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Purpose: In the last decades, the energy cost assessment provided new insight on shuttle or constant running as training modalities. No study, though, quantified the benefit of constant/shuttle running in soccer-players and runners. Therefore, the aim of this study was to clarify if marathon runners and soccer players present specific energy cost values related to their training experience performing constant and shuttle running.Methods: To this aim, eight runners (age 34 ± 7.30y; training experience 5.70 ± 0.84y) and eight soccer-players (age 18.38 ± 0.52y; training experience 5.75 ± 1.84y) were assessed randomly for 6’ on shuttle-running or constant-running with 3 days of recovery in-between. For each condition, the blood lactate (BL) and the energy cost of constant (Cr) and shuttle running (CSh) was determined. To assess differences for metabolic demand in terms of Cr, CSh and BL over the two running conditions on the two groups a MANOVA was used.Results:V·O2max were 67.9 ± 4.5 and 56.8 ± 4.3 ml·min−1 kg−1 (p = 0.0002) for marathon runners and soccer players, respectively. On constant running, the runners had a lower Cr compared to soccer players (3.86 ± 0.16 J kg−1m−1 vs. 4.19 ± 0.26 J kg−1 m−1; F = 9.759, respectively; p = 0.007). On shuttle running, runners had a higher CSh compared to soccer players (8.66 ± 0.60 J kg−1 m−1 vs. 7.86 ± 0.51 J kg−1 m−1; F = 8.282, respectively; with p = 0.012). BL on constant running was lower in runners compared to soccer players (1.06 ± 0.07 mmol L−1 vs. 1.56 ± 0.42 mmol L−1, respectively; with p = 0.005). Conversely, BL on shuttle running was higher in runners compared to soccer players 7.99 ± 1.49 mmol L−1 vs. 6.04 ± 1.69 mmol L−1, respectively; with p = 0.028).Conclusion: The energy cost optimization on constant or shuttle running is strictly related to the sport practiced.

After a short historical account, and a discussion of Hill and Meyerhof’s theory of the energetics of muscular exercise, we analyse steady-state rest and exercise as the condition wherein coupling of respiration to metabolism is most perfect. The quantitative relationships show that the homeostatic equilibrium, centred around arterial pH of 7.4 and arterial carbon dioxide partial pressure of 40 mmHg, is attained when the ratio of alveolar ventilation to carbon dioxide flow ($${\dot{V}}_{A}/{\dot{V}}_{R}{CO}_{2}$$ V ˙ A / V ˙ R CO 2 ) is − 21.6. Several combinations, exploited during exercise, of pertinent respiratory variables are compatible with this equilibrium, allowing adjustment of oxygen flow to oxygen demand without its alteration. During exercise transients, the balance is broken, but the coupling of respiration to metabolism is preserved when, as during moderate exercise, the respiratory system responds faster than the metabolic pathways. At higher exercise intensities, early blood lactate accumulation suggests that the coupling of respiration to metabolism is transiently broken, to be re-established when, at steady state, blood lactate stabilizes at higher levels than resting. In the severe exercise domain, coupling cannot be re-established, so that anaerobic lactic metabolism also contributes to sustain energy demand, lactate concentration goes up and arterial pH falls continuously. The $${\dot{V}}_{A}/{\dot{V}}_{R}{CO}_{2}$$ V ˙ A / V ˙ R CO 2 decreases below − 21.6, because of ensuing hyperventilation, while lactate keeps being accumulated, so that exercise is rapidly interrupted. The most extreme rupture of the homeostatic equilibrium occurs during breath-holding, because oxygen flow from ambient air to mitochondria is interrupted. No coupling at all is possible between respiration and metabolism in this case.

Theoretical 100-m performance times (t100-m) of a top athlete at Mexico-City (2250 m a.s.l.), Alto-Irpavi (Bolivia) (3340 m a.s.l.) and in a science-fiction scenario “in vacuo” were estimated assuming that at the onset of the run: (i) the velocity (v) increases exponentially with time; hence (ii) the forward acceleration (af) decreases linearly with v, iii) its time constant (τ) being the ratio between vmax (for af = 0) and af max (for v = 0). The overall forward force per unit of mass (Ftot), sum of af and of the air resistance (Fa = k v2, where k = 0.0037 J·s2·kg−1·m−3), was estimated from the relationship between af and v during Usain Bolt’s extant world record. Assuming that Ftot is unchanged since the decrease of k at altitude is known, the relationships between af and v were obtained subtracting the appropriate Fa values from Ftot, thus allowing us to estimate in the three conditions considered vmax, τ, and t100-m. These were also obtained from the relationship between mechanical power and speed, assuming an unchanged mechanical power at the end of the run (when af ≈ 0), regardless of altitude. The resulting t100-m amounted to 9.515, 9.474, and 9.114 s, and to 9.474, 9.410, and 8.981 s, respectively, as compared to 9.612 s at sea level. Neglecting science-fiction scenarios, t100-m of a world-class athlete can be expected to undergo a reduction of 1.01 to 1.44% at Mexico-City and of 1.44 to 2.10%, at Alto-Irpavi.

New findings What is the topic of this review? This narrative review explores past and recent findings on the mechanical determinants of energy cost during human locomotion, obtained by using a mechanical approach based on Konig's theorem (Fenn's approach). What advances does it highlight? Recent developments in analytical methods and of their applications allow a better understanding of the mechanical-bioenergetic interaction. Advances are: 1) the determination of "frictional" internal work; 2) the association between tendon work and apparent efficiency; 3) a better understanding of the role of energy recovery and internal work in pathological gait (amputees, stroke and obese); 4) a comprehensive analysis of human locomotion in (simulated) low gravity conditions. Abstract During locomotion, muscles use metabolic energy to produce mechanical work (in a more or less efficient way); as a matter of fact, energetics and mechanics can be considered as two sides of the same coin, the latter being investigated to understand the former. A mechanical approach based on Konig's theorem (Fenn's approach) has proved to be a useful tool to elucidate the determinants of the energy cost of locomotion (e. g. the pendulum-like model of walking and the bouncing model of running) and has resulted in many advances in this field. During the last 60 years, this approach has been refined and applied to explore the determinants of energy cost and efficiency in a variety of conditions (e.g. low gravity, un-steady speed). This narrative review aims to summarise current knowledge about the role that mechanical work has played in our understanding of energy cost to date, and to underline how recent developments in analytical methods and their applications in specific locomotion modalities (on a gradient, at low gravity and in un-steady conditions) and in pathological gaits (asymmetric gait pathologies, obese subjects and in the elderly) could continue to push this understanding further. The recent in vivo quantification of new aspects that should be included in the assessment of mechanical work (e.g. frictional internal work and elastic contribution) deserve future research and would improve our knowledge on the mechanical-bioenergetic interaction during human locomotion, as well as in sport science and space exploration. This article is protected by copyright. All rights reserved.

Comfortable walking speed and energy cost of walking are physiological markers of metabolic activity during gait. People with multiple sclerosis are characterized by altered gait biomechanics and energetics, related to the degree of disability and spasticity, which lead to an increased energy cost of walking. Several studies concerning the energy cost of walking in multiple sclerosis have been published. Nevertheless, differences in protocols and characteristics of the sample have led to different outcomes. The aim of the present meta-analysis is to summarize results from studies with specific inclusion characteristics, and to present data about the comfortable walking speed and the energy cost of walking at that speed. Moreover, a detailed discussion of the potential mechanisms involved in the altered metabolic activity during exercise was included. A total of 19 studies were considered, 12 of which were also part of the quantitative analysis. Despite the strict selection process, high between-group heterogeneity was found for both outcomes. Nevertheless, the overall results suggest a pooled mean comfortable walking speed of 1.12 m/s (95% CI 1.05–1.18) and energy cost of 0.19 mLO2/kg/m (95% CI 0.17–0.21). These findings support the results of previous studies suggesting that energy cost of walking may be increased by 2–3 times compared to healthy controls (HC), and encourage the use of this marker in association with other parameters of the disease.

Bilateral deficit (BLD) occurs when the force (or power) generated by both limbs together is smaller than the sum of the forces (or powers) developed separately by the two limbs. The amount of BLD can be altered by neural adaptations brought about by the repetitive execution of specific motor tasks (training). Prolonged disuse also leads to relevant neural adaptations; however, its effects on BLD are still unknown. Thus, the aim of this study was to investigate the effects of a 35-day bed rest on the BLD of the lower limbs. Ten young healthy volunteers performed maximal explosive efforts on a sledge ergometer with both lower limbs or with the right and the left limb separately. Electromyography (EMG) of vastus lateralis, rectus femoris, biceps femoris and gastrocnemius medialis was also measured. Before bed rest, maximal explosive power and peak force were significantly higher in monolateral than bilateral efforts (+18.7 and +31.0 %, respectively). Conversely, peak velocity was 11.9 % greater in bilateral than monolateral efforts. BLD attained a value of 18.1 % and was accompanied by lower EMG amplitude of knee extensors (−17.0 %) and gastrocnemius medialis (−11.7 %) during bilateral efforts. Bed rest led to a ~28.0 % loss in both bilateral and monolateral maximal explosive power. Neither BLD magnitude nor the difference in EMG amplitudes as well as in peak force and velocity between bilateral and monolateral efforts were affected by bed rest. These results suggest that the neuromuscular factors underlying BLD are unaltered after prolonged disuse.

We tested the linear critical power ( $$\dot{w}_{\text{cr}}$$ ) model for discrete incremental ramp exercise implying recovery intervals at the end of each step. Seven subjects performed incremental (power increment 25 W) stepwise ramps to subject’s exhaustion, with recovery intervals at the end of each step. Ramps’ slopes (S) were 0.83, 0.42, 0.28, 0.21, and 0.08 W s−1; recovery durations (t r) were 0 (continuous stepwise ramps), 60, and 180 s (discontinuous stepwise ramps). We determined the energy store component (W′), the peak power ( $$\dot{w}_{\text{peak}}$$ ), and $$\dot{w}_{\text{cr}}$$ . When t r = 0 s, $$\dot{w}_{\text{cr}}$$ and W′ were 187 ± 26 W and 14.5 ± 5.8 kJ, respectively. When t r = 60 or 180 s, the model for ramp exercise provided inconsistent $$\dot{w}_{\text{cr}}$$ values. A more general model, implying a quadratic $$\dot{w}_{\text{peak}}$$ versus $$\sqrt S$$ relationship, was developed. This model yielded, for t r = 60 s, $$\dot{w}_{\text{cr}}$$ = 189 ± 48 W and W′ = 18.6 ± 17.8 kJ, and for t r = 180 s, $$\dot{w}_{\text{cr}}$$ = 190 ± 34 W, and W′ = 16.4 ± 16.7 kJ. These $$\dot{w}_{\text{cr}}$$ and W′ did not differ from the corresponding values for t r = 0 s. Nevertheless, the overall amount of energy sustaining work above $$\dot{w}_{\text{cr}}$$ , due to energy store reconstitution during recovery intervals, was higher the longer t r, whence higher $$\dot{w}_{\text{peak}}$$ values. The linear $$\dot{w}_{\text{cr}}$$ model for ramp exercise represents a particular case (for t r = 0 s) of a more general model, accounting for energy resynthesis following oxygen deficit payment during recovery.

Our objective was to determine the effects of long-lasting endurance events on the energy cost of running (C r), and the role of maximal oxygen uptake (VO2max), its fractional utilisation (F) and C r in determining the performance. Ten healthy runners (age range 26–59 years) participated in an ultra-endurance competition consisting of three running laps of 22, 48 and 20 km on three consecutive days in the North–East of Italy. Anthropometric characteristics and VO2max by a graded exercise test on a treadmill were determined 5 days before and 5 days after the competition. In addition, C r was determined on a treadmill before and after each running lap. Heart rate (HR) was recorded throughout the three laps. Results revealed that mean C r of the individual laps did not increase significantly with lap number (P = 0.200), thus ruling out any chronic lap effect. Even so, however, at the end of lap 3, C r was 18.0% (P

We investigated whether bilateral deficit (BLD): (1) is observed during explosive lower limb contractions; (2) can be attributed to a reduction of neural drive and/or (3) to a different muscle coordination, and/or (4) to changes of the muscle force-velocity (F-v) relationship. Ten volunteers performed maximal explosive efforts of approximately 450 ms on a sledge ergometer, with both lower limbs (BL), with the right and left limb separately (ML), against different overloads. Peak-force (F, N), peak-power (w, W), sledge peak-velocity (v, m/s) and electromyography (EMG) of vastus lateralis (VL), rectus femoris (RF), biceps femoris (BF) and gastrocnemius medialis (GM) were recorded. Average values over the six overloads of F and w, developed by right or left limb during BL, were significantly lower (883 +/- 200 and 918 +/- 141 N; 1089 +/- 407 and 1099 +/- 325 W) than those developed during ML contractions (1285 +/- 177 and 1306 +/- 147 N; 1536 +/- 408 and 1497 +/- 392 W). VL and RF iEMGs were lower in BL than in ML (74 +/- 28 vs. 91 +/- 21% MVC and 39 +/- 21 vs. 56 +/- 28% MVC). The coordination among the four muscles, as determined from an analysis of the time course of iEMG, expressed as percentage of that attained at the end of the push, was poorer in BL, as compared to ML. BL F-v curves were different as compared to the ML ones, the force and power developed, at a given v, being significantly larger in ML. It is concluded that BLD occurs also during explosive pushes with the lower limbs, and that it is mainly due to different muscle coordination.

At the onset of a square-wave exercise of moderate intensity, in the absence of any detectable lactate production, the hydrolysis of phosphocreatine (PCr) fills the gap between energy requirement and energy yield by oxidative pathways, thus representing a readily available source of energy for the muscle. We verified experimentally the relationships between high-energy phosphates and/or their changes and the time constant of PCr concentration ([PCr]) kinetics in humans (τPCr). High-energy phosphate concentration (by31P-NMR spectroscopy) in the calf muscles were measured during three repetitions of the rest-to-work transition of moderate aerobic square-wave exercise on nine healthy volunteers, while resting [PCr] was estimated from the appropriate spectroscopy data. PCr concentration decreased significantly (22 ± 6%) from rest to steady-state exercise, without differences among the three repetitions. Absolute resting [PCr] and τPCrwere consistent with literature values, amounting to 27.5 ± 2.2 mM and 23.9 ± 2.9 s, respectively. No significant relationships were detected between individual τPCrand mechanical power, fraction or absolute amount of PCr hydrolyzed, or change in ADP concentration. On the contrary, individual τPCr(s) was linearly related to absolute resting [PCr] (mM), the relationship being described by: τPCr= 0.656 + 0.841·[PCr] ( n = 9, R = 0.708, P < 0.05). These data support the view that in humans PCr concentration sets the time course of the oxidative metabolism in skeletal muscle at the start of exercise, being one of the main controllers of oxidative phosphorylation.

This investigation aimed to compare the response of young and older adult men to bed rest (BR) and subsequent rehabilitation (R). Sixteen older (OM, age 55-65 yr) and seven young (YM, age 18–30 yr) men were exposed to a 14-day period of BR followed by 14 days of R. Quadriceps muscle volume (QVOL), force (QF), and explosive power (QP) of leg extensors; single-fiber isometric force (Fo); peak aerobic power (V̇o2peak); gait stride length; and three metabolic parameters, Matsuda index of insulin sensitivity, postprandial lipid curve, and homocysteine plasma level, were measured before and after BR and after R. Following BR, QVOL was smaller in OM (−8.3%) than in YM (−5.7%, P = 0.031); QF (−13.2%, P = 0.001), QP (−12.3%, P = 0.001), and gait stride length (−9.9%, P = 0.002) were smaller only in OM. Fo was significantly smaller in both YM (−32.0%) and OM (−16.4%) without significant differences between groups. V̇o2peak decreased more in OM (−15.3%) than in YM (−7.6%, P < 0.001). Instead, the Matsuda index fell to a greater extent in YM than in OM (−46.0% vs. −19.8%, respectively, P = 0.003), whereas increases in postprandial lipid curve (+47.2%, P = 0.013) and homocysteine concentration (+26.3%, P = 0.027) were observed only in YM. Importantly, after R, the recovery of several parameters, among them QVOL, QP, and V̇o2peak, was not complete in OM, whereas Fo did not recover in either age group. The results show that the effect of inactivity on muscle mass and function is greater in OM, whereas metabolic alterations are greater in YM. Furthermore, these findings show that the recovery of preinactivity conditions is slower in OM.

Previous observations have shown that, in isolated perfused dog gastrocnemii in situ, stimulated to aerobic rhythmic isotonic tetanic contractions (at about 40% of maximal isometric force), only about 20% of the overall metabolic power (proportional to the rate of O2 consumption, VO2) was converted into mechanical power (W). Here we report that, in the same preparation, the maximal velocity during the shortening phase of each tetanus (v, mm s−1) increased with the rate of energy dissipation, as given by the difference between VO2 and W (W kg−1). The relationship between these variables was described by: v=2.85(VO2−W)1.24 (R 2=0.85; n=17). A mathematical analysis of this equation shows that the overall mechanical efficiency (η=WVO2 −1) decreased with increasing v (at constant VO2), whereas it increased with increasing VO2 (at constant v). The net effect of this state of affairs was that the decrease of η over the entire range of work intensities was relatively minor (from 0.22 to 0.15), in spite of a large increase of v, (from 40 to 120 mm s−1), thanks to the concomitant increase of VO2 (from 10 to 25 W kg−1). So, under these experimental conditions, the energetics of work performance seems to be governed by two conflicting needs. The need for a sufficiently high shortening speed (and hence power output), itself requiring a sufficiently large energy dissipation rate, which, however, brings about a fall in η. This is counteracted by the increased VO2, which in turn leads to an increased efficiency at the expense of a fall in shortening speed.

The effects of using different algorithms to estimate the time constant of changes in oxygen uptake at the onset of square-wave 120 W cycloergometric exercise were evaluated in seven subjects. The volume of oxygen taken up at the alveoli (VO(2Ai)) was determined breath-by-breath (BB) from the volume of O(2) transferred at the mouth (VO(2mi)) minus the corresponding volume changes in O(2) stores in the alveoli: VO(2Ai)= VO(2mi)-[V(Ai-1)(FO(2Ai)- FO(2Ai-1))+ FO(2Ai) x Delta V(Ai)], where V(Ai-1) is the alveolar volume at the end of the previous breath, FO(2Ai) and FO(2Ai-1) are estimated from the fractions of end-tidal O(2) in the current and previous breaths, respectively, and Delta V(Ai) is the change in volume during breath i. These quantities can be measured BB, with the exception of V(Ai-1) which must be assumed. The respiratory cycle has been defined as the time elapsing between identical fractions of expiratory gas in two successive breaths. Using this approach, since FO(2Ai)= FO(2Ai-1), any assumption regarding V(Ai-1) becomes unnecessary. In the present study, VO(2Ai) was calculated firstly, by using this approach, and secondly by setting different V(Ai-1) values (from 0 to FRC+0.5 l, where FRC is the functional residual capacity). Values for alveolar O(2) flow (VO(2Ai)), as calculated from the quotient of VO(2Ai) divided by breath duration, were then fitted bi-exponentially. The time constant of the phase II kinetics of VO(2Ai) (tau(2)) was linearly related to V(Ai-1), increasing from 36.6 s (V(Ai-1)=0) to 46.8 s (V(Ai-1)=FRC+0.5 l) while tau(2) estimated using the first approach amounted to 34.3 s. We concluded that, firstly, the first approach allowed us to calculate O(2A) during transitions in step exercise; and secondly, when using methods wherein V(Ai-1) must be assumed, tau(2) depended on V(Ai-1).

To estimate the energetics and biomechanics of accelerated/decelerated running on flat terrain based on its biomechanical similarity to constant speed running up/down an ‘equivalent slope’ dictated by the forward acceleration (a f). Time course of a f allows one to estimate: (1) energy cost of sprint running (C sr), from the known energy cost of uphill/downhill running, and (2) instantaneous (specific) mechanical accelerating power (P sp = a f × speed). In medium-level sprinters (MLS), C sr and metabolic power requirement (P met = C sr × speed) at the onset of a 100-m dash attain ≈50 J kg−1 m−1, as compared to ≈4 for running at constant speed, and ≈90 W kg−1. For Bolt’s current 100-m world record (9.58 s) the corresponding values attain ≈105 J kg−1 m−1 and ≈200 W kg−1. This approach, as applied by Osgnach et al. (Med Sci Sports Exerc 42:170–178, 2010) to data obtained by video-analysis during soccer games, has been implemented in portable GPS devices (GPEXE©), thus yielding P met throughout the match. Actual O2 consumed, estimated from P met assuming a monoexponential VO2 response (Patent Pending, TV2014A000074), was close to that determined by portable metabolic carts. Peak P sp (W kg−1) was 17.5 and 19.6 for MLS and elite soccer players, and 30 for Bolt. The ratio of horizontal to overall ground reaction force (per kg body mass) was ≈20 % larger, and its angle of application in respect to the horizontal ≈10° smaller, for Bolt, as compared to MLS. Finally, we estimated that, on a 10 % down-sloping track Bolt could cover 100 m in 8.2 s. The above approach can yield useful information on the bioenergetics and biomechanics of accelerated/decelerated running.

Microgravity leads to a decline of muscle power especially in the postural muscles of the lower limb. Muscle atrophy primarily contributes to this negative adaptation. Nutritional countermeasures during unloading were shown to possibly mitigate the loss of muscle mass and strength. The aim of this study was to investigate the effects of different diet energy intakes during prolonged inactivity on body composition and lower limbs power output. The effects of lower or higher diet energy intake on the decline of maximal explosive power of the lower limbs, as determined on a sledge ergometer before and after 35 days of bed rest, were investigated on two matched groups of young healthy volunteers. Body composition and lean volume of the lower limb were also measured. After bed rest, fat mass increased (+20.5 %) in the higher energy intake group (N = 9), while it decreased (−4.8 %) in the lower energy intake group (N = 10). Also, the loss of body fat-free mass and lean volume of the lower limb was significantly greater in the higher (−4.6 and −10.8 %, respectively) as compared to the lower (−2.4 and −3.7 %, respectively) diet energy intake group. However, the loss of maximal explosive power was similar between the two groups (−25.2 and −29.5 % in the higher and lower energy intake group, respectively; P = 0.440). The mitigation of loss of muscle mass by means of a moderate caloric diet restriction during prolonged inactivity was not sufficient for reducing the loss of maximal explosive power of the lower limbs.

The mechanical power for cycling (P(c)) at constant ground speed (s), in the absence of wind on smooth hard terrain is the sum of the power dissipated against rolling resistance, gravity and air resistance: P(c)=a x s + M x g x s x sin gamma + b x S3, where a and b are constants, M is the mass of the subject plus bike, g is the acceleration of gravity and gamma is the angle of the terrain with the horizontal. The constant b depends upon the drag coefficient (Cd), the overall area projected on the frontal plane (A(f)), and the air density (rhoa): b = 0.5 x C(d) x A(f) x rhoa. In turn, rhoa depends on air pressure (P(B)) and temperature (T): rhoa=rho0 x 0.359 x P(B) x T(-1), where rho0 is the air density at 760 mmHg (101.3 kPa) and 273 K. The metabolic power developed by the cyclist (E(c)) is related to P(c) E(c) = P(c) x eta(-1), where eta is the mechanical efficiency of cycling. The experimental values of a, b and eta are fairly well known so that, if the maximal metabolic power as a function of the performance time is known for a given cyclist, the following set of data can be individually calculated: (1) best performances over any given distance and for any given altitude above sea level, (2) the effects of posture and body size on maximal speeds, and (3) the maximal incline of the terrain that can be overcome at any given speed or coasting speed for any given downslope. The above set of information makes it possible also to calculate the characteristics of a "Twin Bikes System" (TBS) for preventing microgravity deconditioning during long-term space flight. The TBS consists of two bicycles that are mechanically coupled by a differential gearing, which move at the very same speed, but in the opposite sense, along the inner wall of a cylindrically shaped space module. The circular trajectories induce a centrifugal acceleration vector (a(c)) oriented along the head-to-feet direction of each subject: a(c) = v(t)2 x r(-1) where v(t) is the tangential velocity and r the radius of gyration, which is equal to the inner radius of the space module. So, any desired value of a(c) can be achieved by appropriately selecting v(t), wherefrom the mechanical and metabolic powers that the astronauts must generate can be readily calculated. Experiments performed in a ground-based human centrifuge have shown that the discomfort derived from the rotating environment is reasonably low and well tolerated. If the appropriate atmospheric pressure is provided, cycling on circular or elliptical tracks may be useful to reduce cardiovascular deconditioning that occurs due to the reduced gravity in permanently manned lunar bases. Indeed, on the curved parts of the path a cyclist will generate a horizontal outward acceleration: a(c) = s2 x r(-1), where s is the velocity along the track and r is the radius of curvature. To counterbalance a(c), the subject plus bike must lean inwards so that the vectorial sum of a(c) plus the lunar gravity (g(L) = 1.62 m x s(-2)) is applied along a straight line that includes the centre of mass of the system and the point of wheel contact with the ground. For values of s from 10 to 20 m x s(-1) and r from 50 to 200 m, this vectorial sum ranges from 1.05 to 5.03 g(L) (0.17-0.83 g).

Because the cardiocirculatory response of heart transplant recipients (HTR) to exercise is delayed, we hypothesized that their O2 uptake (V˙o 2) kinetics at the onset of subthreshold exercise are slowed because of an impaired early “cardiodynamic” phase 1, rather than an abnormal subsequent “metabolic” phase 2. Thus we compared the V˙o 2 kinetics in 10 HTR submitted to six identical 10-min square-wave exercises set at 75% (36 ± 5 W) of the load at their ventilatory threshold (VT) to those of 10 controls (C) similarly exercising at the same absolute (40 W; C40W group) and relative load (67 ± 14 W; C67W group). Time-averaged heart rate, breath-by-breathV˙o 2, and O2pulse (O2p) data yielded monoexponential time constants of the V˙o 2 (s) and O2p increase. Separating phase 1 and 2 data permitted assessment of the phase 1 duration and phase 2 V˙o 2 time constant ([Formula: see text]). The V˙o 2 time constant was higher in HTR (38.4 ± 7.5) than in C40W (22.9 ± 9.6; P ≤ 0.002) or C67W (30.8 ± 8.2; P ≤ 0.05), as was the O2p time constant, resulting from a lower phase 1V˙o 2 increase (287 ± 59 vs. 349 ± 66 ml/min; P ≤ 0.05), O2p increase (2.8 ± 0.6 vs. 3.6 ± 1.0 ml/beat; P ≤ 0.0001), and a longer phase 1 duration (36.7 ± 12.3 vs. 26.8 ± 6.0 s; P≤ 0.05), whereas the[Formula: see text]was similar in HTR and C (31.4 ± 9.6 vs. 29.9 ± 5.6 s; P = 0.85). Thus the HTR have slower subthresholdV˙o 2 kinetics due to an abnormal phase 1, suggesting that the heart is unable to increase its output abruptly when exercise begins. We expected a faster[Formula: see text]in HTR because of their prolonged phase 1 duration. Because this was not the case, their muscular metabolism may also be impaired at the onset of subthreshold exercise.

The aim of this study was to: (1) determine directly the energy cost of shuttle running (C Sh) and (2) compare it to the values indirectly estimated from kinematic data. C Sh over distances of ≈10 or ≈20 m was determined on 65 subjects (group 1) from gas exchange measurements over 155 trials, or indirectly estimated on 10 subjects (group 2) from the time course of the speed as follows. (1) The cost to accelerate from zero to peak speed was estimated assuming a 25 % efficiency and added to that of constant-speed running, as obtained on subjects of group 1. (2) Since (i) accelerated running on flat terrain is equivalent to running uphill at constant speed, on a slope dictated by the forward acceleration (di Prampero et al. in J Exp Biol 208:2809-2816, 2005), and (ii) the energy cost of running uphill is known, C Sh was obtained from the time course of the acceleration. C Sh increased with the average speed, at any given speed being significantly greater for the shorter distances; e.g., at ≈4 m/s over 10 m, it amounted to ≈14 J/(kg m), i.e., 3.5-fold larger than that at constant speed. The two indirect methods yielded results not significantly different from C Sh over the longer (≈20 m), but underestimated it over the shorter (≈10 m) distances. From our results, over ≈20 m C Sh can be obtained with sufficient accuracy from actual measurements of peak speed alone, thus, greatly simplifying the experimental procedure. The so-obtained data can then be utilized to assess the athletic status of any subject, as well as to plan appropriate training strategies.

We investigated the relationship between mechanical and energy cost of transport and body mass in running humans. Ten severely obese (body mass ranging from 108.5 to 172.0 kg) and 15 normal-weighted (52.0-89.0 kg) boys and men, aged 16.0-45.8 years, participated in this study. The rate of O(2) consumption was measured and the subjects were filmed with four cameras for kinematic analysis, while running on a treadmill at 8 km h(-1). Mass specific energy cost (C (r)) and external mechanical work (W (ext)) per unit distance were calculated and expressed in joules per kilogram per meter, efficiency (η) was then calculated as W (ext) × C (r) (-1) × 100. Both mass-specific C (r) and W (ext) were found to be independent of body mass (M) (C (r) = 0.002 M + 3.729, n = 25, R (2) = 0.05; W (ext) = -0.001 M + 1.963, n = 25, R (2) = 0.01). It necessarily follows that the efficiency is also independent of M (η = -0.062 M + 53.3298, n = 25, R (2) = 0.05). The results strongly suggest that the elastic tissues of obese subjects can adapt (e.g., thickening) to the increased mass of the body thus maintaining their ability to store elastic energy, at least at 8 km h(-1) speed, at the same level as the normal-weighted subjects.

A functional evaluation of skeletal muscle oxidative metabolism during dynamic knee extension (KE) incremental exercises was carried out following a 35-day bed rest (BR) (Valdoltra 2008 BR campaign). Nine young male volunteers (age: 23.5 ± 2.2 yr; mean ± SD) were evaluated. Pulmonary gas exchange, heart rate and cardiac output (by impedance cardiography), skeletal muscle (vastus lateralis) fractional O2extraction, and brain (frontal cortex) oxygenation (by near-infrared spectroscopy) were determined during incremental KE. Values at exhaustion were considered “peak”. Peak heart rate (147 ± 18 beats/min before vs. 146 ± 17 beats/min after BR) and peak cardiac output (17.8 ± 3.3 l/min before vs. 16.1 ± 1.8 l/min after BR) were unaffected by BR. As expected, brain oxygenation did not decrease during KE. Peak O2uptake was lower after vs. before BR, both when expressed as liters per minute (0.99 ± 0.17 vs. 1.26 ± 0.27) and when normalized per unit of quadriceps muscle mass (46.5 ± 6.4 vs. 56.9 ± 11.0 ml·min−1·100 g−1). Skeletal muscle peak fractional O2extraction, expressed as a percentage of the maximal values obtained during a transient limb ischemia, was lower after (46.3 ± 12.1%) vs. before BR (66.5 ± 11.2%). After elimination, by the adopted exercise protocol, of constraints related to cardiovascular O2delivery, a decrease in peak O2uptake and muscle peak capacity of fractional O2extraction was found after 35 days of BR. These findings suggest a substantial impairment of oxidative function at the muscle level, “downstream” with respect to bulk blood flow to the exercising muscles, that is possibly at the level of blood flow distribution/O2utilization inside the muscle, peripheral O2diffusion, and intracellular oxidative metabolism.

The mechanical power (Wtot, W·kg−1) developed during ten revolutions of all-out periods of cycle ergometer exercise (4–9 s) was measured every 5–6 min in six subjects from rest or from a baseline of constant aerobic exercise [50%–80% of maximal oxygen uptake (VO2max)] of 20–40 min duration. The oxygen uptake [VO2 (W·kg−1, 1 ml O2 = 20.9 J)] and venous blood lactate concentration ([la]b, mM) were also measured every 15 s and 2 min, respectively. During the first all-out period, Wtot decreased linearly with the intensity of the priming exercise (Wtot = 11.9−0.25·VO2). After the first all-out period (i greater than 5–6 min), and if the exercise intensity was less than 60% VO2max, Wtot, VO2 and [la]b remained constant until the end of the exercise. For exercise intensities greater than 60% VO2max, VO2 and [la]b showed continuous upward drifts and Wtot continued decreasing. Under these conditions, the rate of decrease of Wtot was linearly related to the rate of increase of V [(d Wtot/dt) (W·kg−1·s−1) = 5.0·10−5 −0.20·(d VO2/dt) (W·kg−1·s−1)] and this was linearly related to the rate of increase of [la]b [(d VO2/dt) (W·kg−1·s−1) = 2.310−4 + 5.910−5·(d [la]b/dt) (mM·s−1)]. These findings would suggest that the decrease of Wtot during the first all-out period was due to the decay of phosphocreatine concentration in the exercising muscles occurring at the onset of exercise and the slow drifts of VO2 (upwards) and of Wtot (downwards) during intense exercise at constant Wtot could be attributed to the continuous accumulation of lactate in the blood (and in the working muscles).

The present study investigated the effect of 21 days of horizontal bed rest on cutaneous cold and warm sensitivity, and on behavioural temperature regulation. Healthy male subjects (N = 10) were accommodated in a hospital ward for the duration of the study and were under 24-h medical care. All activities (eating, drinking, hygiene, etc.) were conducted in the horizontal position. On the 1st and 22nd day of bed rest, cutaneous temperature sensitivity was tested by applying cold and warm stimuli of different magnitudes to the volar region of the forearm via a Peltier element thermode. Behavioural thermoregulation was assessed by having the subjects regulate the temperature of the water within a water-perfused suit (T (wps)) they were wearing. A control unit established a sinusoidal change in T (wps), such that it varied from 27 to 42 degrees C. The subjects could alter the direction of the change of T (wps), when they perceived it as thermally uncomfortable. The magnitude of the oscillations towards the end of the trial was assumed to represent the upper and lower boundaries of the thermal comfort zone. The cutaneous threshold for detecting cold stimulus decreased (P0.05) from 1.6 (1.0) degrees C on day 1 to 1.0 (0.3) degrees C on day 22. No effect was observed on the ability to detect warm stimuli or on the regulated T (wps). We conclude that although cold sensitivity increased after bed rest, it was not of sufficient magnitude to cause any alteration in behavioural thermoregulatory responses.

The energy cost of running (Cr) is classically determined from steady-state oxygen consumption (V̇o2) at constant speed, divided by running speed. In the present study, Cr was determined during incremental treadmill tests in the course of the assessment of V̇o2maxand related parameters as follows. Assume that the running speed is increased by a constant amount (Δv) at regular short intervals (T) and that, during each intensity transient below the gas exchange threshold, V̇o2increases exponentially, without time delay, toward the steady state. If V̇o2is averaged over homologous times within each speed step, neglecting the initial 10 s, the V̇o2difference between corresponding time values becomes constant and equal to the difference between the appropriate steady states. Thus Cr was obtained from the ratio of the difference between the V̇o2averages for any two homologous times, within subsequent periods, to the corresponding speed difference. Since in aerobic conditions, Cr on the treadmill is independent of the speed, and since Δv and T were constant, the relationship between V̇o2and speed is described by straight lines, where the slope yields Cr above resting. This was indeed experimentally observed, the slopes of the linear regressions ( R2range: 0.78 to 0.97 n = 9 to 16) within the three time windows being essentially equal. In six subjects, the grand-average of Cr amounted to 0.177 ± 0.011 ml O2/(kg·m) [3.70 ± 0.23 J/(kg·m)]. This value is essentially equal to that obtained for the same subjects by applying the “classical” procedure [0.177 ± 0.015 ml O2/(kg·m); 3.70 ± 0.31 J/(kg·m)], so confirming the validity of the incremental approach for assessing the energy cost of treadmill running.

The aim of the present study was to investigate the changes in thickness, fascicle length (L (f)) and pennation angle (theta) of the antigravity gastrocnemius medialis (GM) and vastus lateralis (VL) muscles, and the non-antigravity tibialis anterior (TA) and biceps brachii (BB) muscles measured by ultrasonography in ten healthy males (aged 22.3 +/- 2.2 years) in response to 5 weeks of horizontal bed rest (BR). After BR, muscle thickness decreased by 12.2 +/- 8.8% (P0.05) and 8.0 +/- 9.1% (P0.005) in the GM and VL, respectively. No changes were observed in the TA and BB muscles. L (f) and theta decreased by 4.8 +/- 5.0% (P0.05) and 14.3 +/- 6.8% (P0.005) in the GM and by 5.9 +/- 5.3% (P0.05) and 13.5 +/- 16.2% (P0.005) in the VL, again without any changes in the TA and BB muscles. The finding that amongst the antigravity muscles of the lower limbs, the GM deteriorated to a greater extent than the VL is possibly related to the differences in relative load that this muscle normally experiences during daily loading. The dissimilar response in antigravity and non-antigravity muscles to unloading likely reflects differences in loading under normal conditions. The significant structural alterations of the GM and VL muscles highlight the rapid remodelling of muscle architecture occurring with disuse.

In supra-maximal exercise to exhaustion, the critical velocity (cv) is conventionally calculated from the slope of the distance (d) versus time (t) relationship: d = I + St. I is assumed to be the distance covered at the expense of the anaerobic capacity, S the speed maintained on the basis of the subject’s maximal O2 uptake $$(\dot{V}\hbox{O}_{\rm 2max}).$$ This approach is based on two assumptions: (1) the energy cost of locomotion per unit distance (C) is constant and (2) $$\dot{V}\hbox{O}_{2\rm{max}}$$ is attained at the onset of exercise. Here we show that cv and the anaerobic distance (d anaer) can be calculated also in swimming, where C increases with the velocity, provided that $$\dot{V}\hbox{O}_{2\rm{max}},$$ its on-response, and the C versus v relationship are known. d anaer and cv were calculated from published data on maximal swims for the four strokes over 45.7, 91.4 and 182.9 m, on 20 elite male swimmers (18.9 ± 0.9 years, 75.9 ± 6.4 kg), whose $${\dot{V}}\hbox{O}_{2\rm{max}}$$ and C versus speed relationship were determined, and compared to I and S obtained from the conventional approach. cv was lower than S (4, 16, 7 and 11% in butterfly, backstroke, breaststroke and front crawl) and I (=11.6 m on average in the four strokes) was lower than d anaer. The latter increased with the distance: average, for all strokes: 38.1, 60.6 and 81.3 m over 45.7, 91.4 and 182.9 m. It is concluded that the d versus t relationship should be utilised with some caution when evaluating performance in swimmers.

Theoretical best performance times (t theor) in track running are calculated as follows. Maximal metabolic power (Ė max) is a known function of maximal oxygen uptake (VO2max), of maximal anaerobic capacity (AnS) and of effort duration to exhaustion (t e): Ė max=f (t e). Metabolic power requirement (Ė r) to cover the distance (d) in the performance time t p is the product of the energy cost of locomotion per unit distance (C) and the speed: Ė r=C×d/t p. The time values for which Ė max (t e)=Ė r (t p), assumed to yield t theor, can be obtained for any given subject and distance provided that VO2max, AnS and C are known, and compared with actual best performances (t act). For 15 min≥t e≥100 s, the overall ratio t act/t theor was rather close to 1.0. To estimate the relative role of the different factors limiting VO2max, several resistances to O2 transport are identified, inversely proportional to: alveolar ventilation (R V*), O2 transport by the circulation (R Q), O2 diffusion from capillary blood to mitochondria (R t), mitochondrial capacity (R m). Observed changes of VO2max are accompanied by measured changes of several resistances. The ratio of each resistance to the overall resistance can therefore be calculated by means of the O2 conductance equation. In exercise with large muscle groups (two legs), R Q is the major (75%) limiting factor downstream of the lung, its role being reduced to 50% during exercise with small muscle groups (one leg). R t and R m account for the remaining fractions. In normoxia R V* is negligible; at high altitude it increases progressively, together with R t and R m, at the expense of R Q.

In cycling the gear determines the distance travelled and the mean applied force at each leg thrust. According to Padilla et al. (J Appl Physiol 89:1522-1527, 2000), an elite cyclist was able to cycle for an hour at 14.6 m.s(-1 developing 510 W at a pedal frequency of 101 rpm. Thus, the opposing force was 34 N (=500/14.6), whereas the mean force, developed by the leg muscles, was 144.1 N. It can be calculated that in the same subject cycling on a 20% slope at the same pedal frequency, the velocity would be reduced by about 5 times, i.e. to 2.9 m.s(-1) because of a fivefold increase of the opposing force. In reality, the increase of mean force developed by leg muscles is even larger, because of the fall of the cadence to 60 rpm. In general, during mountain ascents cyclists develop high forces at low cadences that are likely to be more economical; in contrast, on flat ground, they increase the pedalling rates because their aerodynamic posture does not allow high force production. The intermittent pattern of muscular force application generates speed changes that become more evident at great inclines and low cadences. It can be shown that inertial work is appreciable in cycling, increasing with the incline of the road and decreasing with the cadence. However, inertial work does not seem to affect efficiency. Differences in physiologic potential make differences in performance more evident in time trials where the mean incline of the road is not negligible. Cyclists with low body size have an advantageous force versus mass ratio in high mountain ascents.

to the editor: In his letter ([8][1]), Dr. Kemp refers to a model of ATP synthesis control in which the mechanisms during the rest-to-work transient (on-transient) and the work-to-rest transient (off-transient) are the same. Accordingly, only one mathematical representation is used for both