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.

Heart rate and gas exchange dynamic responses to multiple brief exercise bouts (MBEB) in early- and late-pubertal boys and girls.

Natural patterns of physical activity in youth are characterized by brief periods of exercise of varying intensity interspersed with rest. To better understand systemic physiologic response mechanisms in children and adolescents, we examined five responses [heart rate (HR), respiratory rate (RR), oxygen uptake (V̇O2 ), carbon dioxide production (V̇CO2 ), and minute ventilation (V̇E), measured breath-by-breath] to multiple brief exercise bouts (MBEB). Two groups of healthy participants (early pubertal: 17 female, 20 male; late-pubertal: 23 female, 21 male) performed five consecutive 2-min bouts of constant work rate cycle-ergometer exercise interspersed with 1-min of rest during separate sessions of low- or high-intensity (~40% or 80% peak work, respectively). For each 2-min on-transient and 1-min off-transient we calculated the average value of each cardiopulmonary exercise testing (CPET) variable (Y̅). There were significant MBEB changes in 67 of 80 on- and off-transients. Y̅ increased bout-to-bout for all CPET variables, and the magnitude of increase was greater in the high-intensity exercise. We measured the metabolic cost of MBEB, scaled to work performed, for the entire 15 min and found significantly higher V̇O2 , V̇CO2 , and V̇E costs in the early-pubertal participants for both low- and high-intensity MBEB. To reduce breath-by-breath variability in estimation of CPET variable kinetics, we time-interpolated (second-by-second), superimposed, and averaged responses. Reasonable estimates of τ (<20% coefficient of variation) were found only for on-transients of HR and V̇O2 . There was a remarkable reduction in τHR following the first exercise bout in all groups. Natural patterns of physical activity shape cardiorespiratory responses in healthy children and adolescents. Protocols that measure the effect of a previous bout on the kinetics of subsequent bouts may aid in the clinical utility of CPET.

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.

Neuromuscular recovery from severe- and extreme-intensity exercise in men and women.

Maximal voluntary contraction force (MVC), potentiated twitch force (Qpot), and voluntary activation (%VA) recover to baseline within 90 s following extreme-intensity exercise. However, methodological limitations mask important recovery kinetics. We hypothesized reductions in MVC, Qpot, and %VA at task failure following extreme-intensity exercise would be less than following severe-intensity exercise, and Qpot and MVC following extreme-intensity exercise would show significant recovery within 120 s but remain depressed following severe-intensity exercise. Twelve subjects (6 men) completed 2 severe-intensity (40, 50% MVC) and 2 extreme-intensity (70, 80% MVC) isometric knee-extension exercise bouts to task failure (Tlim). Neuromuscular function was measured at baseline, Tlim, and through 150 s of recovery. Each intensity significantly reduced MVC and Qpot compared with baseline. MVC was greater at Tlim (p < 0.01) and at 150 s of recovery (p = 0.004) following exercise at 80% MVC compared with severe-intensity exercise. Partial recovery of MVC and Qpot were detected within 150 s following Tlim for each exercise intensity; Qpot recovered to baseline values within 150 s of recovery following exercise at 80% MVC. No differences in %VA were detected pre- to post-exercise or across recovery for any intensity. Although further analysis showed sex-specific differences in MVC and Qpot, future studies should closely examine sex-dependent responses to extreme-intensity exercise. It is clear, however, that these data reinforce that mechanisms limiting exercise tolerance during extreme-intensity exercise recover quickly. Novelty: Severe- and extreme-intensity exercise cause independent responses in fatigue accumulation and the subsequent recovery time courses. Recovery of MVC and Qpot occurs much faster following extreme-intensity exercise in both men and women.

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.

Influence of muscular contraction on vascular conductance during exercise above versus below critical power.

We tested the hypothesis that limb vascular conductance (LVC) would increase during the immediate recovery phase of dynamic exercise above, but not below, critical power (CP) indicating a threshold for muscular contraction-induced impedance of limb blood flow (LBF). CP (115 ± 26 W) was determined in 7 men and 7 women who subsequently performed ∼5 min of near-supine cycling exercise both below and above CP. LVC demonstrated a greater increase during immediate recovery and remained significantly higher following exercise above, compared to below, CP (all p < 0.001). Power output was associated with the immediate increases in LVC following exercise above, but not below, CP (p < 0.001; r = 0.85). Additionally, variance in percent LBF impedance was significantly lower above (CV: 10.7 %), compared to below (CV: 53.2 %), CP (p < 0.01). CP appears to represent a threshold above which the characteristics of LBF impedance by muscular contraction become intensity-dependent. These data suggest a critical level of LBF impedance relative to contraction intensity exists and, once attained, may promote the progressive metabolic and neuromuscular responses known to occur above CP.

Effects of Caffeine on Exercise Duration, Critical Velocity, and Ratings of Perceived Exertion During Repeated-Sprint Exercise in Physically Active Men.

Caffeine improves short-to-moderate distance running performance, but the effect of caffeine on repeated sprints are equivocal. This research determined if caffeine improved exercise tolerance during repeated-sprint exercise. iCV is a running velocity that distinguishes intermittent running velocities (velocities ≤ iCV) that are sustainable from those resulting in a predictable time to exhaustion (velocities > iCV). Seven physically active men (age = 21.6 ± 1.5 years, body mass = 72.8 ± 5.1 kg, VO2max = 56.9 ± 9.8 mL/kg/min) ingested caffeine (5 mg/kg) or placebo (crossover design) 60 min prior to an intermittent critical velocity (iCV) test. The treadmill grade and velocity at VO2max (vVO2max) were used for iCV testing, and consisted of 3 bouts (10 sec running and 10 sec passive rest) at 130, 110 and 120% vVO2max. Each bout continued until volitional exhaustion and was separated by 20 min of passive rest. Total distance and duration were recorded to determine exercise tolerance using the iCV model. Caffeine ingestion increased running duration at 110% vVO2max (p = 0.02), but not at 120 (p = 0.93) and 130% vVO2max (p = 0.14). Caffeine did not improve iCV model parameters. A single dose of caffeine consumed 60 min before repeated-sprints can improve performance at 110% vVO2max, but not at higher velocities.

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.

Effect of priming exercise and body position on pulmonary oxygen uptake and muscle deoxygenation kinetics during cycle exercise.

We hypothesized that the performance of prior heavy exercise would speed pulmonary oxygen uptake (V̇o2) kinetics (i.e., as described by the time constant, [Formula: see text]) and reduce the amplitude of muscle deoxygenation (deoxy[heme]) kinetics in the supine (S) but not upright (U) body position. Seventeen healthy men completed heavy-intensity constant-work rate exercise tests in S and U consisting of two bouts of 6-min cycling separated by 6-min cycling at 20 W. Pulmonary V̇o2 was measured breath by breath; total and deoxy[heme] were determined via time-resolved near-infrared spectroscopy (NIRS) at three muscle sites. Priming exercise reduced [Formula: see text] in S (bout 1: 36 ± 10 vs. bout 2: 28 ± 10 s, P < 0.05) but not U (bout 1: 27 ± 8 s vs. bout 2: 25 ± 7 s, P > 0.05). Deoxy[heme] amplitude was increased after priming in S (bout 1: 25-28 µM vs. bout 2: 30-35 µM, P < 0.05) and U (bout 1: 13-18 µM vs. bout 2: 17-25 µM, P > 0.05), whereas baseline total[heme] was enhanced in S (bout 1: 110-179 µM vs. bout 2: 121-193 µM, P < 0.05) and U (bout 1: 123-186 µM vs. bout 2: 137-197 µM, P < 0.05). Priming exercise increased total[heme] in both S and U, likely indicating enhanced diffusive O2 delivery. However, the observation that after priming the amplitude of the deoxy[heme] response was increased in S suggests that the reduction in [Formula: see text] subsequent to priming was related to a combination of both enhanced intracellular O2 utilization and increased O2 delivery.NEW & NOTEWORTHY Here we show that oxygen uptake (V̇o2) kinetics are slower in the supine compared with upright body position, an effect that is associated with an increased amplitude of skeletal muscle deoxygenation in the supine position. After priming in the supine position, the amplitude of muscle deoxygenation remained markedly elevated above that observed during upright exercise. Hence, the priming effect cannot be solely attributed to enhanced O2 delivery, and enhancements to intracellular O2 utilization must also be contributory.

Impact of supine exercise on muscle deoxygenation kinetics heterogeneity: mechanistic insights into slow pulmonary oxygen uptake dynamics.

Oxygen uptake (V̇o2) kinetics are slowed in the supine (S) position purportedly due to impaired muscle O2 delivery ([Formula: see text]); however, these conclusions are predicated on single-site measurements in superficial muscle using continuous-wave near-infrared spectroscopy (NIRS). This study aimed to determine the impact of body position [i.e., upright (U) versus S] on deep and superficial muscle deoxygenation (deoxy[heme]) using time-resolved (TR-) NIRS, and how these relate to slowed pulmonary V̇o2 kinetics. Seventeen healthy men completed constant power tests during 1) S heavy-intensity exercise and 2) U exercise at the same absolute work rate, with a subset of 10 completing additional tests at the same relative work rate as S. Pulmonary V̇o2 was measured breath-by-breath and, deoxy- and total[heme] were resolved via TR-NIRS in the superficial and deep vastus lateralis and superficial rectus femoris. The fundamental phase V̇o2 time constant was increased during S compared with U (S: 36 ± 10 vs. U: 27 ± 8 s; P < 0.001). The deoxy[heme] amplitude (S: 25-28 vs. U: 13-18 µM; P < 0.05) and total[heme] amplitude (S: 17-20 vs. U: 9-16 µM; P < 0.05) were greater in S compared with U and were consistent for the same absolute (above data) and relative work rates (n = 10, all P < 0.05). The greater deoxy- and total[heme] amplitudes in S vs. U supports that reduced perfusive [Formula: see text] in S, even within deep muscle, necessitated a greater reliance on fractional O2 extraction and diffusive [Formula: see text]. The slower V̇o2 kinetics in S versus U demonstrates that, ultimately, these adjustments were insufficient to prevent impairments in whole body oxidative metabolism.NEW & NOTEWORTHY We show that supine exercise causes a greater degree of muscle deoxygenation in both deep and superficial muscle and increases the spatial heterogeneity of muscle deoxygenation. Therefore, this study suggests that any O2 delivery gradient toward deep versus superficial muscle is insufficient to mitigate impairments in oxidative function in response to reduced whole muscle O2 delivery. More heterogeneous muscle deoxygenation is associated with slower V̇o2 kinetics.

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.

Prediction of Emergency Capsule Egress Performance.

INTRODUCTION: Critical mission tasks for Martian exploration have been identified and include specific duties that astronauts will have to perform despite any adverse effects of chronic microgravity. Specifically, astronauts may have to perform an emergency capsule egress upon return to Earth, which places specific demands on compromised cardiovascular and neuromuscular systems. Therefore, the purpose of this project was to determine the relationship between cardiorespiratory fitness and simulated capsule egress time.METHODS: There were 15 subjects who volunteered for this study. Vo2peak and peak power output (PPO) were determined on cycle and rowing ergometers. Critical power (CP) was determined by a 3-min all-out rowing test. Subjects then performed an emergency capsule egress on a mock-up of NASA's Orion space capsule. Peak metabolic data were compared between the cycling and rowing tests. Pearson's correlation was used to identify relationships between egress time and Vo2peak, PPO, and CP.RESULTS: Vo2peak, Vco2peak, and minute ventilation were not different between cycling and rowing tests. Cycling elicited a greater PPO than the rowing test. Egress time was negatively correlated to rowing PPO (r = -0.60), but not cycling or rowing Vo2peak, cycling PPO, or CP.CONCLUSIONS: Rowing PPO/kg correlates with egress time. Although individuals with higher PPO/kg were able to finish the task in less time, individuals with low fitness levels (Vo2peak ≤ 20 ml · kg-1 · min-1) could complete the egress within 2 mins. These results suggest that cardiorespiratory fitness should not limit emergency egress and that this can be assessed using rowing exercise.Alexander AM, Sutterfield SL, Kriss KN, Hammer SM, Didier KD, Cauldwell JT, Dzewaltowski AC, Barstow TJ, Ade CJ. Prediction of emergency capsule egress performance. Aerosp Med Hum Perform. 2019; 90(9):782-787.

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.