John Halliwill is an expert on post-exercise hypotension, in which a person's blood pressure drops after workouts. He directs the UO's Exercise and Environmental Physiology Lab, is co-director of the Evonuk Environmental Physiology Core and was a co-founder of the Bowerman Sports Science Clinic. Halliwill has sought to identify hormonal, neural or metabolic factors responsible for heart-related changes during exposure to environmental and physical stresses. He also is seeking to understand the mechanisms that underlie beneficial effects of exercise, particularly in aging populations. He has studied conditions faced by astronauts, helped Olympic athletes prepare to compete in environmental extremes, and tested equipment for the U.S. Marines.
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New study by UO researchers suggests allergy medication may hinder athletic performance
John Halliwill, a leading researcher in post-exercise blood pressure at the UO, is trying to answer that question.
He says that when someone exercises, they activate a certain number of genes in their muscles. This activation is the beginning of a process that creates bigger, stronger muscles. In his research, he found that over a quarter of the genes activated were driven by histamine receptors, the same receptors that allergy medication deactivate.
“[The activation is] that initial step in what eventually helps us become faster, stronger and more fatigue resistant … More than a quarter of those genes were being either driven or modulated by histamine receptors,” Halliwill said...
Are antihistamines worth it before a big workout?
John Halliwill, a professor in the department of human physiology at the University of Oregon, discovered in 2005 that naturally occurring histamines in the body relax blood vessels, increasing blood flow that aids post-exercise recovery. That emerged from his original focus on why some people, including athletes, pass out after vigorous physical exertion. He later found a link between an overactivation of two histamine receptors to drops in blood pressure.
Should exercisers lay off the antihistamines?
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However, a newly published study from the UO lab of John Halliwill has raised such questions. The research found that 795 (about 27 percent) of 3,000 genes activated after vigorous exercise become blunted in their responses during a three-hour recovery period if exercisers had taken strong doses of antihistamines...
Histamine contributes to elevations in skeletal muscle blood flow following exercise, which raises the possibility that histamine is an important mediator of the inflammatory response to exercise. We examined the influence of antihistamines on postexercise blood flow, inflammation, muscle damage, and delayed-onset muscle soreness (DOMS) in a model of moderate exercise-induced muscle damage. Subjects consumed either a combination of fexofenadine and ranitidine (blockade, n = 12) or nothing (control, n = 12) before 45 min of downhill running (-10% grade). Blood flow to the leg was measured before and throughout 120 min of exercise recovery. Markers of inflammation, muscle damage, and DOMS were obtained before and at 0, 6, 12, 24, 48, and 72 h postexercise. At 60 min postexercise, blood flow was reduced ~29% with blockade compared with control (P < 0.05). Markers of inflammation were elevated after exercise (TNF-ɑ, IL-6), but did not differ between control and blockade. Creatine kinase concentrations peaked 12 h after exercise, and the overall response was greater with blockade (18.3 ± 3.2 kU·l-1·h-1) compared with control (11.6 ± 2.0 kU·l-1·h-1; P < 0.05). Reductions in muscle strength in control (-19.3 ± 4.3% at 24 h) were greater than blockade (-7.8 ± 4.8%; P < 0.05) and corresponded with greater perceptions of pain/discomfort in control compared with blockade. In conclusion, histamine-receptor blockade reduced postexercise blood flow, had no effect on the pattern of inflammatory markers, increased serum creatine kinase concentrations, attenuated muscle strength loss, and reduced pain perception following muscle-damaging exercise.NEW & NOTEWORTHY Histamine appears to be intimately involved with skeletal muscle during and following exercise. Blocking histamine's actions during muscle-damaging exercise, via common over-the-counter antihistamines, resulted in increased serum creatine kinase, an indirect marker of muscle damage. Paradoxically, blocking histamine's actions attenuated muscle strength loss and reduced perceptions of muscle pain for 72 h following muscle-damaging exercise. These results indicate that exercise-induced histamine release may have a broad impact on protecting muscle from exercise-induced damage.
In humans, acute aerobic exercise elicits a sustained postexercise vasodilation within previously active skeletal muscle. This response is dependent on activation of histamine H1 and H2 receptors, but the source of intramuscular histamine remains unclear. We tested the hypothesis that interstitial histamine in skeletal muscle would be increased with exercise and would be dependent on de novo formation via the inducible enzyme histidine decarboxylase and/or mast cell degranulation. Subjects performed 1 h of unilateral dynamic knee-extension exercise or sham (seated rest). We measured the interstitial histamine concentration and local blood flow (ethanol washout) via skeletal muscle microdialysis of the vastus lateralis. In some probes, we infused either α-fluoromethylhistidine hydrochloride (α-FMH), a potent inhibitor of histidine decarboxylase, or histamine H1/H2-receptor blockers. We also measured interstitial tryptase concentrations, a biomarker of mast cell degranulation. Compared with preexercise, histamine was increased after exercise by a change (Δ) of 4.2 ± 1.8 ng/ml (P < 0.05), but not when α-FMH was administered (Δ-0.3 ± 1.3 ng/ml, P = 0.9). Likewise, local blood flow after exercise was reduced to preexercise levels by both α-FMH and H1/H2 blockade. In addition, tryptase was elevated during exercise by Δ6.8 ± 1.1 ng/ml (P < 0.05). Taken together, these data suggest that interstitial histamine in skeletal muscle increases with exercise and results from both de novo formation and mast cell degranulation. This suggests that exercise produces an anaphylactoid signal, which affects recovery, and may influence skeletal muscle blood flow during exercise.NEW & NOTEWORTHY Blood flow to previously active skeletal muscle remains elevated following an acute bout of aerobic exercise and is dependent on activation of histamine H1 and H2 receptors. The intramuscular source of histamine that drives this response to exercise has not been identified. Using intramuscular microdialysis in exercising humans, we show both mast cell degranulation and formation of histamine by histidine decarboxylase contributes to the histamine-mediated vasodilation that occurs following a bout of aerobic exercise.
Recovery from exercise refers to the time period between the end of a bout of exercise and the subsequent return to a resting or recovered state. It also refers to specific physiological processes or states, occurring after exercise, which are distinct from the physiology of either the exercising or the resting states. In this context, recovery of the cardiovascular system after exercise occurs across a period of minutes to hours, during which many characteristics of the system, even how it is controlled, are changing over time. Some of these changes may be necessary for long-term adaptation to exercise training, yet some can lead to cardiovascular instability during recovery. Further, some of these changes may provide insight into when the cardiovascular system has recovered from prior training and is physiologically ready for additional training stress. This review focuses on the most consistently observed hemodynamic adjustments and the underlying causes that drive cardiovascular recovery and will highlight how they differ following resistance and aerobic exercise. Primary emphasis will be placed on the hypotensive effect of aerobic and resistance exercise and associated mechanisms that have clinical relevance, but if left unchecked, can progress to symptomatic hypotension and syncope. Finally, we will focus on the practical application of this information to strategies to maximize the benefits of cardiovascular recovery, or minimize the vulnerabilities of this state. We will explore appropriate field measures, and discuss to what extent these can guide an athlete's training.
This study examined the impact of heat acclimation on improving exercise performance in cool and hot environments. Twelve trained cyclists performed tests of maximal aerobic power (V̇o2max), time-trial performance, and lactate threshold, in both cool [13°C, 30% relative humidity (RH)] and hot (38°C, 30% RH) environments before and after a 10-day heat acclimation (∼50% V̇o2max in 40°C) program. The hot and cool condition V̇o2max and lactate threshold tests were both preceded by either warm (41°C) water or thermoneutral (34°C) water immersion to induce hyperthermia (0.8–1.0°C) or sustain normothermia, respectively. Eight matched control subjects completed the same exercise tests in the same environments before and after 10 days of identical exercise in a cool (13°C) environment. Heat acclimation increased V̇o2max by 5% in cool (66.8 ± 2.1 vs. 70.2 ± 2.3 ml·kg−1·min−1, P = 0.004) and by 8% in hot (55.1 ± 2.5 vs. 59.6 ± 2.0 ml·kg−1·min−1, P = 0.007) conditions. Heat acclimation improved time-trial performance by 6% in cool (879.8 ± 48.5 vs. 934.7 ± 50.9 kJ, P = 0.005) and by 8% in hot (718.7 ± 42.3 vs. 776.2 ± 50.9 kJ, P = 0.014) conditions. Heat acclimation increased power output at lactate threshold by 5% in cool (3.88 ± 0.82 vs. 4.09 ± 0.76 W/kg, P = 0.002) and by 5% in hot (3.45 ± 0.80 vs. 3.60 ± 0.79 W/kg, P < 0.001) conditions. Heat acclimation increased plasma volume (6.5 ± 1.5%) and maximal cardiac output in cool and hot conditions (9.1 ± 3.4% and 4.5 ± 4.6%, respectively). The control group had no changes in V̇o2max, time-trial performance, lactate threshold, or any physiological parameters. These data demonstrate that heat acclimation improves aerobic exercise performance in temperate-cool conditions and provide the scientific basis for employing heat acclimation to augment physical training programs.
The study of microvascular function can be performed in humans using laser Doppler flowmetry of the skin. This technology lends itself to a wide range of applications for studying the endothelial function of skin blood vessels. We review the advantages and limitations of postocclusive hyperemia, local thermal hyperemia, acetylcholine iontophoresis, flowmotion and association with microdialysis as tools with which to investigate skin microvascular endothelial function in humans. Postocclusive hyperemia, thermal hyperemia and acetylcholine iontophoresis provide integrated indexes of microvascular function rather than specific endothelial markers. However, they are valuable tools and can be used as surrogate endpoints in clinical trials in which the assessment of microvascular function in humans is required.