H. H. Erickson

Wearable sensor system for wireless state-of-health determination in cattle

Wearable systems for human and animal state-of-health determination share many design requirements. This paper discusses the design of a remote health monitoring system for cattle that hosts a suite of sensors and communicates wirelessly with a base station via Bluetooth telemetry.

Nitric oxide synthase inhibition speeds oxygen uptake kinetics in horses during moderate domain running

Within the moderate exercise intensity domain, the speed of oxygen uptake (V(O(2))) kinetics at the transition to a higher metabolic rate is thought to be limited by an inertia of the oxidative machinery. Nitric oxide (NO)-induced inhibition of O(2) consumption within the electron transport chain may contribute to this inertia. This investigation tested the hypothesis that a reduction or removal of any such NO effect via infusion of N(omega)-nitro-L-arginine methyl ester (L-NAME; a NOS inhibitor) would speed V(O(2)) kinetics at the onset of moderate exercise. Five Thoroughbred geldings underwent four transitions to running speeds of 7 m sec(-1) (two control, C, 2 L-NAME [20 mg kg(-1)]) on an equine treadmill during which pulmonary gas exchange was determined using a bias flow system. Consistent with exercise in the moderate intensity domain, in none of the transitions was a V(O(2)) slow component elicited. The L-NAME treatment significantly accelerated V(O(2)) kinetics via a reduction of the primary amplitude time constant (C, 17.3 +/- 1.7; L-NAME, 11.8 +/- 1.5 sec, P < 0.05) concomitant with faster overall dynamics (i.e. T(50) and T(75) both P < 0.05) and a trend toward a decreased O(2) deficit (C, 6.4 +/- 0.7; L-NAME, 4.7 +/- 1.2 L; P = 0.06). These data support the notion that NO contributes prominently to the oxidative enzyme inertia and thus the speed of V(O(2)) kinetics at the onset of moderate intensity exercise in the horse.

Relationship of pulmonary arterial pressure to pulmonary haemorrhage in exercising horses

Exercise-induced pulmonary haemorrhage (EIPH) is characterised by blood in the airways after strenuous exercise and results from stress failure of the pulmonary capillaries. The purpose of this experiment was to establish a threshold value of transmural pulmonary arterial pressure at which haemorrhage occurs in the exercising horse. Five geldings, age 4-14 years, were run in random order once every 2 weeks at 1 of 4 speeds (9, 11, 13, 15 m/s); one day with no run was used as a control. Heart rate, pulmonary arterial pressure and oesophageal pressure were recorded for the duration of the run. Transmural pulmonary arterial pressure was estimated by electronic subtraction of the oesophageal pressure from the intravascular pulmonary arterial pressure. Within 1 h of the run, bronchoalveolar lavage was performed and the red and white blood cells in the fluid were quantified. Red cell counts in the lavage fluid from horses running at 9, 11 and 13 m/s were not significantly different from the control value, but after runs at 15 m/s, red cell counts were significantly (P<0.05) higher. White cell counts were not different from control values at any speed. Analysis of red cell count vs. transmural pulmonary arterial pressure indicated that haemorrhage occurs at approximately 95 mmHg. Red cell lysis in the lavage fluid was also apparent at transmural pulmonary arterial pressures above 90 mmHg. We conclude that, in the exercising horse, a pulmonary arterial pressure threshold exists above which haemorrhage occurs, and that pressure is often exceeded during high speed sprint exercise.

Cardiorespiratory impact of the nitric oxide synthase inhibitor L-NAME in the exercising horse.

To investigate the role of nitric oxide, NO, in facilitating cardiorespiratory function during exercise, five horses ran on a treadmill at speeds that yielded 50, 80 and 100% of peak pulmonary oxygen uptake (V(O(2)) peak) as determined on a maximal incremental test. Each horse underwent one control (C) and one (NO-synthase inhibitor; N(G)-L-nitro-arginine methyl ester (L-NAME), 20 mg/kg) trial in randomized order. Pulmonary gas exchange (open flow system), arterial and mixed-venous blood gases, cardiac output (Fick Principle), and pulmonary and systemic conductances were determined. L-NAME reduced exercise tolerance, as well as cardiac output (C, 291+/-34; L-NAME, 246+/-38 L/min), body O(2) delivery (C, 74.4+/-5. 5; L-NAME, 62.1+/-5.6 L/min), and both pulmonary (C, 3.07+/-0.26; L-NAME, 2.84+/-0.35 L/min per mmHg) and systemic (C, 1.55+/-0.24; L-NAME, 1.17+/-0.16 L/min per mmHg) effective vascular conductances at peak running speeds (all P<0.05). On the 50 and 80% trials, L-NAME increased O(2) extraction, which compensated for the reduced body O(2) delivery and prevented a fall in V(O(2)). However, at peak running speed in the L-NAME trial, an elevated O(2) extraction (P<0. 05) was not sufficient to prevent V(O(2)) from falling consequent to the reduced O(2) delivery. At the 50 and 80% running speeds (as for peak), L-NAME reduced pulmonary and systemic effective conductances. These data demonstrate that the NO synthase inhibitor, L-NAME, induces a profound hemodynamic impairment at submaximal and peak running speeds in the horse thereby unveiling a potentially crucial role for NO in mediating endothelial function during exercise.

Highly Athletic Terrestrial Mammals: Horses and Dogs

Evolutionary forces drive beneficial adaptations in response to a complex array of environmental conditions. In contrast, over several millennia, humans have been so enamored by the running/athletic prowess of horses and dogs that they have sculpted their anatomy and physiology based solely upon running speed. Thus, through hundreds of generations, those structural and functional traits crucial for running fast have been optimized. Central among these traits is the capacity to uptake, transport and utilize oxygen at spectacular rates. Moreover, the coupling of the key systems--pulmonary-cardiovascular-muscular is so exquisitely tuned in horses and dogs that oxygen uptake response kinetics evidence little inertia as the animal transitions from rest to exercise. These fast oxygen uptake kinetics minimize Intramyocyte perturbations that can limit exercise tolerance. For the physiologist, study of horses and dogs allows investigation not only of a broader range of oxidative function than available in humans, but explores the very limits of mammalian biological adaptability. Specifically, the unparalleled equine cardiovascular and muscular systems can transport and utilize more oxygen than the lungs can supply. Two consequences of this situation, particularly in the horse, are profound exercise-induced arterial hypoxemia and hypercapnia as well as structural failure of the delicate blood-gas barrier causing pulmonary hemorrhage and, in the extreme, overt epistaxis. This chapter compares and contrasts horses and dogs with humans with respect to the structural and functional features that enable these extraordinary mammals to support their prodigious oxidative and therefore athletic capabilities.

Effects of external nasal support on pulmonary gas exchange and EIPH in the horse

Abstract In the horse during high-speed running, partial collapse of the unsupported nasal airways may contribute to elevated inspiratory resistance. This effect would be expected to increase respiratory muscle work and augment negative intrapulmonary pressure swings which in turn might exacerbate exercise-induced pulmonary hemorrhage (EIPH). To investigate this issue, six Thoroughbreds and one Quarter Horse were evaluated while running at high speed (12±1 m/s) under control conditions (C) and wearing an external nasal dilator (ND) in individual, randomly ordered trials two weeks apart. Whole-body gas exchange (oxygen uptake, VO 2 , carbon dioxide output, VCO 2 ), arterial blood gases, acid-base and blood temperature were measured. Compared with C, ND significantly reduced VO 2 (C, 59.9±5.3; ND, 56.4±5.0 L/min, P 2 . However, neither arterial blood gases, acid-base, blood temperature nor plasma lactate were changed significantly. Bronchoalveolar lavage (BAL) revealed a 33% (P 2 and reduce EIPH. It is possible that these effects are secondary to a decreased inspiratory resistance, lowered inspiratory muscle work and altered intrapulmonary pressures.

A distributed infrastructure for veterinary telemedicine

The livestock industry can benefit tremendously from systems that continuously monitor cattle state-of-health, allowing the industry to maintain high meat quality, react to the presence of disease, and predict its spread. Requirements for these monitoring systems are similar to requirements that drive human ambulatory monitoring systems based on wearable sensors and wireless data communication. This paper presents early results from an effort to develop a veterinary telemedicine infrastructure based upon wearable monitoring technology originally developed for home health care. The functional layout of the infrastructure is described, and initial hardware and physiological measurements are presented.

The effect of treadmill incline on maximal oxygen uptake, gas exchange and the metabolic response to exercise in the horse

In healthy man, conditions that change muscle O2 delivery affect the achievable maximum rate of O2 uptake (V̇O2,max) as well as the metabolic (e.g. lactate threshold, LT) and gas exchange (e.g. gas exchange threshold, Tge) responses to incremental exercise. Inclined (I) compared to level (L) running increases locomotory muscle EMG at a given speed in the horse, indicative of elevated metabolic demand. To our knowledge, the effect of treadmill incline on V̇O2,max, LT and Tge has not been addressed in the exercising quadruped. We used blood sampling and breath‐by‐breath expired gas analysis to test the hypothesis that I (10% gradient) would increase V̇O2,max and the rate of O2 uptake (V̇O2) at LT and Tge in six Thoroughbred horses during incremental running to volitional fatigue. V̇O2,max was significantly higher for I (I, 77.8 ± 4.1; L, 65.5 ± 5.3 I min−1; P < 0.05), but peak plasma lactate concentration was not (I, 28.0 ± 3.7; L, 25.9 ± 3.0 mM). Arterial PCO2 increased to 62.1 ± 3.3 and 57.9 ± 2.7 Torr (I vs. L; P < 0.05), yet despite this relative hypoventilation, a distinct Tge was present. This Tge occurred at a significantly different absolute (I, 49.6 ± 3.2; L, 42.4 ± 3.2 I min−1; P < 0.05), but nearly identical relative V̇O2 (I, 63.6 ± 1.2; L, 63.9 ± 1.6% V̇O2,max) in I and L. Similarly, LT occurred at a significantly greater absolute V̇O2 (I, 37.3 ± 2.8; L, 26.9 ± 2.1 1 min−1), but a relative V̇O2 that was not different (I, 47.9 ± 2.1; L, 43.9 ± 4.5% V̇O2,max). In addition, Tge occurred at a significantly higher (P ≤ 0.05) absolute and relative V̇O2 than LT for both I and L tests. In conclusion, V̇O2,max is higher during inclined than level running and both LT and Tge in the horse occur at a similar percentage of V̇O2,max irrespective of the absolute level of V̇O2,max. In contrast to humans, LT is a poor analogue of Tge in the horse.

Inclined running increases pulmonary haemorrhage in the Thoroughbred horse.

REASONS FOR PERFORMING STUDY Capillary stress failure-induced (exercise-induced) pulmonary haemorrhage (EIPH) during intense running in horses is thought to involve both intravascular (i.e. mean pulmonary arterial pressure [Ppa] > 100 mmHg) and extravascular (e.g. negative inspiratory pressure swings) mechanisms. HYPOTHESIS That inclined running would reduce breathing frequency (coupled to stride frequency) and increase tidal volume thus increasing lung volume changes and intrapleural pressure swings resulting in more pronounced EIPH. METHODS Six Thoroughbred horses were run to volitional fatigue (incremental step test) on a level (L) and inclined (I; 10%) treadmill in random order. Pulmonary minute ventilation, arterial blood gases and mean Ppa were obtained during each run while EIPH severity was quantified via bronchoalveolar lavage (BAL) 30 mins post run. RESULTS Time to fatigue did not differ between trials (P > 0.05). At end-exercise, breathing frequency was reduced (L, 127.8 +/- 3.0; I, 122.6 +/- 2.1 breaths/min; P < 0.05) and tidal volume increased (L, 11.5 +/- 0.6; I, 13.1 +/- 0.5 L; P < 0.05) during inclined running. No differences existed in end-exercise plasma [lactate] between trials (L, 24.5 +/- 2.9; I, 26.2 +/- 3.4 mmol/l, P > 0.05); however, the mean peak Ppa was reduced during the inclined run (L, 105+5; I, 96 +/- 4 mmHg, P < 0.05). In the face of reduced Ppa, EIPH severity was increased significantly (P < 0.05) during the inclined vs. level run (L, 37.0 +/- 11.7; I, 49.6 +/- 17.0 x 10(6) red blood cells/ml BAL fluid). CONCLUSIONS Although inclined running lowered peak Ppa, EIPH severity was increased. It is likely that this effect resulted, in part, from an altered ventilatory pattern (i.e. increased tidal volumes and associated intrapleural pressure changes). POTENTIAL RELEVANCE This conclusion supports an important role for extravascular factors in the aetiology of EIPH.

The effect of herbal supplementation on the severity of exercise-induced pulmonary haemorrhage

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 (×10 6 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