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David C Poole,1,2 Howard H Erickson1 1Department of Anatomy and Physiology, 2Department of Kinesiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, USA Abstract: As the Thoroughbreds race for the final stretch, 44 hooves flash and thunder creating a cacophony of tortured air and turf. Orchestrated by selective breeding for physiology and biomechanics, expressed as speed, the millennia-old symphony of man and beast reaches its climax. At nearly 73 kilometers per hour (45 mph) over half a ton of flesh and bone dwarfs its limpet-like jockey as, eyes wild and nostrils flaring, their necks stretch for glory. Beneath each resplendent livery-adorned, latherin-splattered coat hides a monstrous heart trilling at 4 beats per second, and each minute, driving over 400 L (105 gallons) of oxygen-rich blood from lungs to muscles. Matching breath to stride frequency, those lungs will inhale 16 L (4 gallons) of air each stride moving >1,000 L/min in and out of each nostril – and yet failing. Engorged with blood and stretched to breaking point, those lungs can no longer redden the arterial blood but leave it dusky and cyanotic. Their exquisitely thin blood–gas barrier, a mere 10.5 μm thick (1/50,000 of an inch), ruptures, and red cells invade the lungs. After the race is won and lost, long after the frenetic crowd has quieted and gone, that blood will clog and inflame the airways. For a few horses, those who bleed extensively, it will overflow their lungs and spray from their nostrils incarnadining the walls of their stall: a horrifically poignant canvas that strikes at horse racing’s very core. That exercise-induced pulmonary hemorrhage (EIPH) occurs is a medical and physiological reality. That every reasonable exigency is not taken to reduce/prevent it would be a travesty. This review is not intended to provide an exhaustive coverage of EIPH for which the reader is referred to recent reviews, rather, after a brief reminder of its physiologic and pathologic bases, focus is brought on the latest developments in EIPH discovery as this informs state-of-the-art knowledge, the implementation of that knowledge and recommendations for future research and treatment. Keywords: epistaxis, Thoroughbred racehorse, pulmonary capillary rupture, vascular pressure, alveolar pressure, nasal airway collapse

The purpose of this paper is to provide an introduction to the study of oxygen uptake (VO(2)) dynamics or kinetics. Following the onset of exercise, both muscle and pulmonary VO(2) rise in a near-exponential fashion towards the anticipated 'steady-state' VO(2) demand. However, it can take 2-4 min, or even longer at higher work rates, before this steady state is attained. Slow VO(2) kinetics increase the so-called O(2) deficit and obligate a greater contribution from anaerobic mechanisms of ATP production (involving the breakdown of muscle high energy phosphates and lactate production from glycogen) to meet the ATP requirement of the exercise task. A primary goal in this area of research is therefore to elucidate the physiological mechanisms which control and/or limit the rate at which muscle VO(2) increases following the onset of exercise. At higher intensities of exercise, a continued increase in both muscle and pulmonary VO(2) is observed with time despite the external work rate remaining constant. This continued rise in VO(2), beyond the anticipated steady-state requirement for the work rate, has been termed the VO(2) 'slow component,' and establishing the mechanistic basis for this phenomenon is another important goal of research in this field. This paper provides an overview of some of the factors which might contribute to both the fundamental and slow phases of the VO(2) kinetics and, in so doing, provides general background material for the more specific papers that follow. [ABSTRACT FROM AUTHOR]

Exercise-induced pulmonary haemorrhage (EIPH) is a serious condition that affects the health and possibly the performance of all racehorses. However, only two treatments, furosemide and the Flair™ equine nasal strip, both of which reduce capillary transmural pressure, have been successful in reducing EIPH. Alternatively, transient impairment of platelet function and coagulation during exercise has been considered an additional contributor to EIPH. Consequently, herbal formulations designed to enhance platelet function, and hence coagulation, are hypothesized to reduce EIPH. To investigate the validity of this hypothesis, five Thoroughbred horses completed three maximal incremental exercise tests on a 10% inclined treadmill in a randomized cross-over design experiment. Treatments included twice daily oral administration (for 3 days) of a placebo (PL; cornstarch) and two herbal formulas, Yunnan Paiyao (YP) or Single Immortal (SI). Blood samples for coagulation profiles, complete blood counts and biochemistry profiles were collected before each exercise test. During each test, pulmonary arterial pressure, oxygen uptake, arterial blood gases, plasma lactate and time-to-fatigue were measured. Severity of EIPH was quantified via bronchoalveolar lavage (BAL) at 30–60 min post-exercise. The herbal formulations were not effective in decreasing EIPH (×106 red blood cells ml−1 BAL fluid: PL, 27.1±11.6; YP, 33.2±23.4; SI, 35.3±15.4, P>0.05) or in changing any of the other variables measured with the exception of time-to-fatigue, which was slightly but significantly prolonged by Single Immortal compared with placebo and Yunnan Paiyao (PL, 670±9.6 s; YP, 665±5.5 s; SI, 685±7.9 s, P<0.05). Thus, these results do not support the use of these herbal formulations in the prevention of EIPH. [ABSTRACT FROM PUBLISHER]

Furosemide (FUR) and the equine nasal strip (NS) decrease exercise-induced pulmonary haemorrhage (EIPH) compared with control (CON) conditions in the Thoroughbred horse during near-maximal running trials. As FUR and NS have potential performance-enhancing properties, we studied Thoroughbreds running to fatigue to test the hypothesis that time-to-fatigue (TTF) would be increased, yet EIPH reduced, in FUR and NS compared with CON. Thoroughbred geldings (n=6) were run to volitional fatigue on a level treadmill (1 m s−1 increment per minute from an initial trot) every two weeks (order randomized) under CON, NS, FUR (1 mg kg−1; 4 h prior) and FUR+NS conditions. Pulmonary arterial pressure (Ppa) and pulmonary gas exchange were measured throughout exercise, while arterial blood gases were sampled at the end of each 1-min stage. EIPH severity was quantified via bronchoalveolar lavage (BAL) at 30 min post-exercise. TTF was increased for all experimental conditions (i.e. an additional 20±13, 28±8 and 40±6 s for NS, FUR and FUR+NS, respectively; P<0.05) compared with CON. Peak mean Ppa was significantly reduced (P<0.05) for FUR (93.6±6.3 mmHg) and FUR+ NS (95.4±5.1 mmHg), yet unchanged with NS (98.0±5.8 mmHg; P>0.05) compared with CON (100.5±4.9 mmHg). All three experimental conditions exhibited a significant reduction in EIPH compared with CON (64.1±36.8× 6 red blood cells (RBCs) ml−1); however, no significant difference was noted between these conditions (×106 RBCs ml−1: 29.1±16.8, 20.9±13.1 and 26.7±19.8 for NS, FUR and FUR+NS, respectively). Furthermore, no differences for either end-exercise cardiorespiratory (i.e. V˙O2 or V˙CO2) or blood-borne metabolic (i.e. blood gases, lactate or pH) variables were observed. These findings demonstrate that both FUR and NS enhance TTF and reduce EIPH to a similar degree during high-speed treadmill running to fatigue. [ABSTRACT FROM PUBLISHER]

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? [ABSTRACT FROM PUBLISHER]