Interactive effects of exercise intensity and recovery posture on postexercise hypotension.

Postexercise reduction in blood pressure, termed postexercise hypotension (PEH), is relevant for both acute and chronic health reasons and potentially for peripheral cardiovascular adaptations. We investigated the interactive effects of exercise intensity and recovery postures (seated, supine, and standing) on PEH. Thirteen normotensive men underwent a V̇o2max test on a cycle ergometer and five exhaustive constant load trials to determine critical power (CP) and the gas exchange threshold (GET). Subsequently, work-matched exercise trials were performed at two discrete exercise intensities (10% > CP and 10% < GET), with 1 h of recovery in each of the three postures. For both exercise intensities, standing posture resulted in a more substantial PEH (all P < 0.01). For both standing and seated recovery postures, the higher exercise intensity led to larger reductions in systolic [standing: -33 (11) vs. -21 (8) mmHg; seated: -34 (32) vs. -17 (37) mmHg, P < 0.01], diastolic [standing: -18 (7) vs. -8 (5) mmHg; seated: -10 (10) vs. -1 (4) mmHg, P < 0.01], and mean arterial pressures [-13 (8) vs. -2 (4) mmHg, P < 0.01], whereas in the supine recovery posture, the reduction in diastolic [-9 (9) vs. -4 (3) mmHg, P = 0.08) and mean arterial pressures [-7 (5) vs. -3 (4) mmHg, P = 0.06] was not consistently affected by prior exercise intensity. PEH is more pronounced during recovery from exercise performed above CP versus below GET. However, the effect of exercise intensity on PEH is largely abolished when recovery is performed in the supine posture.NEW & NOTEWORTHY The magnitude of postexercise hypotension is greater following the intensity above the critical power in a standing position.

Critical power is a key threshold determining the magnitude of post-exercise hypotension in non-hypertensive young males.

The effect of different exercise intensities on the magnitude of post-exercise hypotension has not been rigorously clarified with respect to the metabolic thresholds that partition discrete exercise intensity domains (i.e., critical power and the gas exchange threshold (GET)). We hypothesized that the magnitude of post-exercise hypotension would be greater following isocaloric exercise performed above versus below critical power. Twelve non-hypertensive men completed a ramp incremental exercise test to determine maximal oxygen uptake and the GET, followed by five exhaustive constant load trials to determine critical power and W' (work available above critical power). Subsequently, criterion trials were performed at four discrete intensities matched for total work performed (i.e., isocaloric) to determine the impact of exercise intensity on post-exercise hypotension: 10% above critical power (10% > CP), 10% below critical power (10% < CP), 10% above GET (10% > GET) and 10% below GET (10% < GET). The post-exercise decrease (i.e., the minimum post-exercise values) in mean arterial (10% > CP: -12.7 ± 8.3 vs. 10% < CP: v3.5 ± 2.9 mmHg), diastolic (10% > CP: -9.6 ± 9.8 vs. 10% < CP: -1.4 ± 5.0 mmHg) and systolic (10% > CP: -23.8 ± 7.0 vs. 10% < CP: -9.9 ± 4.3 mmHg) blood pressures were greater following exercise performed 10% > CP compared to all other trials (all P < 0.01). No effects of exercise intensity on the magnitude of post-exercise hypotension were observed during exercise performed below critical power (all P > 0.05). Critical power represents a threshold above which the magnitude of post-exercise hypotension is greatly augmented. NEW FINDINGS: What is the central questions of this study? What is the influence of exercise intensity on the magnitude of post-exercise hypotension with respect to metabolic thresholds? What is the main finding and its importance? The magnitude of post-exercise hypotension is greatly increased following exercise performed above critical power. However, below critical power, there was no clear effect of exercise intensity on the magnitude of post-exercise hypotension.

Dissociation between exercise intensity thresholds: mechanistic insights from supine exercise.

This study tested the hypothesis that the respiratory compensation point (RCP) and breakpoint in deoxygenated [heme] [deoxy[heme]BP, assessed via near-infrared spectroscopy (NIRS)] during ramp incremental exercise would occur at the same metabolic rate in the upright (U) and supine (S) body positions. Eleven healthy men completed ramp incremental exercise tests in U and S. Gas exchange was measured breath-by-breath and time-resolved-NIRS was used to measure deoxy[heme] in the vastus lateralis (VL) and rectus femoris (RF). RCP (S: 2.56 ± 0.39, U: 2.86 ± 0.40 L·min-1, P = 0.02) differed from deoxy[heme]BP in the VL in U (3.10 ± 0.44 L·min-1, P = 0.002), but was not different in S in the VL (2.70 ± 0.50 L·min-1, P = 0.15). RCP was not different from the deoxy[heme]BP in the RF for either position (S: 2.34 ± 0.48 L·min-1, U: 2.76 ± 0.53 L·min-1, P > 0.05). However, the deoxy[heme]BP differed between muscles in both positions (P < 0.05), and changes in deoxy[heme]BP did not relate to ΔRCP between positions (VL: r = 0.55, P = 0.080, RF: r = 0.26, P = 0.44). The deoxy[heme]BP was consistently preceded by a breakpoint in total[heme], and was, in turn, itself preceded by a breakpoint in muscle surface electromyography (EMG). RCP and the deoxy[heme]BP can be dissociated across muscles and different body positions and, therefore, do not represent the same underlying physiological phenomenon. The deoxy[heme]BP may, however, be mechanistically related to breakpoints in total[heme] and muscle activity.

Impact of supine versus upright exercise on muscle deoxygenation heterogeneity during ramp incremental cycling is site specific.

PURPOSE: We tested the hypothesis that incremental ramp cycling exercise performed in the supine position (S) would be associated with an increased reliance on muscle deoxygenation (deoxy[heme]) in the deep and superficial vastus lateralis (VLd and VLs, respectively) and the superficial rectus femoris (RFs) when compared to the upright position (U). METHODS: 11 healthy men completed ramp incremental exercise tests in S and U. Pulmonary [Formula: see text]O2 was measured breath-by-breath; deoxy[heme] was determined via time-resolved near-infrared spectroscopy in the VLd, VLs and RFs. RESULTS: Supine exercise increased the overall change in deoxy[heme] from baseline to maximal exercise in the VLs (S: 38 ± 23 vs. U: 26 ± 15 µM, P < 0.001) and RFs (S: 36 ± 21 vs. U: 25 ± 15 µM, P < 0.001), but not in the VLd (S: 32 ± 23 vs. U: 29 ± 26 µM, P > 0.05). CONCLUSIONS: The present study supports that the impaired balance between O2 delivery and O2 utilization observed during supine exercise is a regional phenomenon within superficial muscles. Thus, deep muscle defended its O2 delivery/utilization balance against the supine-induced reductions in perfusion pressure. The differential responses of these muscle regions may be explained by a regional heterogeneity of vascular and metabolic control properties, perhaps related to fiber type composition.

August Krogh: Muscle capillary function and oxygen delivery.

The capillary bed constitutes the obligatory pathway for almost all oxygen (O2) and substrate molecules as they pass from blood to individual cells. As the largest organ, by mass, skeletal muscle contains a prodigious surface area of capillaries that have a critical role in metabolic homeostasis and must support energetic requirements that increase as much as 100-fold from rest to maximal exercise. In 1919 Krogh's 3 papers, published in the Journal of Physiology, brilliantly conflated measurements of muscle capillary function at rest and during contractions with Agner K. Erlang's mathematical model of O2 diffusion. These papers single-handedly changed the perception of capillaries from passive vessels serving at the mercy of their upstream arterioles into actively contracting vessels that were recruited during exercise to elevate blood-myocyte O2 flux. Although seminal features of Krogh's model have not withstood the test of time and subsequent technological developments, Krogh is credited with helping found the field of muscle microcirculation and appreciating the role of the capillary bed and muscle O2 diffusing capacity in facilitating blood-myocyte O2 flux. Today, thanks in large part to Krogh, it is recognized that comprehending the role of the microcirculation, as it supports perfusive and diffusive O2 conductances, is fundamental to understanding skeletal muscle plasticity with exercise training and resolving the mechanistic bases by which major pathologies including heart failure and diabetes cripple exercise tolerance and cerebrovascular dysfunction predicates impaired executive function.

Effect of differential muscle activation patterns on muscle deoxygenation and microvascular haemoglobin regulation.

NEW FINDINGS: What is the central question of this study? Does the presence and extent of heterogeneity in the ratio of O2 delivery to uptake across human muscles relate specifically to different muscle activation patterns? What is the main finding and its importance? During ramp incremental knee-extension and cycling exercise, the profiles of muscle deoxygenation (deoxy[haemoglobin + myoglobin]) and diffusive O2 potential (total[haemoglobin + myoglobin]) in the vastus lateralis corresponded to different muscle activation strategies. However, this was not the case for the rectus femoris, where muscle activation and deoxygenation profiles were dissociated and might therefore be determined by other structural and/or functional attributes (e.g. arteriolar vascular regulation and control of red blood cell flux). ABSTRACT: Near-infrared spectroscopy has revealed considerable heterogeneity in the ratio of O2 delivery to uptake as identified by disparate deoxygenation {deoxy[haemoglobin + myoglobin] (deoxy[Hb + Mb])} values in the exercising quadriceps. However, whether this represents a recruitment phenomenon or contrasting vascular and metabolic control, as seen among fibre types, has not been established. We used knee-extension (KE) and cycling (CE) incremental exercise protocols to examine whether differential muscle activation profiles could account for the heterogeneity of deoxy[Hb + Mb] and microvascular haemoconcentration (i.e. total[Hb + Mb]). Using time-resolved near-infrared spectroscopy for the quadriceps femoris (vastus lateralis and rectus femoris) during exhaustive ramp exercise in eight participants, we tested the following hypotheses: (i) the deoxy[Hb + Mb] (i.e. fractional O2 extraction) would relate to muscle activation levels across exercise protocols; and (ii) KE would induce greater total[Hb + Mb] (i.e. diffusive O2 potential) at task failure (i.e. peak O2 uptake) than CE irrespective of muscle site. At a given level of muscle activation, as assessed by the relative integrated EMG normalized to maximal voluntary contraction (%iEMGmax ), the vastus lateralis deoxy[Hb + Mb] profile was not different between exercise protocols. However, at peak O2 uptake and until 20% iEMGmax for CE, rectus femoris exhibited a lower deoxy[Hb + Mb] (83.2 ± 15.5 versus 98.2 ± 19.4 µm) for KE than for CE (P < 0.05). The total[Hb + Mb] at peak O2 uptake was not different between exercise protocols for either muscle site. These data support the hypothesis that the contrasting patterns of convective and diffusive O2 transport correspond to different muscle activation patterns in vastus lateralis but not rectus femoris. Thus, the differential deoxygenation profiles for rectus femoris across exercise protocols might be dependent upon specific facets of muscle architecture and functional haemodynamic events.

Unaltered V̇o2 kinetics despite greater muscle oxygenation during heavy-intensity two-legged knee extension versus cycle exercise in humans.

Relative perfusion of active muscles is greater during knee extension ergometry (KE) than cycle ergometry (CE). This provides the opportunity to investigate the effects of increased O2 delivery (Q̇o2) on deoxygenation heterogeneity among quadriceps muscles and pulmonary oxygen uptake (V̇o2) kinetics. Using time-resolved near-infrared spectroscopy, we hypothesized that compared with CE the superficial vastus lateralis (VL), superficial rectus femoris, and deep VL in KE would have 1) a smaller amplitude of the exercise-induced increase in deoxy[Hb + Mb] (related to the balance between V̇o2 and Q̇o2); 2) a greater amplitude of total[Hb + Mb] (related to the diffusive O2 conductance); 3) a greater homogeneity of regional muscle deoxy[Hb + Mb]; and 4) no difference in pulmonary V̇o2 kinetics. Eight participants performed square-wave KE and CE exercise from 20 W to heavy work rates. Deoxy[Hb + Mb] amplitude was less for all muscle regions in KE (P < 0.05: superficial, KE 17-24 vs. CE 19-40; deep, KE 19 vs. CE 26 µM). Furthermore, the amplitude of total[Hb + Mb] was greater for KE than CE at all muscle sites (P < 0.05: superficial, KE, 7-21 vs. CE, 1-16; deep, KE, 11 vs. CE, -3 µM). Although the amplitude and heterogeneity of deoxy[Hb + Mb] were significantly lower in KE than CE during the first minute of exercise, the pulmonary V̇o2 kinetics was not different for KE and CE. These data show that the microvascular Q̇o2 to V̇o2 ratio, and thus tissue oxygenation, was greater in KE than CE. This suggests that pulmonary and muscle V̇o2 kinetics in young healthy humans are not limited by Q̇o2 during heavy-intensity cycling.

Influence of dietary nitrate supplementation on local sweating and cutaneous vascular responses during exercise in a hot environment.

PURPOSE: We investigated the influence of inorganic nitrate ([Formula: see text]) supplementation on local sweating and cutaneous vascular responses during exercise in hot conditions. METHOD: Eight healthy, young subjects were assigned in a randomized, double-blind, crossover design to receive [Formula: see text]-rich beetroot (BR) juice (140 mL/day, containing ~ 8 mmol of [Formula: see text]) and [Formula: see text]-depleted placebo (PL) juice (140 mL/day, containing ~ 0.003 mmol of [Formula: see text]) for 3 days. On day 3 of supplementation, subjects cycled at an intensity corresponding to 55% of [Formula: see text]O2max for 30 min in hot conditions (30 °C, 50% relative humidity). Chest and forearm sweat rate (SR) and skin blood flow (SkBF), were measured continuously. Cutaneous vascular conductance (CVC) was calculated by SkBF/mean arterial pressure (MAP). RESULTS: Prior to exercise, plasma [Formula: see text] (21 ± 6 and 581 ± 161 µM) and nitrite ([Formula: see text], 87 ± 28 and 336 ± 156 nM) concentrations were higher after BR compared to PL supplementation (P ≤ 0.011, n = 6). Oesophageal, mean skin, and mean body temperatures during exercise were not different between conditions. In addition, BR supplementation did not affect SR, SkBF, and CVC during exercise. A lower MAP was found after 30 min of exercise following BR supplementation (112 ± 6 and 103 ± 6 mmHg for PL and BR, respectively, P = 0.021). CONCLUSION: These results suggest that inorganic [Formula: see text] supplementation, which increases the potential for O2-independent NO production, does not affect local sweating and cutaneous vascular responses, but attenuates blood pressure in young healthy subjects exercising in a hot environment.

Influence of forearm muscle metaboreceptor activation on sweating and cutaneous vascular responses during dynamic exercise.

We examined whether the sustained activation of metaboreceptor in forearm during cycling exercise can modulate sweating and cutaneous vasodilation. On separate days, 12 young participants performed a 1.5-min isometric handgrip exercise at 40% maximal voluntary contraction followed by 1) 9-min forearm ischemia (Occlusion, to activate metaboreceptor) or 2) no ischemia (Control) in thermoneutral conditions (27°C, 50%) with mean skin temperature clamped at 34°C. Thirty seconds after the handgrip exercise, participants cycled for 13.5 min at 40% V̇o2 max For Occlusion, forearm ischemia was maintained for 9 min followed by no ischemia thereafter. Local sweat rate (SR, ventilated capsule) and cutaneous vascular conductance (CVC, laser-Doppler perfusion units/mean arterial pressure) on the contralateral nonischemic arm as well as esophageal and skin temperatures were measured continuously. The period of ischemia in the early stages of exercise increased SR (+0.03 mg·cm(-2)·min(-1), P < 0.05) but not CVC (P > 0.05) above Control levels. No differences were measured in the esophageal temperature at which onset of sweating (Control 37.19 ± 0.09 vs. Occlusion 37.07 ± 0.09°C) or CVC (Control 37.21 ± 0.08 vs. Occlusion 37.08 ± 0.10°C) as well as slopes for these responses (all P > 0.05). However, a greater elevation in SR occurred thereafter such that SR was significantly elevated at the end of the ischemic period relative to Control (0.37 ± 0.05 vs. 0.23 ± 0.05 mg·cm(-2)·min(-1), respectively, P < 0.05) despite no differences in esophageal temperature. We conclude that the activation of forearm muscle metaboreceptor can modulate sweating, but not CVC, during cycling exercise without affecting the core temperature-SR relationship.

The Spatial Distribution of Absolute Skeletal Muscle Deoxygenation During Ramp-Incremental Exercise Is Not Influenced by Hypoxia.

Time-resolved near-infrared spectroscopy (TRS-NIRS) allows absolute quantitation of deoxygenated haemoglobin and myoglobin concentration ([HHb]) in skeletal muscle. We recently showed that the spatial distribution of peak [HHb] within the quadriceps during moderate-intensity cycling is reduced with progressive hypoxia and this is associated with impaired aerobic energy provision. We therefore aimed to determine whether reduced spatial distribution of skeletal muscle [HHb] was associated with impaired aerobic energy transfer during exhaustive ramp-incremental exercise in hypoxia. Seven healthy men performed ramp-incremental cycle exercise (20 W/min) to exhaustion at 3 fractional inspired O2 concentrations (FIO2): 0.21, 0.16, 0.12. Pulmonary O2 uptake ([Formula: see text]) was measured using a flow meter and gas analyser system. Lactate threshold (LT) was estimated non-invasively. Absolute muscle deoxygenation was quantified by multichannel TRS-NIRS from the rectus femoris and vastus lateralis (proximal and distal regions). [Formula: see text] and LT were progressively reduced (p<0.05) with hypoxia. There was a significant effect (p<0.05) of FIO2 on [HHb] at baseline, LT, and peak. However the spatial variance of [HHb] was not different between FIO2 conditions. Peak total Hb ([Hbtot]) was significantly reduced between FIO2 conditions (p<0.001). There was no association between reductions in the spatial distribution of skeletal muscle [HHb] and indices of aerobic energy transfer during ramp-incremental exercise in hypoxia. While regional [HHb] quantified by TRS-NIRS at exhaustion was greater in hypoxia, the spatial distribution of [HHb] was unaffected. Interestingly, peak [Hbtot] was reduced at the tolerable limit in hypoxia implying a vasodilatory reserve may exist in conditions with reduced FIO2.

Effect of stride frequency on thermoregulatory responses during endurance running in distance runners.

Changing stride frequency may influence oxygen uptake and heart rate during running as a function of running economy and central command. This study investigated the influence of stride frequency manipulation on thermoregulatory responses during endurance running. Seven healthy endurance runners ran on a treadmill at a velocity of 15km/h for 60min in a controlled environmental chamber (ambient temperature 27°C and relative humidity 50%), and stride frequency was manipulated. Stride frequency was intermittently manipulated by increasing and decreasing frequency by 10% from the pre-determined preferred frequency. These periods of increase or decrease were separated by free frequency running in the order of free stride frequency, stride frequency manipulation (increase or decrease), free stride frequency, and stride frequency manipulation (increase or decrease) for 15min each. The increased and decreased stride frequencies were 110% and 91% of the free running frequency, respectively (196±6, 162±5, and 178±5steps/min, respectively, P<0.01). Compared to the control, stride frequency manipulation did not affect rectal temperature, heart rate, or the rate of perceived exhaustion during running. Whole-body sweat loss increased significantly when stride frequency was manipulated (1.48±0.11 and 1.57±0.11kg for control and manipulated stride frequencies, respectively, P<0.05), but stride frequency had a small effect on sweat loss overall (Cohen's d=0.31). A higher mean skin temperature was also observed under mixed frequency conditions compared to that in the control (P<0.05). While the precise mechanisms underlying these changes remain unknown (e.g. running economy or central command), our results suggest that manipulation of stride frequency does not have a large effect on sweat loss or other physiological variables, but does increase mean skin temperature during endurance running.

Effects of aerobic exercise in early evening on the following nocturnal sleep and its haemodynamic response.

We determined effect of aerobic exercise in early evening on the quality, quantity, and haemodynamic response of subsequent nocturnal sleep in the home. Ten healthy young participants performed two protocols, with/without cycle ergometer exercise (60 min at 50% heart rate reserve) in early evening. Blood pressure (BP) (Holter) and physical activity (accelerometer) were measured from late afternoon of day 1 until noon of next day (day 2). Additionally, at bedtime participants were equipped with a small device worn on the wrist that identified sleep stage. There were no substantial differences in objective indices of sleep between two protocols (total sleep time: 438 ± 76 vs. 457 ± 64 min; P > 0.10). BP during nocturnal sleep tended to be lowered by prior exercise (MAP: 71 ± 5 vs. 68 ± 6 mmHg; P = 0.08). Aerobic exercise in early evening apparently has no acute effect on sleep per se, but seems to have a residual effect on haemodynamics, i.e. prolongation of post-exercise hypotension.

Modulation of muscle metaboreceptor activation upon sweating and cutaneous vascular responses to rising core temperature in humans.

The present study investigated the role of muscle metaboreceptor activation on human thermoregulation by measuring core temperature thresholds and slopes for sweating and cutaneous vascular responses during passive heating associated with central and peripheral mechanisms. Six male and eight female subjects inserted their lower legs into hot water (43°C) while wearing a water perfusion suit on the upper body (34°C). One minute after immersion, an isometric handgrip exercise--40% of maximum voluntary contraction-was conducted for 1.5 min in both control and experimental conditions, while postexercise occlusion was performed in the experimental condition only for 9 min. The postexercise forearm occlusion during passive heating consistently stimulated muscle metaboreceptors, as implicated by significantly elevated mean arterial blood pressure throughout the experimental period (P <0.05). Stimulation of the forearm muscle metaboreceptors increased sweating and cutaneous vascular responses during passive heating, and was associated with significant reductions in esophageal temperature threshold of sweating and cutaneous vasodilation (Δ threshold, sweating: 0.33 ± 0.05 and 0.16 ± 0.04°C, cutaneous vascular conductance: 0.38 ± 0.08 and 0.16 ± 0.05°C for control and experimental groups, respectively, P < 0.05). The slopes of these responses were not different between the conditions. These results suggest that muscle metaboreceptor activation in the forearm accelerates sweating and cutaneous vasodilation during passive heating associated with a reduction in core temperature thresholds and may be related to central mechanisms controlling heat loss responses.

Heterogeneity of Muscle Blood Flow and Metabolism: Influence of Exercise, Aging, and Disease States.

The systematic increase in V˙O2 uptake and O2 extraction with increasing work rates conceals a substantial heterogeneity of O2 delivery (Q˙O2)-to- V˙O2 matching across and within muscles and other organs. We hypothesize that whether increased/decreased Q˙O2/V˙O2 heterogeneity can be judged as "good" or "bad," for example, after exercise training or in aged individuals or with disease (heart failure, diabetes) depends on the resultant effects on O2 transport and contractile performance.

Effects of increased skin blood flow on muscle oxygenation/deoxygenation: comparison of time-resolved and continuous-wave near-infrared spectroscopy signals.

PURPOSE: We quantified the contribution of skin blood flow (SkBF) to tissue oxygenation/deoxygenation of the flexor digitorum profundus muscle during cutaneous vasodilation. METHODS: Time-resolved near-infrared spectroscopy (TRS-NIRS) was utilized to measure the potential influence of optical factors [mean optical pathlength (PL) and coefficients of absorption (µa) and reduced scattering ([Formula: see text])] on the NIRS-derived signals of eight male subjects. RESULTS: The approximately threefold elevation of SkBF during 1 h whole-body heating (increased internal temperature ~0.9 °C) increased both µa and [Formula: see text] without changing PL. Assuming that the [Formula: see text] coefficient remained constant, i.e., as with continuous-wave (CW) NIRS, resulted in a significant increase in the apparent oxygenation [oxy(Hb + Mb), from 113 ± 13 µM (mean ± SD) for control to 126 ± 13 for the increased SkBF condition, P < 0.01]: this was in marked contrast to the unchanged TRS-derived values. The deoxygenation [deoxy(Hb + Mb)] also increased from control to elevated SkBF (CW-NIRS, from 39 ± 8 to 45 ± 7; TRS, from 38 ± 6 to 44 ± 7 µM; P < 0.01 for both), but less than that seen for oxy(Hb + Mb) and not different between TRS- and CW-NIRS. Further, and in contrast to oxy(Hb + Mb), temporal profiles of deoxy(Hb + Mb) measured by the two NIRS methods were not different. CONCLUSIONS: These findings support use of either NIRS method to estimate local muscle fractional O2 extraction, but not oxygenation, when SkBF is increased at rest.

Sweating response to passive stretch of the calf muscle during activation of forearm muscle metaboreceptors in heated humans.

Activation of muscle metaboreceptors and mechanoreceptors has been shown to independently influence the sweating response, while their integrative control effects remain unclear. We examined the sweating response when the two muscle receptors are concurrently activated in different limbs, as well as the blood pressure response. In total, 27 young males performed passive calf muscle stretches (muscle mechanoreceptor activation) for 30 s in a semisupine position with and without postisometric handgrip exercise muscle ischemia (PEMI, muscle metaboreceptor activation) at exercise intensities of 35 and 50% of maximum voluntary contraction (MVC) under hot conditions (ambient temperature, 35°C, relative humidity, 50%). Passive calf muscle stretching alone increased the mean sweating rate significantly on the forehead, chest, and thigh (SRmean) and mean arterial blood pressure (MAP), but not the heart rate (HR), from prestretching levels by 0.04 ± 0.01 mg·cm(2)·min(-1), 4.0 ± 1.3 mmHg (P < 0.05), and -1.0 ± 0.5 beats/min (P > 0.05), respectively. The SRmean and MAP during PEMI were significantly higher than those at rest. The passive calf muscle stretch during PEMI increased MAP significantly by 3.4 ± 1.0 and 2.0 ± 0.7 mmHg for 35 and 50% of MVC, respectively (P < 0.05), but not that of SRmean or HR at either exercise intensity. These results suggest that sweating and blood pressure responses to concurrent activation of the two muscle receptors in different limbs differ and that the influence of calf muscle mechanoreceptor activation alone on the sweating response disappears during forearm muscle metaboreceptor activation.

Slowed oxygen uptake kinetics in hypoxia correlate with the transient peak and reduced spatial distribution of absolute skeletal muscle deoxygenation.

It remains unclear whether an overshoot in skeletal muscle deoxygenation (HHb; reflecting a microvascular kinetic mismatch of O2 delivery to consumption) contributes to the slowed adjustment of oxidative energy provision at the onset of exercise. We progressively reduced the fractional inspired O2 concentration (F(I,O2)) to investigate the relationship between slowed pulmonary O2 uptake (V(O2)) kinetics and the dynamics and spatial distribution of absolute[HHb]. Seven healthy men performed 8 min cycling transitions during normoxia (F(I,O2) = 0.21),moderate hypoxia (F(I,O2) = 0.16) and severe hypoxia (F(I,O2)= 0.12). V(O2) uptake was measured using a flowmeter and gas analyser system. Absolute [HHb] was quantified by multichannel,time-resolved near-infrared spectroscopy from the rectus femoris and vastus lateralis (proximal and distal regions), and corrected for adipose tissue thickness. The phase II V(O2) time constant was slowed (P <0.05) as F(I,O2) decreased (normoxia, 17 ± 3 s;moderate hypoxia, 22 ± 4 s; and severe hypoxia, 29 ± 9 s). The [HHb] overshoot was unaffected by hypoxia, but the transient peak [HHb] increased with the reduction in F(I,O2) (P <0.05). Slowed V(O2) kinetics in hypoxia were positively correlated with increased peak [HHb] in the transient (r(2) = 0.45; P <0.05), but poorly related to the [HHb] overshoot. A reduction of spatial heterogeneity in peak [HHb]was inversely correlated with slowed V(O2) kinetics (r(2) = 0.49; P <0.05). These data suggest that aerobic energy provision at the onset of exercise may be limited by the following factors: (i) the absolute ratio (i.e. peak [HHb]) rather than the kinetic ratio (i.e. [HHb] overshoot) of microvascular O2 delivery to consumption; and (ii) a reduced spatial distribution in the ratio of microvascular O2 delivery to consumption across the muscle.

Characteristics of sweating responses and peripheral sweat gland function during passive heating in sprinters.

The purpose of this study was to compare sweating function in sprinters who have trained for several years with untrained subjects and trained endurance runners. Two separate experiments were conducted. Nine sprinters, eight untrained men, and nine distance runners (VO2 max 50.9 ± 1.4, 38.2 ± 1.8, and 59.1 ± 1.2 mL/kg/min, respectively; P < 0.05) were passively heated for 50 min (Experiment 1), and ten sprinters, 11 untrained men and nine distance runners (similar VO2 max levels compared with Experiment 1 in each group) had their sweat gland capacity assessed based on acetylcholine-induced sweating rate (SR) (Experiment 2). The slope of the mean non-glabrous SR plotted against change in mean body temperature during passive heating did not differ significantly between sprinters and untrained men (1.21 ± 0.10 and 0.97 ± 0.12 mg cm(-2)/min/°C, respectively); in contrast, compared with untrained men, distance runners exhibited a significantly greater slope (1.42 ± 0.11 mg cm(-2)/min/°C, P < 0.05). The mean body temperature threshold for SR was not significantly different among the groups. Acetylcholine-induced SR did not differ significantly between sprinters and untrained men, whereas distance runners showed a significantly higher induced SR compared with untrained men. The sweating function was not improved in sprinters who have trained 2-3 h/day, 5 days/week, for at least 3 years compared with untrained men, although the VO2 max was markedly greater in sprinters. Thus, there is a case that daily training was not sufficient to improve sweating function in sprinters relative to those in distance runners.