Identification of maximal steady-state metabolic rate by the change in muscle oxygen saturation.

We tested the hypothesis that a %SmO (muscle O saturation) slope can distinguish the heavy-severe exercise domain boundary and the highest steady-state metabolic rate. Thirteen participants (5 women) performed a graded exercise test (GXT) to determine peak oxygen consumption (V̇o) and lactate turn point (LTP). On a separate study day, a %SmO zero-slope prediction trial included completing 5-min cycling bouts in an estimated heavy domain, at an estimated critical power, and in an estimated severe domain.

Transcutaneous delivery of sodium bicarbonate increases intramuscular pH.

Oral bicarbonate loading improves the buffering of metabolic acidosis and may improve exercise performance but can also result in gastric distress. Momentous' PR Lotion contains a novel composition intended to provide a transdermal delivery vehicle for sodium bicarbonate which could allow the same ergogenic effect without the gastric distress. The present study explored the effect of transdermal delivery of sodium bicarbonate in a resting condition.

Interaction of exercise bioenergetics with pacing behavior predicts track distance running performance.

The best possible finishing time for a runner competing in distance track events can be estimated from their critical speed (CS) and the finite amount of energy that can be expended above CS (D´). During tactical races with variable pacing, the runner with the "best" combination of CS and D´ and, therefore, the fastest estimated finishing time prior to the race, does not always win. We hypothesized that final race finishing positions depend on the relationships between the pacing strategies used, the athletes' initial CS, and their instantaneous D´ (i.

The impact of elevated body core temperature on critical power as determined by a 3-min all-out test.

Critical power (CP) delineates the heavy and severe exercise intensity domains, and sustained work rates above CP result in an inexorable progression of oxygen uptake to a maximal value and, subsequently, the limit of exercise tolerance. The finite work capacity above CP, W', is defined by the curvature constant of the power-duration relationship. Heavy or severe exercise in a hot environment generates additional challenges related to the rise in body core temperature (T) that may impact CP and W'.

The balance of muscle oxygen supply and demand reveals critical metabolic rate and predicts time to exhaustion.

We tested the hypothesis that during whole body exercise, the balance between muscle O supply and metabolic demand may elucidate intensity domains, reveal a critical metabolic rate, and predict time to exhaustion. Seventeen active, healthy volunteers (12 males, 5 females; 32 ± 2 yr) participated in two distinct protocols. ( = 7) consisted of constant work rate cycling in the moderate, heavy, and severe exercise intensity domains with concurrent measures of pulmonary V̇o and local %SmO [via near-infrared spectroscopy (NIRS)] on quadriceps and forearm sites.

Physiological demands of running at 2-hour marathon race pace.

The requirements of running a 2-h marathon have been extensively debated but the actual physiological demands of running at ∼21.1 km/h have never been reported. We therefore conducted laboratory-based physiological evaluations and measured running economy (O cost) while running outdoors at ∼21.

Dynamics of the power-duration relationship during prolonged endurance exercise and influence of carbohydrate ingestion.

We tested the hypotheses that the parameters of the power-duration relationship, estimated as the end-test power (EP) and work done above EP (WEP) during a 3-min all-out exercise test (3MT), would be reduced progressively after 40 min, 80 min, and 2 h of heavy-intensity cycling and that carbohydrate (CHO) ingestion would attenuate the reduction in EP and WEP. Sixteen participants completed a 3MT without prior exercise (control), immediately after 40 min, 80 min, and 2 h of heavy-intensity exercise while consuming a placebo beverage, and also after 2 h of heavy-intensity exercise while consuming a CHO supplement (60 g/h CHO). There was no difference in EP measured without prior exercise (260 ± 37 W) compared with EP after 40 min (268 ± 39 W) or 80 min (260 ± 40 W) of heavy-intensity exercise; however, after 2 h EP was 9% lower compared with control (236 ± 47 W; < 0.

Changes in the power-duration relationship following prolonged exercise: estimation using conventional and all-out protocols and relationship with muscle glycogen.

It is not clear how the parameters of the power-duration relationship [critical power (CP) and W'] are influenced by the performance of prolonged endurance exercise. We used severe-intensity prediction trials (conventional protocol) and the 3-min all-out test (3MT) to measure CP and W' following 2 h of heavy-intensity cycling exercise and took muscle biopsies to investigate possible relationships to changes in muscle glycogen concentration ([glycogen]). Fourteen participants completed a rested 3MT to establish end-test power (Control-EP) and work done above EP (Control-WEP).

Critical Velocity during Intermittent Running with Changes of Direction.

Purpose: We tested the hypothesis that critical velocity (CV) during intermittent running with changes of direction is reliably and accurately identified from a simple shuttle field test. We also tested the hypothesis that CV during intermittent running with changes of direction running is not equivalent to continuous linear running.

Methods: Young adults performed a custom shuttle test of intermittent sprint running to reveal CV.

Effects of Two Hours of Heavy-Intensity Exercise on the Power-Duration Relationship.

Introduction: Changes in the parameters of the power-time relationship (critical power (CP) and W') during endurance exercise would have important implications for performance. We tested the hypotheses that CP and W', estimated using the end-test power (EP) and the work done above EP (WEP), respectively, during a the 3-min all-out test (3MT), can be reliably determined, and would be lower, after completing 2 h of heavy-intensity exercise.

Methods: In study 1, six cyclists completed a 3MT immediately after 2 h of heavy-intensity exercise on two occasions to establish the reliability of EP and WEP.

Potentiation of the NO-cGMP pathway and blood flow responses during dynamic exercise in healthy humans.

Purpose: Previous work has shown nitric oxide (NO) contributes to ~15% of the hyperemic response to dynamic exercise in healthy humans. This NO-mediated vasodilation occurs, in part, via increases in intracellular cyclic guanosine monophosphate (cGMP), which is catabolized by phosphodiesterase. We sought to examine the effect of phosphodiesterase-5 (PDE-5) inhibition on forearm blood flow (FBF) responses to dynamic handgrip exercise in healthy humans and the role of NO.

Exercise is medicine in cystic fibrosis.

Exercise activates adrenergic and purinergic pathways that regulate activity of ion channels on airway epithelia cells and sweat glands. Therefore, we hypothesize that exercise is not only an important therapy for cystic fibrosis (CF) patients by facilitating systemic improvements but, more importantly, that exercise can improve the pathophysiological ion dysregulation at a cellular level, thereby enhancing quality of life in CF.

Nitric oxide-mediated vasodilation becomes independent of beta-adrenergic receptor activation with increased intensity of hypoxic exercise.

Hypoxic vasodilation in skeletal muscle at rest is known to include β-adrenergic receptor-stimulated nitric oxide (NO) release. We previously reported that the augmented skeletal muscle vasodilation during mild hypoxic forearm exercise includes β-adrenergic mechanisms. However, it is unclear whether a β-adrenergic receptor-stimulated NO component exists during hypoxic exercise.

Roles of nitric oxide synthase and cyclooxygenase in leg vasodilation and oxygen consumption during prolonged low-intensity exercise in untrained humans.

The vasodilator signals regulating muscle blood flow during exercise are unclear. We tested the hypothesis that in young adults leg muscle vasodilation during steady-state exercise would be reduced independently by sequential pharmacological inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX) with NG-nitro-L-arginine methyl ester (L-NAME) and ketorolac, respectively. We tested a second hypothesis that NOS and COX inhibition would increase leg oxygen consumption (VO2) based on the reported inhibition of mitochondrial respiration by nitric oxide.

Nitric oxide contributes to the augmented vasodilatation during hypoxic exercise.

We tested the hypotheses that (1) nitric oxide (NO) contributes to augmented skeletal muscle vasodilatation during hypoxic exercise and (2) the combined inhibition of NO production and adenosine receptor activation would attenuate the augmented vasodilatation during hypoxic exercise more than NO inhibition alone. In separate protocols subjects performed forearm exercise (10% and 20% of maximum) during normoxia and normocapnic hypoxia (80% arterial O(2) saturation). In protocol 1 (n = 12), subjects received intra-arterial administration of saline (control) and the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA).

Adenosine receptor antagonist and augmented vasodilation during hypoxic exercise.

We tested the hypothesis that adenosine contributes to augmented skeletal muscle vasodilation during hypoxic exercise. In separate protocols, subjects performed incremental rhythmic forearm exercise (10% and 20% of maximum) during normoxia and normocapnic hypoxia (80% arterial O2 saturation). In protocol 1 (n = 8), subjects received an intra-arterial administration of saline (control) and aminophylline (adenosine receptor antagonist).

Exercise intensity-dependent contribution of beta-adrenergic receptor-mediated vasodilatation in hypoxic humans.

We previously reported that hypoxia-mediated reductions in alpha-adrenoceptor sensitivity do not explain the augmented vasodilatation during hypoxic exercise, suggesting an enhanced vasodilator signal. We hypothesized that beta-adrenoceptor activation contributes to augmented hypoxic exercise vasodilatation. Fourteen subjects (age: 29 +/- 2 years) breathed hypoxic gas to titrate arterial O(2) saturation (pulse oximetry) to 80%, while remaining normocapnic via a rebreath system.

Arterial baroreflex control of heart rate during exercise in postural tachycardia syndrome.

Patients with postural tachycardia syndrome (POTS) have excessive tachycardia without hypotension during orthostasis as well as exercise. We tested the hypothesis that excessive tachycardia during exercise in POTS is not related to abnormal baroreflex control of heart rate (HR). Patients (n = 13) and healthy controls (n = 10) performed graded cycle exercise at 25, 50, and 75 W in both supine and upright positions while arterial pressure (arterial catheter) and HR (ECG) were measured.

Exercise hyperaemia: is anything obligatory but the hyperaemia?

Exercise can increase skeletal muscle blood flow by 100-fold over values observed at rest. As this value was 3 to 4 times higher than so-called 'textbook' values at the time it raised a number of issues about cardiovascular control. However, there is a continuing inability to identify the factor or combination of factors that explain this substantial increase in muscle blood flow.

Reduced stroke volume during exercise in postural tachycardia syndrome.

Postural tachycardia syndrome (POTS) is characterized by excessive tachycardia without hypotension during orthostasis. Most POTS patients also report exercise intolerance. To assess cardiovascular regulation during exercise in POTS, patients (n = 13) and healthy controls (n = 10) performed graded cycle exercise at 25, 50, and 75 W in both supine and upright positions while arterial pressure (arterial catheter), heart rate (HR; measured by ECG), and cardiac output (open-circuit acetylene breathing) were measured.

Preserved reflex cutaneous vasodilation in cystic fibrosis does not include an enhanced nitric oxide-dependent mechanism.

In humans, vasoactive intestinal peptide (VIP) may play a role in reflex cutaneous vasodilation during body heating. We tested the hypothesis that the nitric oxide (NO)-dependent contribution to active vasodilation is enhanced in the skin of subjects with cystic fibrosis (CF), compensating for sparse levels of VIP. In 2 parallel protocols, microdialysis fibers were placed in the skin of 11 subjects with CF and 12 controls.