise, and after a high-CHO diet. This regimen has previously been shown to cause changes in the glycogen content of the working muscle. Mean work time for subjects on the first test was 4.87 +/- 1.07 min (mean +/- SD). After the low-CHO diet, the time for which work could be maintained was reduced in an increase to 3.32 +/- 0.93 min, whereas administration of the high-CHO diet resulted in an increase to 6.65 +/- 1.39 min. The resting blood lactate concentration was lower than normal following the low-CHO diet and higher than normal following the high-CHO diet. Post exercise blood lactate concentrations reached a peak between 2 and 6 min after exhaustion and again were lower (8.60 +/- 1.58 mmol/l) after the low-CHO diet and higher (12.86 +/- 1.42 mmol/l) after the high-CHO diet than after performing the same intensity of work to exhaustion on a normal diet (11.66 +/- 1.16 mmol/l). The rate of lactate accumulation appeared to be approximately the same during exercise under all three dietary conditions. If this is the case, it suggests that the alterations in endurance capacity do not result from changes in the rate of anaerobic glycolytic energy production, but possibly from a change in the total capacity of the system.

Alterations in fiber size and capillary diameter were highly correlated with perfusion deficits after myocardial ischemia. After 5 (n = 3) and 30 (n = 5) min of global normothermic ischemia, isolated rabbit hearts were perfused with India ink and then with glutaraldehyde. Morphometric techniques were used to determine mean fiber cross-sectional area [a(f)], mean effective capillary diameter [d(c)], total and perfused capillary number per fiber area, and capillary length per fiber volume in subepicardium (Epi) and subendocardium (Endo). Sarcomere length was measured to differentiate between effects of fiber shortening and intracellular edema on a(f). After 30 min of ischemia, a(f) increased 41 (Epi) and 36% (Endo). Of these percentages, fiber shortening accounted for 2 (Epi) and 25% (Endo). Decreased d(c) was correlated with increased a(f) as well as reductions in perfused capillary number and length. Whereas intracellular edema had the greatest overall effect on a(f), fiber shortening accounted for a significant increase of a(f) in Endo, where perfusion deficits were most pronounced. These data support the hypothesis that microvascular compression consequent to increased a(f) contributes to perfusion deficits after myocardial ischemia.

This brief review examines the athletic potential of mammals in general and the horse in particular as it relates to oxygen (O2) transport and utilization. The horse has been bred selectively for over six millennia based upon its ability to run fast. Whereas this has optimized cardiovascular and muscle function and the capacity to deliver and utilize O2, it has resulted in lung failure during intense exercise. Horses in their athletic prime are considered and attention is focused on their maximal capacities as related to O2 transport, irrespective of age per se. Following a few comments on the history of O2, this review moves from established principles of O2 transport at the integrative organ level to the microcirculation and the processes and principles that govern O2 offloading, where much remains to be discovered. Four principal questions are addressed: (1) as an athlete, what are the most outstanding physiological characteristics of the horse? (2) what anatomical and physiological capacities facilitate this superlative performance and such prodigious O2 fluxes (i.e. maximal VO2)? (3) do cardiovascular dynamics or intramuscular energetic processes limit VO2 kinetics (i.e. the speed at which VO2 increases at the onset of exercise)? VO2 kinetics determine the size of the O2 deficit and as such represent an important determinant of muscle metabolism and fatigue; and (4) what determines the efficacy of muscle microcirculatory O2 exchange?

Aminocaproic acid (ACA) and Premarin w (PRE) are used to treat exercise-induced pulmonary haemorrhage (EIPH) at the racetrack based upon their putative coagulation effects. We hypothesized that neither ACA nor PRE would reduce EIPH because the literature does not substantiate coagulation deficits being manifested in EIPH. Six Thoroughbreds were run from 4 m s 21 until fatigue (1 m s 21 s £ 1 min increments; 68 inclined treadmill) after being treated with placebo, PRE (25 mg) or ACA (5 g) at 2-week intervals in a randomized crossover design. Coagulation and exercise-related variables were measured at rest and maximal effort. EIPH and inflammation were quantified via bronchoalveolar lavage fluid (BALF) 30-60 min post-exercise. EIPH was not altered by either treatment (3.8^1.7 (placebo), 4.6^3.2 (ACA) and 2.4^1.2 (PRE) £ 10 6 RBC ml 21 BALF; p ¼ 0.12), nor was coagulation. However, inflammation was decreased (5.9^0.9 (placebo), 4.4^0.9 (ACA) and 4.2^0.4 (PRE) £ 10 5 WBC ml 21 BALF; both p , 0.05). There was a trend for decreased time-to-fatigue (720^27 (placebo), 709^24 (ACA) and 726^28 (PRE) s; p ¼ 0.09 for placebo vs. ACA) and a reduction in plasma lactate (19.5^3.0 (placebo), 14.7^1.0 (ACA) and 17.6^2.5 (PRE) mmol l 21 ; p , 0.05 for placebo vs. ACA) following ACA administration. ACA and PRE were not effective in reducing EIPH, and ACA may be detrimental to performance. However, both may mitigate exercise-induced pulmonary inflammation.