Wagner diagram for modeling O2pathway - calculation and graphical display by the Helsinki O2pathway tool.

OBJECTIVE: Maximal O2uptake (V̇O2max) reflects the individual's maximal rate of O2transport and utilization through the integrated whole-body pathway composed of the lungs, heart, blood, circulation, and metabolically active tissues. As such, V̇O2maxis strongly associated with physical capacity as well as overall health and thus acts as one predictor of physical performance and as a vital sign in determination of status and progress of numerous clinical conditions. Quantifying the contribution of single parts of the multistep O2pathway to V̇O2maxprovides mechanistic insights into exercise (in)tolerance and into therapy-, training-, or disuse-induced adaptations at individual or group levels. We developed a desktop application (Helsinki O2Pathway Tool - HO2PT) to model numerical and graphical display of the O2pathway based on the "Wagner diagram" originally formulated by Peter D. Wagner and his colleagues. Approach: The HO2PT was developed and programmed in Python to integrate the Fick principle and Fick's law of diffusion into a computational system to import, calculate, graphically display, and export variables of the Wagner diagram. Main results: The HO2PT models O2pathway both numerically and graphically according to the Wagner diagram and pertains to conditions under which the mitochondrial oxidative capacity of metabolically active tissues exceeds the capacity of the O2transport system to deliver O2to the mitochondria. The tool is based on the Python open source code and libraries and freely and publicly available online for Windows, macOS, and Linux operating systems. Significance: The HO2PT offers a novel functional and demonstrative platform for those interested in examining V̇O2maxand its determinants by using the Wagner diagram. It will improve access to and usability of Wagner's and his colleagues' integrated physiological model and thereby benefit users across the wide spectrum of contexts such as scientific research, education, exercise testing, sports coaching, and clinical medicine. .

Effect of Aerobic Exercise and Time-Restricted Feeding on Metabolic Markers and Circadian Rhythm in Mice Fed with the High-Fat Diet.

SCOPE: Diet and exercise are significant players in obesity and metabolic diseases. Time-restricted feeding (tRF) has been shown to improve metabolic responses by regulating circadian clocks but whether it acts synergically with exercise remains unknown. It is hypothesized that forced exercise alone or combined with tRF alleviates obesity and its metabolic complications. METHODS AND RESULTS: Male C57bl6 mice are fed with high-fat or a control diet for 12 weeks either ad libitum or tRF for 10 h during their active period. High-fat diet (HFD)-fed mice are divided into exercise (treadmill for 1 h at 12 m min-1 alternate days for 9 weeks and 16 m min-1 daily for the following 3 weeks) and non-exercise groups. tRF and tRF-Ex significantly decreased body weight, food intake, and plasma lipids, and improved glucose tolerance. However, exercise reduced only body weight and plasma lipids. tRF and tRF-Ex significantly downregulated Fasn, Hmgcr, and Srebp1c, while exercise only Hmgcr. HFD feeding disrupted clock genes, but exercise, tRF, and tRF-Ex coordinated the circadian clock genes Bmal1, Per2, and Rev-Erbα in the liver, adipose tissue, and skeletal muscles. CONCLUSION: HFD feeding disrupted clock genes in the peripheral organs while exercise, tRF, and their combination restored clock genes and improved metabolic consequences induced by high-fat diet feeding.

Endurance capacity impairment in cold air ranging from skin cooling to mild hypothermia.

We tested the effects of cold air (0°C) exposure on endurance capacity to different levels of cold strain ranging from skin cooling to core cooling of Δ-1.0°C. Ten males completed a randomized, crossover, control study consisting of a cycling time to exhaustion (TTE) at 70% of their peak power output following: 1) 30-min of exposure to 22°C thermoneutral air (TN), 2) 30-min exposure to 0°C air leading to a cold shell (CS), 3) 0°C air exposure causing mild hypothermia of -0.5°C from baseline rectal temperature (HYPO-0.5°C), and 4) 0°C air exposure causing mild hypothermia of -1.0°C from baseline rectal temperature (HYPO-1.0°C). The latter three conditions tested TTE in 0°C air. Core temperature and seven-site mean skin temperature at the start of the TTE were: TN (37.0 ± 0.2°C, 31.2 ± 0.8°C), CS (37.1 ± 0.3°C, 25.5 ± 1.4°C), HYPO-0.5°C (36.6 ± 0.4°C, 22.3 ± 2.2°C), HYPO-1.0°C (36.4 ± 0.5°C, 21.4 ± 2.7°C). There was a significant condition effect (P ≤ 0.001) for TTE, which from TN (23.75 ± 13.75 min) to CS (16.22 ± 10.30 min, Δ-30.9 ± 21.5%, P = 0.055), HYPO-0.5°C (8.50 ± 5.23 min, Δ-61.4 ± 19.7%, P ≤ 0.001), and HYPO-1.0°C (6.50 ± 5.60 min, Δ-71.6 ± 16.4%, P ≤ 0.001). Furthermore, participants had a greater endurance capacity in CS compared with HYPO-0.5°C (P = 0.046), and HYPO-1.0°C (P = 0.007), with no differences between HYPO-0.5°C and HYPO-1.0°C (P = 1.00). Endurance capacity impairment at 70% peak power output occurs early in cold exposure with skin cooling, with significantly larger impairments with mild hypothermia up to Δ-1.0°C.NEW & NOTEWORTHY We developed a novel protocol that cooled skin temperature, or skin plus core temperature (Δ-0.5°C or Δ-1.0 °C), to determine a dose-response of cold exposure on endurance capacity at 70% peak power output. Skin cooling significantly impaired exercise tolerance time by ∼31%, whereas core cooling led to a further reduction of 30%-40% with no difference between Δ-0.5°C and Δ-1.0°C. Overall, simply cooling the skin impaired endurance capacity, but this impairment is further magnified by core cooling.

Effects of skin and mild core cooling on cognitive function in cold air in men.

This study tested the effects of skin and core cooling on cognitive function in 0°C cold air. Ten males completed a randomized, repeated measures study consisting of four environmental conditions: (i) 30 min of exposure to 22°C thermoneutral air (TN), (ii) 15 min to 0°C cold air which cooled skin temperature to ~27°C (CS), (iii) 0°C cold air exposure causing mild core cooling of ∆-0.3°C from baseline (C-0.3°C) and (iv) 0°C cold air exposure causing mild core cooling of ∆-0.8°C from baseline (C-0.8°C). Cognitive function (reaction time [ms] and errors made [#]) were tested using a simple reaction test, a two-six item working memory capacity task, and vertical flanker task to assess executive function. There were no condition effects (all p > 0.05) for number of errors made on any task. There were no significant differences in reaction time relative to TN for the vertical flanker and item working memory capacity task. However, simple reaction time was slower in C-0.3°C (297 ± 33 ms) and C-0.8°C (296 ± 41 ms) compared to CS (267 ± 26 ms) but not TN (274 ± 38). Despite small changes in simple reaction time (~30 ms), executive function and working memory was maintained in 0°C cold air with up to ∆-0.8°C reduction in core temperature.

Using Heart Rate Variability Methods for Health-Related Outcomes in Outdoor Contexts: A Scoping Review of Empirical Studies.

Heart rate variability (HRV) is a psychophysiological variable that is often used in applied analysis techniques to indicate health status because it provides a window into the intrinsic regulation of the autonomic nervous system. However, HRV data analysis methods are varied and complex, which has led to different approaches to data collection, analysis, and interpretation of results. Our scoping review aimed to explore the diverse use of HRV methods in studies designed to assess health outcomes in outdoor free-living contexts. Four database indexes were searched, which resulted in the identification of 17,505 candidate studies. There were 34 studies and eight systematic reviews that met the inclusion criteria. Just over half of the papers referenced the 1996 task force paper that outlined the standards of measurement and physiological interpretation of HRV data, with even fewer adhering to recommended HRV recording and analysis procedures. Most authors reported an increase in parasympathetic (n = 23) and a decrease in systematic nervous system activity (n = 20). Few studies mentioned methods-related limitations and challenges, despite a wide diversity of recording devices and analysis software used. We conclude our review with five recommendations for future research using HRV methods in outdoor and health-related contexts.

Exogenous Ketone Salt Supplementation and Whole-Body Cooling Do Not Improve Short-Term Physical Performance.

Exogenous ketone supplementation and whole-body cooling (WBC) have shown to independently influence exercise metabolism. Whether readily available ketone salts, with and without WBC, would provide similar metabolic benefits during steady-state aerobic and time-trial performances was investigated. Nine active males (VO2peak: 56.3 ± 2.2 mL·kg-1·min-1) completed three single-blind exercise sessions preceded by: (1) ingestion of placebo (CON), (2) ketone supplementation (0.3 g·kg-1 ß-OHB) (KET), and (3) ketone supplementation with WBC (KETCO). Participants cycled in steady-state (SS, 60% W max) condition for 30-min, immediately followed by a 15-min time trial (TT). Skin and core temperature, cardio-metabolic, and respiratory measures were collected continuously, whereas venous blood samples were collected before and after supplementation, after SS and TT. Venous ß-OHB was elevated, while blood glucose was lower, with supplementation vs. CON (p < 0.05). TT power output was not different between conditions (p = 0.112, CON: 190 ± 43.5 W, KET: 185 ± 40.4 W, KETCO: 211 ± 50.7 W). RER was higher during KETCO (0.97 ± 0.09) compared to both CON (0.88 ± 0.04, p = 0.012) and KET (0.88 ± 0.05, p = 0.014). Ketone salt supplementation and WBC prior to short-term exercise sufficiently increase blood ß-OHB concentrations, but do not benefit metabolic shifts in fuel utilization or improve time trial performance.

Metabolic flexibility is unimpaired during exercise in the cold following acute glucose ingestion in young healthy adults.

PURPOSE: Metabolic flexibility is compromised in individuals suffering from metabolic diseases, lipo- and glucotoxicity, and mitochondrial dysfunctions. Exercise studies performed in cold environments have demonstrated an increase in lipid utilization, which could lead to a compromised substrate competition, glycotoxic-lipotoxic state, or metabolic inflexibility. Whether metabolic flexibility is altered during incremental maximal exercise to volitional fatigue in a cold environment remains unclear. METHODS: Ten young healthy participants performed four maximal incremental treadmill tests to volitional fatigue, in a fasted state, in a cold (0 °C) or a thermoneutral (22.0 °C) environment, with and without a pre-exercise ingestion of a 75-g glucose solution. Metabolic flexibility was assessed via indirect calorimetry using the change in respiratory exchange ratio (ΔRER), maximal fat oxidation (ΔMFO), and where MFO occurred along the exercise intensity spectrum (ΔFatmax), while circulating lactate and glucose levels were measured pre and post exercise. RESULTS: Multiple linear mixed-effects regressions revealed an increase in glucose oxidation from glucose ingestion and an increase in lipid oxidation from the cold during exercise (p < 0.001). No differences were observed in metabolic flexibility as assessed via ΔRER (0.05 ± 0.03 vs. 0.05 ± 0.03; p = 0.734), ΔMFO (0.21 ± 0.18 vs. 0.16 ± 0.13 g min-1; p = 0.133) and ΔFatmax (13.3 ± 19.0 vs. 0.6 ± 21.3 %V̇O2peak; p = 0.266) in cold and thermoneutral, respectively. CONCLUSIONS: Following glucose loading, metabolic flexibility was unaffected during exercise to volitional fatigue in a cold environment, inducing an increase in lipid oxidation. These results suggest that competing pathways responsible for the regulation of fuel selection during exercise and cold exposure may potentially be mechanistically independent. Whether long-term metabolic influences of high-fat diets and acute lipid overload in cold and warm environments would impact metabolic flexibility remain unclear.

Maximal Fat Oxidation: Comparison between Treadmill, Elliptical and Rowing Exercises.

Fat oxidation during exercise is associated with cardio-metabolic benefits, but the extent of which whole-body exercise modality elicits the greatest fat oxidation remains unclear. We investigated the effects of treadmill, elliptical and rowing exercise on fat oxidation in healthy individuals. Nine healthy males participated in three, peak oxygen consumption tests, on a treadmill, elliptical and rowing ergometer. Indirect calorimetry was used to assess maximal oxygen consumption (V̇O2peak), maximal fat oxidation (MFO) rates, and the exercise intensity MFO occurred (Fatmax). Mixed venous blood was collected to assess lactate and blood gases concentrations. While V̇O2peak was similar between exercise modalities, MFO rates were higher on the treadmill (mean ± SD; 0.61 ± 0.06 g·min-1) compared to both the elliptical (0.41 ± 0.08 g·min-1, p = 0.022) and the rower (0.40 ± 0.08 g·min-1, p = 0.017). Fatmax values were also significantly higher on the treadmill (56.0 ± 6.2 %V̇O2peak) compared to both the elliptical (36.8 ± 5.4 %V̇O2peak, p = 0.049) and rower (31.6 ± 5.0 %V̇O2peak, p = 0.021). Post-exercise blood lactate concentrations were also significantly lower following treadmill exercise (p = 0.021). Exercising on a treadmill maximizes fat oxidation to a greater extent than elliptical and rowing exercises, and remains an important exercise modality to improve fat oxidation, and consequently, cardio-metabolic health.

High-intensity interval exercise in the cold regulates acute and postprandial metabolism.

High-intensity interval exercise (HIIE) has been shown to be more effective than moderate-intensity exercise for increasing acute lipid oxidation and lowering blood lipids during exercise and postprandially. Exercise in cold environments is also known to enhance lipid oxidation; however, the immediate and long-term effects of HIIE exercise in cold are unknown. The purpose of this study was to examine the effects cold stress during HIIE on acute exercise metabolism and postprandial metabolism. Eleven recreationally active individuals (age: 23 ± 3 yr, weight: 80 ± 9.7 kg, V̇O2peak: 39.2 ± 5.73 mL·kg-1·min-1) performed evening HIIE sessions (10 × 60 s cycling, 90% V̇O2peak interspersed with 90 s active recovery, 30% V̇O2peak) in thermoneutral (HIIE-TN, control; 21°C) and cold environment (HIIE-CO; 0°C), following a balanced crossover design. The following morning, participants consumed a high-fat meal. Indirect calorimetry was used to assess substrate oxidation, and venous blood samples were obtained to assess changes in noncellular metabolites. During acute exercise, lipid oxidation was higher in HIIE-CO (P = 0.002) without differences in V̇O2 and energy expenditure (P ≥ 0.162) between conditions. Postprandial V̇O2, lipid and CHO oxidation, plasma insulin, and triglyceride concentrations were not different between conditions (P > 0.05). Postprandial blood LDL-C levels were higher in HIIE-CO 2 h after the meal (P = 0.003). Postprandial glucose area under curve was 49% higher in HIIE-CO versus HIIE-TN (P = 0.034). Under matched energy expenditure conditions, HIIE demonstrated higher lipid oxidation rates during exercise in the cold; but only marginally influenced postprandial lipid metabolism the following morning. In conclusion, HIIE in the cold seemed to be less favorable for postprandial lipid and glycemic responses.NEW & NOTEWORTHY This is the first known study to investigate the effects of cold ambient temperatures on acute metabolism during high-intensity interval exercise, as well as postprandial metabolism the next day. We observed that high-intensity interval exercise in a cold environment does change acute metabolism compared to a thermoneutral environment; however, the addition of a cold stimulus was less favorable for postprandial metabolic responses the following day.

(Neuro) Peptides, Physical Activity, and Cognition.

Regular physical activity (PA) improves cognitive functions, prevents brain atrophy, and delays the onset of cognitive decline, dementia, and Alzheimer's disease. Presently, there are no specific recommendations for PA producing positive effects on brain health and little is known on its mediators. PA affects production and release of several peptides secreted from peripheral and central tissues, targeting receptors located in the central nervous system (CNS). This review will provide a summary of the current knowledge on the association between PA and cognition with a focus on the role of (neuro)peptides. For the review we define peptides as molecules with less than 100 amino acids and exclude myokines. Tachykinins, somatostatin, and opioid peptides were excluded from this review since they were not affected by PA. There is evidence suggesting that PA increases peripheral insulin growth factor 1 (IGF-1) levels and elevated serum IGF-1 levels are associated with improved cognitive performance. It is therefore likely that IGF-1 plays a role in PA induced improvement of cognition. Other neuropeptides such as neuropeptide Y (NPY), ghrelin, galanin, and vasoactive intestinal peptide (VIP) could mediate the beneficial effects of PA on cognition, but the current literature regarding these (neuro)peptides is limited.

Muscle cooling modulates tissue oxidative and biochemical responses but not energy metabolism during exercise.

PURPOSE: This study investigated whether muscle cooling and its associated effects on skeletal muscle oxidative responses, blood gases, and hormonal concentrations influenced energy metabolism during cycling. METHODS: Twelve healthy participants (Males: seven; Females: five) performed two steady-state exercise sessions at 70% of ventilatory threshold on a cycle ergometer. Participants completed one session with pre-exercise leg cooling until muscle temperature (Tm) decreased by 6 °C (LCO), and a separate session without cooling (CON). They exercised until Tm returned to baseline and for an additional 30 min. Cardiovascular, respiratory, metabolic, hemodynamic variables, and skeletal muscle tissue oxidative responses were assessed continuously. Venous blood samples were collected to assess blood gases, and hormones. RESULTS: Heart rate, stroke volume, and cardiac output all increased across time but were not different between conditions. V̇O2 was greater in LCO when muscle temperature was restored until the end of exercise (p < 0.05). Cycling in the LCO condition induced lower oxygen availability, tissue oxygenation, blood pH, sO2%, and pO2 (p < 0.05). Insulin concentrations were also higher in LCO vs. CON (p < 0.05). Importantly, stoichiometric equations from respiratory gases indicated no differences in fat and CHO oxidation between conditions. CONCLUSION: The present study demonstrated that despite muscle cooling and the associated oxidative and biochemical changes, energy metabolism remained unaltered during cycling. Whether lower local and systemic oxygen availability is counteracted via a cold-induced activation of lipid metabolism pathways needs to be further investigated.

Ambient temperature influences metabolic substrate oxidation curves during running and cycling in healthy men.

Fat oxidation in cold environments and carbohydrate (CHO) use in hot environments are increased during exercise at steady-state submaximal workloads. However, the influence of cold and heat on fat and CHO oxidation curves remain unknown. We therefore examined the influence of a cold and warm ambient temperature on fat and CHO oxidation across a wide range of exercise intensities during treadmill and cycle ergometer exercise. Nine, young, healthy, male subjects completed four trials, during which they performed an incremental peak oxygen consumption (⩒O2peak) test on a cycle ergometer or treadmill in a 4.6°C or 34.1°C environment. Substrate oxidation, maximal fat oxidation rate (MFO), and exercise intensity where MFO occurs (Fatmax) were assessed via indirect calorimetry. MFO was significantly greater in the cold vs. warm during the treadmill exercise (0.66 ± 0.31 vs. 0.43 ± 0.23 g min-1; p = 0.02) but not during cycling (0.45 ± 0.24 vs. 0.29 ± 0.11 g min-1; p = 0.076). MFO was also greater during treadmill vs. cycling exercise, irrespective of ambient temperature (0.57 g min-1 vs. 0.37 g min-1; p = 0.04). Fatmax was greater in the cold vs. warm for both treadmill (57 ± 20 vs. 37 ± 17%⩒O2peak; p = 0.025) and cycling (62 ± 28 vs. 36 ± 13%⩒O2peak; p = 0.003). Multiple, linear, mixed-effects regressions revealed a strong influence of ambient temperature on substrate oxidation. We demonstrated that exercising in a cold environment increases MFO and Fatmax, predominantly during treadmill exercise. These results validate the implication of ambient temperature on energy metabolism over a wide range of exercise intensities.

Multi-Day Prolonged Low- to Moderate-Intensity Endurance Exercise Mimics Training Improvements in Metabolic and Oxidative Profiles Without Concurrent Chromosomal Changes in Healthy Adults.

BACKGROUND: Oxidative stress results in lipid, protein, and DNA oxidation, resulting in telomere erosion, chromosomal damage, and accelerated cellular aging. Training promotes healthy metabolic and oxidative profiles whereas the effects of multi-day, prolonged, and continuous exercise are unknown. This study investigated the effects of multi-day prolonged exercise on metabolic and oxidative stress as well as telomere integrity in healthy adults. METHODS: Fifteen participants performed a 14-day, 260-km, wilderness canoeing expedition (12 males) (EXP) (24 ± 7 years, 72 ± 6 kg, 178 ± 8.0 cm, 18.4 ± 8.4% BF, 47.5 ± 9.3 mlO2 kg-1 min-1), requiring 6-9 h of low- to moderate-intensity exercise daily. Ten controls participated locally (seven males) (CON) (31 ± 11 years, 72 ± 15 kg, 174 ± 10 cm, 22.8 ± 10.0% BF, 47.1 ± 9.0 mlO2 kg-1 min-1). Blood plasma, serum, and mononuclear cells were sampled before and after the expedition to assess hormonal, metabolic, and oxidative changes. RESULTS: Serum cholesterol, high- and low-density lipoprotein, testosterone, insulin, sodium, potassium, urea, and chloride concentrations were not different between groups, whereas triglycerides, glucose, and creatinine levels were lower following the expedition (p < 0.001). Malondialdehyde and relative telomere length (TL) were unaffected (EXP: 4.2 ± 1.3 vs. CON: 4.1 ± 0.7 µM; p > 0.05; EXP: 1.00 ± 0.48 vs. CON: 0.89 ± 0.28 TS ratio; p = 0.77, respectively); however, superoxidase dismutase activity was greater in the expedition group (3.1 ± 0.4 vs. 0.8 ± 0.5 U ml-1; p < 0.001). CONCLUSION: These results indicate a modest improvement in metabolic and oxidative profiles with increased superoxidase dismutase levels, suggesting an antioxidative response to counteract the exercise-associated production of free radicals and reactive oxygen species during prolonged exercise, mimicking the effects from long-term training. Although improved antioxidant activity may lead to increased TL, the present exercise stimulus was insufficient to promote a positive cellular aging profile with concordant chromosomal changes in our healthy and young participants.

Association of Physical Activity With Telomere Length Among Elderly Adults - The Oulu Cohort 1945.

Introduction: Physical activity (PA) has been associated with telomere shortening. The association of PA intensity or volume with telomere length (TL) is nonetheless unclear. The aim of our study was to investigate the associations of exercise intensity and volume with TL in elderly adults from Northern Finland (65° latitude North). Methods: Seven hundred elderly subjects born in 1945 in the Oulu region were investigated. PA was measured during a 2-week period with a wrist-worn accelerometer. In addition, a questionnaire was used to assess sedentary time and to achieve a longitudinal PA history and intensity. Relative telomere lengths (RTL) were determined from frozen whole blood samples using a qPCR-based method. Results: Relative telomere lengths were significantly longer in women than men and negatively correlated with age in both genders (men r = -0.210, p = 0.000, women r = -0.174, and p = 0.000). During the 2-week study period, women took more steps than men (p = 0.001), but the association between steps and RTL was only seen in men (p = 0.05). Total steps taken (r = 0.202 and p = 0.04) and sedentary time (r = -0.247 and p = 0.007) significantly correlated with RTLs in 70-year old subjects. Moderate PA was associated with RTL in subjects with the highest quartile of moderate PA compared to the three lower quartiles (p-values: 0.023 between 4th and 1st, 0.04 between 4th and 2nd, and 0.027 between 4th and 3rd) in the 70-year old subjects. Conclusion: Women had longer RTL and a higher step count compared to men. However, exercise volume and RTL correlated positively only in men. Surprisingly, age correlated negatively with RTL already within an age difference of 2 years. This suggests that telomere attrition rate may accelerate in older age. Moderate physical activity at the time of study was associated with RTL.

The effects of skin and core tissue cooling on oxygenation of the vastus lateralis muscle during walking and running.

Skin and core tissue cooling modulates skeletal muscle oxygenation at rest. Whether tissue cooling also influences the skeletal muscle deoxygenation response during exercise is unclear. We evaluated the effects of skin and core tissue cooling on skeletal muscle blood volume and deoxygenation during sustained walking and running. Eleven male participants walked or ran six times on a treadmill for 60 min in ambient temperatures of 22°C (Neutral), 0°C for skin cooling (Cold 1), and at 0°C following a core and skin cooling protocol (Cold 2). Difference between oxy/deoxygenated haemoglobin ([diffHb]: deoxygenation index) and total haemoglobin content ([tHb]: total blood volume) in the vastus lateralis (VL) muscle was measured continuously. During walking, lower [tHb] was observed at 1 min in Cold 1 and Cold 2 vs. Neutral (P˂0.05). Lower [diffHb] was seen at 1 and 10 min in Cold 2 vs. Neutral by 13.5 ± 1.2 µM and 15.3 ± 1.4 µM and Cold 1 by 10.4 ± 3.1 µM and 11.1 ± 4.1 µM, respectively (P˂0.05). During running, [tHb] was lower in Cold 2 vs. Neutral at 10 min only (P = 0.004). [diffHb] was lower at 1 min in Cold 2 by 11.3 ± 3.1 µM compared to Neutral and by 13.5 ± 2.8 µM compared to Cold 1 (P˂0.001). Core tissue cooling, prior to exercise, induced greater deoxygenation of the VL muscle during the early stages of exercise, irrespective of changes in blood volume. Skin cooling alone, however, did not influence deoxygenation of the VL during exercise.

The effects of cold exposure on leukocytes, hormones and cytokines during acute exercise in humans.

The purpose of the study was to examine the effects of exercise on total leukocyte count and subsets, as well as hormone and cytokine responses in a thermoneutral and cold environment, with and without an individualized pre-cooling protocol inducing low-intensity shivering. Nine healthy young men participated in six experimental trials wearing shorts and t-shirts. Participants exercised for 60 min on a treadmill at low (LOW: 50% of peak VO2) and moderate (MOD: 70% VO2peak) exercise intensities in a climatic chamber set at 22°C (NT), and in 0°C (COLD) with and without a pre-exercise low-intensity shivering protocol (SHIV). Core and skin temperature, heart rate and oxygen consumption were collected continuously. Blood samples were collected before and at the end of exercise to assess endocrine and immunological changes. Core temperature in NT was greater than COLD and SHIV by 0.4±0.2°C whereas skin temperature in NT was also greater than COLD and SHIV by 8.5±1.4°C and 9.3±2.5°C respectively in MOD. Total testosterone, adenocorticotropin and cortisol were greater in NT vs. COLD and SHIV in MOD. Norepinephrine was greater in NT vs. other conditions across intensities. Interleukin-2, IL-5, IL-7, IL-10, IL-17, IFN-γ, Rantes, Eotaxin, IP-10, MIP-1ß, MCP-1, VEGF, PDGF, and G-CSF were elevated in NT vs. COLD and/or SHIV. Furthermore, IFN-γ, MIP-1ß, MCP-1, IL-10, VEGF, and PDGF demonstrate greater concentrations in SHIV vs. COLD, mainly in the MOD condition. This study demonstrated that exercising in the cold can diminish the exercise-induced systemic inflammatory response seen in a thermoneutral environment. Nonetheless, prolonged cooling inducing shivering thermogenesis prior to exercise, may induce an immuno-stimulatory response following moderate intensity exercise. Performing exercise in cold environments can be a useful strategy in partially inhibiting the acute systemic inflammatory response from exercise but oppositely, additional body cooling may reverse this benefit.

Fuel selection during short-term submaximal treadmill exercise in the cold is not affected by pre-exercise low-intensity shivering.

Exercise and shivering rely on different metabolic pathways and consequently, fuel selection. The present study examined the effects of a pre-exercise low-intensity shivering protocol on fuel selection during submaximal exercise in a cold environment. Nine male subjects exercised 4 times for 60 min at 50% (LOW) or 70% (MOD) of their peak oxygen consumption on a motorized treadmill in a climatic chamber set at 0 °C with (SHIV) and without (CON) a pre-exercise cooling protocol, inducing low-intensity shivering. Thermal, cardiorespiratory and metabolic responses were measured every 15 min whereas blood samples were collected every 30 min to assess serum nonesterified fatty acids (NEFA), glycerol, glucose, ß-hydroxybutyrate (BHB) and plasma catecholamine concentrations. Rectal and skin temperatures were lower in the SHIV condition, within LOW and MOD conditions, during the first 45 min of exercise. Norepinephrine (NE) concentration was greater in SHIV vs. CON within LOW (1.39 ± 0.17 vs. 0.98 ± 0.17 ng·mL(-1)) and MOD (1.50 ± 0.20 vs. 1.01 ± 0.09 ng·mL(-1)), whereas NEFA, glycerol and BHB were greater in SHIV vs. CON (1060 ± 49 vs. 898 ± 78 µmol·L(-1); 0.27 ± 0.02 vs. 0.22 ± 0.03 mmol·L(-1); 0.39 ± 0.06 vs. 0.27 ± 0.04 mmol·L(-1), respectively) within MOD only. No changes were observed in fat or carbohydrate oxidation between SHIV and CON during exercise. Despite increases in NE, NEFA, glycerol and BHB from pre-exercise low-intensity shivering, fuel selection during short-term submaximal exercise in the cold was unaltered.

Cardiovascular and ventilatory responses to dorsal, facial, and whole-head water immersion in eupnea.

OBJECTIVE: Facial cooling can regulate reflexes of the dive response whereas further body cooling generally induces the cold-shock response. We examined the cardiovascular and ventilatory parameters of these responses during 3-min immersions of the head dorsum, face, and whole head in 17 degrees C water while breathing was maintained. METHODS: From a horizontal position, the head was inserted into a temperature controlled immersion tank in which the water level could be changed rapidly. On four occasions, either the head dorsum, face or whole head (prone and supine) were exposed to water. RESULTS: Mean decrease in heart rate (14%) and increases in systolic (9%) and diastolic (5%) blood pressures were seen during immersion. Relative mean finger skin blood flow had an early transient decrease (31%) for 90 s and then returned to baseline values. A strong transient increase was seen in minute ventilation (92%) at 20 s of immersion via tidal volume (85%). There were no consistent differences between the head dorsum, face, and whole head for all variables in response to immersion. CONCLUSIONS: The cold-shock response (increased minute ventilation and tidal volume) predominated over the dive response in the initial moments of immersion only. The order of emergence of these responses provides further recommendation to avoid head submersion upon cold water entry. It is important to protect the face, with a facemask, and the head dorsum, with an insulative hood, in cold water.

Cold exposure enhances fat utilization but not non-esterified fatty acids, glycerol or catecholamines availability during submaximal walking and running.

Cold exposure modulates the use of carbohydrates (CHOs) and fat during exercise. This phenomenon has mostly been observed in controlled cycling studies, but not during walking and running when core temperature and oxygen consumption are controlled, as both may alter energy metabolism. This study aimed at examining energy substrate availability and utilization during walking and running in the cold when core temperature and oxygen consumption are maintained. Ten lightly clothed male subjects walked or ran for 60-min, at 50% and 70% of maximal oxygen consumption, respectively, in a climatic chamber set at 0°C or 22°C. Thermal, cardiovascular, and oxidative responses were measured every 15-min during exercise. Blood samples for serum non-esterified fatty acids (NEFAs), glycerol, glucose, beta-hydroxybutyrate (BHB), plasma catecholamines, and serum lipids were collected immediately prior, and at 30- and 60-min of exercise. Skin temperature strongly decreased while core temperature did not change during cold trials. Heart rate (HR) was also lower in cold trials. A rise in fat utilization in the cold was seen through lower respiratory quotient (RQ) (-0.03 ± 0.02), greater fat oxidation (+0.14 ± 0.13 g · min(-1)) and contribution of fat to total energy expenditure (+1.62 ± 1.99 kcal · min(-1)). No differences from cold exposure were observed in blood parameters. During submaximal walking and running, a greater reliance on derived fat sources occurs in the cold, despite the absence of concurrent alterations in NEFAs, glycerol, or catecholamine concentrations. This disparity may suggest a greater reliance on intra-muscular energy sources such as triglycerides during both walking and running.

Recovery of hormonal, blood lipid, and hematological profiles from a North Pole expedition.

INTRODUCTION: This study examined the recovery patterns of hormonal, blood lipid, and hematological profiles following strenuous physical loading, continuous extreme cold exposure and energy deficit induced by a North Pole expedition. METHODS: Seven men completed an 850-km North Pole expedition in temperatures varying from -3 degrees C to -47 degrees C. Daily energy intake was approximately 23 MJ x d(-1) and was composed of approximately 60% fat. Blood samples were collected 2 wk before (Pre) the expedition and after 2 wk (Post 1), and 2 mo (Post 2). Additional samples were collected on the first (R1), third (R3), and fifth (R5) return days. RESULTS: Mean weight loss upon return was 10 kg. Energy expenditure was estimated to be 29.6 MJ x d(-1). Declines in cortisol (-237.29 nmol x L(-1)), total testosterone (-5.08 nmol x L(-1)), bioavailable testosterone (-0.37 nmol x L(-1)) and free thyroxin (-5.82 pmol x L(-1)) returned to normal values at R5 or Post 1 (P < 0.05). The increase in sex hormone-binding globulin (+17.5 nmol x L(-1)) rapidly returned to the pre-expedition concentration at R3 (P < 0.05). Significantly greater values were observed at Post 1 in the lipid (high-density lipoprotein +1.86 mmol x L(-1); low-density lipoprotein +4.23 mmol x L(-1)) and hematological (WBC +1.28 x 10(3)/L; platelets +51.86 x 10(3)/L) profiles (P < 0.05). RBC, hemoglobin, and hematocrit were all lower at Post 1 (P < 0.05). CONCLUSION: Although the expedition generated extreme physical stress, this was not directly reflected on hormonal recovery times as it was similar to other much less strenuous events. Despite important variations, all hormones returned to baseline values within 2 wk. Nonetheless, physical stress would appear to have more long-term effects on blood lipid and hematological profiles.