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Aerobic exercise prescription is often set at specific heart rate (HR) values. Previous studies demonstrated that during exercise carried out at a HR slightly above that corresponding to the gas exchange threshold (GET), work rate (WR) has to decrease in order to maintain HR constant. We hypothesized a greater WR decrease at a fixed HR after simulated microgravity/inactivity (bed rest, BR). Ten male volunteers (23 ± 5 yr) were tested before (PRE) and after (POST) a 10-day horizontal BR and performed on a cycle ergometer 1 ) incremental exercise; b ) 15-min HR CLAMPED exercise, in which WR was continuously adjusted to maintain a constant HR, corresponding to that at 120% of GET determined in PRE; 3 ) two moderate-intensity constant WR (MOD) exercises. Breath-by-breath O 2 uptake (V̇o 2 ), HR, and other variables were determined. After BR, peak V̇o 2 (V̇o 2peak ) and GET significantly decreased, by ∼10%. During HR CLAMPED (145 ± 11 beats·min -1 ), the decrease in WR needed to maintain a constant HR was greater in POST versus PRE (-39 ± 10% vs. -29 ± 14%, P < 0.01). In six subjects the decreased WR switched from the heavy- to the moderate-intensity domain. The decrease in WR during HR CLAMPED , in PRE versus POST, was significantly correlated with the V̇o 2peak decrease ( R 2 = 0.52; P = 0.02). A greater amplitude of the slow component of the HR kinetics was observed during MOD following BR. Exercise at a fixed HR is not associated with a specific WR or WR domain; the problem, affecting exercise evaluation and prescription, is greater after BR. The WR decrease during HR CLAMPED is a biomarker of exercise intolerance after BR. NEW & NOTEWORTHY During a 15-min exercise carried out at a heart rate (HR) slightly above that corresponding to the gas exchange threshold, to keep HR constant work rate significantly decreased; the decrease was more pronounced after a 10-day horizontal bed rest. The work rate decrease at a fixed HR can be considered a systemic biomarker of exercise intolerance during microgravity/inactivity and could also be easily and reliably determined during spaceflights or in patients.

In order to identify peripheral biomarkers of impaired oxidative metabolism during exercise following a 10-day bed rest, 10 males performed an incremental exercise (to determine peak pulmonary V̇O 2 (V̇O 2 p)) and moderate-intensity exercises, before (PRE) and after (POST) bed rest. Blood flow response was evaluated in the common femoral artery by Eco-Doppler during 1 min of passive leg movements (PLM). The intramuscular matching between O 2 delivery and O 2 utilization was evaluated by near-infrared spectroscopy (NIRS). Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in isolated muscle fibres, and in vivo by NIRS by the evaluation of skeletal muscle V̇O 2 (V̇O 2 m) recovery kinetics. Resting V̇O 2 m was estimated by NIRS. Peak V̇O 2 p was lower in POST vs. PRE. The area under the blood flow vs. time curve during PLM was smaller (P = 0.03) in POST (274 ± 233 mL) vs. PRE (427 ± 291). An increased (P = 0.03) overshoot of muscle deoxygenation during a metabolic transition was identified in POST. Skeletal muscle citrate synthase activity was not different (P = 0.11) in POST (131 ± 16 nmol min -1  mg -1 ) vs. PRE (138 ± 19). Maximal ADP-stimulated mitochondrial respiration (66 ± 18 pmol s -1  mg -1 (POST) vs. 72 ± 14 (PRE), P = 0.41) was not affected by bed rest. Apparent K m for ADP sensitivity of mitochondrial respiration was reduced in POST vs. PRE (P = 0.04). The V̇O 2 m recovery time constant was not different (P = 0.79) in POST (22 ± 6 s) vs. PRE (22 ± 6). Resting V̇O 2 m was reduced by 25% in POST vs. PRE (P = 0.006). Microvascular-endothelial function was impaired following a 10-day bed rest, whereas mitochondrial mass and function (both in vivo and ex vivo) were unaffected or slightly enhanced. KEY POINTS: Ten days of horizontal bed rest impaired in vivo oxidative function during exercise. Microvascular impairments were identified by different methods. Mitochondrial mass and mitochondrial function (evaluated both in vivo and ex vivo) were unchanged or even improved (i.e. enhanced mitochondrial sensitivity to submaximal [ADP]). Resting muscle oxygen uptake was significantly lower following bed rest, suggesting that muscle catabolic processes induced by bed rest/inactivity are less energy-consuming than anabolic ones., (© 2021 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

New Findings: What is the central question of this study? The role of the cerebral haemodynamic response to either normobaric or hypobaric hypoxia in people susceptible to acute mountain sickness (AMS) is still under debate. Prefrontal cortex near-infrared spectroscopy-derived parameters were monitored in normobaric hypoxia at rest and during moderate-intensity exercise in AMS-prone and non-AMS individuals. What is the main finding and its importance? The AMS-prone individuals did not increase microvascular blood volume and showed lower prefrontal cerebral oxygenation in normobaric hypoxia both at rest and during exercise compared with non-AMS subjects, suggesting that these changes might underpin later development of AMS at altitude., Abstract: The aim of this study was to evaluate changes in prefrontal cerebral oxygenation and microvascular blood volume during exercise in normobaric hypoxia and to investigate possible associations with the occurrence of acute mountain sickness (AMS) at altitude. Twenty-two healthy individuals (age, 26 ± 4 years; peak oxygen uptake, 42 ± 4 ml kg -1  min -1 ) were tested in two different conditions: normoxia (NORM) and normobaric hypoxia (fraction of inspired O 2  = 0.13; HYPO). Data were collected at rest and during submaximal constant-speed exercise. The peripheral oxyhaemoglobin saturation was measured by finger pulse oximeter. Changes in prefrontal cerebral oxygenation (ΔHbO 2 ), deoxygenation (ΔHHb) and microvascular blood volume (ΔHb tot ) were obtained by near-infrared spectroscopy. Within 2 weeks after laboratory testing, subjects rapidly ascended to 3647 m a.s.l., and AMS was evaluated using the Lake Louise scale. Eight subjects were AMS + , whereas 14 were AMS - . During NORM, near-infrared spectroscopy variables did not change from baseline values both at rest and during exercise, with similar results in AMS + and AMS - subjects. During HYPO, ΔHHb increased to a similar extent in both groups, both at rest and during exercise. The ΔHbO 2 was significantly less in AMS + compared with AMS - subjects, both at rest [-3.23 ± 5.90 versus 1.44 ± 2.14 μm, P = 0.04, effect size (ES) = 1.1, respectively] and during exercise (-6.56 ± 5.51 versus 0.37 ± 4.36 μm, P < 0.01, ES = 1.2, respectively). Total haemoglobin did not change from baseline, both at rest (-1.67 ± 9.53 μm) and during exercise (-0.96 ± 9.12 μm) in AMS + subjects, which was significantly different from the AMS - group (5.49 ± 3.99 μm, P = 0.03, ES = 1.0 and 8.17 ± 7.34 μm, P = 0.02, ES = 1.0, respectively). Individuals prone to AMS seem to be unable to increase microvascular blood volume and to maintain oxygenation at the cerebral level during exercise in acute normobaric hypoxia, suggesting that these changes might underpin later development of AMS., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Purpose: Aerobic exercise prescription is often based on a linear relationship between pulmonary oxygen consumption (V˙O2) and heart rate (HR). The aim of the present study was to test the hypothesis that during constant work rate (CWR) exercises at different intensities, the slow component of HR kinetics occurs at lower work rate and is more pronounced that the slow component of V˙O2 kinetics., Methods: Seventeen male (age, 27 ± 4 yr) subjects performed on a cycle ergometer an incremental exercise to voluntary exhaustion and several CWR exercises: 1) moderate CWR exercises, below gas exchange threshold (GET); 2) heavy CWR exercise, at 45% of the difference between GET and V˙O2 peak (Δ); 3) severe CWR exercise, at 95% of Δ; 4) "HRCLAMPED" exercise in which work rate was continuously adjusted to maintain a constant HR, slightly higher than that determined at GET. Breath-by-breath V˙O2, HR, and other variables were determined., Results: In moderate CWR exercises, no slow component of V˙O2 kinetics was observed, whereas a slow component with a relative amplitude (with respect to the total response) of 24.8 ± 11.0% was observed for HR kinetics. During heavy CWR exercise, the relative amplitude of the HR slow component was more pronounced than that for V˙O2 (31.6 ± 11.2% and 23.3 ± 9.0%, respectively). During HRCLAMPED, the decrease in work rate (~14%) needed to maintain a constant HR was associated with a decreased V˙O2 (~10%)., Conclusions: The HR slow component occurred at a lower work rate and was more pronounced than the V˙O2 slow component. Exercise prescriptions at specific HR values, when carried out for periods longer than a few minutes, could lead to premature fatigue.

Aerobic training can be effective in patients with mitochondrial myopathies (MM) and McArdle's disease (McA). The aim of the study was to use noninvasive functional evaluation methods, specifically aimed at skeletal muscle oxidative metabolism, to evaluate the effects of an aerobic exercise training (cycle ergometer, 12 wk, 4 days/wk, ∼65-70% of maximal heart rate) in 6 MM and 7 McA. Oxygen uptake and skeletal muscle vastus lateralis fractional O2 extraction by near-infrared spectroscopy were assessed during incremental and low-intensity constant work rate (CWR) exercises before (BEFORE) and at the end (AFTER) of training. Peak O2 uptake increased significantly with training both in MM [14.7 ± 1.2 vs. 17.6 ± 1.4 ml·kg(-1)·min(-1) (mean ± SD)] and in McA (18.5 ± 1.8 ml·kg(-1)·min(-1) vs. 21.6 ± 1.9). Peak skeletal muscle fractional O2 extraction increased with training both in MM (22.0 ± 6.7 vs. 32.6 ± 5.9%) and in McA (18.5 ± 6.2 vs. 37.2 ± 7.2%). During low-intensity CWR in both MM and McA: V̇o2 kinetics became faster in AFTER, but only in the patients with slow V̇o2 kinetics in BEFORE; the transient overshoot in fractional O2 extraction kinetics disappeared. The level of habitual physical activity was not higher 3 mo after training (FOLLOW-UP vs. PRE). In MM and McA patients a home-based aerobic training program significantly attenuated the impairment of skeletal muscle oxidative metabolism and improved variables associated with exercise tolerance. Our findings indicate that in MM and McA patients near-infrared spectroscopy and V̇o2 kinetics can effectively detect the functional improvements obtained by training., (Copyright © 2016 the American Physiological Society.)

Patients with McArdle's disease (McA) typically show the "second-wind" phenomenon, a sudden decrease in heart rate (HR) and an improved exercise tolerance occurring after a few minutes of exercise. In the present study, we investigated whether in McA a first bout of exercise determines a second wind during a second bout, separated by the first by a few minutes of recovery. Eight McA (44 ± 4 yr) and a control group of six mitochondrial myopathy patients (51 ± 6 yr) performed two repetitions (CWR1 and CWR2) of 6-min constant work rate exercise (∼50% of peak work rate) separated by 6-min (SHORT) or 18-min (LONG) recovery. Pulmonary O2 uptake (Vo2), HR, cardiac output, rates of perceived exertion, vastus lateralis oxygenation {changes in deoxygenated Hb and myoglobin Mb concentrations, Δ[deoxy(Hb+Mb)], by near-infrared spectroscopy} were determined. In McA, Vo2 (0.86 ± 0.2 vs. 0.95 ± 0.1 l/min), HR (113 ± 10 vs. 150 ± 13 beats/min), cardiac output (11.6 ± 0.6 vs. 15.0 ± 0.8 l/min), and rates of perceived exertion (11 ± 2 vs. 14 ± 3) were lower, whereas Δ[deoxy(Hb+Mb)] was higher (14.7 ± 2.3 vs. -0.1 ± 4.6%) in CWR2-SHORT vs. CWR1; the "overshoot" of Δ[deoxy(Hb+Mb)] and the "slow component" of Vo2 kinetics disappeared in CWR2-SHORT. No differences (vs. CWR1) were observed in McA during CWR2-LONG, or in mitochondrial myopathy patients during both CWR2-SHORT and -LONG. A second-wind phenomenon was observed in McA during the second of two consecutive 6-min constant-work rate submaximal exercises. The second wind was associated with changes of physiological variables, suggesting an enhanced skeletal muscle oxidative metabolism. The second wind was not described after a longer (18-min) recovery period.

A recent study has demonstrated that neuromuscular electrical stimulation (NMES) determines, in vitro, a fast-to-slow shift in the metabolic profile of muscle fibers. The aim of the present study was to evaluate if, in the same subjects, these changes would translate, in vivo, into an enhanced skeletal muscle oxidative metabolism. Seven young men were tested (cycle ergometer) during incremental exercises up to voluntary exhaustion and moderate and heavy constant-load exercises (CLE). Measurements were carried out before and after an 8-wk training program by isometric bilateral NMES (quadriceps muscles), which induced an ∼25% increase in maximal isometric force. Breath-by-breath pulmonary O(2) uptake (Vo(2)) and vastus lateralis oxygenation indexes (by near-infrared spectroscopy) were determined. Skeletal muscle fractional O(2) extraction was estimated by near-infrared spectroscopy on the basis of changes in concentration of deoxygenated hemoglobin + myoglobin. Values obtained at exhaustion were considered "peak" values. The following functional evaluation variables were unaffected by NMES: peak Vo(2); gas exchange threshold; the Vo(2) vs. work rate relationship (O(2) cost of cycling); changes in concentration of deoxygenated hemoglobin + myoglobin vs. work rate relationship (related to the matching between O(2) delivery and Vo(2)); peak fractional O(2) extraction; Vo(2) kinetics (during moderate and heavy CLE) and the amplitude of its slow component (during heavy CLE). Thus NMES did not affect several variables of functional evaluation of skeletal muscle oxidative metabolism. Muscle hypertrophy induced by NMES could impair peripheral O(2) diffusion, possibly counterbalancing, in vivo, the fast-to-slow phenotypic changes that were observed in vitro, in a previous work, in the same subjects of the present study.

Our aim was to investigate the relationship between physiological variables (not previously studied) and performance in elite 1,500-m runners. We assessed eight male athletes with an average personal best time of 233.3 ± 6.9 s (110% of the world record) for the 1,500-m race. Ventilatory measurements, maximal oxygen consumption VO2max maximal vastus lateralis muscle deoxygenation (∆[deoxy(Hb+Mb)])max via near-infrared spectroscopy (NIRS), and maximal velocity (V (max)) were obtained during an incremental treadmill test. During subsequent constant-speed exercise at Vmax, we determined the time to exhaustion (Tlim), end-exercise blood lactate concentration ([La]b(max)), VO2 and ∆[deoxy(Hb+Mb)] kinetics parameters. The mean VO2max, [La]b(max) and Vmax were 70.2 ± 3.9 mL kg(-1) min(-1), 12.7 ± 2.4 mmol L(-1), 21.5 ± 0.5 km h(-1), respectively. VO2 at Vmax showed a significant negative correlation with Tlim, whereas [La]b(max) was positively correlated with Tlim. Race speed was found to significantly correlate with ∆[deoxy(Hb+Mb)](max) (79% of maximal value obtained during a transient limb ischemia), ∆[deoxy(Hb+Mb)] slow component (22.9 ± 9.3% of total amplitude) and [La]b(max) at Vmax. [La]b(max) at Vmax was also significantly correlated with ∆[deoxy(Hb+Mb)] slow component, suggesting a greater release of oxygen from the hemoglobin due to the Bohr effect. We conclude that both the maximal capacity of muscle to extract O2 from the blood and the end-exercise blood lactate accumulation are important predictors of best performance in 1,500-m runners.

"Central" and "peripheral" limitations to oxidative metabolism during exercise were evaluated in 10 young males following a 35-day horizontal bed rest (BR). Incremental exercise (IE) and moderate- and heavy-intensity constant-load exercises (CLE) were carried out on a cycloergometer before and 1-2 days after BR. Pulmonary gas exchange, cardiac output (Q; by impedance cardiography), skeletal muscle (vastus lateralis), and brain (frontal cortex) oxygenation (by near-infrared spectroscopy) were determined. After BR, "peak" (values at exhaustion during IE) workload, peak O(2) uptake (Vo(2 peak)), peak stroke volume, Q(peak), and peak skeletal muscle O(2) extraction were decreased (-18, -18, -22, -19, and -33%, respectively). The gas exchange threshold was approximately 60% of Vo(2 peak) both before and after BR. At the highest workloads, brain oxygenation data suggest an increased O(2) extraction, which was unaffected by BR. Vo(2) kinetics during CLE (same percentage of peak workload before and after BR) were slower (time constant of the "fundamental" component: 31.1 +/- 2.0 s before vs. 40.0 +/- 2.2 s after BR); the amplitude of the "slow component" was unaffected by BR, thus it would be greater, after BR, at the same absolute workload. A more pronounced "overshoot" of skeletal muscle O(2) extraction during CLE was observed after BR, suggesting an impaired adjustment of skeletal muscle O(2) delivery. The role of skeletal muscles in the impairment of oxidative metabolism during submaximal and maximal exercise after BR was identified. The reduced capacity of peak cardiovascular O(2) delivery did not determine a "competition" for the available O(2) between skeletal muscles and brain.

Purpose: The aim was to identify additional noninvasive tools allowing to detect and to quantify the metabolic impairment in patients with mitochondrial myopathies (MM) or McArdle's disease (McA)., Methods: Kinetics of adjustment of pulmonary oxygen uptake (VO2 kinetics) during transitions to constant-load moderate-intensity cycle ergometer exercise were determined on 15 MM, 8 McA, 21 patients with signs and/or symptoms of metabolic myopathy but a negative biopsy ("patient controls"; P-CTRL), and 22 healthy untrained controls (CTRL)., Results: VO2 kinetics were slower in MM and in McA versus P-CTRL and CTRL, slower in McA versus MM, and not significantly different between P-CTRL and CTRL. The time constants (tau) of the monoexponential function describing the VO2 kinetics were (X +/- SE) 59.2 +/- 8.5 s in MM, 87.6 +/- 16.4 s in McA, 36.9 +/- 3.1 s in P-CTRL, and 35.4 +/- 1.9 s in CTRL. In a subgroup of the patients (eight MM and seven McA), tau of VO2 kinetics were negatively correlated with two variables determined in a previous study (Grassi B, Marzorati M, Lanfranconi F, et al. Impaired oxygen extraction in metabolic myopathies: detection and quantification by near-infrared spectroscopy. Muscle Nerve. 2007;35:510-20): a) a muscle oxygenation index, obtained by near-infrared spectroscopy, estimating the peak capacity of skeletal muscle fractional O2 extraction; and b) VO2 peak., Conclusions: In MM and McA patients, analysis of pulmonary VO2 kinetics during moderate-intensity exercise allows to identify and to quantify, noninvasively, the impairment of skeletal muscle oxidative metabolism. In these patients, the slower VO2 kinetics can be considered a marker of the impaired exercise tolerance. The present data could be useful for clinicians who need an objective, quantitative, and longitudinal evaluation of the impairment to be used in the follow-up of these patients as well as in the assessment of therapeutic interventions.

Patients with mitochondrial myopathies (MM) or myophosphorylase deficiency (McArdle's disease, McA) show impaired capacity for O(2) extraction, low maximal aerobic power, and reduced exercise tolerance. Non-invasive tools are needed to quantify the metabolic impairment. Six patients with MM, 6 with McA, 25 with symptoms of metabolic myopathy but negative biopsy (patient-controls, P-CTRL) and 20 controls (CTRL) underwent an incremental cycloergometric test. Pulmonary O(2) uptake (VO(2)) and vastus lateralis oxygenation indices (by near-infrared spectroscopy, NIRS) were determined. Concentration changes of deoxygenated hemoglobin and myoglobin (Delta[deoxy(Hb + Mb)]) were considered an index of O(2) extraction. Delta[deoxy(Hb + Mb)] peak (percent limb ischemia) was lower in MM (25.3 +/- 12.0%) and McA (18.7 +/- 7.3) than in P-CTRL (62.4 +/- 3.9) and CTRL (71.3 +/- 3.9) subjects. VO(2) peak and Delta[deoxy(Hb + Mb)] peak were linearly related (r(2) = 0.83). In these patients, NIRS is a tool to detect and quantify non-invasively the metabolic impairment, which may be useful in the follow-up of patients and in the assessment of therapies and interventions.

Tibetan and Andean natives at altitude have allegedly a greater work capacity and stand fatigue better than acclimatized lowlanders. The principal aim of the present review is to establish whether convincing experimental evidence supports this belief and, should this be the case, to analyze the possible underlying mechanisms. The superior work capacity of high altitude natives is not based on differences in maximum aerobic power (V(O2 peak)), mL kg(-1)min(-1)). In fact, average V (O2 peak) of both Tibetan and Andean natives at altitude is only slightly, although not significantly, higher than that of Asian or Caucasian lowlanders resident for more than 1 yr between 3400 and 4700 m (Tibetans, n = 152, vs. Chinese Hans, n = 116: 42.4 +/- 3.4 vs. 39.2 +/- 2.6 mL kg(-1)min(-1), mean +/- SE; Andeans, n = 116, vs. Caucasians, n = 70: 47.1 +/- 1.7 vs. 41.6 +/- 1.2 mL kg(-1)min(-1)). However, compared to acclimatized lowlanders, Tibetans appear to be characterized by a better economy of cycling, walking, and running on a treadmill. This is possibly due to metabolic adaptations, such as increased muscle myoglobin content and antioxidant defense. All together, the latter changes may enhance the efficiency of the muscle oxidative metabolic machinery, thereby supporting a better prolonged submaximal performance capacity compared to lowlanders, despite equal V(O2 peak). With regard to Andeans, data on exercise efficiency is scanty and controversial and, at present, no conclusion can be drawn as to the origin of their superior performance.

The heart rate (HR) and O(2) uptake (VO(2)) responses to cycle ergometer exercise and the role of O(2) transport in limiting submaximal and maximal aerobic performance were assessed in 33 heart transplant recipients (HTR) [14 children (P-HTR), 11 young adults (YA-HTR) and 8 middle-age adults (A-HTR)] and in 28 age-matched control subjects (CTL). In 7 P-HTR ("responders") the HR response to the onset of exercise (on-response) was as fast as that of CTL, whereas in all other patients ("non-responders") the HR on-response was typical of the denervated heart. Compared with non-responder P-HTR, responder P-HTR were also characterized by a normal peak HR (177+/- 16 vs. 151+/- 25 beats/min), an equally slow time constant for the VO(2) on-response (tau: 54 +/- 11 vs. 62+/- 13 s) and a similar low (approximately 60% of that of CTL) peak VO(2) (28 +/- 7 vs. 26 +/- 10 ml/kg per min). On the other hand non-responder YA-HTR and A-HTR were characterized by a relatively low peak HR (151 +/- 21 and 144 +/- 29 beats/min, respectively), a slow tau for the on-response (63 +/- 12 and 70 +/- 11 s) and a low peak (28 +/- 7 and 19 +/- 6 ml/kg per min). In conclusion, a sizeable number of paediatric patients (responder P-HTR) may reacquire the normal HR response to exercise, both in terms of kinetics and maximal level. Despite the almost complete recovery of cardiovascular function, and, probably, oxygen delivery, both the kinetics of the VO(2) on-response and the maximal aerobic power of the responder P-HTR were similar to those of non-responder P-HTR. The latter finding is probably attributable to peripheral limitations, due to inborn and/or pharmacological muscle deterioration.

Success in sprint kayaking depends on the propulsive power generated by trunk, pelvis, shoulder and lower limb movements. However, no studies have examined whole-body kinematics over a simulated distance. We aimed to study the changes in movement patterns of kayakers performing a 500-m kayak sprint. Eleven young K1 sprint kayakers (three females; age: 16.5 ± 1.9 years, height: 174.1 ± 7.1 cm and weight: 66.1 ± 6.2 kg) performed an incremental test on a kayak ergometer to assess their Peak Oxygen Uptake (V̇O2peak). They then performed a 500-m sprint trial on the same ergometer, and the positions of 40 reflective markers were recorded to assess whole-body kinematics. Joint angles over time were computed for the trunk and right shoulder, hip, knee, and ankle. Changes of joint kinematics during the test were assessed with Statistical Parametric Mapping, calculating at each time node the linear regression between joint angles waveforms and the time of the rowing cycle, p <.05. Cardiometabolic responses confirmed that the participants achieved a maximal effort (V̇O2 and HR reached 99 ± 11% and 94 ± 6% of peak values, respectively). Paddle velocity negatively correlated with sprint time. The shoulder (elevation, rotation and flexion), trunk (lateral flexion and rotation) and hip (abduction) angles significantly changed over time in different phases of the stroke cycle during the simulated sprint. No significant differences over time were found for knee and ankle flexion. A high-intensity sprint may affect the shoulder, trunk and hip kinematics of kayak paddling. The kinematic analysis of kayakers' paddling during simulated metabolic-demanding tasks can provide useful insights to coaches and athletes. [ABSTRACT FROM AUTHOR]

Purpose: Recently, some studies have suggested that overall training intensity may be more important than training volume for improving swimming performance. However, those studies focused on very young subjects, and/or the difference between high-volume and high-intensity training was blurred. The aim of this study was to investigate in masters swimmers the effects of manipulation of training volume and intensity on performance and physiological variables. Methods: A group of 10 male masters swimmers (age 32.3 ± 5.1 y) performed 2 different 6-wk training periods followed by 1 wk of tapering. The first period was characterized by high training volume performed at low intensity (HvLi), whereas the second period was characterized by low training volume performed at high intensity (LvHi). Peak oxygen consumption (...O2peak) during incremental arm exercise, individual anaerobic threshold (IAT), and 100-m, 400-m, and 2000-m-freestyle time were evaluated before and at the end of both training periods. Results: HvLi training significant increased ...O2peak (11.9% ± 4.9% [mean change ± 90%CL], P = .002) and performance in the 400-m (-2.8% ± 1.8%, P = .002) and 2000-m (-3.4% ± 2.9%, P = .025), with a likely change in IAT (4.9% ± 4.7%, P > .05). After LvHi training, speed at IAT (12.4% ± 5.3%, P = .004) and 100-m performance (-1.2% ± 0.8%, P = .001) also improved, without any significant changes in ...O2peak, 2000-m, and 400-m. Conclusions: These findings indicate that in masters swimmers an increase of training volume may lead to an improvement of ...O2peak and middle- to long-distance performance. However, a subsequent period of LvHi training maintains previous adjustments and positively affects anaerobic threshold and short-distance performance. [ABSTRACT FROM AUTHOR]

Purpose: Aerobic exercise prescription is often based on a linear relationship between pulmonary oxygen consumption (V˙O2) and heart rate (HR). The aim of the present study was to test the hypothesis that during constant work rate (CWR) exercises at different intensities, the slow component of HR kinetics occurs at lower work rate and is more pronounced that the slow component of V˙O2 kinetics. Methods: Seventeen male (age, 27 ± 4 yr) subjects performed on a cycle ergometer an incremental exercise to voluntary exhaustion and several CWR exercises: 1) moderate CWR exercises, below gas exchange threshold (GET); 2) heavy CWR exercise, at 45% of the difference between GET and V˙O2 peak (Δ); 3) severe CWR exercise, at 95% of Δ; 4) “HRCLAMPED” exercise in which work rate was continuously adjusted to maintain a constant HR, slightly higher than that determined at GET. Breath-by-breath V˙O2, HR, and other variables were determined. Results: In moderate CWR exercises, no slow component of V˙O2 kinetics was observed, whereas a slow component with a relative amplitude (with respect to the total response) of 24.8 ± 11.0% was observed for HR kinetics. During heavy CWR exercise, the relative amplitude of the HR slow component was more pronounced than that for V˙O2 (31.6 ± 11.2% and 23.3 ± 9.0%, respectively). During HRCLAMPED, the decrease in work rate (~14%) needed to maintain a constant HR was associated with a decreased V˙O2 (~10%). Conclusions: The HR slow component occurred at a lower work rate and was more pronounced than the V˙O2 slow component. Exercise prescriptions at specific HR values, when carried out for periods longer than a few minutes, could lead to premature fatigue. [ABSTRACT FROM AUTHOR]

Our objective was to correlate skeletal muscle mass (SM) with cardiopulmonary exercise testing (CPET) descriptors of exercise capacity in patients with amyotrophic lateral sclerosis (ALS) and compare ALS CPET data with those of patients with mitochondrial myopathy (MM) and normal subjects (N). Twenty-four early-stage ALS patients (63±11 years) underwent bioelectrical impedance analysis of body composition, resting spirometry, and ramp CPET. Six MM and six N were used as controls (56 ± 7 and 63 ± 4 years, respectively). Results showed that ALS SM index was similar to that of N (9.0±2.1 kg/m2 vs. 10.4±1.9 kg/m2, respectively; p == n.s.), whereas peak VO2/kg SM was significantly lower (41.5 ± 11.6 ml/kg/min vs. 57.8 ± 7.5 ml/kg/min, respectively; p < 0.01). However, the heart rate/VO2 slope did not differ between ALS and N, being significantly higher in MM than in both ALS and N (6.1 ± 1.4 beats/ml/kg/min vs. 4.2 ± 1.1 beats/ml/kg/min vs. 3.8 ± 2.0 beats/ml/kg/min, respectively; both p < 0.01), excluding a marked skeletal muscle metabolic impairment in ALS. Neither cardiovascular nor ventilatory dysfunction was detected in ALS. Early-stage ALS patients show a SM similar to N, but with a reduced peak VO2/kg SM. Such a reduced peripheral O2 utilization is consistent with deconditioning as the main cause of impaired exercise capacity in this population. [ABSTRACT FROM AUTHOR]

During exercises with relatively small muscle masses, limitations to exercise performance by the cardiovascular system should be significantly reduced, allowing one to fully-test the "oxidative potential" of the investigated muscles. Ten elderly males (E, 77.8 +/- 2.9 years [x +/- SD]) and eight young controls (Y, 26.6 +/- 3.0) underwent incremental exercises to voluntary exhaustion on a dynamic leg-extension (dominant limb) machine (knee-extension, KE) and on a cycloergometer (CYCLO). During KE the load was increased every 3 min to loads corresponding to 20, 40 and 60% of the force of one-repetition maximum (1RM). The following variables were determined (vastus lateralis muscle): concentration changes of deoxygenated haemoglobin and myoglobin (Delta[deoxy(Hb + Mb)]) by near-infrared spectroscopy (NIRS), expressed as percentage of the maximal value obtained during transient limb ischemia, and taken as an index of O2 extraction; root mean square (RMS) and median power frequency (MDF) by electromyography. The total lifted load during KE and peak workload during CYCLO were lower in E versus Y (620.4 +/- 321.9 kg vs. 1347.4 +/- 458.7; 113.5 +/- 23.9 W vs. 224.3 +/- 41.0, respectively). During CYCLO Delta[deoxy(Hb + Mb)] peak (i.e. the value determined at exhaustion) was lower in E (44.5 +/- 17.7%) versus Y (67.1 +/- 22.9), whereas during KE Delta[deoxy(Hb + Mb)] peak was higher in E (56.8 +/- 20.9%) versus Y (38.6 +/- 15.8). "Thresholds", that is abrupt increases in RMS slopes, were detected in Y but not in E, suggesting less recruitment or a preferential atrophy of type 2 fibers in the elderly. These findings, associated with the preserved capacity of O2 extraction, suggest a shift towards oxidative metabolism in skeletal muscles of 78 year-old subjects, which could preserve, at least in part, their capacity to carry out exercise. [ABSTRACT FROM AUTHOR]

The relevance of translational medicine (bringing basic science methods "to the bed of patients") is universally recognized. Too often, however, the tools to be applied translationally are thought to derive only from the "-omics" (genomics, proteomics, transcriptomics, metabolomics, etc.) world. The failures of this "reductionist" approach are widely recognized. In the review, we discuss studies demonstrating that scientifically sound mechanistic insights into diseases, relevant both in terms of basic science and clinically, and very well suited to be utilized within a translational medicine approach, can be obtained from the established field of exercise physiology. Methods originally aimed toward basic physiological mechanisms, and applied for the functional evaluation of athletes and sport performance, can have a valuable translational application in patients with metabolic myopathies; such as myophosphorylase deficiency (McArdle disease) or mitochondrial myopathies, diseases which share the common denominator of an impaired skeletal muscle oxidative metabolism. Several variables can yield pathophysiological insights, can identify and quantify the metabolic impairment and the effects on exercise tolerance (one of the main determinants of the patients' clinical picture and quality of life), and can offer diagnostic clues: the impaired capacity of O2 extraction by skeletal muscle, evaluated by near-infrared spectroscopy; the "exaggerated" cardiovascular response to exercise; the slower speed of adjustment of oxidative metabolism during metabolic transitions; the "slow component" of pulmonary O2 uptake kinetics and the associated reduced efficiency and fatigue; the impaired intramuscular matching between O2 delivery and O2 utilization. The proposed methods are noninvasive, and therefore facilitate repeated or serial evaluations. They provide support for a simple message: physiology and physiological research remain the essential link between genes, molecules, and clinical care. [ABSTRACT FROM AUTHOR]

Purpose: Dietary nitrate supplementation has been shown to reduce O2 cost of submaximal exercise, improve exercise tolerance, and enhance performance in moderately trained individuals. In contrast, data have been provided that elite athletes do not benefit from nitrate supplementation. The aim of this study was to evaluate the effects of short-term nitrate supplementation on endurance performance in subjects with different levels of aerobic fitness. Methods: Twenty-one subjects (mean age, 22.7 ± 1.8 yr) with different aerobic fitness level (...O2peak value ranging from 28.2 to 81.7 mL⋅kg-1⋅min-1) participated in a crossover double-blind placebo-controlled study. Subjects were tested after 6 d of supplementation with either 0.5 1 per day of nitrate (5.5 mmol)-containing water (NITR) or nitrate-free water (PLA). Participants performed an incremental running test until exhaustion and four repetitions of 6-min submaximal (approximately 80% of gas exchange threshold) constant load exercise on a motorized treadmill. Moreover, subjects performed a 3-km running time trial on the field. Results: After NITR, a negative correlation between reduction of O2 cost of submaximal exercise and individual aerobic fitness level was observed (r² = 0.80; P < 0.0001). A significant inverse correlation was also found between aerobic fitness level and improvement in performance for 3-km time trial after NITR (r² = 0.76; P < 0.0001). Additionally, subjects responded differently to dietary nitrate supplementation according to aerobic fitness level with higher-fit subjects showing a lower increase in plasma [NO3-] (r² = 0.86; P < 0.0001) and [NO2-] (r ² = 0.75; P < 0.0001). Conclusions: The results of the present study suggest that the individual aerobic fitness level affects the ergogenic benefits induced by dietary nitrate supplementation. The optimal nitrate loading regimen required to elevate plasma [NO2-] and to enhance performance in elite athletes is different from that of low-fit subjects and requires further studies. [ABSTRACT FROM AUTHOR]

Aerobic exercise prescription is usually set at specific heart rate (HR) values. Previous studies demonstrated that during exercise carried out at a HR slightly above that corresponding to the gas exchange threshold (GET), work rate (w') has to decrease in order to maintain HR constant. Simulated microgravity (bed rest, BR) determines a significant impairment of oxidative metabolism and exercise tolerance. PURPOSE: To test the hypothesis that the w' decrease at a fixed HR would be greater after BR. METHODS: Ten male volunteers (23±5 yr) were tested before (PRE) and after (POST) a 10-day horizontal BR, and performed on a cycle ergometer: a) an incremental exercise up to voluntary exhaustion (INCR); b) a 15-min "HRCLAMPED" exercise, in which w' was continuously adjusted to maintain a constant HR, slightly higher than that determined at GET. Pulmonary gas exchange was assessed breath-by-breath. Fractional O2 extraction (Δ[deoxy(Hb+Mb)]) was evaluated at different sites of the quadriceps by near-infrared spectroscopy (NIRS) RESULTS: During INCR peak pulmonary O2 uptake (...O2peak) (40.3±6.1 vs. 44.4±7.2 ml/kg/min, p<0.001) and Δ[deoxy(Hb+Mb)]peak (p<0.05) were significantly lower in POST vs. PRE. w' at GET was not different in POST (113±33 W) vs. PRE (118±33 W). During HRCLAMPED exercise (set at 145±11 b/min), the decrease in w' needed to maintain a constant HR was significantly more pronounced in POST vs. PRE (-39±10 vs. -29±14%, p<0.01), and it was associated with decreases (both in POST and in PRE) of V...O2 (-14 and -13%), Δ[deoxy(Hb+Mb)] (-41 and -18%), gas exchange ratio (R) and blood lactate ([La]b). Net mechanical efficiency decreased by 38 and 36%, in POST and PRE, respectively. CONCLUSIONS: During 15-min exercise initially set at a w' corresponding to a HR slightly above GET (as frequently done for aerobic exercise prescription), in order to keep HR constant w' had to decrease by ~29% and ~39%, respectively, before and after a 10-day BR. Exercise prescription at fixed submaximal HR is not associated with a specific w'; the problem is greater in microgravity. The w' decrease at a fixed HR is a useful tool to identify an impaired exercise tolerance. The w' decrease was more pronounced than that necessary to prevent "slow components" of ...O2, Δ[deoxy(Hb+Mb)], R and [La]b. Funding: ASI, MARS-PRE Project, n. DC-VUM-2017-006. [ABSTRACT FROM AUTHOR]

PURPOSE: Impairments of oxidative metabolism after exposure to microgravity are documented, but the sites of impairment are still debated. Aim of this study was to identify markers of impaired oxidative metabolism along the O2 pathway, following 10-day of horizontal bed rest (BR). METHODS: fore (PRE) and after (POST) BR, 10 young males performed on a cycle ergometer an incremental exercise (to determine peak pulmonary V...O2 [V...O2p] and peak cardiac output [CO]), and moderate-intensity exercise (MOD). Vastus lateralis muscle fractional O2 extraction was measured by near-infrared spectroscopy (NIRS). Blood flow response was evaluated in the common femoral artery by Eco-Doppler during 1-min passive leg movements (PLM). Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in isolated muscle fibers obtained by biopsy, and non-invasively in vivo by NIRS, by calculating skeletal muscle V...O2 (...O2m) recovery kinetics (repeated occlusions method) following MOD. Resting V...O2m was estimated by NIRS by the rate of muscle oxygenation during limb blood flow occlusions at rest. RESULTS: Peak V...O2p and peak cardiac output were lower in POST vs. PRE (41.5±6.5 ml/kg/min vs. 44.5±7.4, P=0.001; 19.0±3.2 L/min vs. 25.2±5.5, P=0.004). The area under the blood flow vs. time curve during PLM was lower (P=0.038) in POST (274±233 mL) vs. PRE (427±291). Skeletal muscle citrate synthase activity, estimate of mitochondrial mass, was not different (P=0.115) in POST (131.2±15.9 UI/mg) vs. PRE (137.9±18.8). Maximal ADP-stimulated mitochondrial respiration (66.4±17.5 pmol/s/mg [POST] vs. 72.3±14.0 [PRE], P=0.127) was not affected by BR. Apparent Km for ADP sensitivity was reduced in POST vs. PRE (P=0.04). The time-constant of V...O2m recovery was not different (P=0.079) in POST (22.2±5.9 s) vs. PRE (21.7±5.7). ...O2m at rest was reduced by about 25% in POST vs. PRE (P<0.01). CONCLUSIONS: Cardiovascular and peripheral vascular-endothelial functions were impaired following a 10-day BR, whereas mitochondrial mass and function (both in vivo and ex vivo) were unaffected, or even improved (enhanced mitochondrial sensitivity to submaximal [ADP]). Resting V...O2m was lower after BR; muscle catabolic processes induced by BR are less energyconsuming than anabolic ones. Funding: ASI, MARS-PRE, n. DC-VUM-2017-006. [ABSTRACT FROM AUTHOR]