Showing papers in "Journal of Applied Physiology in 2013"
TL;DR: There is no additional improvement in exercise tolerance after ingesting BR containing 16.8 compared with 8.4 mmol NO3(-).
Abstract: Dietary supplementation with beetroot juice (BR), containing approximately 5-8 mmol inorganic nitrate (NO3(-)), increases plasma nitrite concentration ([NO2(-)]), reduces blood pressure, and may positively influence the physiological responses to exercise. However, the dose-response relationship between the volume of BR ingested and the physiological effects invoked has not been investigated. In a balanced crossover design, 10 healthy men ingested 70, 140, or 280 ml concentrated BR (containing 4.2, 8.4, and 16.8 mmol NO3(-), respectively) or no supplement to establish the effects of BR on resting plasma [NO3(-)] and [NO2(-)] over 24 h. Subsequently, on six separate occasions, 10 subjects completed moderate-intensity and severe-intensity cycle exercise tests, 2.5 h postingestion of 70, 140, and 280 ml BR or NO3(-)-depleted BR as placebo (PL). Following acute BR ingestion, plasma [NO2(-)] increased in a dose-dependent manner, with the peak changes occurring at approximately 2-3 h. Compared with PL, 70 ml BR did not alter the physiological responses to exercise. However, 140 and 280 ml BR reduced the steady-state oxygen (O2) uptake during moderate-intensity exercise by 1.7% (P = 0.06) and 3.0% (P < 0.05), whereas time-to-task failure was extended by 14% and 12% (both P < 0.05), respectively, compared with PL. The results indicate that whereas plasma [NO2(-)] and the O2 cost of moderate-intensity exercise are altered dose dependently with NO3(-)-rich BR, there is no additional improvement in exercise tolerance after ingesting BR containing 16.8 compared with 8.4 mmol NO3(-). These findings have important implications for the use of BR to enhance cardiovascular health and exercise performance in young adults.
405 citations
TL;DR: Increases in mitochondrial content following six HIT sessions may facilitate improvements in respiratory capacity and oxygen extraction, and ultimately are responsible for the improvements in maximal whole body exercise capacity and endurance performance in previously untrained individuals.
Abstract: Six sessions of high-intensity interval training (HIT) are sufficient to improve exercise capacity. The mechanisms explaining such improvements are unclear. Accordingly, the aim of this study was t...
229 citations
TL;DR: EM data suggest that mitochondrial membranes interact in vivo among mitochondria, possibly to induce morphology transitions, for kiss-and-run behavior, or other processes involving contact between mitochondrial membranes.
Abstract: Dynamic remodeling of mitochondrial morphology through membrane dynamics are linked to changes in mitochondrial and cellular function. Although mitochondrial membrane fusion/fission events are frequent in cell culture models, whether mitochondrial membranes dynamically interact in postmitotic muscle fibers in vivo remains unclear. Furthermore, a quantitative assessment of mitochondrial morphology in intact muscle is lacking. Here, using electron microscopy (EM), we provide evidence of interacting membranes from adjacent mitochondria in intact mouse skeletal muscle. Electron-dense mitochondrial contact sites consistent with events of outer mitochondrial membrane tethering are also described. These data suggest that mitochondrial membranes interact in vivo among mitochondria, possibly to induce morphology transitions, for kiss-and-run behavior, or other processes involving contact between mitochondrial membranes. Furthermore, a combination of freeze-fracture scanning EM and transmission EM in orthogonal planes was used to characterize and quantify mitochondrial morphology. Two subpopulations of mitochondria were studied: subsarcolemmal (SS) and intermyofibrillar (IMF), which exhibited significant differences in morphological descriptors, including form factor (means ± SD for SS: 1.41 ± 0.45 vs. IMF: 2.89 ± 1.76, P < 0.01) and aspect ratio (1.97 ± 0.83 vs. 3.63 ± 2.13, P < 0.01) and circularity (0.75 ± 0.16 vs. 0.45 ± 0.22, P < 0.01) but not size (0.28 ± 0.31 vs. 0.27 ± 0.20 μm2). Frequency distributions for mitochondrial size and morphological parameters were highly skewed, suggesting the presence of mechanisms to influence mitochondrial size and shape. In addition, physical continuities between SS and IMF mitochondria indicated mixing of both subpopulations. These data provide evidence that mitochondrial membranes interact in vivo in mouse skeletal muscle and that factors may be involved in regulating skeletal muscle mitochondrial morphology.
188 citations
TL;DR: Data suggest that measurement of fascicle lengths and pennation angles are accurate under certain conditions, such as when large limb muscles are imaged in a relaxed state and the limb or joint remains stationary.
Abstract: Ultrasound imaging is widely used to measure architectural features of human skeletal muscles in vivo. We systematically reviewed studies of the reliability and validity of two-dimensional ultrasound measurement of muscle fascicle lengths or pennation angles in human skeletal muscles. A comprehensive search was conducted in June 2011. Thirty-six reliability studies and six validity studies met the inclusion criteria. Data from these studies indicate that ultrasound measurements of muscle fascicle lengths are reliable across a broad range of experimental conditions [intraclass correlation coefficient (ICC) and r values were always > 0.6, and coefficient of variation values were always 0.5 and coefficient of variation values were always 0.7) under certain conditions, such as when large limb muscles are imaged in a relaxed state and the limb or joint remains stationary. Future studies on validity should consider ways to test for the validity of two-dimensional ultrasound imaging in contracted or moving muscles and the best method of probe alignment.
187 citations
TL;DR: Evidence is provided that peripheral fatigue and associated afferent feedback limits the development of peripheral fatiguing and compromises endurance exercise performance by inhibiting CMD.
Abstract: This study sought to determine whether afferent feedback associated with peripheral muscle fatigue inhibits central motor drive (CMD) and thereby limits endurance exercise performance. On two separ...
178 citations
TL;DR: The present review examines the current state of the art of the pathophysiology of muscle dysfunction in COPD and finds that deconditioning seems to play a key role in peripheral muscle dysfunction.
Abstract: Muscle dysfunction often occurs in patients with chronic obstructive pulmonary disease (COPD) and may involve both respiratory and locomotor (peripheral) muscles. The loss of strength and/or endurance in the former can lead to ventilatory insufficiency, whereas in the latter it limits exercise capacity and activities of daily life. Muscle dysfunction is the consequence of complex interactions between local and systemic factors, frequently coexisting in COPD patients. Pulmonary hyperinflation along with the increase in work of breathing that occur in COPD appear as the main contributing factors to respiratory muscle dysfunction. By contrast, deconditioning seems to play a key role in peripheral muscle dysfunction. However, additional systemic factors, including tobacco smoking, systemic inflammation, exercise, exacerbations, nutritional and gas exchange abnormalities, anabolic insufficiency, comorbidities and drugs, can also influence the function of both respiratory and peripheral muscles, by inducing modifications in their local microenvironment. Under all these circumstances, protein metabolism imbalance, oxidative stress, inflammatory events, as well as muscle injury may occur, determining the final structure and modulating the function of different muscle groups. Respiratory muscles show signs of injury as well as an increase in several elements involved in aerobic metabolism (proportion of type I fibers, capillary density, and aerobic enzyme activity) whereas limb muscles exhibit a loss of the same elements, injury, and a reduction in fiber size. In the present review we examine the current state of the art of the pathophysiology of muscle dysfunction in COPD.
172 citations
TL;DR: A substantial revision of a method for measuring several physiological traits causing obstructive sleep apnea, which is a relatively simple way of defining mechanisms underlying OSA and could potentially be used in a clinical setting to individualize therapy.
Abstract: We previously published a method for measuring several physiological traits causing obstructive sleep apnea (OSA). The method, however, had a relatively low success rate (76%) and required mathemat...
171 citations
TL;DR: Mitochondrial-specific respiration capacities during β-oxidation, maximal oxidative phosphorylation, and electron transport system capacity all correspondingly improve with aerobic capacity, independent of mitochondrial content in human skeletal muscle.
Abstract: Changes in skeletal muscle respiratory capacity parallel that of aerobic fitness. It is unknown whether mitochondrial content, alone, can fully account for these differences in skeletal muscle resp...
169 citations
TL;DR: Regular physical activity prevents the development of chronic muscle pain and exercise-induced muscle pain by reducing phosphorylation of the NR1 subunit of the NMDA receptor in the central nervous system, however, regular physical activity has no effect on development of acute pain.
Abstract: Chronic musculoskeletal pain is a significant health problem and is associated with increases in pain during acute physical activity. Regular physical activity is protective against many chronic di...
154 citations
TL;DR: It is suggested that light exercise has the potential to enhance the effectiveness of motor learning or recovery following brain damage, and low-intensity cycling promoted the neuroplastic response to cTBS within the motor cortex of healthy adults.
Abstract: Regular physical activity is associated with enhanced plasticity in the motor cortex, but the effect of a single session of aerobic exercise on neuroplasticity is unknown. The aim of this study was to compare corticospinal excitability and plasticity in the upper limb cortical representation following a single session of lower limb cycling at either low or moderate intensity, or a control condition. We recruited 25 healthy adults to take part in three experimental sessions. Cortical excitability was examined using transcranial magnetic stimulation to elicit motor-evoked potentials in the right first dorsal interosseus muscle. Levels of serum brain-derived neurotrophic factor and cortisol were assessed throughout the experiments. Following baseline testing, participants cycled on a stationary bike at a workload equivalent to 57% (low intensity, 30 min) or 77% age-predicted maximal heart rate (moderate intensity, 15 min), or a seated control condition. Neuroplasticity within the primary motor cortex was then examined using a continuous theta burst stimulation (cTBS) paradigm. We found that exercise did not alter cortical excitability. Following cTBS, there was a transient inhibition of first dorsal interosseus motor-evoked potentials during control and low-intensity conditions, but this was only significantly different following the low-intensity state. Moderate-intensity exercise alone increased serum cortisol levels, but brain-derived neurotrophic factor levels did not increase across any condition. In summary, low-intensity cycling promoted the neuroplastic response to cTBS within the motor cortex of healthy adults. These findings suggest that light exercise has the potential to enhance the effectiveness of motor learning or recovery following brain damage.
149 citations
TL;DR: This synthesis summarizes and integrates knowledge derived from papers relating acute impacts of exercise on artery function, specifically endothelial function assessed by flow-mediated dilatation, and proposes that an immediate decrease in FMD occurs soon after exercise cessation and that this is followed by a (supra)normalization response.
Abstract: Although the effects of exercise training on vascular function have been well studied, less is known about the effects of acute exercise bouts. This synthesis summarizes and integrates knowledge de...
TL;DR: Nasal high flow may be utilized to increase tidal breathing during wakefulness and to relieve respiratory loads during sleep and the mechanisms of action differ from those of CPAP and are sleep/wake-state dependent.
Abstract: Nasal high flow (NHF) has been shown to increase expiratory pressure and reduce respiratory rate but the mechanisms involved remain unclear. Ten healthy participants [age, 22 ± 2 yr; body mass inde...
TL;DR: Alterations in mechanisms of muscle mass maintenance in COPD are reviewed and the involvement of oxidative stress, inflammation, and myostatin as potential triggers of cachexia are discussed.
Abstract: Pulmonary cachexia is a prevalent, debilitating, and well-recognized feature of COPD associated with increased mortality and loss of peripheral and respiratory muscle function. The exact cause and underlying mechanisms of cachexia in COPD are still poorly understood. Increasing evidence, however, shows that pathological changes in intracellular mechanisms of muscle mass maintenance (i.e., protein turnover and myonuclear turnover) are likely involved. Potential factors triggering alterations in these mechanisms in COPD include oxidative stress, myostatin, and inflammation. In addition to muscle wasting, peripheral muscle in COPD is characterized by a fiber-type shift toward a more type II, glycolytic phenotype and an impaired oxidative capacity (collectively referred to as an impaired oxidative phenotype). Atrophied diaphragm muscle in COPD, however, displays an enhanced oxidative phenotype. Interestingly, intrinsic abnormalities in (lower limb) peripheral muscle seem more pronounced in either cachectic patients or weight loss-susceptible emphysema patients, suggesting that muscle wasting and intrinsic changes in peripheral muscle's oxidative phenotype are somehow intertwined. In this manuscript, we will review alterations in mechanisms of muscle mass maintenance in COPD and discuss the involvement of oxidative stress, inflammation, and myostatin as potential triggers of cachexia. Moreover, we postulate that an impaired muscle oxidative phenotype in COPD can accelerate the process of cachexia, as it renders muscle in COPD less energy efficient, thereby contributing to an energy deficit and weight loss when not dietary compensated. Furthermore, loss of peripheral muscle oxidative phenotype may increase the muscle's susceptibility to inflammation- and oxidative stress-induced muscle damage and wasting.
TL;DR: Airway smooth muscle (ASM) plays an integral part in the pathophysiology of asthma and is an important target in the treatment of asthma.
Abstract: Airway smooth muscle (ASM) plays an integral part in the pathophysiology of asthma. It is responsible for acute bronchoconstriction, which is potentiated by constrictor hyperresponsiveness, impaired relaxation and length adaptation. ASM also contributes to airway remodeling and inflammation in asthma. In light of this, ASM is an important target in the treatment of asthma.
TL;DR: Good agreement between N IRS and (31)P-MRS indexes of skeletal muscle oxidative capacity suggest that NIRS is a valid method for assessing mitochondrial function, and that direct comparisons between NIRs and ( 31)MRS measurements may be possible.
Abstract: The purpose of this study was to cross-validate measurements of skeletal muscle oxidative capacity made with near-infrared spectroscopy (NIRS) measurements to those made with phosphorus magnetic re
TL;DR: The results suggest that the increased aerobic capacity shown with AE+RE was accompanied by a more robust increase in muscle size compared with RE, and it remains that intense AE can be executed prior to RE without compromising performance outcome.
Abstract: This study tested the hypothesis that chronic aerobic and resistance exercise (AE+RE) would elicit greater muscle hypertrophy than resistance exercise only (RE). Ten men (25 ± 4 yr) performed 5 wk ...
TL;DR: Insight is provided into the muscle regulatory systems and molecular processes underlying the physiological benefits induced by interrupting prolonged sitting and the effects of chronic inactivity on expression of some specific genes.
Abstract: Breaking up prolonged sitting has been beneficially associated with cardiometabolic risk markers in both observational and intervention studies. We aimed to define the acute transcriptional events induced in skeletal muscle by breaks in sedentary time. Overweight/obese adults participated in a randomized three-period, three-treatment crossover trial in an acute setting. The three 5-h interventions were performed in the postprandial state after a standardized test drink and included seated position with no activity and seated with 2-min bouts of light- or moderate-intensity treadmill walking every 20 min. Vastus lateralis biopsies were obtained in eight participants after each treatment, and gene expression was examined using microarrays validated with real-time quantitative PCR. There were 75 differentially expressed genes between the three conditions. Pathway analysis indicated the main biological functions affected were related to small-molecule biochemistry, cellular development, growth and proliferation, and carbohydrate metabolism. Interestingly, differentially expressed genes were also linked to cardiovascular disease. For example, relative to prolonged sitting, activity bouts increased expression of nicotamide N-methyltransferase, which modulates anti-inflammatory and anti-oxidative pathways and triglyceride metabolism. Activity bouts also altered expression of 10 genes involved in carbohydrate metabolism, including increased expression of dynein light chain, which may regulate translocation of the GLUT-4 glucose transporter. In addition, breaking up sedentary time reversed the effects of chronic inactivity on expression of some specific genes. This study provides insight into the muscle regulatory systems and molecular processes underlying the physiological benefits induced by interrupting prolonged sitting.
TL;DR: Interestingly, phosphorylation levels were restored after 12 days of detraining in the DT group, indicating that, with chronic resistance training, anabolic signaling becomes less sensitive to resistance exercise stimuli but is restored after a short detraining period.
Abstract: Resistance training-induced muscle anabolism and subsequent hypertrophy occur most rapidly during the early phase of training and become progressively slower over time. Currently, little is known about the intracellular signaling mechanisms underlying changes in the sensitivity of muscles to training stimuli. We investigated the changes in the exercise-induced phosphorylation of hypertrophic signaling proteins during chronic resistance training and subsequent detraining. Male rats were divided into four groups: 1 bout (1B), 12 bouts (12B), 18 bouts (18B), and detraining (DT). In the DT group, rats were subjected to 12 exercise sessions, detrained for 12 days, and then were subjected to 1 exercise session before being killed. Isometric training consisted of maximum isometric contraction, which was produced by percutaneous electrical stimulation of the gastrocnemius muscle every other day. Muscles were removed 24 h after the final exercise session. Levels of total and phosphorylated p70S6K, 4E-BP1, rpS6, and p90RSK levels were measured, and phosphorylation of p70S6K, rpS6, and p90RSK was elevated in the 1B group compared with control muscle (CON) after acute resistance exercise, whereas repeated bouts of exercise suppressed those phosphorylation in both 12B and 18B groups. Interestingly, these phosphorylation levels were restored after 12 days of detraining in the DT group. On the contrary, phosphorylation of 4E-BP1 was not altered with chronic training and detraining, indicating that, with chronic resistance training, anabolic signaling becomes less sensitive to resistance exercise stimuli but is restored after a short detraining period.
TL;DR: It is concluded that 1) lactate MCR reaches an apex below the LT, 2) LT corresponds to a limitation in MCR, and 3) endurance training augments capacities for lactate production, disposal and clearance.
Abstract: To understand the meaning of the lactate threshold (LT) and to test the hypothesis that endurance training augments lactate kinetics [i.e., rates of appearance and disposal (Ra and Rd, respectively...
TL;DR: Results confirm previous findings that treatment with a mitochondrial-targeted antioxidant is sufficient to prevent casting-induced skeletal muscle atrophy, mitochondrial dysfunction, and activation of the proteases calpain and caspase-3 and reveal that inactivity-induced increases in mitochondrial ROS emission play a required role in activation of key proteolytic systems and the downregulation of important anabolic signaling molecules in muscle fibers exposed to prolonged inactivity.
Abstract: Long periods of skeletal muscle disuse result in muscle fiber atrophy, and mitochondrial production of reactive oxygen species (ROS) appears to be a required signal for the increase in protein degradation that occurs during disuse muscle atrophy. The experiments detailed here demonstrate for the first time in limb muscle that the inactivity-induced increases in E3 ligase expression and autophagy biomarkers result from increases in mitochondrial ROS emission. Treatment of animals with a mitochondrial-targeted antioxidant also prevented the disuse-induced decrease in anabolic signaling (Akt/mammalian target of rapamycin signaling) that is normally associated with prolonged inactivity in skeletal muscles. Additionally, our results confirm previous findings that treatment with a mitochondrial-targeted antioxidant is sufficient to prevent casting-induced skeletal muscle atrophy, mitochondrial dysfunction, and activation of the proteases calpain and caspase-3. Collectively, these data reveal that inactivity-induced increases in mitochondrial ROS emission play a required role in activation of key proteolytic systems and the downregulation of important anabolic signaling molecules in muscle fibers exposed to prolonged inactivity.
TL;DR: With the knowledge gained through this metaanalysis, noninvasive tools could measure elastic modulus in vivo and reasonably predict ultimate stress (or structural compromise) for diseased or injured tendon.
Abstract: Tendon is a highly specialized, hierarchical tissue designed to transfer forces from muscle to bone; complex viscoelastic and anisotropic behaviors have been extensively characterized for specific
TL;DR: The mechanisms by which bone, tendon, and enthesis healing occurs, and the effects of NSAID therapy on each of these processes are summarized.
Abstract: Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for the treatment of skeletal injuries. The ability of NSAIDs to reduce pain and inflammation is well-established. However, the effects of NSAID therapy on healing of skeletal injuries is less defined. NSAIDs inhibit cyclooxygenase activity to reduce synthesis of prostaglandins, which are proinflammatory, lipid-signaling molecules. Inhibition of cyclooxygenase activity can impact many physiological processes. The effects of NSAID therapy on healing of bone, tendon, and the tendon-to-bone junction (enthesis) have been studied in animal and cell culture models, but human studies are few. Use of different NSAIDs with different pharmacological properties, differences in dosing regimens, and differences in study models and outcome measures have complicated comparisons between studies. In this review, we summarize the mechanisms by which bone, tendon, and enthesis healing occurs, and describe the effects of NSAID therapy on each of these processes. Determining the impact of NSAID therapy on healing of skeletal tissues will enable clinicians to appropriately manage the patient's condition and improve healing outcomes.
TL;DR: The results suggest that the FF pattern is not more economical than the RF pattern.
Abstract: It continues to be argued that a forefoot (FF) strike pattern during running is more economical than a rearfoot (RF) pattern; however, previous studies using one habitual footstrike group have foun...
TL;DR: Findings provide direct evidence for a peripheral modulation of sudomotor activity in females, in contrast to sex, which does not modulate cutaneous vasodilation.
Abstract: The current study aimed to determine whether a peripheral modulation of sweating contributes to the lower sudomotor thermosensitivity previously observed in females during exercise. We examined dos...
TL;DR: The results support the hypothesis that age-related alterations in the myosin molecule contribute to skeletal muscle dysfunction and physical disability and indicate that this effect is stronger in women.
Abstract: We hypothesize that age-related skeletal muscle dysfunction and physical disability may be partially explained by alterations in the function of the myosin molecule. To test this hypothesis, skeletal muscle function at the whole muscle, single fiber, and molecular levels was measured in young (21–35 yr) and older (65–75 yr) male and female volunteers with similar physical activity levels. After adjusting for muscle size, older adults had similar knee extensor isometric torque values compared with young, but had lower isokinetic power, most notably in women. At the single-fiber and molecular levels, aging was associated with increased isometric tension, slowed myosin actin cross-bridge kinetics (longer myosin attachment times and reduced rates of myosin force production), greater myofilament lattice stiffness, and reduced phosphorylation of the fast myosin regulatory light chain; however, the age effect was driven primarily by women (i.e., age-by-sex interaction effects). In myosin heavy chain IIA fibers, single-fiber isometric tension and molecular level mechanical and kinetic indexes were correlated with whole muscle isokinetic power output. Collectively, considering that contractile dysfunction scales up through various anatomical levels, our results suggest a potential sex-specific molecular mechanism, reduced cross-bridge kinetics, contributes to the reduced physical capacity with aging in women. Thus these results support our hypothesis that age-related alterations in the myosin molecule contribute to skeletal muscle dysfunction and physical disability and indicate that this effect is stronger in women.
TL;DR: The notion that mitochondrial membrane dynamics are actively remodelled in skeletal muscle, which may be regulated by contractile activity and the metabolic state, is supported.
Abstract: A unique property of mitochondria in mammalian cells is their ability to physically interact and undergo dynamic events of fusion/fission that remodel their morphology and possibly their function. ...
TL;DR: Reduced muscle endurance associated with underlying loss of muscle oxphen is already present in patients with mild-to-moderate COPD without muscle wasting.
Abstract: Being well-established in advanced chronic obstructive pulmonary disease (COPD), skeletal muscle dysfunction and its underlying pathology have been scarcely investigated in patients with mild-to-mo...
TL;DR: Circulating muscle-specific and muscle-related miRNAs primarily responded to a downhill exercise (high eccentric component) and could potentially be alternative biomarkers of muscle damage and two muscle- related miRN as well as markers or mediators of physiological adaptations were dependent on the exercise mode.
Abstract: Here, we studied muscle-specific and muscle-related miRNAs in plasma of exercising humans. Our aim was to determine whether they are affected by eccentric and/or concentric exercise modes and could...
TL;DR: In this paper, the vascular consequences of short-term reductions in daily physical activity were examined, and it was shown that physical inactivity promotes the development of cardiovascular diseases, however, few data exist examining the vascular effects.
Abstract: Physical inactivity promotes the development of cardiovascular diseases. However, few data exist examining the vascular consequences of short-term reductions in daily physical activity. Thus we tes...
TL;DR: A thermal manikin, (MTNW, Seattle, WA) was used to determine the effective cooling power of moisture evaporation, and a general formula for the calculation of λeff was developed.
Abstract: Calculation of evaporative heat loss is essential to heat balance calculations. Despite recognition that the value for latent heat of evaporation, used in these calculations, may not always reflect the real cooling benefit to the body, only limited quantitative data on this is available, which has found little use in recent literature. In this experiment a thermal manikin, (MTNW, Seattle, WA) was used to determine the effective cooling power of moisture evaporation. The manikin measures both heat loss and mass loss independently, allowing a direct calculation of an effective latent heat of evaporation (λeff). The location of the evaporation was varied: from the skin or from the underwear or from the outerwear. Outerwear of different permeabilities was used, and different numbers of layers were used. Tests took place in 20°C, 0.5 m/s at different humidities and were performed both dry and with a wet layer, allowing the breakdown of heat loss in dry and evaporative components. For evaporation from the skin, λeff is close to the theoretical value (2,430 J/g) but starts to drop when more clothing is worn, e.g., by 11% for underwear and permeable coverall. When evaporation is from the underwear, λeff reduction is 28% wearing a permeable outer. When evaporation is from the outermost layer only, the reduction exceeds 62% (no base layer), increasing toward 80% with more layers between skin and wet outerwear. In semi- and impermeable outerwear, the added effect of condensation in the clothing opposes this effect. A general formula for the calculation of λeff was developed.