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 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.

Limitations to exercise tolerance in type 1 diabetes: the role of pulmonary oxygen uptake kinetics and priming exercise.

We compared the time constant (τV̇O2) of the fundamental phase of pulmonary oxygen uptake (V̇o2) kinetics between young adult men with type 1 diabetes and healthy control subjects. We also assessed the impact of priming exercise on τV̇O2, critical power, and muscle deoxygenation in a subset of participants with type 1 diabetes. Seventeen men with type 1 diabetes and 17 healthy male control subjects performed moderate-intensity exercise to determine τV̇O2. A subset of seven participants with type 1 diabetes performed an additional eight visits, in which critical power, τV̇O2, and muscle deoxyhemoglobin + myoglobin ([HHb+Mb], via near-infrared spectroscopy) kinetics (described by a time constant, τ[HHb+Mb]) were determined with (PRI) and without (CON) a prior 6-min bout of heavy exercise. τV̇O2 was greater in participants with type 1 diabetes compared with control subjects (type 1 diabetes 50 ± 13 vs. control 32 ± 12 s; P < 0.001). Critical power was greater in PRI compared with CON (PRI 161 ± 25 vs. CON 149 ± 22 W; P < 0.001), whereas τV̇O2 (PRI 36 ± 15 vs. CON 50 ± 21 s; P = 0.006) and τ[HHb+Mb] (PRI 10 ± 5 vs. CON 17 ± 11 s; P = 0.037) were reduced in PRI compared with CON. Type 1 diabetes patients showed slower pulmonary V̇o2 kinetics compared with control subjects; priming exercise speeded V̇o2 and [HHb + Mb] kinetics and increased critical power in a subgroup with type 1 diabetes. These data therefore represent the first characterization of the power-duration relationship in type 1 diabetes and the first experimental evidence that τV̇O2 is an independent determinant of critical power in this population.NEW & NOTEWORTHY Patients with type 1 diabetes demonstrated slower oxygen uptake (V̇o2) kinetics compared with healthy control subjects. Furthermore, a prior bout of high-intensity exercise speeded V̇o2 kinetics and increased critical power in people with type 1 diabetes. Prior exercise speeded muscle deoxygenation kinetics, indicating that V̇o2 kinetics in type 1 diabetes are limited primarily by oxygen extraction and/or intracellular factors. These findings highlight the potential for interventions that decrease metabolic inertia for enhancing exercise tolerance in this condition.

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.

Effects of muscle cooling on kinetics of pulmonary oxygen uptake and muscle deoxygenation at the onset of exercise.

This study investigated effects of skeletal muscle cooling on the metabolic response and kinetics of pulmonary oxygen uptake ( V˙ O2 ) and skeletal muscle deoxygenation during submaximal exercise. In the cooling condition (C), after immersion of the lower body into 12°C water for 30 min, eight healthy males performed 30-min cycling exercise at the lactate threshold while undergoing thigh cooling by a water-circulating pad. In the normal condition (N) as control, they conducted the same exercise protocol without cooling. Blood lactate concentration was significantly higher in C than N at 10 min after onset of exercise (4.0 ± 1.7 and 2.4 ± 1.2 mmol/L in C and N, P < 0.05). The percent change in the tissue oxygen saturation of the vastus lateralis, measured by a near-infrared spectroscopy, was significantly lower in C at 2, 8, 10, and 20 min after the exercise onset compared with N (P < 0.05). The percent change in deoxy hemoglobin+myoglobin concentration (Deoxy[Hb+Mb]) showed a transient peak at the onset of exercise and significantly higher value in C at 10, 20, and 30 min after the exercise onset (P < 0.05). Compared to N, slower V˙ O2 kinetics (mean response time) was observed in C (45.6 ± 7.8 and 36.1 ± 7.7 sec in C and N, P < 0.05). The mean response time in C relative to N was significantly correlated with the transient peak of Deoxy[Hb+Mb] in C (r = 0.84, P < 0.05). These results suggest that lower oxygen delivery to the hypothermic skeletal muscle might induce greater glycolytic metabolism during exercise and slower V˙ O2 kinetics at the onset of exercise.

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.

Blood flow occlusion-related O2 extraction "reserve" is present in different muscles of the quadriceps but greater in deeper regions after ramp-incremental test.

It was recently demonstrated that an O2 extraction reserve, as assessed by the near-infrared spectroscopy (NIRS)-derived deoxygenation signal ([HHb]), exists in the superficial region of vastus lateralis (VL) muscle during an occlusion performed at the end of a ramp-incremental test. However, it is unknown whether this reserve is present and/or different in magnitude in other portions and depths of the quadriceps muscles. We tested the hypothesis that an O2 extraction reserve would exist in other regions of this muscle but is greater in deep compared with more superficial portions. Superficial (VL-s) and deep VL (VL-d) as well as superficial rectus femoris (RF-s) were monitored by a combination of low- and high-power time-resolved (TRS) NIRS. During the occlusion immediately post-ramp-incremental test there was a significant overshoot in the [HHb] signal ( P < 0.05). However, the magnitude of this increase was greater in VL-d (93.2 ± 42.9%) compared with VL-s (55.0 ± 19.6%) and RF-s (47.8 ± 14.0%) ( P < 0.05). The present study demonstrated that an O2 extraction reserve exists in different pools of active muscle fibers of the quadriceps at the end of a ramp exercise to exhaustion. The greater magnitude in the reserve observed in the deeper portion of VL, however, suggests that this portion of muscle may present a greater surplus of oxygenated blood, which is likely due to a greater population of slow-twitch fibers. These findings add to the notion that the plateau in the [HHb] signal toward the end of a ramp-incremental exercise does not indicate the upper limit of O2 extraction. NEW & NOTEWORTHY Different portions of the quadriceps muscles exhibited an untapped O2 extraction reserve during a blood flow occlusion performed at the end of a ramp-incremental exercise. In the deeper portion of the vastus lateralis muscle, this reserve was greater compared with superficial vastus lateralis and rectus femoris. These data suggest that the O2 extraction reserve may be dependent on the vascular and/or oxidative capacities of the muscles.

Brachial artery blood flow dynamics during sinusoidal leg cycling exercise in humans.

To explore the control of the peripheral circulation of a nonworking upper limb during leg cycling exercise, blood flow (BF) dynamics in the brachial artery (BA) were determined using a sinusoidal work rate (WR) exercise. Ten healthy subjects performed upright leg cycling exercise at a constant WR for 30 min, followed by 16 min of sinusoidal WR consisting of 4-min periods of WR fluctuating between a minimum output of 20 W and a maximum output corresponding to ventilatory threshold (VT). Throughout the protocol, pulmonary gas exchange, heart rate (HR), mean arterial blood pressure (MAP), blood velocity (BV), and cross-sectional area of the BA, forearm skin BF (SBF), and sweating rate (SR) were measured. Each variable was fitted to a sinusoidal model with phase shift (θ) and amplitude (A). Nearly all variables closely fit a sinusoidal model. Variables relating to oxygen transport, such as VO2 and HR, followed the sinusoidal WR pattern with certain delays (θ: VO2; 51.4 ± 4.0°, HR; 41.8 ± 5.4°, mean ± SD). Conversely, BF response in the BA was approximately in antiphase (175.1 ± 28.9°) with a relatively large A, whereas the phase of forearm SBF was dissimilar (65.8 ± 35.9°). Thus, the change of BF through a conduit artery to the nonworking upper limb appears to be the reverse when WR fluctuates during sinusoidal leg exercise, and it appears unlikely that this could be ascribed exclusively to altering the downstream circulation to forearm skin.

Near-infrared spectroscopy of superficial and deep rectus femoris reveals markedly different exercise response to superficial vastus lateralis.

To date our knowledge of skeletal muscle deoxygenation as measured by near-infrared spectroscopy (NIRS) is predicated almost exclusively on sampling of superficial muscle(s), most commonly the vastus lateralis (VL-s). Recently developed high power NIRS facilitates simultaneous sampling of deep (i.e., rectus femoris, RF-d) and superficial muscles of RF (RF-s) and VL-s. Because deeper muscle is more oxidative with greater capillarity and sustains higher blood flows than superficial muscle, we used time-resolved NIRS to test the hypotheses that, following exercise onset, the RF-d has slower deoxy[Hb+Mb] kinetics with reduced amplitude than superficial muscles. Thirteen participants performed cycle exercise transitions from unloaded to heavy work rates. Within the same muscle (RF-s vs. RF-d) deoxy[Hb+Mb] kinetics (mean response time, MRT) and amplitudes were not different. However, compared with the kinetics of VL-s, deoxy[Hb+Mb] of RF-s and RF-d were slower (MRT: RF-s, 51 ± 23; RF-d, 55 ± 29; VL-s, 18 ± 6 s; P < 0.05). Moreover, the amplitude of total[Hb+Mb] was greater for VL-s than both RF-s and RF-d (P < 0.05). Whereas pulmonary V˙O2 kinetics (i.e., on vs. off) were symmetrical in heavy exercise, there was a marked on-off asymmetry of deoxy[Hb+Mb] for all three sites i.e., MRT-off > MRT-on (P < 0.05). Collectively these data reveal profoundly different O2 transport strategies, with the RF-s and RF-d relying proportionately more on elevated perfusive and the VL-s on diffusive O2 transport. These disparate O2 transport strategies and their temporal profiles across muscles have previously been concealed within the "global" pulmonary V˙O2 response.

The effect of dietary nitrate supplementation on the spatial heterogeneity of quadriceps deoxygenation during heavy-intensity cycling.

This study investigated the influence of dietary inorganic nitrate (NO3-) supplementation on pulmonary O2 uptake (V˙O2) and muscle deoxyhemoglobin/myoglobin (i.e. deoxy [Hb + Mb]) kinetics during submaximal cycling exercise. In a randomized, placebo-controlled, cross-over study, eight healthy and physically active male subjects completed two step cycle tests at a work rate equivalent to 50% of the difference between the gas exchange threshold and peak V˙O2 over separate 4-day supplementation periods with NO3--rich (BR; providing 8.4 mmol NO3-∙day-1) and NO3--depleted (placebo; PLA) beetroot juice. Pulmonary V˙O2 was measured breath-by-breath and time-resolved near-infrared spectroscopy was utilized to quantify absolute deoxy [Hb + Mb] and total [Hb + Mb] within the rectus femoris, vastus lateralis, and vastus medialis There were no significant differences (P > 0.05) in the primary deoxy [Hb + Mb] mean response time or amplitude between the PLA and BR trials at each muscle site. BR significantly increased the mean (three-site) end-exercise deoxy [Hb + Mb] (PLA: 91 ± 9 vs. BR: 95 ± 12 µmol/L, P < 0.05), with a tendency to increase the mean (three-site) area under the curve for total [Hb + Mb] responses (PLA: 3650 ± 1188 vs. BR: 4467 ± 1315 µmol/L sec-1, P = 0.08). The V˙O2 slow component reduction after BR supplementation (PLA: 0.27 ± 0.07 vs. BR: 0.23 ± 0.08 L min-1, P = 0.07) correlated inversely with the mean increases in deoxy [Hb + Mb] and total [Hb + Mb] across the three muscle regions (r2 = 0.62 and 0.66, P < 0.05). Dietary NO3- supplementation increased O2 diffusive conductance across locomotor muscles in association with improved V˙O2 dynamics during heavy-intensity cycling transitions.

Greater V˙O2peak is correlated with greater skeletal muscle deoxygenation amplitude and hemoglobin concentration within individual muscles during ramp-incremental cycle exercise.

It is axiomatic that greater aerobic fitness (V˙O2peak) derives from enhanced perfusive and diffusive O2 conductances across active muscles. However, it remains unknown how these conductances might be reflected by regional differences in fractional O2 extraction (i.e., deoxy [Hb+Mb] and tissue O2 saturation [StO2]) and diffusive O2 potential (i.e., total[Hb+Mb]) among muscles spatially heterogeneous in blood flow, fiber type, and recruitment (vastus lateralis, VL; rectus femoris, RF). Using quantitative time-resolved near-infrared spectroscopy during ramp cycling in 24 young participants (V˙O2peak range: ~37.4-66.4 mL kg-1 min-1), we tested the hypotheses that (1) deoxy[Hb+Mb] and total[Hb+Mb] at V˙O2peak would be positively correlated with V˙O2peak in both VL and RF muscles; (2) the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) during submaximal exercise would not differ among subjects differing in V˙O2peak Peak deoxy [Hb+Mb] and StO2 correlated with V˙O2peak for both VL (r = 0.44 and -0.51) and RF (r = 0.49 and -0.49), whereas for total[Hb+Mb] this was true only for RF (r = 0.45). Baseline deoxy[Hb+Mb] and StO2 correlated with V˙O2peak only for RF (r = -0.50 and 0.54). In addition, the deoxy[Hb+Mb] slopes were not affected by aerobic fitness. In conclusion, while the pattern of deoxygenation (the deoxy[Hb+Mb] slopes) did not differ between fitness groups the capacity to deoxygenate [Hb+Mb] (index of maximal fractional O2 extraction) correlated significantly with V˙O2peak in both RF and VL muscles. However, only in the RF did total[Hb+Mb] (index of diffusive O2 potential) relate to fitness.