Loss of α-actinin-3 during human evolution provides superior cold resilience and muscle heat generation.

The protein α-actinin-3 expressed in fast-twitch skeletal muscle fiber is absent in 1.5 billion people worldwide due to homozygosity for a nonsense polymorphism in ACTN3 (R577X). The prevalence of the 577X allele increased as modern humans moved to colder climates, suggesting a link between α-actinin-3 deficiency and improved cold tolerance. Here, we show that humans lacking α-actinin-3 (XX) are superior in maintaining core body temperature during cold-water immersion due to changes in skeletal muscle thermogenesis. Muscles of XX individuals displayed a shift toward more slow-twitch isoforms of myosin heavy chain (MyHC) and sarcoplasmic reticulum (SR) proteins, accompanied by altered neuronal muscle activation resulting in increased tone rather than overt shivering. Experiments on Actn3 knockout mice showed no alterations in brown adipose tissue (BAT) properties that could explain the improved cold tolerance in XX individuals. Thus, this study provides a mechanism for the positive selection of the ACTN3 X-allele in cold climates and supports a key thermogenic role of skeletal muscle during cold exposure in humans.

Cell-free DNA kinetics in response to muscle-damaging exercise: A drop jump study.

A significant increase in circulating cell-free DNA (cfDNA) occurs with physical exercise, which depends on the type of exertion and the duration. The aims of this study were as follows: (1) to investigate the time course of cfDNA and conventional markers of muscle damage from immediately after to 96 h after muscle-damaging exercise; and (2) to investigate the relationship between cfDNA and indicators of primary (low-frequency fatigue and maximal voluntary isometric contraction) and secondary (creatine kinase and delayed-onset muscle soreness) muscle damage in young healthy males. Fourteen participants (age, 22 ± 2 years; weight, 84.4 ± 11.2 kg; height, 184.0 ± 7.4 cm) performed 50 intermittent drop jumps at 20 s intervals. We measured cfDNA and creatine kinase concentrations, maximal voluntary isometric contraction torque, low-frequency fatigue and delayed-onset muscle soreness before and at several time points up to 96 h after exercise. Plasma cfDNA levels increased from immediately postexercise until 72 h postexercise (P < 0.01). Elevation of postexercise cfDNA was correlated with both more pronounced low-frequency fatigue (r = -0.52, P = 3.4 × 10-11) and delayed-onset muscle soreness (r = 0.32, P = 0.00019). Levels of cfDNA change in response to severe primary and secondary muscle damage after exercise. Levels of cfDNA exhibit a stronger correlation with variables related to primary muscle damage than to secondary muscle damage, suggesting that cfDNA is a more sensitive marker of acute loss of muscle function than of secondary inflammation or damaged muscle fibres.

Fasting for 48 h induced similar glucose intolerance in both sexes despite greater perceived stress and decreased estradiol levels in females.

PURPOSE: The purpose of this study was to compare the effects of fasting for 48 h on the evoked insulin and glucose responses in males and females, and to explore factors such as stress and estrogen levels that might influence these responses. METHODS: Healthy, nonobese male (n = 14) and female (n = 14) subjects underwent 48-h fasting trial. Changes in glucose tolerance and insulin levels in response to the oral glucose tolerance test, subjectively perceived stress and catecholamine concentrations were measured in all participants. Estrogen levels were also measured in the female participants during the 48-h fast. RESULTS: Glucose area under the curve (AUC) values increased similarly in both sexes after 48-h fasting (P < 0.05), but females displayed a greater rise in insulin AUC values than males (P < 0.05). Fasting increased plasma epinephrine concentrations in both sexes (P < 0.05), whereas plasma norepinephrine concentrations and subjective stress increased only in females (P < 0.05). Plasma 17-ß-estradiol concentrations in females decreased after fasting (P < 0.05). CONCLUSION: Fasting for 48 h induced a similar glucose intolerance in females and males, despite decreased 17-ß-estradiol levels and greater psychological and physiological stress in females. These differences represent a plausible explanation for the gender-based differences observed in insulin responses. TRIAL REGISTRATION: Retrospectively registered on ClinicalTrials.gov (NCT05545943) in September 19, 2022.

Three-week sprint interval training (SIT) reduces cell-free DNA and low-frequency fatigue but does not induce VO2max improvement in older men.

PURPOSE: This study aimed to investigate the impact of sprint interval training (SIT) on both the acute and 3-week modulations of cell-free DNA (cfDNA), as well as its association with neuromuscular fatigue and physical performance in healthy young and old men. METHODS: Ten young (20-25 year old) and nine elderly (63-72 year old) healthy men performed nine SIT sessions consisting of 4-to-6-all-out cycling repetitions of 30 s interspaced with 4-min rest intervals. We compared the maximal voluntary contractions torque, central activation ratio, low-frequency fatigue (LFF), and cfDNA concentrations between the groups before, immediately after, 1 h after, and 24 h after the first and ninth SIT sessions. RESULTS: The plasma cfDNA levels were increased post-exercise (from 1.4 ± 0.258 to 1.91 ± 0.278 ng/ml (P < 0.01) on a log10 scale), without significant differences between the groups. However, older individuals showed a slight decrease in the baseline cfDNA values, from 1.39 ± 0.176 to 1.29 ± 0.085 ng/ml on a log10 scale, after 3 weeks (P = 0.043). Importantly, the elevation of the post-exercise cfDNA values was correlated with an increase in LFF in both groups. Three weeks of SIT induced an improvement in the recovery of LFF (main session effect, P = 0.0029); however, only the young group showed an increase in aerobic capacity (VO2max) (from 40.8 ± 6.74 to 43.0 ± 5.80 ml/kg/min, P = 0.0039). CONCLUSION: Three weeks of SIT diminished the baseline cfDNA values in the old group, together with an improvement in the recovery of LFF. However, VO2max was increased only in the young group.

Near-InfraRed Spectroscopy Provides a Reproducible Estimate of Muscle Aerobic Capacity, but Not Whole-Body Aerobic Power.

Near-infrared spectroscopy (NIRS) during repeated limb occlusions is a noninvasive tool for assessing muscle oxidative capacity. However, the method's reliability and validity remain under investigation. This study aimed to determine the reliability of the NIRS-derived mitochondrial power of the musculus vastus lateralis and its correlation with whole-body (cycling) aerobic power (V̇O2 peak). Eleven healthy active men (28 ± 10 y) twice (2 days apart) underwent repeated arterial occlusions to induce changes in muscle oxygen delivery after 15 s of electrical muscle stimulation. The muscle oxygen consumption (mV̇O2) recovery time and rate (k) constants were calculated from the NIRS O2Hb signal. We assessed the reliability (coefficient of variation and intraclass coefficient of correlation [ICC]) and equivalency (t-test) between visits. The results showed high reproducibility for the mV̇O2 recovery time constant (ICC = 0.859) and moderate reproducibility for the k value (ICC = 0.674), with no significant differences between visits (p > 0.05). NIRS-derived k did not correlate with the V̇O2 peak relative to body mass (r = 0.441, p = 0.17) or the absolute V̇O2 peak (r = 0.366, p = 0.26). In conclusion, NIRS provides a reproducible estimate of muscle mitochondrial power, which, however, was not correlated with whole-body aerobic capacity in the current study, suggesting that even if somewhat overlapping, not the same set of factors underpin these distinct indices of aerobic capacity at the different (peripheral and whole-body systemic) levels.

Prolonged fasting outperforms short-term fasting in terms of glucose tolerance and insulin release: a randomised controlled trial.

Fasting is related to glucose intolerance and insulin resistance, but it is unknown whether the duration of fasting influences these factors. We explored whether prolonged fasting increases norepinephrine and ketone concentrations and decreases core temperature to a greater extent than short-term fasting; if so, this should lead to improved glucose tolerance. Forty-three healthy young adult males were randomly assigned to undergo a 2-d fast, 6-d fast or the usual diet. Changes in rectal temperature (TR), ketone and catecholamine concentrations, glucose tolerance and insulin release in response to an oral glucose tolerance test were assessed. Both fasting trials increased ketone concentration, and the effect was larger after the 6-d fast (P < 0·05). TR and epinephrine concentration increased only after the 2-d fast (P < 0·05). Both fasting trials increased the glucose area under the curve (AUC) (P < 0·05), but the AUC remained higher than the baseline value after participants returned to their usual diet in the 2-d fast group (P < 0·05). Neither fasting had an immediate effect on the insulin AUC, although it increased after return to their usual diet in the 6-d fast group (P < 0·05). These data suggest that the 2-d fast elicited residual impaired glucose tolerance, which may be linked to greater perceived stress during short-term fasting, as shown by the epinephrine response and change in core temperature. By contrast, prolonged fasting seemed to evoke an adaptive residual mechanism that is related to improved insulin release and maintained glucose tolerance.

Short-duration cold exposure decreases fasting-induced glucose intolerance but has no effect on resting energy expenditure.

The aim of the present study was to investigate whether brief cold exposure can reverse fasting-induced glucose intolerance and insulin resistance, and improve resting energy expenditure (REE). Twelve young non-obese women were randomly assigned to undergo the following conditions: 2 days of fasting with two 10-min whole-body cold-water immersions on separate days (FAST-COLD), 2 days of fasting without cold-water immersions (FAST), 2 days of usual diet with two 10-min whole-body cold-water immersions on separate days (COLD), or 2 days of usual diet without cold-water immersions (CON) in a randomised crossover fashion. Changes in REE and substrate utilisation, and glucose tolerance and insulin sensitivity from the oral glucose tolerance test were examined. The results showed that FAST-COLD and FAST trials increased (P < 0.05) REE and decreased (P < 0.05) respiratory quotient, but these variables did not differ significantly between the FAST-COLD and FAST trials. The glucose and insulin area under the curves (AUCs) were higher (P < 0.05) in the FAST-COLD and FAST trials than in the CON and COLD trials, and these AUCs were lower (P < 0.05) in the FAST-COLD than in the FAST trial. Matsuda index was lower in the FAST trial than in the CON trial (P < 0.05), and tended to be greater after the FAST-COLD trial than after the FAST trial (P = 0.060). In conclusion, cold exposure had no effect on REE but decreased fasting-induced glucose intolerance which was accompanied by a maintained insulin sensitivity.

Age-related differences in the neuromuscular performance of fatigue-provoking exercise under severe whole-body hyperthermia conditions.

PURPOSE: The purpose of this study was to determine if aging would lead to greater decline in neuromuscular function during a fatiguing task under severe whole-body hyperthermia conditions. METHODS: Twelve young (aged 19-21 years) and 11 older (aged 65-80 years) males were enrolled in the study, which comprised a randomized control trial under a thermoneutral condition at an ambient temperature of 23°C (CON) and an experimental trial with passive lower body heating in 43°C water (HWI-43°C). Changes in neuromuscular function and fatigability, and physical performance-influencing factors such as psychological, thermoregulatory, neuroendocrine, and immune responses to whole-body hyperthermia were measured. RESULTS: A slower increase in rectal temperature, and a lower heart rate, thermal sensation, and sweating rate were observed in older males than young males in response to HWI-43°C trial (p < 0.05). Nevertheless, prolactin increased more in response to hyperthermia in young males, while interleukin-6 and cortisol levels increased more in older males (p < 0.05). Peripheral dopamine levels decreased in older males and increased in young males in response to hyperthermia (p < 0.05). Surprisingly, older males demonstrated greater neuromuscular fatigability resistance and faster maximal voluntary contraction (MVC) torque recovery after a 2-min sustained isometric MVC task under thermoneutral and severe hyperthermic conditions (p < 0.05). CONCLUSION: Neuromuscular performance during fatigue-provoking sustained isometric exercise under severe whole-body hyperthermia conditions appears to decline in both age groups, but a lower relative decline in torque production for older males may relate to lower psychological and thermophysiological strain along with a diminished dopamine response and prolactin release.

Age-Related Difference in Cognitive Performance under Severe Whole-Body Hyperthermia Parallels Cortisol and Physical Strain Responses.

Background and Objectives: To date, understanding age-related changes in cognitive processes during heat exposure still needs to be better-understood. Thus, the main aim of the current study was to evaluate the effects of whole-body hyperthermia (WBH), i.e., a ≈ 2.5 °C increase in rectal temperature (Tre) from overnight-fast baseline value, on cognitive functioning in old and young men and to explore factors, such as stress and thermophysiological strain, that could influence such changes. Materials and Methods: Ten young (19-21 years of age) and nine old (61-80 years of age) healthy men underwent an experimental trial with passive lower-body heating in hot water immersion (HWI) at 43 °C (HWI-43 °C) until Tre reached 39 °C in old adults and 39.5 °C in young adults. Cognitive performance and cortisol concentration were assessed before and after HWI, and the physiological strain index (PSI) was assessed during HWI-43 °C. Results: PSI was lower and cortisol concentration was greater after HWI-43 °C in the old group compared with the young group (p < 0.05). Surprisingly, hyperthermia improved cognitive flexibility only in old adults, whereas short-term and visual recognition memories were maintained in both age groups. Conclusions: A ≈ 2.5 °C increase in rectal temperature can improve executive function in old adults, and this increase parallels the increased cortisol concentration and the lower thermophysiological strain under severe WBH conditions.

Two-day fasting affects kynurenine pathway with additional modulation of short-term whole-body cooling: a quasi-randomised crossover trial.

Metabolites of the kynurenine (KYN) pathway of tryptophan (TRP) degradation have attracted interest as potential pathophysiological mediators and future diagnostic biomarkers. A greater knowledge of the pathological implications of the metabolites is associated with a need for a better understanding of how the normal behaviour and physiological activities impact their concentrations. This study aimed to investigate whether fasting (FAST) and whole-body cold-water immersion (CWI) affect KYN pathway metabolites. Thirteen young women were randomly assigned to receive the 2-d FAST with two 10-min CWI on separate days (FAST-CWI), 2-d FAST without CWI (FAST-CON), 2-d two CWI on separate days without FAST (CON-CWI) or the 2-d usual diet without CWI (CON-CON) in a randomised crossover fashion. Changes in plasma concentrations of TRP, kynurenic acid (KYNA), 3-hydroxy-kynurenine (3-HK), picolinic acid (PIC), quinolinic acid (QUIN) and nicotinamide (NAA) were determined with ultra-performance liquid chromatography-tandem mass spectrometer. FAST-CWI and FAST-CON lowered TRP concentration (P < 0·05, ηp2 = 0·24), and increased concentrations of KYNA, 3-HK and PIC (P < 0·05, ηp2 = 0·21-0·71) with no additional effects of CWI. The ratio of PIC/QUIN increased after FAST-CWI and FAST-CON trials (P < 0·05) but with a blunted effect in the FAST-CWI trial (P < 0·05) compared with the FAST-CON trials (ηp2 = 0·67). Concentrations of QUIN and NAA were unaltered. This study demonstrated that fasting for 2 d considerably impacts the concentration of several metabolites in the KYN pathway. This should be considered when discussing the potential of KYN pathway metabolites as biomarkers.

Exposure to acute noxious heat evokes a cardiorespiratory shock response in humans.

Background: Noxious acute cold stimuli cause cold shock via the sympathetic nervous system. However, no studies have investigated respiratory "heat shock" in response to noxious acute heat stimuli (≥ 42 °C).Methods: In the present study, we examined whether short-duration whole-body immersion (for 5 min) in noxious hot water (45 °C) is a sufficient stimulus to induce a respiratory acute shock response.Results and conclusion: Our results indicate that short-duration whole-body immersion in noxious 45 °C water produces a significantly greater body temperature, heart rate, and perceptual and respiratory strain than immersion in innocuous warm 37 °C water (p < .05). The initial first minute of hot water immersion (HWI) at 45 °C (vs. immersion at 37 °C) caused a cardiorespiratory shock response, which manifested as acute hyperventilation, and increased ventilatory tidal volume, respiratory exchange ratio, and heart rate (p < .05). Adjustment to this initial respiratory heat shock response within the first minute of immersion was observed as compared with remaining HWI time (1-5 min). Intriguingly, the time-course kinetics of breathing frequency, oxygen uptake, and carbon dioxide washout did not differ between whole-body immersion at 37 °C and immersion at 45 °C, but were higher than in control thermoneutral conditions of an empty bath (p < .05). This may be because of events initiated not only by the water temperature but also by the change in the hydrostatic pressure acting upon the body when immersed in the water bath.

Kinetics of lipid indicators in response to short- and long-duration whole-body, cold-water immersion.

Cold exposure-induced secretion of stress hormones activates cold-defense responses and mobilizes substrates for increased energy demands to fuel thermogenesis. However, it is unclear whether acute cold exposure-induced stress hormone response kinetics affect circulating lipid parameter kinetics. Therefore, we aimed to investigate the 2-day kinetics of stress hormones (i.e., cortisol, epinephrine, and norepinephrine) and the lipid profile (i.e., total cholesterol [TC], high-density lipoprotein [HDL] cholesterol, low-density lipoprotein [LDL] cholesterol, and triglycerides) in response to whole-body long- (intermittent 170 min; 170-CWI) or short-duration (10 min; 10-CWI) cold-water immersion (CWI; 14 °C water) in 17 healthy, young, adult men. Both CWI trials induced a marked release of the stress hormones, epinephrine, and norepinephrine, with higher concentrations detected after 170-CWI (p < 0.05) and a disrupted diurnal peak of cortisol lasting for a few hours. 170-CWI increased triglyceride levels from immediately after until 2 h after CWI, thereafter the concentration decreased at 4 h, 6 h, 1 day and 2 days after CWI (p < 0.05). Furthermore, the HDL-cholesterol level increased immediately after and at 6 h after 170-CWI (p < 0.05), while TC and LDL-cholesterol levels were not altered within 2 days. Lipid parameters were not affected within the 2 days after 10-CWI. Although both CWIs decreased deep body temperature and increased stress hormone levels for a few hours, only long-duration CWI induced changes in the circulating lipid profile within 2 days after CWI. This should be considered when discussing therapeutic protocols to improve circulating lipid profiles and ameliorate diseases associated with such profiles.

Recovering body temperature from acute cold stress is associated with delayed proinflammatory cytokine production in vivo.

A poor outcome of whole-body hypothermia often results from a late complication, rather than from acute effects of hypothermia. A low body (cell) temperature or the increase in the concentrations of the stress hormones cortisol, epinephrine, and norepinephrine in response to acute cold stress have been proposed as potent proinflammatory cytokine suppressant. In the current study, we tested the hypothesis that the recovery of body temperature from a whole-body intermittent cold-water immersion (CWI, at 13-14 °C for a total 170 min) is associated with a delayed response of proinflammatory cytokines in young healthy men. Our results revealed a delay in the increase in the proinflammatory interleukin 6 and interleukin 1ß cytokines after the CWI, which paralleled the changes in cortisol, epinephrine, norepinephrine, and body temperature. CWI decreased tumor necrosis factor α (TNF-α) immediately and 1 h after the CWI. Although TNF-α had recovered to the pre-immersion level at 2 h after CWI, its natural circadian cycle kinetics was disrupted until 12 h after the CWI. Furthermore, we showed that CWI strongly modified the white blood cell counts, with changes reaching a peak between 1 and 2 h after the CWI.

Exposure to total 36-hr sleep deprivation reduces physiological and psychological thermal strain to whole-body uncompensable passive heat stress in young adult men.

Total sleep deprivation (TSD) is associated with endothelial dysfunction and a consequent decrease in vascular reactivity and increase in peripheral vascular resistance. These effectors compromise the body's ability to thermoregulate in hot and cold stress conditions. We investigated heat-unacclimated young adult men (26 ± 2 years) to determine whether 36 hr of TSD compared to an 8 or 4-hr sleep condition, would suppress the responses of the autonomic system (body rectal temperature [Tre ], heart rate [HR], root mean square of successive interbeat intervals, physiological strain, blood pressure [BP], circulating blood catecholamines, sweating rate and subjective sensations) to whole-body uncompensable passive heat stress in traditional Finnish sauna heat (Tair  = 80-90°C, rh = 30%). Sauna bathing that induced whole-body hyperthermia had a residual effect on reducing BP in the 8-hr and 4-hr sleep per night conditions according to BP measurements. By contrast, 36 hr of total wakefulness led to an increase in BP. These observed sleep deprivation-dependent differences in BP modifications were not accompanied by changes in the blood plasma epinephrine and norepinephrine concentrations. However, during sauna bathing, an increase in BP following 36 hr of TSD was accompanied by significant decreases in body Tre , HR and physiological strain, together with a diminished sweating rate, enhanced vagus-mediated autonomic control of HR variability, and improved thermal perception by the subjects. Our results suggest the impaired ability of the body to accumulate external heat in the body's core under uncompensable passive heat conditions following 36 hr of TSD, because of the TSD-attenuated autonomic system response to acute heat stress.

Residual effects of short-term whole-body cold-water immersion on the cytokine profile, white blood cell count, and blood markers of stress.

Background: One of the most challenging environmental extremes is immersion in cold/icy water, and consequent common assumption is that even a brief exposure to cold can lead to cold-related illnesses. The increase in the concentrations of the stress hormones cortisol, epinephrine (Epi), and norepinephrine (NE) in response to acute cold stress are thought to suppress the release of proinflammatory cytokines. No previous study has explored the residual consequences of whole-body short-term cold-water immersion (CWI; 14 °C for 10 min) on the immune response in healthy non-acclimated young adult men (aged 20-30 years).Materials and methods: In the current study, we tested the hypothesis that short-term acute whole-body CWI would induce high blood levels of cortisol, NE, and Epi, which in turn would increase circulating leukocyte numbers and delay the production of proinflammatory cytokines (tumor necrosis factor α (TNF-α), interleukin 1ß (IL-1ß), and IL-6). Results: Short-term whole-body CWI produced a stressful physiological reaction, as manifested by hyperventilation and increased muscle shivering, metabolic heat production, and heart rate. CWI also induced the marked release of the stress hormones Epi, NE, and cortisol. The change in IL-6 concentration after CWI was delayed and TNF-α production was decreased, but IL-1ß was not affected within 48 h after CWI. A delayed increase in neutrophil percentage and decrease in lymphocyte percentage occurred after CWI.Conclusion: These findings suggest that, even though CWI caused changes in stress and immune markers, the participants showed no predisposition to symptoms of the common cold within 48 h after CWI.

Carbohydrate restriction following strenuous glycogen-depleting exercise does not potentiate the acute molecular response associated with mitochondrial biogenesis in human skeletal muscle.

PURPOSE: Carbohydrate (CHO) restriction could be a potent metabolic regulator of endurance exercise-induced muscle adaptations. Here, we determined whether post-exercise CHO restriction following strenuous exercise combining continuous cycling exercise (CCE) and sprint interval exercise could affect the gene expression related to mitochondrial biogenesis and oxidative metabolism in human skeletal muscle. METHODS: In a randomized cross-over design, 8 recreationally active males performed two cycling exercise sessions separated by 4 weeks. Each session consisted of 60-min CCE and six 30-s all-out sprints, which was followed by ingestion of either a CHO or placebo beverage in the post-exercise recovery period. Muscle glycogen concentration and the mRNA levels of several genes related to mitochondrial biogenesis and oxidative metabolism were determined before, immediately after, and at 3 h after exercise. RESULTS: Compared to pre-exercise, strenuous cycling led to a severe muscle glycogen depletion (> 90%) and induced a large increase in PGC1A and PDK4 mRNA levels (~ 20-fold and ~ 10-fold, respectively) during the acute recovery period in both trials. The abundance of the other transcripts was not changed or was only moderately increased during this period. CHO restriction during the 3-h post-exercise period blunted muscle glycogen resynthesis but did not increase the mRNA levels of genes associated with muscle adaptation to endurance exercise, as compared with abundant post-exercise CHO consumption. CONCLUSION: CHO restriction after a glycogen-depleting and metabolically-demanding cycling session is not effective for increasing the acute mRNA levels of genes involved in mitochondrial biogenesis and oxidative metabolism in human skeletal muscle.

Carbohydrates do not accelerate force recovery after glycogen-depleting followed by high-intensity exercise in humans.

Prolonged low-frequency force depression (PLFFD) induced by fatiguing exercise is characterized by a persistent depression in submaximal contractile force during the recovery period. Muscle glycogen depletion is known to limit physical performance during prolonged low- and moderate-intensity exercise, and accelerating glycogen resynthesis with post-exercise carbohydrate intake can facilitate recovery and improve repeated bout exercise performance. Short-term, high-intensity exercise, however, can cause PLFFD without any marked decrease in glycogen. Here, we studied whether recovery from PLFFD was accelerated by carbohydrate ingestion after 60 minutes of moderate-intensity glycogen-depleting cycling exercise followed by six 30-seconds all-out cycling sprints. We used a randomized crossover study design where nine recreationally active males drank a beverage containing either carbohydrate or placebo after exercise. Blood glucose and muscle glycogen concentrations were determined at baseline, immediately post-exercise, and during the 3-hours recovery period. Transcutaneous electrical stimulation of the quadriceps muscle was performed to determine the extent of PLFFD by eliciting low-frequency (20 Hz) and high-frequency (100 Hz) stimulations. Muscle glycogen was severely depleted after exercise, with a significantly higher rate of muscle glycogen resynthesis during the 3-hours recovery period in the carbohydrate than in the placebo trials (13.7 and 5.4 mmol glucosyl units/kg wet weight/h, respectively). Torque at 20 Hz was significantly more depressed than 100 Hz torque during the recovery period in both conditions, and the extent of PLFFD (20/100 Hz ratio) was not different between the two trials. In conclusion, carbohydrate supplementation enhances glycogen resynthesis after glycogen-depleting exercise but does not improve force recovery when the exercise also involves all-out cycling sprints.

Local knee heating increases spinal and supraspinal excitability and enhances plantar flexion and dorsiflexion torque production of the ankle in older adults.

PURPOSE: Aging is associated with progressive loss of active muscle mass and consequent decreases in resting metabolic rate and body temperature, and slowing of nerve conduction velocities and muscle contractility. These effectors compromise the ability of the elderly to maintain an upright posture during sudden balance perturbation, increase the risk of falls, and lead to self-imposed reduction in physical activity. Short-term superficial acute heating can modulate the neural drive transmission to exercising muscles without any marked change in deep-muscle temperature. METHODS: To determine whether the short-term (5 min) application of local passive knee-surface heating (next-to-skin temperature, ~ 44 °C) in healthy older subjects of both sexes (64-74 years; eight men/eight women) enhances reflex excitability, we compared the voluntarily and electrically induced ankle muscle torque production and contractile properties with those of healthy younger subjects of both sexes (21-35 years, 10 men/10 women). RESULTS: The application of local heating (vs. control) increased the maximal Hoffman reflex (Hmax), the maximal volitional wave (Vsup) amplitude, and the Hmax/Mmax amplitude ratio, and decreased Vsup latency only in older adults. In the older adults (vs. younger adults), the application of local heating (vs. control trial) was accompanied by a significant increase in maximal voluntary peak torque, rate of torque development, and isokinetic peak torque of plantar flexion/dorsiflexion muscle contraction. CONCLUSION: The spinal and supraspinal reflex excitability of older adults increased during local knee-heating application. The improved motor drive transmission observed in older adults was accompanied by increased voluntarily induced torque production of the ankle muscles during isometric/isokinetic contractions.

"Two sides of the same coin": constant motor learning speeds up, whereas variable motor learning stabilizes, speed-accuracy movements.

PURPOSE: The aim of this study was to determine the time course of the trade-off between speed and accuracy, intraindividual variability, and movement transfer and retention (4 weeks after learning) of speed-accuracy tasks. METHODS: The participants in this study were healthy adults randomly divided into three groups (control versus constant versus variable). They were aged 19-24 years, and 30 (15 men and 15 women) were in each group. Participants had to perform various tasks with the right dominant hand: (a) simple reaction test; (b) maximal velocity measurement; and (c) a speed-accuracy task. RESULTS: During constant and variable learning, the trade-off in a speed-accuracy task in specific situations shifted toward improved motor planning and motor execution speed, and to reduced intraindividual variability. However, during variable learning, the maximal velocity and variability of motor planning time did not change. Constant learning effectively transferred into variable tasks in terms of reaction time, average velocity and maximal velocity, and these effects were greater than those associated with variable learning. However, the effects of constant learning did not transfer fully into the performance variability of variable movements. Variable learning effectively transferred into constant tasks for the coefficient of variation of the path of movement, average velocity, maximal velocity and reaction time. The retention effect depended neither on learning nor task specificity (constant versus variable tasks). CONCLUSION: Constant learning speeds up but does not stabilize speed-accuracy movements in variable tasks; whereas, variable learning stabilizes but does not speed up speed-accuracy movements in constant tasks.