Impact of Topical Capsaicin Cream on Thermoregulation and Perception While Walking in the Cold.

INTRODUCTION: Capsaicin, a chili pepper extract, can stimulate increased skin blood flow (SkBF) with a perceived warming sensation on application areas. Larger surface area application may exert a more systemic thermoregulatory response. Capsaicin could assist with maintaining heat transport to the distal extremities, minimizing cold weather injury risk. However, the thermoregulatory and perceptual impact of topical capsaicin cream application prior to exercise in the cold is unknown. METHODS: Following application of either a 0.1% capsaicin or control cream to the upper and lower extremities (10 g total, ∼40-50% body surface area), 11 participants in shorts and a t-shirt were exposed to 30 min of cold (0 °C, 40% relative humidity). Exposures comprised of 5 min seated rest, 20 min walking (1.6 m·s-1, 5% grade), and 5 min seated rest. Temperature (skin, core), SkBF, skin conductivity, heart rate, thermal sensation, and thermal comfort were measured throughout. RESULTS: The capsaicin treatment did not differ from the control treatment in skin temperature (treatment mean: 30.0 ± 2.5, 30.1 ± 2.4 °C, respectively, p = 0.655), core temperature (treatment mean: 37.3 ± 0.5, 37.4 ± 0.4 °C, respectively, p = 0.113), SkBF (treatment mean: -8.4 ± 10.0, -11.1 ± 10.7 A.U., respectively, p = 0.492), skin conductivity (treatment mean: -0.7 ± 5.1, 0.4 ± 6.4 µS, respectively, p = 0.651), or heart rate (treatment mean: 83 ± 29, 85 ± 28 beats·minute-1, respectively, p = 0.234). The capsaicin and control treatments also did not differ in thermal sensation (p = 0.521) and thermal comfort (p = 0.982), with perceptual outcomes corresponding with feeling "cool" and "just uncomfortable," respectively. CONCLUSIONS: 0.1% topical capsaicin application to exposed limbs prior to walking in a cold environment does not alter whole-body thermoregulation or thermal perception.

Influence of topical menthol gel on thermoregulation and perception while walking in the heat.

PURPOSE: Menthol is known to elicit opposing thermoregulatory and perceptual alterations during intense exercise. The current purpose was to determine the thermoregulatory and perceptual effects of topical menthol application prior to walking in the heat. METHODS: Twelve participants walked (1.6 m s-1, 5% grade) for 30 min in the heat (38 °C, 60% relative humidity) with either a 4% menthol or control gel on the upper (shoulder to wrist) and lower (mid-thigh to ankle) limbs. Skin blood flow (SkBF), sweat (rate, composition), skin conductivity, heart rate, temperature (skin, core), and thermal perception were measured prior to and during exercise. RESULTS: Skin conductivity expressed as time to 10, 20, 30, and 40 µS was delayed due to menthol (559 ± 251, 770 ± 292, 1109 ± 301, 1299 ± 335 s, respectively) compared to the control (515 ± 260, 735 ± 256, 935 ± 300, 1148 ± 298 s, respectively, p = 0.048). Sweat rate relative to body surface area was lower due to menthol (0.55 ± 0.16 L h-1 m(2)-1) than the control (0.64 ± 0.16 L h-1 m(2)-1, p = 0.049). Core temperature did not differ at baseline between the menthol (37.4 ± 0.3 °C) and control (37.3 ± 0.4 °C, p = 0.298) but was higher at 10, 20, and 30 min due to menthol (37.5 ± 0.3, 37.7 ± 0.2, 38.1 ± 0.3 °C, respectively) compared to the control (37.3 ± 0.4, 37.4 ± 0.3, 37.7 ± 0.3 °C, respectively, p < 0.05). The largest rise in core temperature from baseline was at 30 min during menthol (0.7 ± 0.3 °C) compared to the control (0.4 ± 0.2 °C, p = 0.004). Overall, the menthol treatment was perceived cooler, reaching "slightly warm" whereas the control treatment reached "warm" (p < 0.001). CONCLUSION: Menthol application to the limbs impairs whole-body thermoregulation while walking in the heat despite perceiving the environment as cooler.

The isolated effects of local cold application on proteolytic and myogenic signaling.

Post-exercise cooling studies reveal inhibitory effects on markers of skeletal muscle growth. However, the isolated effect of local cold application has not been adequately addressed. It is unclear if the local cold or the combination of local cold and exercise is driving negatively altered skeletal muscle gene expression. The purpose was to determine the effects of a 4 h local cold application to the vastus lateralis on the myogenic and proteolytic response. Participants (n = 12, 27 ± 6 years, 179 ± 9 cm, 82.8 ± 13.0 kg, 18.4 ± 7.1 %BF) rested with a thermal wrap placed on each leg with either circulating cold fluid (10 °C, COLD) or no fluid circulation (room temperature, RT). Muscle samples were collected to quantify mRNA (RT-qPCR) and proteins (Western Blot) associated with myogenesis and proteolysis. Temperatures in COLD were lower than RT at the skin (13.2 ± 1.0 °C vs. 34.8 ± 0.9 °C; p < 0.001) and intramuscularly (20.5 ± 1.3 °C vs. 35.6 ± 0.8 °C, p < 0.001). Myogenic-related mRNA, MYO-G and MYO-D1, were lower in COLD (p = 0.001, p < 0.001, respectively) whereas myogenic-mRNA, MYF6, was greater in COLD (p = 0.002). No other myogenic associated genes were different between COLD and RT (MSTN, p = 0.643; MEF2a, p = 0.424; MYF5, p = 0.523; RPS3, p = 0.589; RPL3-L, p = 0.688). Proteolytic-related mRNA was higher in COLD (FOXO3a, p < 0.001; Atrogin-1, p = 0.049; MURF-1, p < 0.001). The phosphorylation:total protein ratio for the translational repressor of muscle mass, 4E-BP1Thr37/46, was lower in COLD (p = 0.043), with no differences in mTORser2448 (p = 0.509) or p70S6K1Thr389 (p = 0.579). Isolated local cooling over 4 h exhibits inhibited myogenic and higher proteolytic skeletal muscle molecular response.

The independent effects of local heat application on muscle growth program associated mRNA and protein phosphorylation.

The development and maintenance of skeletal muscle is crucial for the support of daily function. Recent evidence suggests that genes coded for proteins associated with the human muscle growth program (myogenic and proteolytic genes) are sensitive to local heat application. Therefore, the purpose of this investigation was to determine the effect of 4 h of local heat application to the vastus lateralis at rest on acute phosphorylation (mTORSer2448, p70-S6K1Thr389, and 4E-BP1Thr47/36) and gene expression changes for proteins associated with the muscle growth program. Intramuscular temperature of the HOT limb was 1.2 ± 0.2 °C higher than CON limb after 4 h of local heating. However, this local heat stimulus did not influence transcription of genes associated with myogenesis (MSTN, p = 0.321; MYF5, p = 0.445; MYF6, p = 0.895; MEF2a, p = 0.809; MYO-G, p = 0.766; MYO-D1, p = 0.118; RPS3, p = 0.321; and RPL-3L, p = 0.577), proteolysis (Atrogin-1, p = 0.573; FOXO3a, p = 0.452; MURF-1, p = 0.284), nor protein phosphorylation (mTORSer2448, p = 0.981; P70-S6K1Thr389, p = 0.583; 4E-BP1Thr37/46, p = 0.238) associated with the muscle growth program. These findings suggest little to no association between the local application of heat, at rest, and the activation of the observed muscle growth program-related markers.

Influence of topical capsaicin cream on thermoregulation and perception during acute exercise in the heat.

PURPOSE: Determine if topical capsaicin, a transient receptor potential vanilloid heat thermoreceptor activator, alters thermoregulation and perception when applied topically prior to thermal exercise. METHODS: Twelve subjects completed 2 treatments. Subjects walked (1.6 m s-1, 5% grade) for 30 min in the heat (38 °C, 60% relative humidity) with either a capsaicin (0.025% capsaicin) or control cream applied to the upper (shoulder to wrist) and lower (mid-thigh to ankle) limbs covering ∼50% body surface area. Skin blood flow (SkBF), sweat (rate, composition), heart rate, temperature (skin, core), and perceived thermal sensation were measured prior to and during exercise. RESULTS: The relative change in SkBF was not different between treatments at any time point (p = 0.284). There were no differences in sweat rate between the capsaicin (1.23 ± 0.37 L h-1) and control (1.43 ± 0.43 L h-1, p = 0.122). There were no differences in heart rate between the capsaicin (122 ± 38 beats·min-1) and control (125 ± 39 beats·min-1, p = 0.431). There were also no differences in weighted surface (p = 0.976) or body temperatures (p = 0.855) between the capsaicin (36.0 ± 1.7 °C, 37.0 ± 0.8 °C, respectively) and control (36.0 ± 1.6 °C, 36.9 ± 0.8 °C, respectively). The capsaicin treatment was not perceived as hotter than the control treatment until minute 30 of exercise (2.8 ± 0.4, 2.5 ± 0.5, respectively, p = 0.038) CONCLUSIONS: Topical capsaicin application does not alter whole-body thermoregulation during acute exercise in the heat despite perceiving the treatment as hotter late in exercise.

Independent effects of acute normobaric hypoxia and hypobaric hypoxia on human physiology.

The purpose of this study was to examine the effects of acute normobaric (NH, decreased FiO2) and hypobaric (HH, 4200 m ascent) hypoxia exposures compared to sea level (normobaric normoxia, NN). Tissue oxygenation, cardiovascular, and body fluid variables measured during rest and a 3-min step-test following 90-min exposures (NH, HH, NN). Muscle oxygenated hemoglobin (O2Hb) decreased, and muscle deoxygenated hemoglobin (HHb) increased environmentally independent from rest to exercise (p < 0.001). During exercise, brain O2Hb was lower at HH compared to NN (p = 0.007), trending similarly with NH (p = 0.066), but no difference between NN and NH (p = 0.158). During exercise, HR at NH (141 ± 4 beats·min-1) and HH (141 ± 3 beats·min-1) were higher than NN (127 ± 44 beats·min-1, p = 0.002), but not each other (p = 0.208). During exercise, stroke volume at HH (109.6 ± 4.1 mL·beat-1) was higher than NH (97.8 ± 3.3 mL·beat-1) and NN (99.8 ± 3.9 mL·beat-1, p ≤ 0.010) with no difference between NH and NN (p = 0.481). During exercise, cardiac output at NH (13.8 ± 0.6 L) and HH (15.5 ± 0.7 L) were higher than NN (12.6 ± 0.5 L, p ≤ 0.006) with HH also higher than NH (p = 0.001). During acute hypoxic stimuli, skeletal muscle maintains oxygenation whereas the brain does not. These differences may be mediated by environmentally specific cardiovascular compensation. Thus, caution is advised when equating NH and HH.

Influence of Local Muscle Cooling on Mitochondrial-Related Gene Expression at Rest.

The purpose of this study was to determine the impact of localized cooling of the skeletal muscle during rest on mitochondrial related gene expression. Thermal wraps were applied to the vastus lateralis of each limb of 12 participants. One limb received a cold application (randomized) (COLD), while the other did not (RT). Wraps were removed at the 4 h time point and measurements of skin temperature, blood flow, and intramuscular temperature were taken prior to a muscle biopsy. RT-qPCR was used to measure expression of genes associated with mitochondrial development. Skin and muscle temperatures were lower in COLD than RT (p < 0.05). Femoral artery diameter was lower in COLD after 4 h (0.62 ± 0.05 cm, to 0.60 ± 0.05 cm, p = 0.018). Blood flow was not different in COLD compared to RT (259 ± 69 mL·min-1 vs. 275 ± 54 mL·min-1, p = 0.20). PGC-1α B and GABPA expression was higher in COLD relative to RT (1.57-fold, p = 0.037 and 1.34-fold, p = 0.006, respectively). There was no difference (p > 0.05) in the expression of PGC-1α, NT-PGC-1α, PGC-1α A, TFAM, ESRRα, NRF1, GABPA, VEGF, PINK1, PARK 2, or BNIP3-L. The impact of this small magnitude of difference in gene expression of PGC-1α B and GABPA without alterations in other genes are unknown. There appears to be only limited impact of local muscle cooling on the transcriptional response related to mitochondrial development.

Does the Heel's Dissipative Energetic Behavior Affect Its Thermodynamic Responses During Walking?

Most of the terrestrial legged locomotion gaits, like human walking, necessitate energy dissipation upon ground collision. In humans, the heel mostly performs net-negative work during collisions, and it is currently unclear how it dissipates that energy. Based on the laws of thermodynamics, one possibility is that the net-negative collision work may be dissipated as heat. If supported, such a finding would inform the thermoregulation capacity of human feet, which may have implications for understanding foot complications and tissue damage. Here, we examined the correlation between energy dissipation and thermal responses by experimentally increasing the heel's collisional forces. Twenty healthy young adults walked overground on force plates and for 10 min on a treadmill (both at 1.25 ms-1) while wearing a vest with three different levels of added mass (+0%, +15%, & +30% of their body mass). We estimated the heel's work using a unified deformable segment analysis during overground walking. We measured the heel's temperature immediately before and after each treadmill trial. We hypothesized that the heel's temperature and net-negative work would increase when walking with added mass, and the temperature change is correlated with the increased net-negative work. We found that walking with +30% added mass significantly increased the heel's temperature change by 0.72 ± 1.91   ℃ (p = 0.009) and the magnitude of net-negative work (extrapolated to 10 min of walking) by 326.94 ± 379.92 J (p = 0.005). However, we found no correlation between the heel's net-negative work and temperature changes (p = 0.277). While this result refuted our second hypothesis, our findings likely demonstrate the heel's dynamic thermoregulatory capacity. If all the negative work were dissipated as heat, we would expect excessive skin temperature elevation during prolonged walking, which may cause skin complications. Therefore, our results likely indicate that various heat dissipation mechanisms control the heel's thermodynamic responses, which may protect the health and integrity of the surrounding tissue. Also, our results indicate that additional mechanical factors, besides energy dissipation, explain the heel's temperature rise. Therefore, future experiments may explore alternative factors affecting thermodynamic responses, including mechanical (e.g., sound & shear-stress) and physiological mechanisms (e.g., sweating, local metabolic rate, & blood flow).

Effects of passive and active leg movements to interrupt sitting in mild hypercapnia on cardiovascular function in healthy adults.

Prolonged sitting in a mild hypercapnic environment impairs peripheral vascular function. The effects of sitting interruptions using passive or active skeletal muscle contractions are still unclear. Therefore, we sought to examine the vascular effects of brief periods (2 min every half hour) of passive and active lower limb movement to interrupt prolonged sitting with mild hypercapnia in adults. Fourteen healthy adults (24 ± 2 yr) participated in three experimental visits sitting for 2.5 h in a mild hypercapnic environment (CO2 = 1,500 ppm): control (CON, no limb movement), passive lower limb movement (PASS), and active lower limb movement (ACT) during sitting. At all visits, brachial and popliteal artery flow-mediated dilation (FMD), microvascular function, plasmatic levels of nitrate/nitrite and endothelin-1, and heart rate variability were assessed before and after sitting. Brachial and popliteal artery FMDs were reduced in CON and PASS (P < 0.05) but were preserved (P > 0.05) in ACT. Microvascular function was blunted in CON (P < 0.05) but was preserved in PASS and ACT (P > 0.05). In addition, total plasma nitrate/nitrite was preserved in ACT (P > 0.05) but was reduced in CON and PASS (P < 0.05), and endothelin-1 levels were decreased in ACT (P < 0.05). Both passive and active movement induced a greater ratio between the low-frequency and high-frequency bands for heart rate variability (P < 0.05). For the first time, to our knowledge, we found that brief periods of passive leg movement can preserve microvascular function, but that an intervention that elicits larger increases in shear rate, such as low-intensity exercise, is required to fully protect both macrovascular and microvascular function and circulating vasoactive substance balance.NEW & NOTEWORTHY Passive leg movement could not preserve macrovascular endothelial function, whereas active leg movement could protect endothelial function. Attenuated microvascular function can be salvaged by passive movement and active movement. Preservation of macrovascular hemodynamics and plasma total nitrate/nitrite and endothelin-1 during prolonged sitting requires active movement. These findings dissociate the impacts induced by mechanical stress (passive movement) from the change in metabolism (active movement) on the vasculature during prolonged sitting in a mild hypercapnic environment.

Acute effects of functional dry needling on skeletal muscle function.

INTRODUCTION: Functional dry needling (FDN) is commonly used to treat soft tissue pain-related conditions. Previous research has demonstrated benefits to chronic resistance training; however, objective physiological measures sensitive to acute exercise have not been found. The purpose of this study was to evaluate the acute effects of FDN on muscle strength and endurance. METHODS: Ten subjects (height 168 ± 9 cm, mass 68.2 ± 11.3 kg) were tested bilaterally (pre and post) for vastus lateralis (VL) isometric strength, isokinetic fatigue index, muscle electrical activity, and muscle oxygenation. FDN was administered to one leg, while the other served as a control. RESULTS: Limited acute effects of functional dry needling were observed (p < 0.05). DISCUSSION: FDN does not appear to acutely improve muscle function in healthy young adults. Although there were no improvements in muscle function, there were no adverse effects either, contributing to the safety of FDN healthy populations. CONCLUSION: Acute FDN does not appear to enhance muscle performance in a healthy, non-clinical population. Thus, clinicians should consider the population and desired outcome when applying FDN.

Skeletal Muscle mRNA Response to Hypobaric and Normobaric Hypoxia After Normoxic Endurance Exercise.

Background: The physiological effects of hypoxia may be influenced by how hypoxia is achieved. The purpose of this study was to determine the effects of recovery in hypobaric hypoxia (HH), normobaric hypoxia (NH), and normobaric normoxia (NN) after endurance exercise on gene expression related to mitochondrial biogenesis, myogenesis, and proteolysis. Methods: Fifteen recreationally trained subjects each cycled for 1 hour before recovering for 4 hours in NN (laboratory atmospheric conditions, 975 m), HH (depressurized to simulate 4420 m), and NH (fraction of O2 reduced to simulate 4420 m). Muscle biopsy samples were obtained before exercise and after 4 hours of recovery. Results: Blood oxygenation (SpO2) was lower in HH (76.02 ± 0.58%) than NH (79.45 ± 0.56, p < 0.001), which were both lower than in NN (96.3 ± 0.17, p < 0.001). Heart rate was higher in HH (82 ± 2 bpm) than NH (77 ± 1 bpm, p < 0.001), which were both higher than in NN (67 ± 1 bpm, p < 0.001). Mitochondrial transcription factor A (TFAM) mRNA was lower after NN than HH (p = 0.034) or NH (p = 0.005), but was not different between HH and NH (p = 0.460). Myostatin (MSTN) mRNA decreased from pre- to postexercise (p < 0.001) in all conditions and was lower in HH compared with NH (p = 0.035) and NN (p = 0.017). No other differences were noted in genes related to mitochondrial biogenesis, myogenesis, or proteolysis (p > 0.05). Conclusion:TFAM mRNA is lower with hypoxia exposure, but effected by the type of hypoxia. MSTN gene expression is lower after exposure to HH than NH or NN. These data support previous work and caution the translation of NH data obtained in a NH environment to a HH environment.

Skeletal muscle cold shock and heat shock protein mRNA response to aerobic exercise in different environmental temperatures.

The response of cold shock proteins to exercise and environmental temperature in human skeletal muscle is not known. The purpose of this study was to determine the early mRNA response of human stress proteins to endurance exercise and environmental temperatures. Seven recreationally trained males cycled for 1 hour at 60% VO2peak in 7°C, 20°C, and 33°C with biopsies taken pre- and 3 hours post-exercise. Gene expression for heat shock and cold shock proteins were analyzed using qRT-PCR on muscle biopsy samples from the vastus lateralis. RBM3 mRNA was reduced 1.43 ± 0.10 fold (p = 0.006) while there was a trend for CIRP to decrease1.27 ± 0.14 fold (p = 0.059) from pre- to 3 h post-exercise. CIRP and RBM3 mRNA were not different between temperatures (p = 0.273 and p = 0.686, respectively). HSP70 mRNA was 2.27 ± 0.23 fold higher 3 h post-exercise when compared to pre-exercise (p = 0.002) but was not significantly different between temperatures (p = 0.103). HSP27, HSP90, and HSF1 mRNA did not change from pre- to post-exercise (p = 0.052, p = 0.324, p = 0.795) and were not different between temperatures (p = 0.247, p = 0.134, p = 0.808). These data indicate that exposure to mild heat and cold during aerobic exercise have limited effect on the skeletal muscle mRNA expression of heat shock and cold shock proteins. However, skeletal muscle mRNA of cold shock proteins decrease, while HSP70 mRNA increases in response to a low to moderate intensity aerobic exercise bout.

Effects of exercise in a cold environment on transcriptional control of PGC-1α.

Peroxisome proliferator-activated receptor-α coactivator-1α (PGC-1α) mRNA is increased with both exercise and exposure to cold temperature. However, transcriptional control has yet to be examined during exercise in the cold. Additionally, the need for environmental cold exposure after exercise may not be a practical recovery modality. The purpose of this study was to determine mitochondrial-related gene expression and transcriptional control of PGC-1α following exercise in a cold compared with room temperature environment. Eleven recreationally trained males completed two 1-h cycling bouts in a cold (7°C) or room temperature (20°C) environment, followed by 3 h of supine recovery in standard room conditions. Muscle biopsies were taken from the vastus lateralis preexercise, postexercise, and after a 3-h recovery. Gene expression and transcription factor binding to the PGC-1α promoter were analyzed. PGC-1α mRNA increased from preexercise to 3 h of recovery, but there was no difference between trials. Estrogen-related receptor-α (ERRα), myocyte enhancer factor-2 (MEF2A), and nuclear respiratory factor-1 (NRF-1) mRNA were lower in cold than at room temperature. Forkhead box class-O (FOXO1) and cAMP response element-binding protein (CREB) binding to the PGC-1α promoter were increased postexercise and at 3 h of recovery. MEF2A binding increased postexercise, and activating transcription factor 2 (ATF2) binding increased at 3 h of recovery. These data indicate no difference in PGC-1α mRNA or transcriptional control after exercise in cold versus room temperature and 3 h of recovery. However, the observed reductions in the mRNA of select transcription factors downstream of PGC-1α indicate a potential influence of exercise in the cold on the transcriptional response related to mitochondrial biogenesis.

Irisin and Fibronectin Type III Domain-Containing 5 Responses to Exercise in Different Environmental Conditions.

Fibronectin type III domain-containing 5 (FNDC5) is a skeletal muscle membrane-bound precursor to the myokine irisin. Irisin is involved in stimulating adipose tissue to become more metabolically active in order to produce heat. The purpose of this study was to determine the effects of exercise in a hot (33 °C), cold (7 °C), and room temperature (RT, 20 °C) environment on the skeletal muscle gene expression of FNDC5 and the plasma concentrations of irisin. Twelve recreationally trained males completed three separate, 1 h cycling bouts at 60% of Wmax in a hot, cold, and RT environment followed by three hours of recovery at room temperature. Blood samples were taken from the antecubital vein and muscle biopsies were taken from the vastus lateralis pre-, post-, and 3 h post-exercise. Plasma concentrations of irisin did not change from pre- (9.23 ± 2.68 pg·mL-1) to post-exercise (9.6 ± 0.2 pg·mL-1, p = 0.068), but did decrease from post-exercise to 3 h post-exercise (8.9 ± 0.5 pg·mL-1, p = 0.047) regardless of temperature. However, when plasma volume shifts were considered, no differences were found in irisin (p = 0.086). There were no significant differences between trials for irisin plasma concentrations (p > 0.05). No significant differences in FNDC5 were observed between the hot, cold, or RT or pre-, post-, or 3 h post-exercise time points (p > 0.05). These data indicate that the temperature in which exercise takes place does not influence FNDC5 transcription or circulating irisin in a human model.

The effect of environmental temperature on exercise-dependent release of brain-derived neurotrophic factor.

Brain-derived neurotrophic factor (BDNF) is a biomarker of cognitive function that is released into the blood stream following exercise, and cognitive function is impaired by environmental temperatures that are hot and cold. Purpose: To evaluate the exercise-dependent release of BDNF in different environmental temperatures. Methods: Recreationally trained males each completed three trials consisting of cycling for 1 h at 60% Wmax at three different temperatures: 33°C (hot), 7°C (cold), and 20°C (moderate room temperature). Blood was taken from the antecubital vein pre-exercise, immediately post-exercise, and 3 h post-exercise. Respiratory gases were collected periodically throughout exercise and recovery. Results: BDNF was elevated immediately following an exercise bout (1711 ± 766 pg·ml-1) regardless of temperature from pre-exercise (1257 ± 653 pg·ml-1, p = 0.001) and returned to basal levels following 3 h of recovery (1289 ± 650 pg·ml-1, p = 0.786). There was no effect (p > 0.05) of temperature on BDNF following the exercise bout. Plasma glucose was elevated in hot (6.2 ± 0.9 mmol) over cold (5.3 ± 0.6 mmol, p = 0.035) and moderate room temperature (5.2 ± 0.5, p = 0.008). VO2 was elevated during exercise in hot (3.01 ± 0.45 L·min-1) over cold (2.67 ± 0.35 L·min-1, p = 0.005) and moderate room temperature (2.80 ± 0.38 L·min-1, p = 0.001). There was no relationship between BDNF and plasma glucose (p > 0.05) or VO2 across any time point or temperature (p > 0.05). Conclusion: With aerobic exercise, BDNF is elevated; however, the release of BDNF is not impacted by different environmental temperatures during exercise.

Leptin, adiponectin, and ghrelin responses to endurance exercise in different ambient conditions.

Excessive positive energy balance is a major factor leading to obesity. The ability to alter the appetite-regulating hormones leptin, adiponectin, and ghrelin may help decrease excessive energy intake. Exercise and exposure to extreme temperatures can independently affect these appetite-regulating hormones. PURPOSE: To determine the effect of exercising in different environmental conditions on the circulating concentrations of leptin, adiponectin, and ghrelin. METHODS: Eleven recreationally-trained male participants completed 3 separate 1 h cycling bouts at 60% Wmax in hot, cold, and room temperature conditions (33°C, 7°C, 20°C), followed by a 3 h recovery at room temperature. Blood was drawn pre-exercise, post-exercise, and 3 h post-exercise. Hematocrit and hemoglobin were measured to account for change in plasma volume. RESULTS: Leptin concentrations were lower at post and 3 h post-exercise compared with pre-exercise, with and without correction for plasma volume shifts, regardless of temperature (p < 0.05). Adiponectin was higher post-exercise compared with pre-exercise (p = 0.021) but not 3 h post-exercise (p = 0.084) without correction for plasma volume shifts. However, adiponectin concentrations were not different at any time point when plasma volume shifts were accounted for (p > 0.05). Total ghrelin and acylated ghrelin concentrations were not affected at post and 3 h post-exercise compared with pre-exercise, with and without correcting for plasma volume shifts, regardless of ambient temperature (p > 0.05). No differences in leptin, adiponectin, or ghrelin were found between trials (p > 0.05). CONCLUSION: Temperature does not affect the circulating concentrations of appetite-regulating hormones during an acute bout of endurance exercise.

Impact of hot and cold exposure on human skeletal muscle gene expression.

Many human diseases lead to a loss of skeletal muscle metabolic function and mass. Local and environmental temperature can modulate the exercise-stimulated response of several genes involved in mitochondrial biogenesis and skeletal muscle function in a human model. However, the impact of environmental temperature, independent of exercise, has not been addressed in a human model. Thus, the purpose of this study was to compare the effects of exposure to hot, cold, and room temperature conditions on skeletal muscle gene expression related to mitochondrial biogenesis and muscle mass. Recreationally trained male subjects (n = 12) had muscle biopsies taken from the vastus lateralis before and after 3 h of exposure to hot (33 °C), cold (7 °C), or room temperature (20 °C) conditions. Temperature had no effect on most of the genes related to mitochondrial biogenesis, myogenesis, or proteolysis (p > 0.05). Core temperature was significantly higher in hot and cold environments compared with room temperature (37.2 ± 0.1 °C, p = 0.001; 37.1 ± 0.1 °C, p = 0.013; 36.9 ± 0.1 °C, respectively). Whole-body oxygen consumption was also significantly higher in hot and cold compared with room temperature (0.38 ± 0.01 L·min-1, p < 0.001; 0.52 ± 0.03 L·min-1, p < 0.001; 0.35 ± 0.01 L·min-1, respectively). In conclusion, these data show that acute temperature exposure alone does not elicit significant changes in skeletal muscle gene expression. When considered in conjunction with previous research, exercise appears to be a necessary component to observe gene expression alterations between different environmental temperatures in humans.

Transcriptional control, but not subcellular location, of PGC-1α is altered following exercise in a hot environment.

The purpose of this study was to determine mitochondrial biogenesis-related mRNA expression, binding of transcription factors to the peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC-1α) promoter, and subcellular location of PGC-1α protein in human skeletal muscle following exercise in a hot environment compared with a room temperature environment. Recreationally trained males (n = 11) completed two trials in a temperature- and humidity-controlled environmental chamber. Each trial consisted of cycling in either a hot (H) or room temperature (C) environment (33 and 20°C, respectively) for 1 h at 60% of maximum wattage (Wmax) followed by 3 h of supine recovery at room temperature. Muscle biopsies were taken from the vastus lateralis pre-, post-, and 3 h postexercise. PGC-1α mRNA increased post (P = 0.039)- and 3 h postexercise in C (P = 0.002). PGC-1α, estrogen-related receptor-α (ERRα), and nuclear respiratory factor 1 (NRF-1) mRNA was all lower in H than C post (P = 0.038, P < 0.001, and P = 0.030, respectively)- and 3 h postexercise (P = 0.035, P = 0.007, and P < 0.001, respectively). Binding of cAMP response element-binding protein (CREB) (P = 0.005), myocyte enhancer factor 2 (MEF2) (P = 0.047), and FoxO forkhead box class-O1 (FoxO1) (P = 0.010) to the promoter region of the PGC-1α gene was lower in H than C. Nuclear PGC-1α protein increased postexercise in both H and C (P = 0.029) but was not different between trials (P = 0.602). These data indicate that acute exercise in a hot environment blunts expression of mitochondrial biogenesis-related mRNA, due to decreased binding of CREB, MEF2, and FoxO1 to the PGC-1α promoter.

The effects of constant vs. variable workload cycling on performance and perception.

BACKGROUND: The purpose of this study was to determine whether constant load (CL) cycling or variable load (VL) cycling stimulates different physiological and psychological responses. METHODS: Recreationally-trained male cyclists (N.=8, age 32±5 yr, weight 75.7±10.9 kg, body fat 13.4±5.6%, VO2peak 4.60±0.62 L/min) completed two experimental trials. During the VL trial, participants alternated between 3 minutes at 45% and 3 minutes at 85% of maximal aerobic power during the 63-minute trial. During the CL trial, participants cycled at a constant 65% of maximal aerobic power for 63 minutes. The total amount of work was held constant for the two trials. Immediately following each trial, participants completed a maximal 10-km performance trial. Blood lactate was measured at 6, 30, and 60 minutes of cycling as well as at the beginning and conclusion of the performance trial. RESULTS: Time trial performance was not different between VL (16.97±2.07 min) and CL (16.81±1.47 min, P=0.624). There was no difference in VO2 (P=0.429), heart rate (P=0.640), blood lactate (P=0.520), rated perceived exertion (RPE) (P=0.216), Feeling Scale (P=0.626), or attentional focus (P=0.315) between VL and CL 10-km performance time trials. However, RPE (P=0.003) and attentional focus (P=0.016) were elevated in VL. CONCLUSIONS: These data indicate that VL and CL cycling have no differential effect on subsequent performance or physiology despite differences in perception during the experimental trials.

Comparison of V[Combining Dot Above]O2peak and Achievement of V[Combining Dot Above]O2peak Criteria in Three Modes of Exercise in Female Triathletes.

Snoza, CT, Berg, KE, and Slivka, DR. Comparison of V[Combining Dot Above]O2peak and achievement of V[Combining Dot Above]O2peak criteria in three modes of exercise in female triathletes. J Strength Cond Res 30(10): 2816-2822, 2016-The purpose of this study was to compare peak aerobic capacity in female triathletes in 3 modes of exercise: treadmill, cycle, and arm ergometer. A second purpose was to determine the extent that physiologic criteria for achieving V[Combining Dot Above]O2peak were reached in each mode of exercise. Six criteria were examined: V[Combining Dot Above]O2 plateau, heart rate (HR), blood lactate concentration (BLC), respiratory exchange ratio, oxygen saturation, and rating of perceived exertion (RPE). Twelve recreational level female triathletes completed maximal tests on the treadmill, stationary bike, and arm ergometer. Results indicated V[Combining Dot Above]O2peak (ml·kg·min) is highest on a treadmill (46.8 ± 2.1), intermediate in cycling (40.7 ± 5.0), and lowest in arm ergometry (28.2 ± 3.3) with mean differences being significant (p ≤ 0.05). Blood lactate concentration and RPE criteria were met by the highest number of subjects across the 3 modes of testing while the HR criterion was not achieved in any participant in arm ergometry and only 2 in cycling. It was concluded that in moderately trained recreational level triathletes, V[Combining Dot Above]O2peak is highest in running and lowest in arm ergometry. Criteria for achieving V[Combining Dot Above]O2peak most frequently were blood lactate level and RPE. Coaches and researchers should appreciate that V[Combining Dot Above]O2peak values of moderately trained triathletes differ considerably in contrast to elite triathletes and tend to be highest on the treadmill and lowest in arm ergometry. Also, criteria used to determine achievement of V[Combining Dot Above]O2peak should be carefully selected and seem to be best achieved using BLC and RPE.