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The mechanisms responsible for increased metabolic cost of walking in older adults are poorly understood. We recently proposed a theoretical premise by which age-related reductions in Achilles tendon stiffness (kAT) can disrupt the neuromechanics of calf muscle force production and contribute to faster rates of oxygen consumption during walking. The purpose of this study was to objectively evaluate this premise. We quantified kAT at a range of matched relative activations prescribed using electromyographic biofeedback and walking metabolic cost and ankle joint biomechanics in a group of 15 younger (age: 23 ± 4 yr) and 15 older (age: 72 ± 5 yr) adults. Older adults averaged 44% lower kAT than younger adults at matched triceps surae activations during isokinetic dorsiflexion tasks on a dynamometer (P = 0.046). Older adults also walked with a 17% higher net metabolic power (P = 0.017) but indistinguishable peak Achilles tendon forces than younger adults. Thus, data implicate altered tendon length-tension relations with age more than differences in the operating region of those length-tension relations between younger and older adults. In addition, we discovered empirical evidence that lesser kAT—likely due to the shorter muscle lengths and thus higher relative activations it imposes—was positively correlated with higher net metabolic power during walking (r = −0.365, P = 0.048). These results pave the way for interventions focused on restoring ankle muscle-tendon unit structural stiffness to improve walking energetics in aging. NEW & NOTEWORTHY: This study provides the first empirical evidence to our knowledge that age-related decreases in kAT exact a potentially significant metabolic penalty during walking. These results pave the way for interventions focused on restoring ankle muscle-tendon unit structural stiffness to improve walking energetics in aging. [ABSTRACT FROM AUTHOR]

Walking is a fundamental aspect of daily life and exercise, with clinical benefits for cardiovascular health and muscle strength. However, accurately measuring energy efficiency during walking poses challenges due to equipment and spatial constraints. In this study, we proposed the cadence-based energy expenditure index (cEEI) and analyzed its correlation with the previously proposed index for measuring energy expenditure under various gait conditions. We enrolled 15 healthy participants and conducted an experimental protocol on a treadmill to measure the following energy expenditure-related indices: oxygen cost index (OCI), energy expenditure index (EEI), and cEEI. The participants underwent stages of walking at different speeds and inclinations that comply with the modified Bruce protocol, whereas their heart rate, oxygen uptake, and cadence were recorded. Participants showed significant increases in heart rate, oxygen uptake, and cadence with higher walking speeds and inclinations. Correlation analysis revealed strong associations between cEEI and OCI, especially during walking conditions. Bland–Altman plots and interclass correlation coefficient analysis demonstrated a favorable agreement between cEEI and OCI, outperforming EEI. In conclusion, this study proposes cEEI as a reliable metric for estimating energy expenditure during walking by proving a strong correlation and agreement with OCI across various gait conditions. This suggests the potential for cEEI to provide real-time, individualized feedback on energy expenditure during walking, facilitating more personalized exercise prescriptions. NEW & NOTEWORTHY: We proposed cEEI as a reliable metric for estimating energy expenditure under various walking conditions. Its demonstrated accuracy and potential for real-time individualized feedback could revolutionize personalized exercise prescriptions for diverse sexes and age groups, as well as individuals with disabilities requiring real-time physical monitoring and home care. [ABSTRACT FROM AUTHOR]

Endurance performance declines with advancing age. Of the three main physiological factors that determine endurance running performance [maximal oxygen consumption (V̇ o 2max), lactate threshold, and running economy (RE)], V̇ o 2max appears to be most affected by age. Although endurance performance declines with age, recently, endurance performance has rapidly improved in master athletes as the number of master athletes competing in endurance events has increased. Master athletes represent an intriguing model to study healthy aging. In this case study, we reassessed the physiological profile of a 76-yr-old distance runner who broke the marathon world record for men over 70 yr of age in 2018. This runner was tested a few months before breaking the world record and retested in 2024. Between 2018 and 2024, his marathon running velocity decreased significantly. Therefore, the purpose of this case study was to determine the physiological changes that explain his performance decline. RE remained similar to 2018, and while there was not a clear breakpoint in blood lactate, he still likely runs marathons at a high percentage (∼90%) of his V̇ o 2max. However, V̇ o 2max declined by 15.1%. HRmax declined by 3.2% and maximal O2 pulse declined by 12.4%, suggesting that maximal stroke volume and/or arteriovenous O2 difference decreased. Altogether, although this marathoner continues to compete at an elite level, his performance has declined since his record-breaking marathon due to a reduction in V̇ o 2max. This is likely caused by reductions in maximal stroke volume and/or arteriovenous O2 difference. We speculate that these changes reflect primarily age-related processes. NEW & NOTEWORTHY: We performed 6-yr follow-up testing on a world record-breaking master marathon runner. We determined that his performance declined since his record-breaking marathon in 2018 primarily due to a reduction in V̇ o 2max. His max heart rate (HR) changed minimally, but his peak O2 pulse decreased, suggesting that his maximal stroke volume and/or arteriovenous O2 difference decreased. These changes likely reflect primarily age-related effects in the absence of an overt pathological disease process. [ABSTRACT FROM AUTHOR]

Prior studies of muscle blood flow and muscle-specific oxygen consumption have required invasive injection of dye and magnetic resonance imaging, respectively. Such measures have limited utility for continuous monitoring of the respiratory muscles. Frequency-domain near-infrared spectroscopy and diffuse correlation spectroscopy (FD-NIRS & DCS) can provide continuous surrogate measures of blood flow index (BFi) and metabolic rate of oxygen consumption (MRO2). This study aimed to validate sternocleidomastoid FD-NIRS & DCS outcomes against electromyography (EMG) and mouth pressure (Pm) during incremental inspiratory threshold loading (ITL). Six female and six male healthy adults (means ± SD; 30 ± 7 yr, maximum inspiratory pressure 118 ± 61 cmH2O) performed incremental ITL starting at low loads (8 ± 2 cmH2O) followed by 50-g increments every 2 min until task failure. FD-NIRS & DCS continuously measured sternocleidomastoid oxygenated and deoxygenated hemoglobin + myoglobin (oxy/deoxy[Hb + Mb]), tissue saturation of oxygen (StO2), BFi, and MRO2. Ventilatory parameters including inspiratory Pm were also evaluated. Pm increased during incremental ITL (P < 0.05), reaching −47[−74 to −34] cmH2O (median [IQR: 25%–75%]) at task failure. Ventilatory parameters were constant throughout ITL (all P > 0.05). Sternocleidomastoid BFi and MRO2 increased from the start of the ITL (both P < 0.05). Deoxy[Hb + Mb] increased close to task failure, concomitantly with a constant increase in MRO2, and decreased StO2. Sternocleidomastoid deoxy[Hb + Mb], BFi, StO2, and MRO2 obtained during ITL via FD-NIRS & DCS correlated with sternocleidomastoid EMG (all P < 0.05). In healthy adults, FD-NIRS & DCS can provide continuous surrogate measures of respiratory BFi and MRO2. Increasing sternocleidomastoid oxygen consumption near task failure was associated with increased oxygen extraction and reduced tissue saturation. NEW & NOTEWORTHY: This study introduces a novel approach, frequency-domain near-infrared spectroscopy and diffuse correlation spectroscopy (FD-NIRS & DCS), for noninvasive continuous monitoring of respiratory muscle blood flow and metabolic rate of oxygen consumption. Unlike prior methods involving invasive dye injection and magnetic resonance imaging, FD-NIRS & DCS offers the advantage of continuous measurement without the need for invasive procedures. It holds promise for advancing muscle physiology understanding and opens avenues for real-time monitoring of respiratory muscles. [ABSTRACT FROM AUTHOR]

Understanding post-stroke changes in skeletal muscle oxidative metabolism and microvascular reactivity could help create therapeutic targets that optimize rehabilitative interventions. Due to disuse atrophy, we hypothesized that basal muscle oxygen consumption rate and microvascular endothelial function would be impaired in the tibialis anterior (TA) muscle of the affected leg of chronic stroke survivors compared with the nonaffected leg and versus matched controls. Fifteen chronic stroke survivors (10 females) and 15 matched controls (9 females) completed this study. A near-infrared spectroscopy oximeter measured tissue oxygen saturation (StO2) of the TA in both legs of stroke survivors and the dominant leg of controls. A cuff was placed around the thigh and inflated to 225 mmHg for 5 min while StO2 was continuously measured. The rate of change in StO2 was calculated during cuff occlusion and immediately post-cuff release. The rate of oxygen desaturation was similar between the legs of the stroke survivors (paretic –0.12 ± 0.04%·s−1 vs. nonparetic –0.16 ± 011%·s−1; P = 0.49), but the paretic leg had a reduced desaturation rate versus controls (–0.25 ± 0.18%·s−1; P = 0.007 vs. paretic leg). After cuff release, there was a greater oxygen resaturation rate in the nonparetic leg compared with the paretic leg (3.13 ± 2.08%·s−1 vs. 1.60 ± 1.11%·s−1, respectively; P = 0.01). The control leg had a similar resaturation rate versus the nonparetic leg (control = 3.41 ± 1.79%·s−1; P = 0.69) but was greater than the paretic leg (P = 0.003). The TA in the paretic leg had an impaired muscle oxygen consumption rate and reduced microvascular endothelial function compared with controls. NEW & NOTEWORTHY: Secondary consequences of stroke are not well described. In this study, we show that basal muscle oxidative consumption and microvascular endothelial function are reduced in the paretic tibialis anterior muscle of chronic stroke survivors compared with matched controls using near-infrared spectroscopy and the vascular occlusion technique. There was a moderately strong correlation between microvascular endothelial function and paretic leg strength. [ABSTRACT FROM AUTHOR]

This systematic review and meta-analysis examined the physiological mechanisms responsible for lower peak exercise leg oxygen uptake (V̇ o 2) in patients with chronic disease. Studies measuring peak leg V̇ o 2 (primary outcome) and its physiological determinants during large (cycle) or small muscle mass exercise (single-leg knee extension, SLKE) in patients with chronic disease were included in this meta-analysis. Pooled estimates for each outcome were reported as a weighted mean difference (WMD) between chronic disease and controls. We included 10 studies that measured peak leg V̇ o 2 in patients with chronic disease (n = 109, mean age: 45 yr; encompassing chronic obstructive pulmonary disease, COPD, heart failure with reduced ejection fraction, HFrEF, or chronic renal failure, RF) and age-matched controls (n = 88). In pooled analysis, peak leg V̇ o 2 (WMD; −0.23 L/min, 95% CI: −0.32 to −0.13), leg oxygen (O2) delivery (WMD: −0.27 L/min, 95% CI: −0.37 to −0.17), and muscle O2 diffusive conductance (WMD: −5.2 mL/min/mmHg, 95% CI: −7.1 to −3.2) were all significantly lower during cycle and SLKE exercise in chronic disease versus controls. These results highlight that during large and small muscle mass exercise in patients with COPD, HFrEF, or RF, there is no single factor causing peak V̇ o 2 limitations. Specifically, the lower peak V̇ o 2 in these pathologies is due to not only the expected impairments in convective O2 delivery but also impairments in muscle oxygen diffusive transport from capillary to mitochondria. Whether impaired muscle O2 transport is caused solely by inactivity or additional muscle pathology remains in question. NEW & NOTEWORTHY: Peripheral (skeletal muscle and vasculature) factors contribute significantly to reduced exercise capacity during both large and small muscle mass exercise in chronic diseases such as COPD, HFrEF, or RF and should be important targets of therapy in addition to the primary organs (lungs, heart, and kidneys) affected by disease. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that a %SmO2 (muscle O2 saturation) slope can distinguish the heavy-severe exercise domain boundary and the highest steady-state metabolic rate. Thirteen participants (5 women) performed a graded exercise test (GXT) to determine peak oxygen consumption (V O2peak) and lactate turn point (LTP). On a separate study day, a %SmO2 zero-slope prediction trial included completing 5-min cycling bouts in an estimated heavy domain, at an estimated critical power, and in an estimated severe domain. Linear regression then determined the work rate at the predicted %SmO2 zero-slope, before a fourth 5-min confirmation trial. Two separate validation study days included confirmed steady-state (heavy domain) and nonsteady-state (severe domain) constant work rate trials. The power at the predicted %SmO2 zero-slope was 204 ± 36 W and occurred at a % SmO2 slope of 0.7 ± 1.4%/min (P = 0.12 relative to zero). There was no difference between the power at LTP (via GXT) and the predicted %SmO2 zero-slope linked power (P = 0.74). From validation study days, the %SmO2 slope was 0.32 ± 0.73%/min during confirmed heavy-domain constant work rate exercise and -0.75 ± 1.94%/min during confirmed severe-domain exercise (P < 0.05). The %SmO2 zero-slope consistently delineated steady state from nonsteady-state metabolic parameters (V O2 and blood lactate) and the heavy-severe domain boundary. Our data suggest the %SmO2 slope can identify the highest steady-state metabolic rate and the physiological boundary between the heavy-severe domain, independent of work rate. [ABSTRACT FROM AUTHOR]

Physiologists commonly use single-value energy equivalents (e.g., 20.1 kJ/LO2 and 20.9 kJ/LO2) to convert oxygen uptake (VO2) to energy, but doing so ignores how the substrate oxidation ratio (carbohydrate:fat) changes across aerobic intensities. Using either 20.1 kJ/LO2 or 20.9 kJ/LO2 can incur systematic errors of up to 7%. In most circumstances, the best approach for estimating energy expenditure is to measure both VO2 and VCO2 and use accurate, species-appropriate stoichiometry. However, there are circumstances when VCO2 measurements may be unreliable. In those circumstances, we recommend that the research report or compare only VO2. [ABSTRACT FROM AUTHOR]

Responses to exercise at a given percentage of one’s maximum rate of oxygen consumption (VO2max), or percentage of the power associated with VO2max during a graded exercise test (i.e., PGXT), vary. The purpose of this study was to determine if differences in critical power (PCRIT, maximum metabolic steady state) and work-prime (W0, the amount of work tolerated above steady state) are related to training-induced changes in endurance. PCRIT, W' VO2max, and other variables were determined before and after 22 adults completed 8 wk of either moderate-intensity continuous training (MICT) or high-intensity interval training (HIIT) performed at fixed percentages of PGXT. On average, PCRIT increased to a greater extent following HIIT (MICT: 15.7 ± 3.1% vs. HIIT: 27.5 ± 4.3%; P = 0.03), but the magnitude of change varied widely within each group (MICT: 4%–36%, HIIT: 4%–61%). The intensity of the prescribed exercise relative to pretraining PCRIT, not PGXT, accounted for most of the variance in changes to PCRIT in response to a given protocol (R² = 0.61–0.64; P < 0.01). Although PCRIT and VO2max were related before training (R² = 0.92, P < 0.01), the training-induced change in PCRIT was not significantly related to the change in VO2max (R² = 0.06, P = 0.26). Before training, time-to-failure at PGXT was related to W0 (R2 = 0.52; P < 0.01), but not VO2max (R² = 0.13; P = 0.10). Traininginduced changes in time-to-failure at the initial PGXT were better captured by the combined changes in W0 and PCRIT (R² = 0.77, P < 0.01), than by the change in VO2max (R² = 0.24; P = 0.02). Differences in PCRIT and W' account for some of the variability in responses to endurance exercise. NEW & NOTEWORTHY As the highest percentage of VO2max at which steady state conditions can be achieved, a person’s critical power (PCRIT) strongly influences the metabolic strain of a given exercise. In this study we demonstrate that training-induced changes in endurance are more strongly related to the intensity of an exercise training program, relative to PCRIT than relative to VO2max. Thus, exercise may be more homogenously and effectively prescribed in relation to PCRIT than traditional factors like VO2max. [ABSTRACT FROM AUTHOR]

Few noninvasive therapies currently exist to improve functional capacity in people with lower extremity peripheral artery disease (PAD). The goal of the present study was to test the hypothesis that unsupervised, home-based leg heat therapy (HT) using water-circulating trousers perfused with warm water would improve walking performance in patients with PAD. Patients with symptomatic PAD were randomized into either leg HT (n = 18) or a sham treatment (n = 16). Patients were provided with water- circulating trousers and a portable pump and were asked to apply the therapy daily (7 days/wk, 90 min/session) for 8 wk. The primary study outcome was the change from baseline in 6-min walk distance at 8-wk follow-up. Secondary outcomes included the claudication onset-time, peak walking time, peak pulmonary oxygen consumption and peak blood pressure during a graded treadmill test, resting blood pressure, the ankle-brachial index, postocclusive reactive hyperemia in the calf, cutaneous microvascular reactivity, and perceived quality of life. Of the 34 participants randomized, 29 completed the 8-wk follow-up. The change in 6-min walk distance at the 8-wk follow-up was significantly higher (P = 0.029) in the group exposed to HT than in the shamtreated group (Sham: median: -0.9; 25%, 75% percentiles: -5.8, 14.3; HT: median: 21.3; 25%, 75% percentiles: 10.1, 42.4, P = 0.029). There were no significant differences in secondary outcomes between the HT and sham group at 8-wk follow-up. The results of this pilot study indicate that unsupervised, home-based leg HT is safe, well-tolerated, and elicits a clinically meaningful improvement in walking tolerance in patients with symptomatic PAD. NEW & NOTEWORTHY This is the first sham-controlled trial to examine the effects of home-based leg heat therapy (HT) on walking performance in patients with peripheral artery disease (PAD). We demonstrate that unsupervised HT using water-circulating trousers is safe, well-tolerated, and elicits meaningful changes in walking ability in patients with symptomatic PAD. This home-based treatment option is practical, painless, and may be a feasible adjunctive therapy to counteract the decline in lower extremity physical function in patients with PAD. [ABSTRACT FROM AUTHOR]

Phase 2 pulmonary oxygen uptake kinetics (ϕ2 τV̇o2P) reflect muscle oxygen consumption dynamics and are sensitive to changes in state of training or health. This study identified an unbiased method for data collection, handling, and fitting to optimize V̇o2P kinetics estimation. A validated computational model of V̇o2P kinetics and a Monte Carlo approach simulated 2 × 105 moderate-intensity transitions using a distribution of metabolic and circulatory parameters spanning normal health. Effects of averaging (interpolation, binning, stacking, or separate fitting of up to 10 transitions) and fitting procedures (biexponential fitting, or ϕ2 isolation by time removal, statistical, or derivative methods followed by monoexponential fitting) on accuracy and precision of V̇o2P kinetics estimation were assessed. The optimal strategy to maximize accuracy and precision of τV̇o2P estimation was 1-s interpolation of 4 bouts, ensemble averaged, with the first 20 s of exercise data removed. Contradictory to previous advice, we found optimal fitting procedures removed no more than 20 s of ϕ1 data. Averaging method was less critical: interpolation, binning, and stacking gave similar results, each with greater accuracy compared with analyzing repeated bouts separately. The optimal procedure resulted in ϕ2 τV̇o2P estimates for transitions from an unloaded or loaded baseline that averaged 1.97 ± 2.08 and 1.04 ± 2.30 s from true, but were within 2 s of true in only 47-62% of simulations. Optimized 95% confidence intervals for τV̇o2P ranged from 4.08 to 4.51 s, suggesting a minimally important difference of ~5 s to determine significant changes in τV̇o2P during interventional and comparative studies.NEW & NOTEWORTHY We identified an unbiased method to maximize accuracy and precision of oxygen uptake kinetics (τV̇o2P) estimation. The optimum number of bouts to average was four; interpolation, bin, and stacking averaging methods gave similar results. Contradictory to previous advice, we found that optimal fitting procedures removed no more than 20 s of phase 1 data. Our data suggest a minimally important difference of ~5 s to determine significant changes in τV̇o2P during interventional and comparative studies.

The pulmonary O2 uptake (V̇o2p) response to ramp-incremental (RI) exercise increases linearly with work rate (WR) after an early exponential phase, implying that a single time constant (τ) and gain (G) describe the response. However, variability in τ and G of V̇o2p kinetics to different step increments in WR is documented. We hypothesized that the "linear" V̇o2p-WR relationship during RI exercise results from the conflation between WR-dependent changes in τ and G. Nine men performed three or four repeats of RI exercise (30 W/min) and two step-incremental protocols consisting of four 60-W increments beginning from 20 W or 50 W. During testing, breath-by-breath V̇o2p was measured by mass spectrometry and volume turbine. For each individual, the V̇o2p RI response was characterized with exponential functions containing either constant or variable τ and G values. A relationship between τ and G vs. WR was determined from the step-incremental protocols to derive the variable model parameters. τ and G increased from 21 ± 5 to 98 ± 20 s and from 8.7 ± 0.6 to 12.0 ± 1.9 ml·min(-1)·W(-1) for WRs of 20-230 W, respectively, and were best described by a second-order (τ) and a first-order (G) polynomial function of WR (lowest Akaike information criterion score). The sum of squared residuals was not different (P > 0.05) when the V̇o2p RI response was characterized with either the constant or variable models, indicating that they described the response equally well. Results suggest that τ and G increase progressively with WR during RI exercise. Importantly, these relationships may conflate to produce a linear V̇o2p-WR response, emphasizing the influence of metabolic heterogeneity in determining the apparent V̇o2p-WR relationship during RI exercise.

Despite several attempts to quantify the metabolic savings resulting from the use of passive back-support exoskeletons (BSEs), no study has modeled the metabolic change while wearing an exoskeleton during lifting. The objectives of this study were to: 1) quantify the metabolic reductions due to the VT-Lowe's exoskeleton during lifting; and 2) provide a comprehensive model to estimate the metabolic reductions from using a passive BSE. In this study, 15 healthy adults (13 males, 2 females) of ages 20--34 yr (mean = 25.33, SD = 4.43) performed repeated freestyle lifting and lowering of an empty box and a box with 20% of their bodyweight. Oxygen consumption and metabolic expenditure data were collected. A model for metabolic expenditure was developed and fitted with the experimental data of two prior studies and the without-exoskeleton experimental results. The metabolic cost model was then modified to reflect the effect of the exoskeleton. The experimental results revealed that VT-Lowe's exoskeleton significantly lowered the oxygen consumption by ~9% for an empty box and 8% for a 20% bodyweight box, which corresponds to a net metabolic cost reduction of ~12% and ~9%, respectively. The mean metabolic difference (i.e., without-exo minus with-exo) and the 95% confidence interval were 0.36 and (0.2-0.52) W/kg for 0% body weight and 0.43 and (0.18-0.69) W/kg for 20% body weight. Our modeling predictions for with-exoskeleton conditions were precise, with absolute freestyle prediction errors of <2.1%. The model developed in this study can be modified based on different study designs, and can assist researchers in enhancing designs of future lifting exoskeletons. [ABSTRACT FROM AUTHOR]

This study examined the impact of aging on the elastic and resistive components of the work of breathing (Wb) during locomotor exercise at a given 1) ventilatory rate, 2) metabolic rate, and 3) operating lung volume. Eight healthy younger (25 ± 4 yr) and 8 older (72 ± 6 yr) participants performed incremental bicycle exercise, from which retrospective analyses identified similar ventilatory rates (approximately 40, 70, and 100 L·min-1), similar metabolic rates (VO2: approximately 1.2, 1.6, and 1.9 L·min-1), and similar lung volumes [inspiratory and expiratory reserve volumes (IRV/ERV: approximately 25/34%, 16/33%, and 13-34% of vital capacity]. Wb at each level was quantified by integrating the averaged esophageal pressure-volume loop, which was then partitioned into elastic and resistive components of inspiratory and expiratory work using the modified Campbell diagram. IRV was smaller in the older participants during exercise at ventilations of 70 and 100 L·min-1 and during exercise at the three metabolic rates (P < 0.05). Mainly because of a greater inspiratory elastic and resistive Wb in the older group (P < 0.05), total Wb was augmented by 40%-50% during exercise at matched ventilatory and matched metabolic rates. When examined during exercise evoking similar lung volumes, total Wb was not different between the groups (P = 0.86). Taken together, although aging exaggerates total Wb during locomotor exercise at a given ventilatory or a given metabolic rate, this difference is abolished during exercise at a given operating lung volume. These findings highlight the significance of operating lung volume in determining the age-related difference in Wb during locomotor exercise. [ABSTRACT FROM AUTHOR]

Muscle deoxygenation (i.e., deoxy[Hb + Mb]) during exercise assesses the matching of oxygen delivery (Q̇O2) to oxygen utilization (V̇O2). Until now limitations in near-infrared spectroscopy (NIRS) technology did not permit discrimination of deoxy[Hb + Mb] between superficial and deep muscles. In humans, the deep quadriceps is more highly vascularized and oxidative than the superficial quadriceps. Using high-power time-resolved NIRS, we tested the hypothesis that deoxygenation of the deep quadriceps would be less than in superficial muscle during incremental cycling exercise in eight males. Pulmonary V̇O2 was measured and muscle deoxy[Hb + Mb] was determined in the superficial vastus lateralis (VL), vastus medialis (VM), and rectus femoris (RF-s) and the deep rectus femoris (RF-d). deoxy[Hb + Mb] in RF-d was significantly less than VL at 70% (67.2 ± 7.0 vs. 75.5 ± 10.7 μM) and 80% (71.4 ± 11.0 vs. 79.0 ± 15.4 μM) of peak work rate (WR(peak)), but greater than VL and VM at WR(peak) (87.7 ± 32.5 vs. 76.6 ± 17.5 and 75.1 ± 19.9 μM). RF-s was intermediate at WR(peak) (82.6 ± 18.7 μM). Total hemoglobin and myoglobin concentration and tissue oxygen saturation were significantly greater in RF-d than RF-s throughout exercise. The slope of deoxy[Hb + Mb] increase (proportional to Q̇O2/V̇O2) in VL and VM slowed markedly above 70% WR(peak), whereas it became greater in RF-d. This divergent deoxygenation pattern may be due to a greater population of slow-twitch muscle fibers in the RF-d muscle and the differential recruitment profiles and vascular and metabolic control properties of specific fiber populations within superficial and deeper muscle regions.

Near-infrared assessment of skeletal muscle is restricted to superficial tissues due to power limitations of spectroscopic systems. We reasoned that understanding of muscle deoxygenation may be improved by simultaneously interrogating deeper tissues. To achieve this, we modified a high-power (∼8 mW), time-resolved, near-infrared spectroscopy system to increase depth penetration. Precision was first validated using a homogenous optical phantom over a range of inter-optode spacings (OS). Coefficients of variation from 10 measurements were minimal (0.5-1.9%) for absorption (μa), reduced scattering, simulated total hemoglobin, and simulated O2 saturation. Second, a dual-layer phantom was constructed to assess depth sensitivity, and the thickness of the superficial layer was varied. With a superficial layer thickness of 1, 2, 3, and 4 cm (μa = 0.149 cm(-1)), the proportional contribution of the deep layer (μa = 0.250 cm(-1)) to total μa was 80.1, 26.9, 3.7, and 0.0%, respectively (at 6-cm OS), validating penetration to ∼3 cm. Implementation of an additional superficial phantom to simulate adipose tissue further reduced depth sensitivity. Finally, superficial and deep muscle spectroscopy was performed in six participants during heavy-intensity cycle exercise. Compared with the superficial rectus femoris, peak deoxygenation of the deep rectus femoris (including the superficial intermedius in some) was not significantly different (deoxyhemoglobin and deoxymyoglobin concentration: 81.3 ± 20.8 vs. 78.3 ± 13.6 μM, P > 0.05), but deoxygenation kinetics were significantly slower (mean response time: 37 ± 10 vs. 65 ± 9 s, P ≤ 0.05). These data validate a high-power, time-resolved, near-infrared spectroscopy system with large OS for measuring the deoxygenation of deep tissues and reveal temporal and spatial disparities in muscle deoxygenation responses to exercise.

Skeletal muscle deoxygenated hemoglobin and myoglobin concentration ([HHb]), assessed by near-infrared spectroscopy (NIRS), is commonly used as a surrogate of regional O2 extraction (reflecting the O2 delivery-to-consumption ratio, Q̇/V̇o2). However, [HHb] change (Δ[HHb]) is also influenced by capillary-venous heme concentration, and/or small blood vessel volume (reflected in total heme; [THb]). We tested the hypotheses that Δ[HHb] is associated with O2 extraction, and insensitive to [THb], over a wide range of Q̇/V̇o2 elicited by passive head-up tilt (HUT; 10-min, 15° increments, between -10° and 75°). Steady-state common femoral artery blood flow (FBF) was measured by echo-Doppler, and time-resolved NIRS measured [HHb] and [THb] of vastus lateralis (VL) and gastrocnemius (GS) in 13 men. EMG confirmed muscles were inactive. During HUT in VL [HHb] increased linearly (57 ± 10 to 101 ± 16 μM; P < 0.05 above 15°) and was associated (r(2) ∼ 0.80) with the reduction in FBF (618 ± 75 ml/min at 0° to 268 ± 52 ml/min at 75°; P < 0.05 above 30°) and the increase in [THb] (228 ± 30 vs. 252 ± 32 μM; P < 0.05 above 15°). GS response was qualitatively similar to VL. However, there was wide variation within and among individuals, such that the overall limits of agreement between Δ[HHb] and ΔFBF ranged from -35 to +19% across both muscles. Neither knowledge of tissue O2 saturation nor vascular compliance could appropriately account for the Δ[HHb]-ΔFBF dissociation. Thus, under passive tilt, [HHb] is influenced by Q̇/V̇o2, as well as microvascular hematocrit and/or tissue blood vessel volume, complicating its use as a noninvasive surrogate for muscle microvascular O2 extraction.

The rise in oxygen consumption during the transition from rest to exercise is faster in those who are endurance-trained than those who have sedentary lifestyles, partly due to a more efficient cardiac response. However, data regarding this acute cardiac response in trained individuals are limited to heart rate (HR), stroke volume, and cardiac output. Considering this, we compared cardiac kinetics, including left ventricular (LV) strains and twist/untwist mechanics, between endurance-trained cyclists and their sedentary counterparts. Twenty young, male, trained cyclists and 23 untrained participants aged 18-25 yr performed five similar constant workload exercises on a cyclo-ergometer (target HR: 130 beats/min). During each session, LV myocardial diastolic and systolic linear strains, as well as torsional mechanics, were assessed using speckle-tracking echocardiography. Cardiac function was evaluated every 15 s during the first minute and every 30 s thereafter, until 240 s. Stroke volume increased during the first 30-45 s in both groups but to a significantly greater extent in trained cyclists (31% vs. 24%). Systolic parameters were similar in both groups. Transmitral peak filling velocity and peak filling rate responded faster to exercise and with greater amplitude in trained cyclists. Left ventricular filling pressure was lower in the former, whereas LV relaxation was greater but only at the base of the left ventricle. Basal rotation and peak untwisting rate responded faster and to a greater extent in the cyclists. This study provides new mechanical insights into the key role of LV untwisting in the more efficient acute cardiac response of endurancetrained athletes at onset of exercise. NEW & NOTEWORTHY Our study assessed for the first time, to our knowledge, the kinetics of left ventricular function during the transition from rest to constant-load exercise in endurance-trained subjects. We observed a faster cardiac response in cyclists characterized by a faster response of cardiac output, left ventricular transmitral filling, basal rotation, and untwisting. This study highlighted the key role of left ventricular twisting mechanics in the more efficient acute cardiac response of endurancetrained athletes at onset of exercise. [ABSTRACT FROM AUTHOR]

Critical power (CP) delineates the heavy and severe exercise intensity domains, and sustained work rates above CP result in an inexorable progression of oxygen uptake to a maximal value and, subsequently, the limit of exercise tolerance. The finite work capacity above CP, W0, is defined by the curvature constant of the power-duration relationship. Heavy or severe exercise in a hot environment generates additional challenges related to the rise in body core temperature (Tc) that may impact CP and W0. The purpose of this study was to determine the effect of elevated Tc on CP and W0. CP and W0 were estimated by end-test power (EP; mean of final 30 s) and work above end-test power (WEP), respectively, from 3-min "all-out" tests performed on a cycle ergometer. Volunteers (n = 8, 4 female) performed the 3-min tests during a familiarization visit and two experimental visits (thermoneutral vs. hot, randomized crossover design). Before experimental 3-min tests, the subjects were immersed in water (thermoneutral: 36°C for 30 min; hot: 40.5°C until Tc was ~38.5°C). Mean Tc was significantly greater in the hot condition than in the thermoneutral condition (38.5 ± 0.0°C vs. 37.4 ± 0.2°C; means ± SD, P < 0.01). All 3-min tests were performed in an environmental chamber [thermoneutral: 18°C, 45% relative humidity (RH); hot: 38 °C, 40% RH]. EP was similar between thermoneutral (239 ± 57 W) and hot (234 ± 66 W; P = 0.55) conditions. WEP was similar between thermoneutral (10.9 ± 3.0 kJ) and hot conditions (9.3 ± 3.6; P = 0.19). These results suggest that elevated Tc has no significant impact on EP or WEP. NEW & NOTEWORTHY The parameters of the power-duration relationship (critical power and W0) estimated by a 3-min all-out test were not altered by elevated body core temperature as compared with a thermoneutral condition. [ABSTRACT FROM AUTHOR]

The baroreflex integrity in early-stage pulmonary arterial hypertension (PAH) remains uninvestigated. A potential baroreflex impairment could be functionally relevant and possibly mediated by enhanced peripheral chemoreflex activity. Thus, we investigated 1) the cardiac baroreflex in nonhypoxemic PAH; 2) the association between baroreflex indexes and peak aerobic capacity [i.e., peak oxygen consumption (Vo2peak)]; and 3) the peripheral chemoreflex contribution to the cardiac baroreflex. Nineteen patients and 13 age- and sex-matched healthy adults (HA) randomly inhaled either 100% O2 (peripheral chemoreceptor inhibition) or 21% O2 (control session) while at rest and during a repeated sit-to-stand maneuver. Beat-by-beat analysis of R-R intervals and systolic blood pressure provided indexes of cardiac baroreflex sensitivity (cBRS) and effectiveness (cBEI). The PAH group had lower cBEI for all sequences (cBEIALL) at rest [means ± SD: PAH = 0.5 ± 0.2 vs. HA = 0.7 ± 0.1 arbitrary units (a.u.), P = 0.02] and lower cBRSALL (PAH = 6.8 ± 7.0 vs. HA = 9.7 ± 5.0 ms·mmHg-1, P < 0.01) and cBEIALL (PAH = 0.4 ± 0.2 vs. HA= 0.6 ± 0.1 a.u., P < 0.01) during the sit-to-stand maneuver versus the HA group. The cBEI during the sit-to-stand maneuver was independently correlated to Vo2peak (partial r = 0.45, P < 0.01). Hyperoxia increased cBRS and cBEI similarly in both groups at rest and during the sit-to-stand maneuver. Therefore, cardiac baroreflex dysfunction was observed under spontaneous and, most notably, provoked blood pressure fluctuations in nonhypoxemic PAH, was not influenced by the peripheral chemoreflex, and was associated with lower Vo2peak, suggesting that it could be functionally relevant. [ABSTRACT FROM AUTHOR]

Sepsis-induced diaphragm dysfunction is a major contributor to respiratory failure in mechanically ventilated patients. There are no pharmacological treatments for this syndrome, but studies suggest that diaphragm weakness is linked to mitochondrial free radical generation. We hypothesized that administration of mitoquinone mesylate (MitoQ), a mitochondrially targeted free radical scavenger, would prevent sepsis-induced diaphragm dysfunction. We compared diaphragm function in 4 groups of male mice: 1) sham-operated controls treated with saline (0.3 mL ip), 2) sham-operated treated with MitoQ (3.5 mg/kg/day given intraperitoneally in saline), 3) cecal ligation puncture (CLP) mice treated with saline, and 4) CLP mice treated with MitoQ. Forty-eight hours after surgery, we assessed diaphragm force generation, myosin heavy chain content, state 3 mitochondrial oxygen consumption (OCR), and aconitase activity. We also determined effects of MitoQ in female mice with CLP sepsis and in mice with endotoxininduced sepsis. CLP decreased diaphragm specific force generation and MitoQ prevented these decrements (e.g. maximal force averaged 30.2 ± 1.3, 28.0 ± 1.3, 12.8 ± 1.9, and 30.0 ± 1.0 N/cm2 for sham, sham þ MitoQ, CLP, and CLP þ MitoQ groups, respectively, P < 0.001). CLP also reduced diaphragm mitochondrial OCR and aconitase activity; MitoQ blocked both effects. Similar responses were observed in female mice and in endotoxin-induced sepsis. Moreover, delayed MitoQ treatment (by 6 h) was as effective as immediate treatment. These data indicate that MitoQ prevents sepsis-induced diaphragm dysfunction, preserving force generation. MitoQ may be a useful therapeutic agent to preserve diaphragm function in critically ill patients with sepsis. [ABSTRACT FROM AUTHOR]

Exercise often causes skeletal muscle hyperthermia, likely resulting in decreased efficiency of mitochondrial respiration. We hypothesized that athletic conditioning would improve mitochondrial tolerance to hyperthermia. Skeletal muscle biopsies were obtained from six Alaskan sled dogs under light general anesthesia before and after a full season of conditioning and racing, and respiration of permeabilized muscle fibers was measured at 38, 40, 42, and 44 °C. There was no effect of temperature on phosphorylating respiration, and athletic conditioning increased maximal phosphorylating respiration by 19%. Leak respiration increased and calculated efficiency of oxidative phosphorylation decreased with increasing incubation temperature, and athletic conditioning resulted in higher leak respiration and lower calculated oxidative phosphorylation efficiency at all temperatures. Conditioning increased skeletal muscle expression of putative mitochondrial leak pathways adenine nucleotide transporter 1 and uncoupling protein 3, both of which were correlated with the magnitude of leak respiration. We conclude that athletic conditioning in elite canine endurance athletes results in increased capacity for mitochondrial proton leak that potentially reduces maximal mitochondrial membrane potential during periods of high oxidative phosphorylation. This effect may provide a mechanistic explanation for previously reported decreases in exercise-induced muscle damage in well-conditioned subjects. [ABSTRACT FROM AUTHOR]

Computer simulations, using the “Pi double-threshold” mechanism of muscle fatigue postulated previously (the first threshold initiating progressive reduction in work efficiency and the second threshold resulting in exercise intolerance), demonstrated that several parameters of the skeletal muscle bioenergetic system can affect maximum oxygen consumption (V_ O2max), critical power (CP), and oxygen consumption (V_ O2) on-kinetics in skeletal muscle. Simulations and experimental observations together demonstrate that endurance exercise training increases oxidative phosphorylation (OXPHOS) activity and/or each-step activation (ESA) intensity, the latter, especially in the early stages of training. Here, new computer simulations demonstrate that an endurance training-induced increase in OXPHOS activity and decrease in peak Pi (Pipeak), at which exercise is terminated because of exercise intolerance, result in increased V_ O2max and CP, speeding of the primary phase II of V_ O2 on-kinetics, and decreases V_ O2 slow component magnitude, consistent with their observed behavior in vivo. It is possible, but remains unknown, whether there is a contribution to this behavior of an increase in the critical Pi (Picrit), above which the additional ATP usage underlying the slow component begins, and a decrease in the activity of the additional ATP usage (kadd). Thus, we offer a mechanism, involving Pi accumulation, Picrit and Pipeak, of the training-induced adaptations in V_ O2max, CP, and the primary and slow component phases of V_ O2 on-kinetics that was absent in the literature. [ABSTRACT FROM AUTHOR]

Efforts to better understand cardiorespiratory health are relevant for the future development of optimized physical activity programs. We aimed to explore the impact of the signal quality on the expected associations between the ability of the aerobic system in supplying energy as fast as possible during moderate exercise transitions with its maximum capacity to supply energy during maximal exertion. It was hypothesized that a slower aerobic system response during moderate exercise transitions is associated with a lower maximal aerobic power; however, this relationship relies on the quality of the oxygen uptake dataset. Forty-three apparently healthy participants performed a moderate constant work rate (CWR) followed by a pseudorandom binary sequence (PRBS) exercise protocol on a cycle ergometer. Participants also performed a maximum incremental cardiopulmonary exercise testing (CPET). The maximal aerobic power was evaluated by the peak oxygen uptake during the CPET and the aerobic fitness was estimated from different approaches for oxygen uptake dynamics analysis during the CWR and PRBS protocols at different levels of signal-to-noise ratio. The product moment correlation coefficient was used to evaluate the correlation level between variables. Aerobic fitness was correlated with maximum aerobic power, but this correlation increased as a function of the signal-to-noise ratio. Aerobic fitness is related to maximal aerobic power; however, this association appeared to be highly dependent on the data quality and analysis for aerobic fitness evaluation. Our results show that simpler moderate exercise protocols might be as good as maximal exertion exercise protocols to obtain indexes related to cardiorespiratory health. [ABSTRACT FROM AUTHOR]

Near-infrared spectroscopy (NIRS) has been utilized as a noninvasive method to evaluate skeletal muscle mitochondrial function in humans, by calculating muscle V O2 (V O2m) recovery (off-) kinetics following short light-intensity plantar flexion exercise. The aim of the present study was to determineV O2m off- kinetics following standard cycle ergometer exercise of different intensities. Fifteen young physically active healthy men performed an incremental exercise (INCR) up to exhaustion and two repetitions of constant work-rate (CWR) exercises at 80% of gas exchange threshold (GET; MODERATE) and at 40% of the difference between GET and peak pulmonary V O2 (V O2p; HEAVY). V O2p and vastus lateralis muscle fractional O2 extraction by NIRS [deoxy(HbMb)]) were recorded continuously. Transient arterial occlusions were carried out at rest and during the recovery for V O2m calculation. All subjects tolerated the repeated occlusions protocol without problems. The quality of the monoexponential fitting for V O2m off-kinetics analysis was excellent (0.93≤r2≤0.99). According to interclass correlation coefficient, the test-retest reliability was moderate to good. V O2m values at the onset of recovery were ~27, ~38, and ~35 times higher (in MODERATE, HEAVY, and INCR, respectively) than at rest. The time constants (τ) of V O2m off-kinetics were lower (P < 0.001) following MODERATE (29.1 ± 6.8 s) vs. HEAVY (40.8 ± 10.9) or INCR (42.9 ± 10.9), suggesting an exercise intensity dependency of V O2m off-kinetics. Only following MODERATE theV O2m off-kinetics were faster than the V O2p off-kinetics. V O2m off-kinetics, determined noninvasively by the NIRS repeated occlusions technique, can be utilized as a functional evaluation tool of skeletal muscle oxidative metabolism also following conventional cycle ergometer exercise. [ABSTRACT FROM AUTHOR]

Exercise capacity and training response are limited in chronic obstructive pulmonary disease (COPD), but the extent to which this is related to altered skeletal muscle function is not fully understood. To test the hypothesis that muscle gene expression is altered in COPD, we performed needle biopsies from the vastus lateralis of six COPD patients and five sedentary age-matched healthy men, before and after 3 mo of exercise training. RNA was hybridized to Affymetrix U133A Genechip arrays. In addition, peak O(2) uptake and other functional parameters (e.g., 6-min walk) were measured before and after training. The 6-min walk test increased significantly following training in both groups (53.6 +/- 18.6 m in controls, P = 0.045; 37.1 +/- 6.7 m in COPD, P = 0.002), but peak O(2) uptake increased only in controls (19.4 +/- 4.5%, P = 0.011). Training significantly altered muscle gene expression in both groups, but the number of affected genes was lower in the COPD patients (231) compared with controls (573). Genes related to energy pathways had higher expression in trained controls. In contrast, oxidative stress, ubiquitin proteasome, and COX gene pathways had higher expression in trained COPD patients, and some genes (e.g., COX11, COX15, and MAPK-9) were upregulated by training only in COPD patients. We conclude that both COPD and control subjects demonstrated functional responses to training but with somewhat different patterns in muscle gene expression. The pathways that are uniquely induced by exercise in COPD (e.g., ubiquitin proteasome and COX) might indicate a greater degree of tissue stress (perhaps by altered O(2) and CO(2) dynamics) than in controls.

Obesity blunts catecholamine and growth hormone (GH) responses to exercise in adults, but the effect of obesity on these exercise-associated hormonal responses in children is unclear. Therefore, the aim of the present study was to asses the effect of childhood obesity on the counterregulatory hormonal response to acute exercise. Twenty-five obese children (Ob; body mass index > 95%), and 25 age, gender, and maturity-matched normal-weight controls (NW) participated in the study. Exercise consisted of ten 2-min bouts of constant-cycle ergometry above the anaerobic threshold, with 1-min rest intervals between each bout. Pre-, post-, and 120-min postexercise blood samples were collected for circulating components of the GH-IGF-I axis and catecholamines. There were no differences in peak exercise heart rate, serum lactate, and peak O2 uptake normalized to lean body mass between the groups. Obesity attenuated the GH response to exercise (8.9 +/- 1.1 vs. 3.4 +/- 0.7 ng/ml in NW and Ob participants, respectively; P < 0.02). No significant differences in the response to exercise were found for other components of the GH-IGF-I axis. Obesity attenuated the catecholamine response to exercise (epinephrine: 52.5 +/- 12.7 vs. 18.7 +/- 3.7 pg/ml, P < 0.02; norepinephrine: 479.5 +/- 109.9 vs. 218.0 +/- 26.0 pg/ml, P < 0.04; dopamine: 17.2 +/- 2.9 vs. 3.5 +/- 1.9 pg/ml, P < 0.006 in NW and Ob, respectively). Insulin levels were significantly higher in the obese children and dropped significantly after exercise in both groups. Despite the elevated insulin levels and the blunted counterregulatory response, none of the participants developed hypoglycemia. Childhood obesity was associated with attenuated GH and catecholamine response to acute exercise. These abnormalities were compensated for, so that exercise was not associated with hypoglycemia, despite increased insulin levels in obese children.

Little is known about the relationship among training, energy expenditure, muscle volume, and fitness in prepubertal girls. Because physical activity is high in prepubertal children, we hypothesized that there would be no effect of training. Forty pre- and early pubertal (mean age 9.1 +/- 0.1 yr) nonobese girls enrolled in a 5 day/wk summer school program for 5 wk and were randomized to control (n = 20) or training groups (n = 20; 1.5 h/day, endurance-type exercise). Total energy expenditure (TEE) was measured using doubly labeled water, thigh muscle volume using magnetic resonance imaging, and peak O(2) uptake (VO(2 peak)) using cycle ergometry. TEE was significantly greater (17%, P < 0.02) in the training girls. Training increased thigh muscle volume (+4.3 +/- 0.9%, P < 0.005) and VO(2 peak) (+9.5 +/- 6%, P < 0.05), effects surprisingly similar to those observed in adolescent girls using the same protocol (Eliakim A, Barstow TJ, Brasel JA, Ajie H, Lee W-NP, Renslo R, Berman N, and Cooper DM, J Pediatr 129: 537-543, 1996). We further compared these two sample populations: thigh muscle volume per weight was much lower in adolescent compared with prepubertal girls (17.0 +/- 0.3 vs. 27.8 +/- 0.6 ml/kg body mass; P < 0.001), and allometric analysis revealed remarkably low scaling factors relating muscle volume (0.34 +/- 0.05, P < 0.0001), TEE (0.24 +/- 0. 06, P < 0.0004), and VO(2 peak) (0.28 +/- 0.07, P < 0.0001) to body mass in all subjects. Muscle and cardiorespiratory functions were quite responsive to brief training in prepubertal girls. Moreover, a retrospective, cross-sectional analysis suggests that increases in muscle mass and VO(2 peak) may be depressed in nonobese American girls as they mature.

The aim of this study was to examine the physiological profiles and the pacing strategies of the father (59 yr old) and son (34 yr old) who broke the World Record time (4:59:22; father: 2:27:52, son: 2:31:30) for combined father and son marathon in 2019. Oxygen uptake (V O2), heart rate (HR), ventilation (V E), blood lactate concentration (La), and running economy (RE) were measured during treadmill- running tests. The total distance of the marathon was divided into eight sections of 5 km and one last section of 2.195 km, and the relative average running velocity on each section was calculated individually. V O2max, HRmax, V? Emax, and Lamax were 65.4 mL· kg-1·min-1, 165 beats/min, 115 L/min, 5.7 mmol/L for the father and 66.9 mL·kg-1·min-1, 181 beats/min, 153 L/min, 11.5 mmol/L for the son, respectively. At 17 km/h, RE was 210 mL·kg-1·km-1 for the father and 200 mL·kg-1·km-1 for the son, and % V ? O2max sustained was 90.9% for the father and 84.5% for the son, respectively. The father maintained an even running velocity during the marathon (running velocity CV -1%), while the son ran the second halfmarathon 7% slower than the first one, and his running velocity markedly dropped from the 35th kilometer. Father and son who broke the World record time for combined father and son marathon had a similar level of performance, but their physiological profiles and pacing strategies during the marathon were different. A more even speed for the son could help them to improve their own record in the near future. [ABSTRACT FROM AUTHOR]

In aged rats, diaphragm muscle (DIAm) reduced specific force and fiber cross-sectional area, sarcopenia, is selective for vulnerable type IIx and/or IIb DIAm fibers, with type I and IIa fibers being resilient. In humans, the oxidative capacity [as measured by maximum succinate dehydrogenase (SDHmax) activity] of fast-type muscle is reduced with aging, with slow-type muscle being unaffected. We hypothesized that in aged Fischer rat DIAm exhibiting sarcopenia, reduced SDHmax activity would occur in type IIx and/or IIb fibers. Rats obtained from the NIA colony (6, 18, and 24 mo old) were euthanized, and ~2-mmwide DIAm strips were obtained. For SDHmax and fiber type assessments, DIAm strips were stretched (approximately optimal length), fresh frozen in isopentane, and sectioned on a cryostat at 6 m. SDHmax, quantified by intensity of nitroblue tetrazolium diformazan precipitation, was assessed in a fiber type-specific manner by comparing serial sections labeled with myosin heavy chain (MyHC) antibodies differentiating type I (MyHCSlow), IIa (MyHC2A), and IIx and/or IIb fibers. Isometric DIAm force and fatigue were assessed in DIAm strips by muscle stimulation with supramaximal pulses at a variety of frequencies (5-100 Hz) delivered in 1-s trains. By 24 mo, DIAm sarcopenia was apparent and SDHmax in type IIx and/or IIb fibers activity was reduced ~35% compared with 6-mo-old control DIAm. These results underscore the remarkable fiber type selectivity of type IIx and/or IIb fibers to age-associated perturbations and suggest that reduced mitochondrial oxidative capacity is associated with DIAm sarcopenia. [ABSTRACT FROM AUTHOR]

Near-infrared diffuse correlation spectroscopy (DCS) is a rapidly evolving optical imaging technique for the assessment of skeletal muscle O2 utilization (mVO2). We compared DCS-derived determinants of mVO2 with conventional measures [blood flow by brachial artery Doppler ultrasound and venous O2 saturation (SVO2 )] in eight volunteers at rest and during incremental handgrip exercise. Brachial artery blood flow and DCS-derived blood flow index (BFI) were linearly related (R2 = 0.57) and increased with each workload, whereas SVO2 decreased from 65.3 ± 2.5% (rest) to 39.9 ± 3.0% (light exercise; P < 0.01) with no change thereafter. In contrast, DCS-derived tissue O2 saturation decreased progressively with each incremental stage (P < 0.01), driven almost entirely by an initial steep rise in deoxyhemoglobin/myoglobin, followed by a linear increase thereafter. Whereas seemingly disparate at first glance, we believe these two approaches provide similar information. Indeed, by plotting the mean convective O2 delivery and diffusive O2 conductance, we show that the initial increase in mVO2 during the transition from rest to exercise was achieved by a greater increase in diffusive O2 conductance versus convective O2 delivery (10-fold vs. 4-fold increase, respectively), explaining the initial decline in SVO2 . In contrast, the increase in mVO2 from light to heavy exercise was achieved by equal increases (1.8-fold) in convective O2 delivery and diffusive O2 conductance, explaining the plateau in SVO2 . That DCS-derived BFI and deoxyhemoglobin/myoglobin (surrogate measure of O2 extraction) share the same general biphasic pattern suggests that both DCS and conventional approaches provide complementary information regarding the determinants of mVO2. NEW & NOTEWORTHY Near-infrared diffuse correlation spectroscopy (DCS) is an emerging optical imaging technique for quantifying skeletal muscle O2 delivery and utilization at the microvascular level. Here, we show that DCS provides complementary insight into the determinants of muscle O2 consumption across a wide range of exercise intensities, further establishing the utility of DCS. [ABSTRACT FROM AUTHOR]

Heat and hypobaric hypoxia independently compromise exercise performance; however, their combined impact on exercise performance has yet to be quantified. This study examined the effects of heat, hypobaric hypoxia, and the combination of these environments on self-paced cycling time trial (TT) performance. Twelve subjects [2 female, 10 male; sea level (SL) peak oxygen consumption (VO2peak), 41.5 ± 4.4 mL·kg-1·min-1, mean ± SD] completed 30 min of steady-state cycling exercise (50% SL VO2peak), followed by a 15-min self-paced TT in four environmental conditions: SL thermoneutral [SLTN; 250 m, 20°C, 30-50% relative humidity (rh)], SL hot (SLH; 250 m, 35°C, 30% rh), hypobaric hypoxia thermoneutral (HTN; 3,000 m, 20°C, 30-50% rh), and hypobaric hypoxia hot (HH; 3,000 m, 35°C, 30% rh). Performance was assessed by the total work (kJ) completed. TT performance was lower (P < 0.05) in SLH, HTN, and HH relative to SLTN (-15.4 ± 9.7, <24.1 ± 16.2, and <33.1 ± 13.4 kJ, respectively). Additionally, the total work completed in HTN and HH was lower (P < 0.05) than that in SLH. In SLH, HTN, and HH, work rate was reduced versus SLTN (P < 0.05) within the first 3 min of exercise and was consistent for the remainder of the bout. No differences (P = 0.05) existed for heart rate or Ratings of Perceived Exertion at the end of exercise among conditions. The decrease in self-paced TT performance in the heat and/or hypobaric hypoxia conditions compared with SLTN conditions resulted from a nearly immediate reduction in work rate that may have been regulated by environmentally induced changes in physiological strain and perception of effort in response to TT exercise. [ABSTRACT FROM AUTHOR]

The present study tested whether, during moderate exercise, 1) the dynamic responses of ADP and changes in free energy of ATP hydrolysis (delta GATP) were similar to those of phosphocreatine [PCr; as would be expected for a simple controller of muscle respiration (QO2)] and 2) the rise in pulmonary O2 uptake (VO2) during cycle exercise would reflect the rise in muscle QO2 indicated by the calf PCr kinetics. The responses of PCr, Pi, ADP, and delta GATP were measured from the calf in five subjects during supine treadle exercise using 31P-magnetic resonance spectroscopy and compared with those for VO2, measured breath by breath during upright cycle exercise. The time constants for delta GATP [24.2 +/- 14.2 (SE) s] were not significantly different from those for PCr (26.3 +/- 17.3 s) and Pi (30.7 +/- 22.5 s) (P > 0.05). The time constants for phase 2 VO2 (29.9 +/- 16.8 s) were also similar to those of PCr. In contrast, the dynamics of ADP were distorted from those of PCr due to dynamic changes in pH. These results are consistent with mechanisms of respiratory control that feature substrate control by PCr or thermodynamic control through changes in delta GATP. However, these results are not consistent with substrate control by ADP in a simple fashion. Furthermore, the similarity of time constants for phase 2 VO2 and muscle PCr suggests that phase 2 VO2 kinetics reflect those of muscle QO2 in healthy subjects during moderate exercise.

An acute insulin-like growth factor I (IGF-I) response to 10 min of above-lactate threshold cycle ergometer exercise was studied in 10 subjects (age 22-35 yr). Each subject exercised on three separate mornings after ingesting one of two isocaloric isovolemic liquid meals high in either fat or glucose or an isovolemic noncaloric placebo. The high-fat meal attenuated the growth hormone (GH) response (Cappon et al., J. Clin. Endocrinol. Metab. 76: 1418-1422, 1993). In contrast, IGF-I increased equally for all protocols [e.g., after the placebo meal IGF-I increased from 21,716 (SE) ng/ml preexercise to 25,316 ng/ml at 10 min of exercise; P < 0.05]. IGF-I peaked by the 10th min of exercise, like GH, and remained significantly elevated for only 20 min of recovery. We tested for possible GH-dependent mechanisms in which circulating IGF-I would increase 12-24 h after exercise. Ten subjects (age 23-32 yr) performed 10 min of above-lactate threshold exercise at 9, 10, and 11 A.M. GH was elevated after the first exercise bout (peak GH 6.05 +/- 1.45 ng/ml; P < 0.001) but was significantly reduced for the second and third bouts (peak GH 2.52 +/- 0.76 and 1.50 +/- 0.40 ng/ml, respectively). No increase in IGF-I was observed by 8 A.M. on the following day. Heavy ergometer exercise led to brief and small increases in circulating IGF-I that were independent of circulating GH.(ABSTRACT TRUNCATED AT 250 WORDS)

Gas exchange response to high-intensity exercise differs in children and adults. We hypothesized that these findings are related to a lower anaerobic ATP supply in children. We predicted therefore a maturation of muscle high-energy phosphate metabolism during exercise. To test this hypothesis, we measured calf muscle Pi, phosphocreatine (PCr), and pH with 31P-nuclear magnetic resonance spectroscopy during rest and progressive exercise in 10 children and 8 adults. No differences were found at rest in pH and Pi/PCr between children and adults. Exercise resulted in a greater increase in Pi/PCr (P < 0.001) and decrease in pH (P < 0.0001) in adults than in children. Six adults and five children exhibited a transition from a slow to a faster rate of Pi/PCr increase and pH decrease during exercise. No significant differences were found between the two groups in the initial slow-phase slopes of Pi/PCr and pH as a function of work rate. In contrast, during the fast phase, Pi/PCr increased (slope: adults 23.6 +/- 9.8, children 10.7 +/- 2.5; P < 0.05) and pH decreased (slope: adults -6.0 +/- 1.9, children -3.7 +/- 1.2; P < 0.05) more rapidly in adults than in children. In conclusion, high-intensity exercise results in different kinetics of Pi/PCr and pH between children and adults. These results suggest that children are less able than adults to affect ATP rephosphorylation by anaerobic metabolic pathways during high-intensity exercise.

To test the hypothesis that O2 uptake (VO2) dynamics are different in adults and children, we examined the response to and recovery from short bursts of exercise in 10 children (7-11 yr) and 13 adults (26-42 yr). Each subject performed 1 min of cycle ergometer exercise at 50% of the anaerobic threshold (AT), 80% AT, and 50% of the difference between the AT and the maximal O2 uptake (VO2max) and 100 and 125% VO2max. Gas exchange was measured breath by breath. The cumulative O2 cost [the integral of VO2 (over baseline) through exercise and 10 min of recovery (ml O2/J)] was independent of work intensity in both children and adults. In above-AT exercise, O2 cost was significantly higher in children [0.25 +/- 0.05 (SD) ml/J] than in adults (0.18 +/- 0.02 ml/J, P less than 0.01). Recovery dynamics of VO2 in above-AT exercise [measured as the time constant (tau VO2) of the best-fit single exponential] were independent of work intensity in children and adults. Recovery tau VO2 was the same in both groups except at 125% VO2max, where tau VO2 was significantly smaller in children (35.5 +/- 5.9 s) than in adults (46.3 +/- 4 s, P less than 0.001). VO2 responses (i.e., time course, kinetics) to short bursts of exercise are, surprisingly, largely independent of work rate (power output) in both adults and children. In children, certain features of the VO2 response to high-intensity exercise are, to a small but significant degree, different from those in adults, indicating an underlying process of physiological maturation.

We hypothesized that the O2 uptake (Vo2) response to high-intensity exercise would be different in children than in adults. To test this hypothesis, 22 children (6-12 yr old) and 7 adults (27-40 yr old) performed 6 min of constant-work-rate cycle-ergometer exercise. Sixteen children performed a single test above their anaerobic threshold (AT). In a separate protocol, six children and all adults exercised at low and high intensity. Low-intensity exercise corresponded to the work rate at 80% of each subject's AT. High-intensity exercise (above the AT) was determined first by calculating the difference in work rate between the AT and the maximal Vo2 (delta). Twenty-five, 50, and 75% of this difference were added to the work rate at the subject's AT, and these work rates were referred to as 25% delta, 50% delta, and 75% delta. For exercise at 50% delta and 75% delta, Vo2 increased throughout exercise (O2 drift, linear regression slope of Vo2 as a function of time from 3 to 6 min) in all the adults, and the magnitude of the drift was correlated with increasing work rates in the above-AT range (r = 0.91, P less than 0.0001). In contrast, no O2 drift was observed in over half of the children during above-AT exercise. The O2 drifts were much higher in adults (1.76 +/- 0.63 ml O2.kg-1.min-2 at 75% delta) than in children (0.20 +/- 0.42, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

The present study investigated whether intrinsic exercise capacity affects the changes in thermoregulation, metabolism and central dopamine (DA) induced by treadmill running. Male Wistar rats were subjected to three incremental exercises and ranked as low-performance (LP), standard-performance (SP), and high-performance (HP) rats. In the first experiment, abdominal (TABD) and tail (TTAIL) temperatures were registered in these rats during submaximal exercise (SE) at 60% of maximal speed. Immediately after SE, rats were decapitated and concentrations of DA and 3,4-dihydroxyphenylacetic acid (DOPAC) were determined in the preoptic area (POA). In the second experiment, oxygen consumption was measured and mechanical efficiency (ME) was calculated in these rats during an incremental exercise. HP rats ran for longer periods and were fatigued with higher TABD values, with no difference in TTAIL. Nevertheless, thermoregulatory efficiency was higher in HP rats, compared with other groups. DA and DOPAC concentrations in the POA were increased by SE, with higher levels in HP compared with LP and SP rats. V̇o2 also differed between groups, with HP rats displaying a lower consumption throughout the incremental exercise but a higher V̇o2 at fatigue. ME, in turn, was consistently higher in HP than in LP and SP rats. Thus, our results show that HP rats have greater TABD values at fatigue, which seem to be related to a higher dopaminergic activity in the POA. Moreover, HP rats exhibited a greater thermoregulatory efficiency during exercise, which can be attributed to a lower V̇o2, but not to changes in tail heat loss mechanisms. NEW & NOTEWORTHY Our findings reveal that rats with higher intrinsic exercise capacities have greater thermoregulatory efficiencies and increased dopaminergic activity in the preoptic area, a key brain area in thermoregulatory control, while exercising. Moreover, higher intrinsic exercise capacities are associated with decreased oxygen consumption for a given exercise intensity, which indicates greater mechanical efficiencies. Collectively, these findings help to advance our knowledge of why some rats of a given strain can exercise for longer periods than others. [ABSTRACT FROM AUTHOR]

This study aims to investigate the cardiorespiratory responses to different vibration frequencies to characterize the intensity of exercise, as well as to compare the effect of two types of squatting exercises (static and dynamic) on the whole body vibration (WBV) exercise in individuals with chronic obstructive pulmonary disease (COPD). Twenty-six subjects were divided and paired into healthy and COPD groups that performed static squatting associated with WBV (frequencies: 30, 35, and 40 Hz; amplitude: 2 mm) and dynamic squatting associated with WBV (frequency: 35 Hz; amplitude 2 mm) on a vertical vibration platform. Oxygen consumption (V̇o2), heart rate (HR), minute ventilation (V̇e), ratio of minute ventilation to oxygen production (V̇e/V̇o2), ratio of minute ventilation to carbon dioxide production (V̇e/V̇co2), oxygen saturation (SpO2), and rating of perceived exertion were measured. For both groups, there was a decrease in V̇e/V̇o2 and V̇e/V̇co2 ratios during static and dynamic squats, as well as an increase in other cardiorespiratory parameters, and no significant difference existed between them. There was an effect of the type of squat on the HR variation; the values in the static squat were higher than those of the dynamic squat in both groups. There was a significant difference with a reduction in SpO2 at 40 Hz frequency when compared with 30 Hz in the COPD group. The other variables behaved similarly between the frequencies. The WBV exercise, regardless of the frequencies used, represented a mild effort that promoted cardiorespiratory response in COPD, with greater responses in the static squat and no adverse effect. NEW & NOTEWORTHY This study showed that an acute session of light exercise of whole body vibration (WBV) can increase the cardiorespiratory responses in patients with chronic obstructive pulmonary disease (COPD), reaching values similar to that of the control group. The results might contribute, therefore, to the elaboration of exercise protocols with WBV for the treatment of patients with COPD during rehabilitation. Thus, future studies referring to training on the vibratory platform could use these exercise parameters and demonstrate possible long-term benefits. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the later effects of daily NO3- supplementation over 3 wk of training on the relationship between O2 uptake and power at different intensities with an incremental test (IT), a double-wingate test (WT), and an endurance capacity test at 80% Wmax (ECT) before and after the supplementation period. Seventeen male recreational athletes participated in this double-blind placebo (PL)-controlled study. Subjects participated in a 3-wk intermittent high-intensity, high-volume training period with 45 intervals of Wmax − 10 W and an active recovery period of 10 W in between with dietary NO3- (NaNO3) or placebo supplementation (NaCl) (both 8.5 mg·kg−1·day−1) on a cycle ergometer. During a training session, plasma [NO3-] (P < 0.001) and plasma [NO2-] (P < 0.01) were higher in nitrate (N), whereas in pre- and posttests mean plasma [NO3-] and [NO2-] were not different between groups. In the WT [48 h after cessation of supplementation (C)], the ratio between V̇o2 and power decreased in N (P < 0.01) with no changes in PL. Endurance capacity (4–5 days after C) similarly increased in both groups (P < 0.01). However, the total oxygen consumption decreased by 5% (P < 0.01) in N, with no change in PL. The slope of V̇o2·W−1 in IT (5–7 days after C) decreased in N (P < 0.01), whereas no changes were found in PL. During low- and moderate-intensity workloads, no changes and differences in V̇o2 could be detected. We conclude that nitrate supplementation causes a sustaining reduction of the oxygen cost per watt during exercise with a large recruitment of type II muscle fibers without affecting endurance capacity. NEW & NOTEWORTHY Because most studies focused on the acute effects of NO3- supplementation on exercise performance during a supplementation period, the sustainability of the effects of the NO3- supplementation remain unknown. We followed the development of V̇o2/W at different intensities during the first week after cessation of daily NO3- supplementation over 3 wk. The results indicate that NO3- supplementation has a long-term effect for at least 7 days after cessation during heavy all-out workloads without affecting endurance capacity. [ABSTRACT FROM AUTHOR]

Nitrate-rich beetroot juice (BR) supplementation has been shown to increase biomarkers of nitric oxide availability with implications for the physiological responses to exercise. We hypothesized that BR supplementation before and during prolonged moderate-intensity exercise would maintain an elevated plasma nitrite concentration ([[Formula: see text]]), attenuate the expected progressive increase in V̇o2 over time, and improve performance in a subsequent time trial (TT). In a double-blind, randomized, crossover design, 12 men completed 2 h of moderate-intensity cycle exercise followed by a 100-kJ TT in three conditions: 1) BR before and 1 h into exercise (BR + BR); 2) BR before and placebo (PL) 1 h into exercise (BR + PL); and 3) PL before and 1 h into exercise (PL + PL). During the 2-h moderate-intensity exercise bout, plasma [NO-2] declined by ~17% in BR + PL but increased by ~8% in BR + BR such that, at 2 h, plasma [NO-2] was greater in BR + BR than both BR + PL and PL + PL ( P < 0.05). V̇o2 was not different among conditions over the first 90 min of exercise but was lower at 120 min in BR + BR (1.73 ± 0.24 l/min) compared with BR + PL (1.80 ± 0.21 l/min; P = 0.08) and PL + PL (1.83 ± 0.27 l/min; P < 0.01). The decline in muscle glycogen concentration over the 2-h exercise bout was attenuated in BR + BR (~28% decline) compared with BR + PL (~44% decline) and PL + PL (~44% decline; n = 9, P < 0.05). TT performance was not different among conditions ( P > 0.05). BR supplementation before and during prolonged moderate-intensity exercise attenuated the progressive rise in V̇o2 over time and appeared to reduce muscle glycogen depletion but did not enhance subsequent TT performance. NEW & NOTEWORTHY We show for the first time that ingestion of nitrate during exercise preserves elevated plasma [nitrite] and negates the progressive rise in O2 uptake during prolonged moderate-intensity exercise. [ABSTRACT FROM AUTHOR]