The acute effects of passive heating on endothelial function, muscle microvascular oxygen delivery, and expression of serum HSP90α.

Passive heating has been a therapeutic tool used to elevate core temperature and induce increases in cardiac output, blood flow, and shear stress. We aimed to determine the effects of a single bout of passive heating on endothelial function and serum heat shock protein 90α (HSP90α) levels in young, healthy subjects. 8 healthy subjects were recruited to participate in one bout of whole-body passive heating via immersion in a 40 °C hot tub to maintain a 1 °C increase in rectal temperature for 60 min. Twenty-four hours after heating, shear-rate corrected endothelium-dependent dilation increased (pre: 0.004 ± 0.002%SRAUC; post: 0.006 ± 0.003%SRAUC; p = 0.034) but serum [HSP90α] was not changed (pre: 36.7 ± 10.3 ng/mL; post: 40.6 ± 15.9 ng/mL; p = 0.39). Neither resting muscle O2 utilization (pre: 0.17 ± 0.11 mL O2 min-1 (100 g)-1; post: 0.14 ± 0.09 mL O2 min-1 (100 g)-1); p = 0.28) nor mean arterial pressure (pre: 74 ± 11 mmHg; post: 73 ± 11 mmHg; p = 0.79) were influenced by the heating intervention. Finally, time to peak after cuff release was significantly delayed for % O2 sat (TTPpre = 39 ± 8.9 s and TTPpost = 43.5 ± 8.2 s; p = 0.007) and deoxy-[heme] (TTPpre = 41.3 ± 18.1 s and TTPpost = 51.4 ± 16.3 s; p = 0.018), with no effect on oxy-[heme] (p = 0.19) and total-[heme] (p = 0.41). One bout of passive heating improved endothelium-dependent dilation 24 h later in young, healthy subjects. This data suggests that passive heat treatments may provide a simple intervention for improving vascular health.

Post-occlusive reactive hyperemia and skeletal muscle capillary hemodynamics.

Post-occlusive reactive hyperemia (PORH) is an accepted diagnostic tool for assessing peripheral macrovascular function. While conduit artery hemodynamics have been well defined, the impact of PORH on capillary hemodynamics remains unknown, despite the microvasculature being the dominant site of vascular control. Therefore, the purpose of this investigation was to determine the effects of 5 min of feed artery occlusion on capillary hemodynamics in skeletal muscle. We tested the hypothesis that, upon release of arterial occlusion, there would be: 1) an increased red blood cell flux (fRBC) and red blood cell velocity (VRBC), and 2) a decreased proportion of capillaries supporting RBC flow compared to the pre-occlusion condition. METHODS: In female Sprague-Dawley rats (n = 6), the spinotrapezius muscle was exteriorized for evaluation of capillary hemodynamics pre-occlusion, 5 min of feed artery occlusion (Occ), and 5 min of reperfusion (Post-Occ). RESULTS: There were no differences in mean arterial pressure (MAP) or capillary diameter (Dc) between pre-occlusion and post-occlusion (P > 0.05). During 30 s of PORH, capillary fRBC was increased (pre: 59 ± 4 vs. 30 s-post: 77 ± 2 cells/s; P < 0.05) and VRBC was not changed (pre: 300 ± 24 vs. 30 s post: 322 ± 25 µm/s; P > 0.05). Capillary hematocrit (Hctcap) was unchanged across the pre- to post-occlusion conditions (P > 0.05). Following occlusion, there was a 20-30% decrease in the number of capillaries supporting RBC flow at 30 s and 300 s-post occlusion (pre: 92 ± 2%; 30 s-post: 66 ± 3%; 300 s-post: 72 ± 6%; both P < 0.05). CONCLUSION: Short-term feed artery occlusion (i.e. 5 min) resulted in a more heterogeneous capillary flow profile with the presence of capillary no-reflow, decreasing the percentage of capillaries supporting RBC flow. A complex interaction between myogenic and metabolic mechanisms at the arteriolar level may play a role in the capillary no-reflow with PORH. Measurements at the level of the conduit artery mask significant alterations in blood flow distribution in the microcirculation.

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.

Influence of blood flow occlusion on muscular recruitment and fatigue during maximal-effort small muscle-mass exercise.

KEY POINTS: The heavy-to-severe intensity exercise threshold (i.e. critical force) distinguishes between steady-state and progressive metabolic and neuromuscular responses to exercise. High levels of skeletal muscle sensory feedback related to peripheral fatigue development are thought to restrict motor unit activation and limit exercise tolerance. Utilizing limb blood flow occlusion, we demonstrate that critical force reflects an oxygen-delivery-dependent balance between motor unit activation and peripheral fatigue development. Our findings suggest that mechanisms which determine the total force-producing capacity of exercising skeletal muscle are significantly altered during blood flow occlusion. These findings may have widespread implications for exercise tolerance in patient populations who experience partial vascular occlusion or altered neuromuscular reflexes. ABSTRACT: High levels of muscle sensory feedback restrict motor unit activation and limit exercise tolerance. The roles of muscle fatigue development and motor unit activation in determining the heavy- to severe-intensity threshold (critical force; CF) remain unclear. This study utilized blood flow occlusion (OCC) to determine relationships between muscle fatigue development and motor unit activation during the determination of CF. We hypothesized that (1) OCC would exacerbate peripheral fatigue development and increase the rate of motor unit deactivation, and (2) blood flow reperfusion (REP) would result in muscle recovery and re-recruitment of motor units despite continuous maximal effort, (3) resulting in an end-exercise force not different from CF. Seven young, healthy subjects performed maximal-effort rhythmic handgrip exercise for 5 min under control conditions (CON) and during OCC and REP. Peripheral fatigue development and motor unit activation were measured via electrical stimulation and electromyography, respectively, during each test. OCC resulted in significantly greater peripheral fatigue development than CON (54.3 ± 34.8%; P < 0.001). Motor unit deactivation was only observed during OCC (P < 0.001). REP resulted in significant peripheral recovery (P < 0.001) and the re-recruitment of motor units (P < 0.001) to levels not different from CON. While OCC resulted in a significantly greater reduction in force production compared to CON (65.7 ± 35.6%; P < 0.001), REP resulted in the restoration of maximal-effort force production (266 ± 19 N; P < 0.001) to levels not different from CF (276 ± 55 N). These data suggest that CF reflects an oxygen-delivery-dependent balance between motor unit activation and peripheral fatigue development. Furthermore, this study established that mechanisms which determine the total force-producing capacity of exercising skeletal muscle are altered during OCC.

Limb blood flow and muscle oxygenation responses during handgrip exercise above vs. below critical force.

This study compared the brachial artery blood flow (Q̇BA) and microvascular oxygen delivery responses during handgrip exercise above vs. below critical force (CF; the isometric analog of critical power). Q̇BA and microvascular oxygen delivery are important determinants of oxygen utilization and metabolite accumulation during exercise, both of which increase progressively during exercise above CF. However the Q̇BA and microvascular oxygen delivery responses above vs. below CF remain unknown. We hypothesized that Q̇BA, deoxygenated-heme (deoxy-[heme]; an estimate of microvascular fractional oxygen extraction), and total-heme concentrations (total-[heme]; an estimate of changes in microvascular hematocrit) would demonstrate physiological maximums above CF despite increases in exercise intensity. Seven men and six women performed 1) a 5-min rhythmic isometric-handgrip maximal-effort test (MET) to determine CF and 2) two constant target-force tests above (severe-intensity; S1 and S2) and two constant target-force tests below (heavy-intensity; H1 and H2) CF. CF was 189.3 ± 16.7 N (29.7 ± 1.6%MVC). At end-exercise, Q̇BA was greater for tests above CF (S1: 418 ± 147 mL/min; S2: 403 ± 137 mL/min) compared to tests below CF (H1: 287 ± 97 mL/min; H2: 340 ± 116 mL/min; all p < 0.05) but was not different between S1 and S2. Further, end-test Q̇BA during both tests above CF was not different from Q̇BA estimated at CF (392 ± 37 mL/min). At end-exercise, deoxy-[heme] was not different between tests above CF (S1: 150 ± 50 µM; S2: 155 ± 57 µM), but was greater during tests above CF compared to tests below CF (H1: 101 ± 24 µM; H2: 111 ± 21 µM; all p < 0.05). At end-exercise, total-[heme] was not different between tests above CF (S1: 404 ± 58 µM; S2: 397 ± 73 µM), but was greater during tests above CF compared to H1 (352 ± 58 µM; p < 0.01) but not H2 (371 ± 57 µM). These data suggest limb blood flow limitations exist and maximal levels of muscle microvascular oxygen delivery and extraction occur during exercise above, but not below, CF.

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.

Microvascular blood flow during vascular occlusion tests assessed by diffuse correlation spectroscopy.

NEW FINDINGS: What is the central question of this study? What are the characteristics of the time courses of blood flow in the brachial artery and microvascular beds of the skin and skeletal muscle following transient ischaemia? What is the main finding and its importance? Skeletal muscle blood flow was significantly slower than the transient increase in the cutaneous tissue, suggesting mechanistic differences between cutaneous and muscular blood flow distribution after transient ischaemia. These results challenge the use of the cutaneous circulation as globally representative of vascular function. ABSTRACT: Vascular function can be assessed by measuring post-occlusion hyperaemic responses along the arterial tree (vascular occlusion test; VOT). It is currently unclear if responses are similar across vascular beds following cuff release, given potential differences in compliance. To examine this, we compared laser Doppler-derived blood flux in the cutaneous circulation (LDFcut ) and skeletal muscle microvascular blood flux (BFI) using diffuse correlation spectroscopy (DCS), to brachial artery blood flow (BABF) during VOT. We hypothesized that during a VOT following cuff release, (1) BFI response would be delayed compared to the brachial artery response, and (2) time to peak blood flux in the cutaneous vasculature would be slower than both brachial artery and skeletal muscle responses. Seven healthy men (26 ± 4 years) performed three trials of a brachial artery VOT protocol with 10 min of rest between trials. A combined DCS and near-infrared spectroscopy probe provided BFI and oxygenation characteristics (total-[haem]), respectively, of skeletal muscle. BABF was determined via Doppler ultrasound and microvascular cutaneous blood flux was determined via LDFcut . Following cuff release, time to peak of BFI (32.3 ± 6.0 s) was significantly longer than BABF (7.3 ± 2.5 s), LDFcut (10.0 ± 6.4 s) and total-[haem] (14.2 ± 8.3 s) (all P < 0.001). However, time to peak of BABF, LDFcut and total-[haem] were not significantly different (P > 0.05). These results suggest mechanistic differences in control of cutaneous and muscular blood flow distribution after transient ischaemia.

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.

Reduced insulin sensitivity in young, normoglycaemic subjects alters microvascular tissue oxygenation during postocclusive reactive hyperaemia.

NEW FINDINGS: What is the central question of the study? Are measures of reduced insulin sensitivity in young, normoglycaemic subjects correlated with near-infrared spectroscopy-derived microvascular responsiveness [tissue oxygen saturation reperfusion rate (STO2 upslope)] during postocclusive reactive hyperaemia? What is the main finding and its importance? A sevenfold range of hepatic insulin sensitivity is significantly correlated (r = 0.44, P = 0.02) with STO2 upslope after transient tissue ischaemia. Near-infrared spectroscopy may be an important tool for determining altered microvascular function before onset of hyperglycaemia. Identification of pre-type 2 diabetes much earlier than with the present clinical criteria is important for pre-emptive measures against microvascular deterioration. ABSTRACT: Near-infrared spectroscopy (NIRS) measurement of postocclusive reactive hyperaemia (PORH) tissue oxygen saturation reperfusion rate [STO2 upslope (as a percentage per minute)] has recently been correlated with the percentage of flow-mediated dilatation (%FMD). Cardiovascular disease is associated with impairments in %FMD. Reduced insulin sensitivity may negatively affect the vascular system for many years before prediabetes/type 2 diabetes states. The aim of this study was to determine whether static and dynamic STO2 parameters during PORH are correlated with reduced insulin sensitivity in young, normoglycaemic subjects. Glucose and insulin were measured during an oral glucose tolerance test in 18- to 26-year-old, healthy subjects (11 men and 11 women), and STO2 was measured during PORH of antebrachial muscle. Hepatic (ISIHOMA ) and whole-body (ISICOMP ) insulin sensitivities were calculated. The STO2 upslope was negatively correlated with minimal STO2 (r = -0.5, P = 0.01). The change of STO2 from minimum to baseline (ΔSTO2 ) was significantly negatively correlated with fasting insulin (r = -0.5, P = 0.01) and a positively correlated with ISIHOMA (r = 0.65, P = 0.001). The minimum STO2 was significantly negatively correlated with ISIHOMA , and STO2 upslope was significantly positively correlated with ISIHOMA (r = 0.44, P = 0.02). The minimum STO2 (a measure of O2 extraction while the cuff was inflated), ΔSTO2 (a measure of the amount of reperfusion) and STO2 upslope (a measure of responsiveness of the microcirculation to ischaemia) were all positively correlated with ISIHOMA , one of the longest-used measures of insulin sensitivity. The NIRS-derived STO2 might be a useful tool for assessing how levels of reduced insulin sensitivity in young, normoglycaemic adults affect the microvasculature.

Cardiovascular consequences of the inspiratory muscle metaboreflex: effects of age and sex.

With inspiratory muscle metaboreflex activation, we hypothesized that, compared with their younger counterparts, older men and women would exhibit greater 1) increases in mean arterial pressure (MAP) and limb vascular resistance (LVR) and 2) decreases in limb blood flow (Q̇L) but 3) no sex differences would be present in older adults. Sixteen young adults [8 young men (YM) and 8 young women (YW), 18-24 yr] and 16 older adults [8 older men (OM) and 8 older women (OW), 60-73 yr] performed inspiratory resistive breathing tasks (IRBTs) at 2% and 65% of their maximal inspiratory pressure. During the IRBTs, breathing frequency was 20 breaths/min with a 50% duty cycle. At baseline and during the IRBTs, MAP was measured via automated oscillometry, Q̇L was determined via Doppler ultrasound, and LVR was calculated. The 65% IRBT led to significantly greater increases in MAP in OW (15.9 ± 8.1 mmHg) compared with YW (6.9 ± 1.4 mmHg) but not (P > 0.05) between OM (12.3 ± 5.7 mmHg) and YM (10.8 ± 5.7 mmHg). OW (-20.2 ± 7.2%) had greater (P < 0.05) decreases in Q̇L compared with YW (-9.4 ± 10.2%), but no significant differences were present between OM (-22.8 ± 9.7%) and YM (-22.7 ± 11.3%) during the 65% IRBT. The 65% IRBT led to greater (P < 0.05) increases in LVR in OW (48.2 ± 25.5%) compared with YW (19.7 ± 15.0%), but no differences (P > 0.05) existed among OM (54.4 ± 17.8%) and YM (47.1 ± 23.3%). No significant differences were present in MAP, Q̇L, or LVR between OM and OW. These data suggest that OW exhibit a greater inspiratory muscle metaboreflex compared with YW, whereas no differences between OM and YM existed. Finally, sex differences in the inspiratory muscle metaboreflex are not present in older adults.NEW & NOTEWORTHY Premenopausal women exhibit an attenuated inspiratory muscle metaboreflex compared with young men; however, it is unknown whether these sex differences are present in older adults. Older women exhibited a greater inspiratory muscle metaboreflex compared with premenopausal women, whereas no differences were present between older and younger men.

Sex differences in the cardiovascular consequences of the inspiratory muscle metaboreflex.

It is currently unknown whether sex differences exist in the cardiovascular consequences of the inspiratory muscle metaboreflex. We hypothesized that the activation of the inspiratory muscle metaboreflex will lead to less of an increase in mean arterial pressure (MAP) and limb vascular resistance (LVR) and less of a decrease in limb blood flow (Q̇L) in women compared with men. Twenty healthy men (n = 10, 23 ± 2 yr) and women (n = 10, 22 ± 3 yr) were recruited for this study. Subjects performed inspiratory resistive breathing tasks (IRBTs) at 2% or 65% of their maximal inspiratory mouth pressure (PIMAX). During the IRBTs, the breathing frequency was 20 breaths/min with a 50% duty cycle. At rest and during the IRBTs, MAP was measured via automated oscillometry, Q̇L was measured via Doppler ultrasound, and LVR was calculated. EMG was recorded on the leg to ensure no muscle contraction occurred. The 65% IRBT led to attenuated increases (P < 0.01) from baseline in women compared with men for MAP (W: 7.3 ± 2.0 mmHg; M: 11.1 ± 5.0 mmHg) and LVR (W: 17.7% ± 14.0%; M: 47.9 ± 21.0%), as well as less of a decrease (P < 0.01) in Q̇L (W: -7.5 ± 9.9%; M: -23.3 ± 10.2%). These sex differences in MAP, Q̇L, and LVR were still present in a subset of subjects matched for PIMAX The 2% IRBT resulted in no significant changes in MAP, Q̇L, or LVR across time or between men and women. These data indicate premenopausal women exhibit an attenuated inspiratory muscle metaboreflex compared with age-matched men.

The effect of resting blood flow occlusion on exercise tolerance and W'.

It has previously been postulated that the anaerobic work capacity (W') may be utilized during resting blood flow occlusion in the absence of mechanical work. We tested the hypothesis that W' would not be utilized during an initial range of time following the onset of resting blood flow occlusion, after which W' would be utilized progressively more. Seven men completed blood flow occlusion constant power severe intensity handgrip exercise to task failure following 0, 300, 600, 900, and 1,200 s of resting blood flow occlusion. The work performed above critical power (CP) was not significantly different between the 0-, 300-, and 600-s conditions and was not significantly different from the total W' available. Significantly less work was performed above CP during the 1,200-s condition than the 900-s condition (P < 0.05), while both conditions were significantly less than the 0-, 300-, and 600-s conditions (P < 0.05). The work performed above CP during these conditions was significantly less than the total W' available (P < 0.05). The utilization of W' during resting blood flow occlusion did not begin until 751 ± 118 s, after which time W' was progressively utilized. The current findings demonstrate that W' is not utilized during the initial ∼751 s of resting blood flow occlusion, but is progressively utilized thereafter, despite no mechanical work being performed. Thus, the utilization of W' is not exclusive to exercise, and a constant amount of work that can be performed above CP is not the determining mechanism of W'.

The impact of pedal rate on muscle oxygenation, muscle activation and whole-body VO2 during ramp exercise in healthy subjects.

PURPOSE: The aim of this project was to study the impact of pedal rate on breakpoints in muscle oxygenation (deoxy[Hb + Mb] and total[Hb + Mb]) and activation (iEMG and MPF) at high intensities during ramp exercise. METHODS: Twelve physically active students performed incremental ramp exercises at 60 rpm, starting either at 50 or 80 W (i.e., 60rpm50 and 60rpm80), and at 100 rpm, starting at 50 W (100rpm50). Pulmonary VO2, muscle activation (iEMG and MPF) and oxygenation were recorded with EMG and NIRS, respectively. IEMG, MPF, deoxy[Hb + Mb] and total[Hb + Mb] were expressed as functions of work rate (WR) and pulmonary VO2 (%VO2peak) and analyzed with double-linear models. RESULTS: The breakpoints (BP) of iEMG, MPF, total[Hb + Mb] and deoxy[Hb + Mb] in %VO2peak did not differ among the pedal rate conditions (P > 0.05), whereas the BPs in WR were significantly lower in 100rpm50 compared to 60rpm50 and 60rpm80 (P < 0.01). Across the pedal rate conditions the BP (in %VO2peak) of total[Hb + Mb] (82.7 ± 1.5 %VO2peak) was significantly lower (P < 0.01) compared to the BP in iEMG (84.3 ± 1.7 %VO2peak) and MPF (84.2 ± 1.6 %VO2peak), whereas the BP in deoxy[Hb + Mb] (87.4 ± 1.4 %VO2peak) and respiratory compensation point (89.9 ± 1.8 %VO2peak) were significantly higher (P < 0.01) compared to the BP in total[Hb + Mb], iEMG and MPF. Additionally, the BPs in iEMG, MPF, total[Hb + Mb] and deoxy[Hb + Mb], and the RCP were highly correlated (r > 0.90; P < 0.001). CONCLUSIONS: The present study showed that muscle activation and oxygenation at high intensities during incremental exercise are related to pulmonary VO2 rather than external WR, with a close interrelationship between that muscle activation, oxygenation and pulmonary VO2.

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.

Relationship between brachial artery blood flow and total [hemoglobin+myoglobin] during post-occlusive reactive hyperemia.

The associations between macrovascular and microvascular responses reported previously during post-occlusive reactive hyperemia have been inconsistent. The purpose of this study was therefore to determine the temporal relationship between the reactive hyperemic responses within a conduit artery and the downstream microvessels. Conduit artery blood flow was measured in the brachial artery with pulsed Doppler ultrasound. A potential analog of microvascular flow, changes in skeletal muscle total[hemoglobin+myoglobin] (T[Hb+Mb]), was assessed with near-infrared spectroscopy (NIRS). We found a high degree of correlation between these two measures (r=0.91). Cross-correlation analysis revealed two distinct response patterns. In 10 of our 15 subjects there was time displacement between peak brachial artery blood flow (BABF) and T[Hb+Mb] responses; in the remaining 5 the peaks were coincident. Granger causality testing suggested that reactive hyperemia in the macrovessel determined hyperemia in the downstream microvessels in all 15 study subjects. Time constants for the on (τ1) and off (τ2) kinetics of each response were calculated; our initial hypothesis was that τ1 and τ2 for T[Hb+Mb] would correlate with τ1 and τ2 for BABF, respectively. However, only for τ2 was this observed (r=0.52; p<0.05). No similar relationship was observed for τ1. Adipose tissue thickness did not influence either time constant for T[Hb+Mb]. Taken together, our results show that the temporal characteristics of the hyperemic response in the conduit artery are qualitatively reflected in the downstream microvasculature, but mechanisms for quantitative differences remain to be identified.

Influence of exercise intensity on respiratory muscle fatigue and brachial artery blood flow during cycling exercise.

PURPOSE: During high intensity exercise, both respiratory muscle fatigue and cardiovascular reflexes occur; however, it is not known how inactive limb blood flow is influenced. The purpose of this study was to determine the influence of moderate and high exercise intensity on respiratory muscle fatigue and inactive limb muscle and cutaneous blood flow during exercise. METHODS: Twelve men cycled at 70 and 85 % [Formula: see text] for 20 min. Subjects also performed a second 85 % [Formula: see text] test after ingesting 1,800 mg of N-acetylcysteine (NAC), which has been shown to reduce respiratory muscle fatigue (RMF). Maximum inspiratory pressures (P Imax), brachial artery blood flow (BABF), cutaneous vascular conductance (CVC), and mean arterial pressure were measured at rest and during exercise. RESULTS: Significant RMF occurred with 85 % [Formula: see text] (P Imax, -12.8 ± 9.8 %), but not with 70 % [Formula: see text] (P Imax, -5.0 ± 5.9 %). BABF and BA vascular conductance were significantly lower at end exercise of the 85 % [Formula: see text] test compared to the 70 % [Formula: see text] test. CVC during exercise was not different (p > 0.05) between trials. With NAC, RMF was reduced (p < 0.05) and BABF was significantly higher (~30 %) compared to 85 % [Formula: see text] (p < 0.05). CONCLUSIONS: These data suggest that heavy whole-body exercise at 85 % [Formula: see text] leads to RMF, decreases in inactive arm blood flow, and vascular conductance, but not cutaneous blood flow.

Sex differences in the intensity-duration relationships of the severe- and extreme-intensity exercise domains.

Extreme-intensity exercise is described by W'ext (analogous to J' for isometric exercise) that is smaller than W' of severe-intensity exercise (W'sev) in males. Sex differences in exercise tolerance appear to diminish at near-maximal exercise, however, there is evidence of greater contributions of peripheral fatigue (i.e. potentiated twitch force; Qpot) in males during extreme-intensity exercise. Therefore, the current study tested the hypotheses that J'ext would not be different between males and females, however, males would exhibit a greater reduction in neuromuscular function (i.e. maximal voluntary contraction, MVC; Qpot) following extreme-intensity exercise. Seven males and 7 females completed three severe- (Tlim: 2-4 min, S3; 5-8 min, S2; 9-15 min, S1) and three extreme-intensity (70, 80, 90%MVC) knee-extension bouts. MVC and Qpot relative to baseline were compared at task failure and at 150 s of recovery. J'ext was significantly less than J'sev in males (2.4 ± 1.2kJ vs 3.9 ± 1.3kJ; p = 0.03) and females (1.6 ± 0.8kJ vs 2.9 ± 1.7kJ; p = 0.05); however, there were no sex differences in J'ext or J'sev. MVC (%Baseline) was greater at task failure following extreme-intensity exercise (76.5 ± 20.0% vs 51.5 ± 11.5% in males, 75.7 ± 19.4% vs 66.7 ± 17.4% in females), but was not different at 150 s of recovery (95.7 ± 11.8% in males, 91.1 ± 14.2% in females). Reduction in Qpot, however, was greater in males (51.9 ± 16.3% vs 60.6 ± 15.5%) and was significantly correlated with J'ext (r2 = 0.90, p < 0.001). Although there were no differences in the magnitude of J'ext, differences in MVC and Qpot are evidence of sex-specific responses and highlight the importance of appropriately characterizing exercise intensity regarding exercise domains when comparing physiological responses in males and females.Highlights We have previously shown evidence that extreme-intensity dynamic exercise is described by W'ext in males and smaller than W'sev. We currently tested for potential sex differences in J'ext (isometric analogue to W') and neuromuscular responses (i.e. maximal voluntary contraction, MVC; potentiated twitch force, Qpot) during extreme-intensity exercise.J'ext and extreme-intensity exercise tolerance was not different between males and females. The reduction in MVC was not different across extreme-intensity exercise across males and females, whereas the reduction in Qpot was greater in males following all extreme-intensity exercises, although not after exercise at 90%MVC.Together, although extreme-intensity exercise tolerance is not different, these data highlight differences in the contributing mechanisms of fatigue during severe- and extreme-intensity exercise between males and females.

Influence of priming exercise on muscle deoxy[Hb + Mb] during ramp cycle exercise.

The aim of the present study was to gain better insight into the mechanisms underpinning the sigmoid pattern of deoxy[Hb + Mb] during incremental exercise by assessing the changes in the profile following prior high-intensity exercise. Ten physically active students performed two incremental ramp (25 W min(-1)) exercises (AL and LL, respectively) preceded on one occasion by incremental arm (10 W min(-1)) and on another occasion by incremental leg exercise (25 W min(-1)), which served as the reference test (RT). Deoxy[Hb + Mb] was measured by means of near-infrared spectroscopy and surface EMG was recorded at the Vastus Lateralis throughout the exercises. Deoxy[Hb + Mb], integrated EMG and Median Power Frequency (MdPF) were expressed as a function of work rate (W) and compared between the exercises. During RT and AL deoxy[Hb + Mb] followed a sigmoid increase as a function of work rate. However, during LL deoxy[Hb + Mb] increased immediately from the onset of the ramp exercise and thus no longer followed a sigmoid pattern. This different pattern in deoxy[Hb + Mb] was accompanied by a steeper slope of the iEMG/W-relationship below the GET (LL: 0.89 ± 0.11% W(-1); RT: 0.74 ± 0.08% W(-1); AL: 0.72 ± 0.10% W(-1)) and a more pronounced decrease in MdPF in LL (17.2 ± 4.5%) compared to RT (5.0 ± 2.1%) and AL (3.9 ± 3.2%). It was observed that the sigmoid pattern of deoxy[Hb + Mb] was disturbed when the ramp exercise was preceded by priming leg exercise. Since the differences in deoxy[Hb + Mb] were accompanied by differences in EMG it can be suggested that muscle fibre recruitment is an important underlying mechanism for the pattern of deoxy[Hb + Mb] during ramp exercise.