Peripheral triiodothyronine (T(3)) levels during escapable and inescapable footshock

Changes in peripheral thyroid hormone levels are associated with changes in human affective disorders, particularly depression. In the current study we used an animal stress paradigm, proposed to be an animal model of depression, to examine peripheral T(3) levels during and after escapable or inescapable stress in adult male rats. In this model, one animal can control the termination of foot-shock stress by performing a lever press, and therefore experiences escapable stress. His lever press also terminates the shock for his yoked partner, who has no control over the stressor, and therefore experiences inescapable stress. In three separate experiments, blood samples were collected during and after one or two sessions of escapable/inescapable stress. We found that exposure to inescapable stress, but not escapable stress, caused a decrease in T(3) levels 120 min post-stress initiation. Peripheral T(3) levels were not significantly altered in animals exposed to escapable stress. In sum, these results add to a large body of previous data indicating that psychological coping can prevent the effects of physical stress on many diverse systems.     

Absence of long-term modulation of ventilation by dead-space loading during moderate exercise in humans

The stability of arterial PCO₂ (P_aCO₂) during moderate exercise in humans suggests a CO₂-linked control that matches ventilation (_E) to pulmonary CO₂ clearance (CO₂). An alternative view is that _E is subject to long-term modulation (LTM) induced by hyperpnoeic history. LTM has been reported with associative conditioning via dead-space (V_D) loading in exercising goats (Martin and Mitchell 1993). Whether this prevails in humans is less clear, which may reflect differences in study design (e.g. subject familiarisation; V_D load; whether or not _E is expressed relative to CO₂; choice of P_aCO₂ estimator). After familiarisation, nine healthy males performed moderate constant-load cycle-ergometry (20 W-80 W-20 W; <lactate threshold, _L): day 1, pre-conditioning, n=3; day 2, conditioning (V_D=1.59 l, doubling _E at 20 W and 80 W), n=8 with 10 min rest between tests; and, after 1 h rest, post-conditioning, n=3. Gas exchange was determined breath-by-breath. Post-conditioning, neither the transient [phase 1, phase 2 (1, 2)] nor steady-state _E exercise responses, nor their proportionality to CO₂, differed from pre-conditioning. For post-conditioning trial 1, steady-state _E was 28.1 (4.7) l min^–1 versus 29.1 (3.8) l min^–1 pre-conditioning, and mean-alveolar PCO₂ (a validated P_aCO₂ estimator) was 5.53 (0.48) kPa [41.5 (3.6) mmHg] versus 5.59 (0.49) kPa [41.9 (3.7) mmHg]; the 1 _E increment was 4.2 (2.9) l min^–1 versus 5.2 (1.9) l min^–1; the 2 _E time-constant () was 64.4 (24.1) s versus 64.1 (25.3) s; _E/CO₂ was 1.12 (0.04) versus 1.10 (0.04); and the _E-CO₂ slope was 21.7 (3.4) versus 21.2 (3.2). In conclusion, we could find no evidence to support ventilatory control during moderate exercise being influenced by hyperpnoeic history associated with dead-space loading in humans.     

Comparison of arterial,end-tidal and transcutaneous PCO2 during moderate exercise and external C02 loading in humans

Summary Static relationships between arterial, transcutaneous[/p] and end-tidal PCO₂ (P _aCO₂, P _tc CO ₂, P _etCO₂) as well as the dynamic relationship between P _etCO₂ and P _tcCO₂ were studied during moderate bicycle ergometer exercise with and without external C0₂ loading. The exercise pattern consisted of 5-min intervals of constant power at 40 W and 100 W and 900 s of randomised changes between these two power levels. The external CO₂ loading was achieved by means of controlled variations of inspiratory gas compositions aimed at a constant P _etCO₂ of 6.5 kPa (49 mm Hg). The P_etO2 was regulated at 17.3 kPa (130 mm Hg). Under steady-state conditions all PCO₂ parameters showed close linear relationships. P _aCO₂/P _tcCO₂ was near to identity while the P _etCO₂ systematically overestimated changes in P _aCO₂. No relationship showed a significant influence of the exercise intensity. Transients of P _tcCO₂ are considerably slower than P _etCO₂ transients. The dynamic relationship between both parameters was found to be independent of whether internal or external C0₂ loadings were applied. It is concluded that the combination of P _etCO₂ and P _tcCO₂ measurements allows an improved non-invasive assessment of P _aCO₂. While P _etC0₂ better reflects the transients, P _tcCO₂ can be employed to determine slow changes of the absolute P _aCO₂.     

The relation of ventilation to metabolic rate during moderate exercise in man

Summary To characterize more precisely the relationship between ventilation (V _E) and CO₂ output (VCO₂) during incremental exercise, 35 healthy males were studied at rest and during upright cycle ergometry, with the work rate incremented every 4 min up to each subject's anaerobic threshold ( _an). Twenty-one subjects had arterial blood sampled at rest and in the steady state at each work rate to determine the relationship between physiological dead space ventilation (V _D) and VCO₂. At these work rates arterial PCO₂ was regulated at the resting, control value. V _E (BTPS) was linearly related to VCO₂ from rest to _an with a slope of 24.6. However, the regression had a significant positive intercept of 3.2 L·min^–1. This causes the ventilatory equivalent for CO₂ (i.e., V _E/VCO₂) to decrease with increasing work rates. V _D also increased linearly with increasing VCO₂. However, this was consequent to increased breathing frequency as V _D remained constant. Thus, the observed fall in V _E/VCO₂ with increasing work rates is due to the positive intercept but the inherent relationship between V _E and VCO₂, reflected by the linear regression slope, remains unchanged from rest through moderate exercise.This investigation was supported by National Institutes of Health Grant HL-11907     

Thyroid function and thyroid hormone metabolism in elderly people low T3-syndrome in old age?

Summary T₄-, T₃- and reverse-T₃ concentrations were measured in the sera of 365 subjects beyond the age of 65 in order to evaluate if the decrease of serum T₃ frequently observed in old age can be attributed to old age per se or to concomitant non-thyroidal disease. The results obtained from a carefully selected healthy group of elderly people show that 1) total and free T₃ levels are lower in senescence but well within the range for euthyroidism in younger healthy controls; 2) the decrease of serum T₃ is more pronounced and occurs earlier in healthy old males than in females, so that for subjects over the age of 75, the upper limit for euthyroidism has to be adjusted by 10% in women and by 20% in men; and 3) there is no low T₃ syndrome characterized by decreased serum T₃ and increased serum reverse T₃, solely due to old age.Turnover kinetics have shown the daily production of T₄ and T₃ in old age to decrease by 20 µg and 10 µg, respectively, and an increased T₃ metabolic clearance not to account for the reduction of serum T₃ concentrations. Combined stimulation tests with TSH and TRH showed that the functional reserve of the thyroid gland to produce T₃ is maintained in old age. The first step in the sequence of events may be seen in an impairment of TSH secretion leading to an adaptation of the amount of thyroid hormones to a reduced mass of metabolically active body tissue in old age.     

The effect of prolonged submaximal exercise on gas exchange kinetics and ventilation during heavy exercise in humans

This study compared ventilation, gas exchange (oxygen uptake, V̇O₂) and the surface electromyogram (EMG) activity of four major lower limb muscles during heavy exercise before (Pre-Ex) and after (Post-Ex) a sustained 90-min cycling exercise at 60% V̇O_2peak. The 90-min exercise was incorporated under the hypothesis that sustained exercise would alter substrate availability in the second exercise bout causing differences in fibre recruitment patterns, gas exchange and ventilation. Nine trained male subjects [V̇O_2peak=60.2 (1.7) ml·kg⁻¹·min⁻¹] completed two identical 6-min bouts of cycling performed at high intensity [~90% V̇O_2peak; 307 (6) W, mean (SE)]. Ventilation and gas exchange were measured breath-by-breath and the EMG was recorded during the last 12 s of each minute of the two 6-min bouts. EMG signals were analysed to determine integrated EMG (iEMG) and mean power frequency (MPF). V̇O₂ at min 3 and min 6 in Post-Ex were significantly higher (i.e., +201 and 141 ml·min⁻¹, respectively, P<0.05) than in Pre-Ex but there was a ~25% decrease of the slow component, taken as the difference between min 6 and min 3 [187 (27) vs 249 (35) ml·min⁻¹, respectively, P<0.05]. The greater whole-body V̇O₂ after 3 min of exercise in Post-Ex was not accompanied by clear alterations in the iEMG and MPF of the examined leg muscles. Ventilation and heart rate were elevated (~12–16 l·min⁻¹ and ~10 beats·min⁻¹, respectively, P<0.05) as were the ratios V̇ _E/O₂ and V̇ _E/V̇CO₂ in the Post-Ex tests. It was concluded that the V̇O₂ and ventilation responses to high-intensity exercise can be altered following prolonged moderate intensity exercise in terms of increased amplitude without associated major changes in either iEMG or MPF values among conditions.     

The influences of thermal stress on serum biochemical parameters of Iranian fat-tailed sheep and their correlation with triiodothyronine (T3), thyroxine (T4) and cortisol concentrations

In order to study the influences of thermal stress on serum biochemical parameters of Iranian fat-tailed sheep and their correlation with triiodothyronine (T₃), thyroxine (T₄) and cortisol concentrations, an experiment was conducted using 45 clinically healthy Iranian fat-tailed sheep. These animals were divided into three experimental groups: group I, 15 sheep at 4 °C, group II 15 sheep at 21 °C and group III 15 sheep at 40 °C. Blood samples were taken from the jugular vein of all animals after 7 days exposure to the appropriate environmental temperature. The concentrations of total protein, glucose, cholesterol, total lipid, calcium, inorganic phosphorus, magnesium, creatine kinase, lactate dehydrogenase, triiodothyronine and thyroxine in cold stress conditions were higher than in heat stress; in contrast, the activities of aspartate aminotransferase and alanine aminotransferase were higher in heat stress conditions than in cold (p = <0.05). Although there were no significant differences in the concentrations of blood urea nitrogen, triglyceride, alkaline phosphatase and cortisol at either heat stress or cold stress, the first three assays were significantly lower than in animals kept at optimum temperatures, with cortisol having significantly higher values. These results revealed that very hot and very cold conditions had a profound effect on serum biochemical parameters.Abbreviations ALT alanine aminotransferase - AST aspartate aminotransferase - BUN blood urea nitrogen - LD lactate dehydrogenase - CK creatine kinase - ALP alkaline phosphatase     

TRH-refraktäre TSH-Werte,Trijodthyroninspiegel und T3/T4-Quotienten bei mit T3/T4-Kombinationspräparaten behandelten hypothyreoten Kindern

Zusammenfassung Bei 23 Kindern mit primärer Hypothyreose, die mit Thyroxin (T₄) und Trijodthyronin (T₃) enthaltenden Kombinationspräparaten behandelt worden waren, wurden TRH-Teste, TBI, T₃- und T₄-Bestimmungen durchgeführt. Die T₃/T₄-Quotienten wurden berechnet. 7 von 10 Patienten mit TRH-refraktären TSH-Werten und normalen T₄-Spiegeln wiesen überhöhte T₃-Werte auf. Bei 6 von diesen Patienten konnten pathologisch überhöhte T₃/T₄-Quotienten beobachtet werden. Eine TRH-refraktäre TSH-Suppression wurde nur bei hohen T₄-Werten gefunden. Nach einer Reduktion der Substitutionsdosis normalisierten sich die überhöhten T₃-Spiegel. Die Befunde zeigen, daß nicht nur die T₄-Werte sondern auch die TSH- und T₃-Spiegeln unter der Behandlung mit Schilddrüsenhormonen kontrolliert werden sollten. Die Durchführung der Substitutionstherapie der Hypothyreose mit T₃/T₄-Kombinationspräparaten im Verhältnis 1:4 sollte überdacht werden.     

Die T3-Hyperthyreose unter den Aspekten der Sekretion und peripheren Produktion der Schilddrüsenhormone

Zusammenfassung Bei der T₃-Hyperthyreose ist im Vergleich zu der T₄/T₃-Hyperthyreose nur das T₃ erhöht, während das T₄ und das r-T₃ im Normbereich liegen. Die endogene Markierung des T₄ ist auch bei der T₃-Hyperthyreose erhöht, so daß eine vermehrte T₄-Sekretion angenommen werden muß. Die normalen T₄-Konzentrationen dürften aus einer verstärkten T₄-Dejodination resultieren. Als Ursache für das hohe T₃ bei gleichzeitig normalem r-T₃ wird eine Richtungsumkehr der Dejodination des T₄ zum T₃ zu ungunsten des r-T₃ diskutiert.Mit Unterstützung durch die Deutsche Forschungsgemeinschaft (SFB87/B6 und H₁)     

T8-positive lymphocytes in inflammatory infiltrates of the vessel wall in nonspecific aorto-arteritis

Institute of Experimental Cardiology, All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR. A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR D. S. Sarkisov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 105, No. 6 pp. 718–720, June, 1988.     

A method for assessing muscle fatigue during sprint exercise in humans using a friction-loaded cycle ergometer

This study investigated the mechanical changes induced by muscle fatigue caused by repeated sprints and determined whether a friction-loaded cycle ergometer has any advantages for assessing muscle fatigue. Nine subjects performed 15 sprints, each of 5 s with a 25-s rest, on a friction-loaded cycle ergometer. The averaged force, power and velocity of each push-off were calculated. Maximal power decreased by 17.9%, with a concomittent slowing of muscle contraction, but without any change in the maximal force. These results demonstrated that repeated sprints slow down muscle contraction, leading to a fall in maximal power without any loss of force. This would suggest that fast twitch fibres are selectively fatigued by repeated sprints. However, the ergometer used in the present study made it difficult to evaluate the relative influences of contraction velocity and sprinting time. This was certainly the most important limitation. On the other hand, it showed the advantage of measuring instantaneous power and total work dissipated in the environment simultaneously. It also permitted a force-velocity relationship to be obtained from a single sprint and this relationship is known to be closely related to the muscle fibre composition. Accepted: 5 March 1998     

Arterial H+ regulation during exercise in humans

Resting arterial H+ concentration ([H+]a) is in the nanomolar range (40±2 nm/L) while its production is in the millimolar range/min, with little variation from subject to subject. To determine the precision with which [H(+)]a is regulated during exercise, [H+]a, PaCO2 and ventilation (V˙(E)) were measured during progressively increasing work rate exercise in 16 normal subjects. (V˙(E)) increased with [H+]a, the latter attributable to PaCO2 increase below the lactic acidosis threshold (LAT) (ΔV˙(E)/Δ[H+]a ≈ 15 L min(-1) nanomol(-1)). [H+]a and PaCO2 increased, simultaneously, as work rate was increased below LAT. PaCO2 reversed direction of change between LAT and ventilatory compensation point (VCP). Above LAT, [H+]a increase relative to (V˙(E)) increase was greater than below LAT. PaCO2 decreased above the LAT, while [H+]a continued to increase. Thus the exercise acidosis was converted from respiratory, below, to a metabolic, above the LAT. We conclude that [H+]a is increased and regulated over the full range of exercise, but with less sensitivity above the LAT.     

A comparison of various methods for the determination of VO2max

Summary Previous studies have shown that true maximal oxygen uptake (VO₂max) obtained by means of cycle ergometer and step test are lower than the VO₂max measured during uphill treadmill running. The predicted VO₂max measured by ergometer was even lower. Four different methods for the determination of VO₂max within the same group of examinees were compared: True VO₂max by treadmill, ergometer, step test, and predicted VO₂max (Astrand-Rhyming). This study was performed on 15 healthy non-professional sportsmen. They underwent progressive test protocols on alternating days and the results were as follows — VO₂max expressed in ml O₂ kg BW/min (mean±SD): treadmill running 63.8±4.7; ergometer cycling 60.2±5.6; step test 59.6±5.2 and predicted VO₂max 59.9±6.9.The VO₂max as determined by uphill treadmill running was significantly higher than with the other methods. No significant difference was found between true VO₂max determined by the ergometer and step test. However, step test and properly executed Astrand-Rhyming test again proved to be reliable and deviate from the treadmill test by only 6%. Maximal heart rate was sgnificantly higher in the treadmill and step tests than in the direct ergometer test.     

Thyrotropic hormone (TSH) regulation of triiodothyronine (T3) concentration in immune cells

Objective:  Cells of the immune system (peritoneal lymphocytes, monocytes, granulocytes and mast cells as well as thymocytes) contain triiodothyronine (T₃). The aim of the present experiments was to study whether thyrotropic hormone (TSH) regulates or not the T₃ concentration of these cells. Methods:  Peritoneal fluid and thymus cells of adult rats were studied by immunocytochemistry, combined with flow cytometry for triiodothyronine content with or without in-vitro TSH treatment. In addition, adult female CD1 mice were treated in vivo with 10 or 40 mU TSH and after 1 hour peritoneal immune cells were studied using the above mentioned method. Results:  Both in vitro (in rat) and in vivo (in mice) TSH treatments significantly elevated the T₃ content in each cell type. In vitro TSH 0.1 mU/ml cell suspension was enough to provoke about 50 % increase in T₃ production. Conclusion:  T₃ concentration in immune cells seems to be regulated by TSH, similarly to the T₃ in the thyroid. Considering the large number of immune cells in an organism, TSH regulation of their T₃ content could have an important physiological and pathological role, both in and beyond the immune system. Received 15 April 2008; returned for revision 19 May 2008; received from final revision 20 May 2008; accepted by I. Ahnfeld-R?nne 23 June 2008     

Circulating cytokines and hormones with immunosuppressive but neutrophil-priming potentials rise after endurance exercise in humans

To investigate the mechanisms of exercise-induced immune perturbations, we measured promising immunomodulatory hormones and cytokines in plasma of 16 male marathon runners before and after a competitive 42.195-km race. Interleukin 1-beta (IL-1β) and interferon gamma (IFN-γ) concentrations remained unchanged after the marathon. The cytokines IL-12, IFN-α and tumour necrosis factor alpha (TNF-α) could not be detected even using highly sensitive specific immunoassays, indicating at least that overshooting responses of these cytokines had not occurred after exercise. As mechanisms for the small changes in these cytokines, we demonstrated for the first time a significant rise in concentrations of inhibitory cytokine IL-10 in addition to the immunosuppressive hormone cortisol, although concentrations of IL-4 and transforming growth factor-beta (TGF-β) were unaffected by the race. Furthermore, concentrations of IL-1 receptor antagonist (IL-1ra) and IL-6, which are negative-feedback inhibitors of cytokine production, increased by more than 100 times. As for humoral mediators of neutrophil mobilization, concentrations of growth hormone (GH), cortisol and granulocyte colony-stimulating factor (G-CSF) increased significantly. In addition, concentrations of neutrophil-priming substances (IL-6, IL-8, G-CSF, GH and prolactin) also increased significantly and the induction of IL-8 and G-CSF with exercise was demonstrated for the first time in the present study. In contrast, IL-2 concentration decreased, by 32%, and this was correlated with the induction of nitric oxide (NO) production. Muscle damage, monitored using changes in concentrations of creatine kinase and myoglobin, was also observed. These results suggested that exercise-induced pathogenesis including previously reported immunosuppression and neutrophil hyper-reactivity might be attributed, at least partly, to the systemic dynamics of the above bioactive substances. Accepted: 30 August 1999     

Arterial carbon dioxide estimates during upper body exercise

Summary The purpose of this investigation was to develop a regression equation to predict arterial carbon dioxide tensions (PaCO₂) from end-tidal carbon dioxide tensions (PETCO₂) during upper body exercise. A secondary purpose was to examine the ability of an existing regression equation developed for lower body exercise (Jones et al. 1979) to predict PaCO₂ during upper body exercise. Nine male subjects completed a progressive intensity, discontinuous test on an arm crank ergometer with submaximal power output (PO) levels of 25, 74, and 98 W. During each submaximal PO level, steady state oxygen uptake was achieved and appropriate physiological responses were measured. PETCO₂ was found to be significantly (p<0.05) higher than PaCO₂ at both the 74 and 98 W levels. In addition, when PETCO₂'s were regressed against their corresponding PaCO₂ tensions a correlation coefficient of r=0.66 was found. Based upon our subjects' PETCO₂ and tidal volume (V_T) responses, a multiple regression equation was constructed to predict their PaCO₂ (SPaCO₂), this being SPaCO₂=24.7+0.43 PETCO₂–3.3 V_T. When SPaCO₂ was regressed against the corresponding PaCO₂ tension, a correlation coefficient of r=0,84 was found. When the equation of Jones et al. (1979) was used to predict PaCO₂ a correlation coefficient of r=0.77 was found. No significant differences were found between tensions predicted by either equation and the actual PaCO₂ at any PO level. These results indicate that either prediction equation can be satisfactorily used to estimate PaCO₂ tensions during upper body exercise.Supported by the Medical Research Services of the Veterans Administration, NIH Grant No. 7RO1NS16003-01 and by Air Force Contract No. F33615-78-0501     

Immunocytochemical detection of effects of TRH and T4 on prolactin- and TSH-producing cells in the pituitary gland of Rana ridibunda

Effects of synthetic thyrotropin-releasing hormone (TRH) and various doses of thyroxin (T4) on prolactin (PRL)-producing cells and thyrotropic cells in the pituitary were investigated in adult male and female Rana ridibunda frogs. Animals were given 200 microg TRH once a week for 4 weeks and 0.2-0.5 mg T4 during 3 days per week for a period of 2 weeks by injections in the groin. PRL-producing cells and thyrotropic cells were identified with light microscopical and electron microscopical immunocytochemical methods, using rabbit anti-PRL and rabbit anti-thyroid stimulating hormone (TSH) as primary antibodies. TRH caused cytological changes in both cell types, which were consistent with increased synthesis and release of both PRL and TSH. Treatment with 0.5 mg T4 activated both cell types less than TRH treatment did, whereas 0.2 and 0.4 mg T4 caused inactivation of both cell types. In conclusion, mammalian TRH is effective on both types of frog pituitary cells. Our study suggests that T4 has a positive rather than a negative effect when concentrations above a certain threshold are given.     

Transcutaneous,noninvasiveP O 2 monitoring in adults during exercise and hypoxemia

A new, commercially available, transcutaneous (tc)P _{O 2} monitor was tested in adult females and in laboratory animals to assess its applicability in measuring arterial oxygen tension during physiological stress. Observed values on dogs correlated well with direct measurements of arterialP _{O 2} and with previous data obtained from measurements of arterial blood during exercise and hypoxemia. In our female subjects the unit responded rapidly to changes in inspired ambient oxygen and electrical stability was excellent during maximal exercise tests. TranscutaneousP _{O 2} decreased to an average of 87.8 Torr during maximum exercise breathing 20.9% O₂, and to 32 Torr while breathing 12.6% O₂ at maximum work. Two distinct patterns of response in tcP _{O 2} were observed during hypoxic and normoxic exercise. The technique appears to have substantial future application both in clinical and physiological investigation involving adult subjects.     

CO2 dissociation curves of oxygenated whole blood obtained at rest and in exercise

Summary In vitro CO₂ dissociation curves for oxygenated whole blood were determined in 19 healthy male subjects at rest and during submaximal and maximal bicycle work. Hemoglobin concentration and blood lactate increased with increasing work load and accordingly buffer value of the whole blood increased while bicarbonate and Base Excess (BE) decreased, resulting in a downward shift of the CO₂ dissociation curve during exercise. Despite the marked increase in buffer values of the blood, the slopes of the CO₂ dissociation curves during exercise were found to be about the same as those obtained at rest. It was inferred that the increasing effect of increased buffer value, on the dissociation slope, was essentially compensated by the decreasing effect of diminished bicarbonate content. The advantages of this relatively constant CO₂ dissociation slope for the indirect measurement of cardiac output by the Fick principle are discussed.     

Recovery dynamics of skeletal muscle oxygen uptake during the exercise off-transient

The time course of muscle recovery from contractions (i.e., muscle off-kinetics), measured directly at the site of O₂ exchange, i.e., in the microcirculation, is unknown. Whereas biochemical models based upon creatine kinase flux rates predict slower off- than on-transients [Kushmerick, M.J., 1998. Comp. Biochem. Physiol. B: Biochem. Mol. Biol.] whole muscle data [Krustrup, et al. J. Physiol.] suggest on–off symmetry.

Purpose

We tested the hypothesis that the slowed recovery blood flow (Qm) kinetics profile in the spinotrapezius muscle [Ferreira et al., 2006. J. Physiol.] was associated with a slowed muscle recovery compared with that seen at the onset of contractions (time constant, τ  23 s, Behnke et al., 2002. Resp. Physiol.), i.e., on–off asymmetry.

Methods

Measurements of capillary red blood cell flux and microvascular pressure of O₂ (P_O2mv) were combined to resolve the temporal profile of muscle across the moderate intensity contractions-to-rest transition.

Results

Muscle decreased from an end-contracting value of 7.7 ± 0.2 ml/100 g/min to 1.7 ± 0.1 ml/100 g/min at the end of the 3 min recovery period, which was not different from pre-stimulation . Contrary to our hypothesis, muscle in recovery began to decrease immediately (i.e., time delay <2 s) and demonstrated rapid first-order kinetics (τ, 25.5 ± 2.6 s) not different (i.e., symmetrical to) to those during the on-transient. This resulted in a systematic increase in microvascular P_O2 during the recovery from contractions.

Conclusions

The slowed Qm kinetics in recovery serves to elevate the ratio and thus microvascular P_O2. Whether this Qm response is obligatory to the rapid muscle kinetics and hence speeds the repletion of high-energy phosphates by maximizing conductive and diffusive O₂ flux is an important question that awaits resolution.